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Psychological and Physiological Trauma Research
Seize Your Journeys
_______________________ Traumatic stress is found in many competent, healthy, strong, good people. No one can completely protect themselves from traumatic experiences. Many people have long-lasting problems following exposure to trauma. Up to 8% of persons will have PTSD at some time in their lives. People who react to traumas are not going crazy. What is happening to them is part of a set of common symptoms and problems that are connected with being in a traumatic situation, and thus, is a normal reaction to abnormal events and experiences. Having symptoms after a traumatic event is NOT a sign of personal weakness. Given exposure to a trauma that is bad enough, probably all people would develop PTSD. By understanding trauma symptoms better, a person can become less fearful of them and better able to manage them. By recognizing the effects of trauma and knowing more about symptoms, a person will be better able to decide about getting treatment. _______________________
FUNCTIONAL NEUROANATOMY In order to best understand this atlas it is important to have a sense of the functional neuroanatomy of the brain. Over the next several pages there is a brief summary of the 5 major brain systems that relate to behavior, along with the general location seen on SPECT of these areas.
The Deep Limbic System
Functions
Problems
The Basal Ganglia System
Functions
Problems
The Prefrontal Cortex
Functions
Problems
The Cingulate Gyrus
Problems
The Temporal Lobes
Functions
Problems
Non-dominant Side (usually the right)
Secure Attachments as a Defense Against Trauma “All people mature and thrive in a social context that has profound effects on how they cope with life’s stresses. Particularly early in life, the social context plays a critical role in fuffering an individual against stressful situations, and in building the psychological and biological capacities to deal with further stresses. The primary function of parents can be thought of as helping children modulate their arousal by attuned and well-timed provision of playing, feeding, comforting, touching, looking, cleaning, and resting—in short, by teaching them skills that will gradually help them modulate their own arousal. Secure attachment bonds serve as primary defenses against trauma-induced psychopathology in both children and adults (Finkelhor & Browne, 1984). In children who have been exposed to severe stressors, the quality of the parental bond is probably the single most important determinant of long-term damage (McFarlane, 1988).” van der Kolk, Bessel, Alexander C. McFarlane, and Lars Weisaeth, eds. 1996. Traumatic stress: The effects of overwhelming experience on mind, body, and society. New York and London: Guilford Press. .p. 185 _______________________
Sleep Disorders
“The sleep disorders are organized into four major sections according to presumed etiology. Primary Sleep Disorders are those in which none of the etiologies listed below (i.e., another mental disorder, a general medical condition, or a substance) is responsible. Primary Sleep Disorders are presumed to arise from endogenous abnormalities in sleep-wake generating or timing mechanisms, often complicated by conditioning factors. Primary Sleep Disorders in turn are divided into Dyssomnias (characterized by abnormalities in the amount, quality, or timing of sleep) and Parasomnias (characterized by abnormal behavioral or physiological events occurring in association with sleep, specific sleep stages, or sleep-awake transitions). Sleep Disorder Related to Another Mental Disorder involves a prominent complaint of sleep disturbance that results from a diagnosable mental disorder (often a Mood Disorder or Anxiety Disorder) but that is sufficiently severe to warrant independent clinical attention. Presumably, the pathophysiological mechanisms responsible for the mental disorder also affect sleep-awake regulation. Sleep Disorder Due to a General Medical Condition involves a prominent complaint of sleep disturbance that results from the direct physiological effects of a general medical condition on the sleep-wake system. Substance-Induced Sleep Disorder involves prominent complaints of sleep disturbance that result from the concurrent use, or recent discontinuation of use, of a substance (including medications). That systematic assessment in individuals who present with prominent complaints of sleep disturbance includes an evaluation of the specific type of sleep complaint and a consideration of concurrent mental disorders, general medical conditions, and substance (including medication) use that may be responsible for the sleep disturbance. Five distinct sleep stages can be measured by polysomnography: rapid eye movement (REM) sleep and four stages of non-rapid eye movement (NREM) sleep (stages 1, 2, 3, and 4). Stage 1 NREM sleep is a transition from wakefulness to sleep and occupies about 5% of time spent asleep in healthy adults. Stage 2 NREM sleep, which is characterized by specific EEG waveforms (sleep spindles and K complexes), occupies about 50% of time spent asleep. Stages 3 and 4 NREM sleep (also known collectively as slow-wave sleep) are the deepest levels of sleep and occupy about 10%-20% of sleep time. REM sleep, during which the majority of typical storylike dreams occur, occupies about 20%-25% of total sleep. These sleep stages have a characteristic temporal organization across the night. NREM stages 3 and 4 tend to occur in the first one-third to one-half of the night and increase in duration in response to sleep deprivation. REM sleep occurs cyclically throughout the night, alternating with NREM sleep about every 80-100 minutes. REM sleep periods increase in duration toward the morning. Human sleep also varies characteristically across the life span. After relative stability with large amounts of slow-wave sleep in childhood and early adolescence, sleep continuity and depth deteriorate across the adult age range. This deterioration is reflected by increased wakefulness and stage 1 sleep and decreased stages 3 and 4 sleep. Because of this, age must be considered in the diagnosis of a Sleep Disorder in any individual. Polysomnography is the monitoring of multiple electrophysiological parameters during sleep and generally includes measurement of EEG activity, electroculographic activity, and electromyographic activity. Additional polysomnographic measures may include oral or nasal airflow, respiratory effort, chest and abdominal wall movement, oxyhemoglobin saturation, or exhaled carbon dioxide concentration; these measures are used to monitor respiration during sleep and to detect the presence and severity of sleep apnea. Measurement of peripheral electromyographic activity may be used to detect abnormal movements during sleep. Most polysomnographic studies are conducted during the person’s usual sleeping hours—that is, at night. However, daytime polysomnographic studies also are used to quantify daytime sleepiness. The most common daytime procedure is the Multiple Sleep Latency Test (MSLT), in which the individual is instructed to lie down in a dark room and not resist falling asleep; this protocol is repeated fives times during the day. Sleep latency (the amount of time required to fall asleep) is measured on each trial and is used as an index of physiological sleepiness. The converse of the MSLT is also used: In the Repeated Test of Sustained Wakefulness (RTSW), the individual is placed in a quiet, dimly lit room and instructed to remain awake; this protocol is repeated several times during the day. Again, sleep latency is measured, but is it used here as an index of the individual’s ability to maintain wakefulness. Standard terminology for polysomnographic measures is used throughout the test in this section. Sleep continuity refers to the overall balance of sleep and wakefulness during a night of sleep. “Better” sleep continuity indicates consolidated sleep and wakefulness; “worse” sleep continuity indicates disrupted sleep with more wakefulness. Specific sleep continuity measures include sleep latency—the amount of time required to fall asleep (expressed in minutes); intermittent wakefulness—the amount of awake time after initial sleep onset (expressed in minutes); and sleep efficiency—the ratio of actual time spent asleep to time spent in bed (expressed as a percentage, with higher numbers indicating better sleep continuity). Sleep architecture refers to the amount and distribution of specific sleep stages. Sleep architecture measures include absolute amount of REM sleep and each NREM sleep stage (in minutes), relative amount of REM seep and NREM sleep stages (expressed as a percentage of total sleep time), and latency between sleep onset and the first REM period (REM latency). The text for each of the Sleep Disorders contains a section describing its relationship to corresponding disorders in The International Classification of Sleep Disorders: (ICSD) diagnostic and Coding Manual, published in 1990 by the American Sleep Disorders Association. _________________
Substance Dependence “Features The essential feature of Substance Dependence is a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues use of the substance despite significant substance-related problems. There is a pattern of repeated self-administration that can result in tolerance, withdrawal, and compulsive drug-taking behavior. A diagnosis of Substance Dependence can be applied to every class of substances except caffeine. The symptoms of Dependence are similar across the various categories of substances, but for certain classes some symptoms are less salient, and in a few instances not all symptoms apply (e.g., withdrawal symptoms are not specified for Hallucinogenic Dependence). Although not specifically listed as a criterion item, “craving” (a strong subjective drive to use the substance) is likely to be experienced by most (if not all) individuals with Substance Dependence. Dependence is defined as a cluster of three or more of the symptoms listed below occurring at any time in the same 12-month-period. Tolerance (Criterion 1) is the need for greatly increased amounts of the substance to achieve intoxication (or the desired effect) or a markedly diminished effect with continued use of the same amount of the substance. The degree to which tolerance develops varies greatly across substances. Furthermore, for a specific drug, varied degrees of tolerance may develop for its different central nervous system effects. For example, for opioids, tolerance to respiratory depression and tolerance to analgesia develop at different rates. Individuals with heavy use of opioids and stimulants can develop substantial (e.g., 10-f0ld) levels of tolerance, often to a dosage that would be lethal to a nonuser. Alcohol tolerance can also be pronounced, but is usually less extreme than for amphetamine. Many individuals who smoke cigarettes consume more than 20 cigarettes a day, an amount that would have produced symptoms of toxicity when they first started smoking. Individuals with heavy use of cannabis or phencyclidine (PCP) are generally not aware of having developed tolerance (although it has been demonstrated in animal studies and in some individuals). Tolerance may be difficult to determine by history alone when the substance used is illegal and perhaps mixed with various diluents or with other substances. In such situations, laboratory tests may be helpful (e.g., high blood levels of the substance coupled with little evidence of intoxication suggest that tolerance is likely). Tolerance must also be distinguished from individual variability in the initial sensitivity to the effects of particular substances. For example, some first-time drinkers show very little evidence of intoxication with three or four drink, whereas others of similar weight and drinking histories had slurred speech and incoordination. Withdrawal (Criterion 2a) is a maladaptive behavioral change, with physiological and cognitive concomitants, that occurs when blood or tissue concentrations of a substance decline in an individual who had maintained prolonged heavy use of the substance. After developing unpleasant withdrawal symptoms, the persons is likely to take the substance to relieve or to avoid those symptoms (Criterion 2b), typically using the substance throughout the day beginning soon after awakening. Withdrawal symptoms, which are generally the opposite of the acute effects of the substance, vary greatly across the calluses of substances, and separate criteria sets for Withdrawal are provided for most of the classes. Marked and generally easily measured physiological signs of withdrawal are common with alcohol, opioids, and sedatives, hypnotics, and anxiolytics. Withdrawal signs and symptoms are often present, but may be less apparent, with stimulants such as amphetamines and cocaine, as well as with nicotine and cannabis. No significant withdrawal is seen even after repeated use of hallucinogens. Withdrawal from phencyclidine and related substances has not yet been described in humans (although it has been demonstrated in animals). Neither tolerance nor withdrawal is necessary or sufficient for a diagnosis of Substance Dependence. However, for most classes of substances, a past history of tolerance or withdrawals is associated with a more severe clinical course (i.e., an earlier onset of Dependence, higher levels of substance intake, and a greater number of substance-related problems). Some individuals (e.g., those with Cannabis Dependence) show a pattern of compulsive use without obvious signs of tolerance or withdrawal. Conversely, some general medical and postsurgical patients without Opioid Dependence may develop a tolerance to prescribed opioids and experience withdrawal symptoms without showing any signs of compulsive use. The specifiers With Physiological Dependence and Without Physiological Dependence are provided to indicate the presence or absence of tolerance or withdrawal. The following items describe the pattern of compulsive substance use that is characteristic of Dependence. The individual may take the substance in larger amounts or over a longer period than was originally intended (e.g., continuing to drink until severely intoxicated despite having set a limit of only one drink) (Criterion 3). The individual may express a persistent desire to cut down or regulate substance use. Often, there have been many unsuccessful efforts to decrease or discontinue use (Criterion 4). The individual may spend a great deal of time obtaining the substance, using the substance, or recovering from its effects (Criterion 5). In some instances of Substance Dependence, virtually all of the person’s daily activities revolve around the substance. Important social, occupational, ore recreational activities may be given up or reduced because of substance use (Criterion 6). The individual may withdraw from family activities and hobbies in order to use the substance in private or to spend more time with substance-using friends. Despite recognizing the contributing role of the substance to a psychological or physical problem (e.g., sever depressive symptoms or damage to organ systems), the person continues to use the substance (Criterion 7). The key issue in evaluating this criterion is not eh existence of the problem, but rather the individual’s failure to abstain from using the substance despite having evidence of the difficulty it is causing.
Specifiers Tolerance and withdrawal may be associated with a higher risk for immediate general medical problems and a higher relapse rate. Specifiers are provided to note their presence or absence: With Physiological Dependence. This specifier should be used when Substance Dependence is accompanied by evidence of tolerance (Criterion 1) or withdrawal (Criterion 2). Without Physiological Dependence. This specifier should be used when there is no evidence of tolerance (Criterion 1) or withdrawal (Criterion 2). In these individuals, Substance Dependence is characterized by a pattern of compulsive use (at least three items from Criteria 3-7).”
Diagnostic and Statistical Manual of Mental Disorders. 2000. 4th ed. Washington, D.C.: American Psychiatric Association. P. 193-195.
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PTSD, DID, and EMDR Posttraumatic Stress Disorder "The essential feature of Posttraumatic Stress Disorder us the development of characteristic symptoms following exposure to an extreme traumatic stressor involving direct personal experience of an event that involves actual or threatened death or serious injury, or other threat to one's physical integrity; or witnessing an event that involves death, injury, or a threat to the physical integrity of another person; or learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate (Criteria A1). The person's response to the event must involve intense fear, helplessness, or horror (or in children, the response must involve disorganized or agitated behavior) (Criterion A2). The characteristic symptoms resulting from the exposure to the extreme trauma include persistent reexperiencing of the traumatic event (Criterion E), and the disturbance must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion F). Traumatic events that are experienced directly include, but are not limited to, military combat, violent personal assault (sexual assault, physical attack, robbery, mugging), being kidnapped, being taken hostage, terrorist attack, torture, incarceration as a prisoner of war or in a concentration camp, natural or manmade disasters, severe automobile accidents, or being diagnosed with a life-threatening illness. For children, sexually traumatic events may include developmentally inappropriate sexual experiences without threatened or actual violence or injury. Witnessed events include, but are not limited to, observing the serious injury or unnatural death of another person due to violent assault, accident, war, or disaster or unexpectedly witnessing a dead body or body parts. Events experienced by others that are learned about include, but are not limited to, violent personal assault, serious accident, or serious injury experienced y a family member or a close friend; learning about the sudden, unexpected death of a family member or a close friend; or learning that one's child has a life threatening disease. The disorder may be especially sever or long lasting when the stressor is of human design (e.g., torture, rape). the likelihood of developing this disorder may increase as the intensity of and physical proximity to the stressor increase. The traumatic event can be reexperienced in various ways. Commonly the person has recurrent and intrusive recollections of the event (Criterion B1) or recurrent distressing dreams during which the event can be replayed or otherwise represented (Criterion B2). In rare instances, the person experiences dissociative states that last from a few seconds to several hours, or even days, during which components of the event are relived and the person behaves as though experiencing the event at that moment (Criterion B3). These episodes, often referred to as "flashbacks," are typically brief but can be associated with prolonged distress and heightened arousal. Intense psychological distress (Criterion B4) or physiological reactivity (Criterion B5) often occurs when the person is exposed to triggering events that resemble or symbolize an aspect of the traumatic event (e.g., anniversaries of the traumatic event; cold, snowy weather or uniformed guards for survivors of death camps in cold climates; hot, humid weather for combat veterans of the South Pacific; entering any elevator for an woman who was reaped in an elevator). Stimuli associated with the trauma are persistently avoided. The person commonly makes deliberate efforts to avoid thoughts, feelings, or conversations about the traumatic event (Criterion C1) and to avoid activities, situations, or people who around recollections of it (Criterion C2). This avoidance of reminders may include amnesia for an important aspect of the traumatic event (Criterion C3). Diminished responsiveness to the external work, referred to as "psychic numbing" or "emotional anesthesia," usually begins soon after the traumatic event. The individual may complain of having markedly diminished interest or participation in previously enjoyed activities (Criterion C4), of feeling detached or estranged from other people (Criterion C5), or of having markedly reduced ability to feel emotions (especially those associated with intimacy, tenderness and sexuality) (Criterion C6). The individual may have a sense of a foreshortened future (e.g., not expecting to have a career, marriage, children, or a normal life span) (Criterion C7). The individual has persistent symptoms of anxiety or increased arousal that were not present before the trauma. these symptoms may include difficulty falling or staying asleep that may be to recurrent nightmares during which the traumatic event is relived (Criterion D1), hypervigilance (Criterion D4), and exaggerated startle response (Criterion D5). Some individuals report irritability or outburst of anger (Criterion D2) or difficulty concentrating or completing tasks (Criterion D3)."
Dissociative Identity Disorder (DID) "The essential feature of Dissociative identity Disorder is the presence of two or more distinct identities or personality states (Criterion A) that recurrently take control of behavior (Criterion B). There is an inability to recall important personal information, the extent of which is too great to be explained by ordinary forgetfulness (Criterion C). The disturbance is not due tot eh direct physiological effects of a substance or a general medical condition (Condition D.). In children, the symptoms cannot be attributed to imaginary playmates or other fantasy play. Dissociative Identity Disorder reflects a failure to integrate various aspects of identity, memory, and consciousness. Each personality state may be experienced as if it has a distinct personal history, self-image, and identity, including a separate name. Usually there is a primary identity that carries the individual's given name and is passive, dependent, guilty, and depressed. The alternate identities frequently have different names and characteristics that contrast with the primary identity (e.g., are hostile, controlling, and self-destructive). Particular identities may emerge in specific circumstances and may differ in reported age and gender, vocabulary, general knowledge, or predominant affect. Alternate identities are experienced as taking control in sequence, ore at the expense of the other, and may deny knowledge of one another, be critical of one another, or appear to be in open conflict. Occasionally, one or more powerful identities allocate time to the others. Aggressive or hostile identities may at times interrupt activities or place the others in uncomfortable situations. Individuals with this disorder experience frequent gaps in memory for personal history, both remote and recent. The amnesia is frequently asymmetrical. The more passive identities tend to have more constricted memories, whereas the more hostile, controlling, or "protector" identities have more complete memories. An identity that is not in control may nonetheless gain access to consciousness by producing auditory or visual hallucinations (e.g., a voice giving instructions). Evidence of amnesia may be uncovered by reports from others who have witnessed behavior that is disavowed by the individual or by the individual's own discoveries (e.g., finding items of clothing at home that the individual cannot remember having bought). There may be loss of memory not only for recurrent periods of time, but also an overall loss of biographical memory for some extended period of childhood, adolescence, or even adulthood. Transitions among identities are often triggered by psychosocial stress. The time required to switch from one identity to another is usually a matter of seconds, but, less frequently, may b gradual. Behavior that may be frequently associated with identity switches include rapid blinking, facial changes, changes in voice or demeanor, or disruption in the individual's train of thoughts. The number of identities reported ranges from 2 to more than 100. Half of reported cases include the individuals with 10 or fewer identities." Diagnostic and Statistical Manual of Mental Disorders. 2000. 4th ed. Washington, D.C.: American Psychiatric Association. EMDR Eye Movement Desensitization and Reprocessing "Eye Movement Desensitization and Reprocessing (EMDR)1 integrates elements of many effective psychotherapies in structured protocols that are designed to maximize treatment effects. These include psychodynamic, cognitive behavioral, interpersonal, experiential, and body-centered therapies2. EMDR is an information processing therapy and uses an eight phase approach. During EMDR1 the client attends to past and present experiences in brief sequential doses while simultaneously focusing on an external stimulus. Then the client is instructed to let new material become the focus of the next set of dual attention. This sequence of dual attention and personal association is repeated many times in the session. Eight Phases of Treatment The first phase is a history taking session during which the therapist assesses the client's readiness for EMDR and develops a treatment plan. Client and therapist identify possible targets for EMDR processing. These include recent distressing events, current situations that elicit emotional disturbance, related historical incidents, and the development of specific skills and behaviors that will be needed by the client in future situations. During the second phase of treatment, the therapist ensures that the client has adequate methods of handling emotional distress and good coping skills, and that the client is in a relatively stable state. If further stabilization is required, or if additional skills are needed, therapy focuses on providing these. The client is then able to use stress reducing techniques whenever necessary, during or between sessions. However, one goal is not to need these techniques once therapy is complete. In phase three through six, a target is identified and processed using EMDR procedures. These involve the client identifying the most vivid visual image related to the memory (if available), a negative belief about self, related emotions and body sensations. The client also identifies a preferred positive belief. The validity of the positive belief is rated, as is the intensity of the negative emotions. After this, the client is instructed to focus on the image, negative thought, and body sensations while simultaneously moving his/her eyes back and forth following the therapist's fingers as they move across his/her field of vision for 20-30 seconds or more, depending upon the need of the client. Athough eye movements are the most commonly used external stimulus, therapists often use auditory tones, tapping, or other types of tactile stimulation. The kind of dual attention and the length of each set is customized to the need of the client. The client is instructed to just notice whatever happens. After this, the clinician instructs the client to let his/her mind go blank and to notice whatever thought, feeling, image, memory, or sensation comes to mind. Depending upon the client's report the clinician will facilitate the next focus of attention. In most cases a client-directed association process is encouraged. This is repeated numerous times throughout the session. If the client becomes distressed or has difficulty with the process, the therapist follows established procedures to help the client resume processing. When the client reports no distress related to the targeted memory, the clinician asks him/her to think of the preferred positive belief that was identified at the beginning of the session, or a better one if it has emerged, and to focus on the incident, while simultaneously engaging in the eye movements. After several sets, clients generally report increased confidence in this positive belief. The therapist checks with the client regarding body sensations. If there are negative sensations, these are processed as above. If there are positive sensations, they are further enhanced. In phase seven, closure, the therapist asks the client to keep a journal during the week to document any related material that may arise and reminds the client of the self-calming activities that were mastered in phase two. The next session begins with phase eight, re-evaluation of the previous work, and of progress since the previous session. EMDR treatment ensures processing of all related historical events, current incidents that elicit distress, and future scenarios that will require different responses. The overall goal is produce the most comprehensive and profound treatment effects in the shortest period of time, while simultaneously maintaining a stable client within a balanced system. After EMDR processing, clients generally report that the emotional distress related to the memory has been eliminated, or greatly decreased, and that they have gained important cognitive insights. Importantly, these emotional and cognitive changes usually result in spontaneous behavioral and personal change, which are further enhanced with standard EMDR procedures." www.emdr.com __________________ Major Depressive Disorder “Diagnostic Features The essential feature of Major Depressive Disorder is a clinical course that is characterized by one or more Major Depressive Episodes without a history of Manic, Mixed, or Hypomanic Episodes (Criteria A and C). Episodes of Substance-Induced Mood Disorder (due to the direct physiological effects of a drug of abuse, a medication, or toxin exposure) or of Mood Disorder Due to a General Medical Condition do not count toward a diagnosis of Major Depressive Disorder. In addition, the episodes must not be better accounted for by Schizoaffective Disorder and are not superimposed on Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified (Criterion B). The fourth digit in the diagnostic code for Major Depressive Disorder indicates whether it is a Single Episode (used only for first episodes) or Recurrent. It is sometimes difficult to distinguish between a single episode with waxing and waning symptoms and two separate episodes. For purposes of this manual, an episode is considered to have ended when the full criteria for eh Major Depressive Episode have not been met for at least 2 consecutive months. During this 2-month period, there is either complete resolution of symptoms or the presence of depressive symptoms that no longer meet the full criteria for a Major Depressive Episode (In Partial Remission). The fifth digit in the diagnostic code for Major Depressive Disorder indicates the current state of the disturbance. If the criteria for a Major Depressive Disorder are met, the severity of the episode is notes as Mild, Moderate, Severe Without Psychotic Features, or Severe With Psychotic Features. If the criteria for a Major Depressive Episode are not currently met, the fifth digit is used to indicate whether the disorder is In Partial Remission or In Full Remission. If Manic, Mixed, or Hypomanic Episodes develop in the course of Major Depressive Disorder, the diagnosis is changed to a Bipolar Disorder. However, if manic or hypomanic symptoms occur as a direct effect of antidepressant treatment, use of other medications, substance use, or toxin exposure, the diagnosis of Major Depressive Disorder remains appropriate and an addition diagnosis of Substance-induced Mood Disorder, With Manic features (or With Mixed Features), should be noted. Similarly, if manic or hypomanic symptoms occur as a direct effect of a general medical condition, the diagnosis of Major Depressive Disorder remains appropriate and an additional diagnosis of Mood Disorder Due to a General Medical Condition, With Manic Features (or With Mixed Features), should be noted.” p. 369 “Course Major Depressive Disorder may begin at any age, with an average age at onset in the mid-20s. Epidemiological data suggest that the age at onset is decreasing for those born more recently. The course of Major Depressive Disorder, Recurrent, is variable. Some people have isolated episodes that are separated by many years without any depressive symptoms, whereas others have clusters of episodes, and still others have increasingly frequent episodes as they grow older. Some evidence suggests that the periods of remission generally last longer early in the course of the disorder. The number of prior episodes predicts the likelihood of developing a subsequent Major Depressive Episode. At least 60% of individuals with Major Depresssive Disorder, Single Episode, can be expected to have a second episode. Individuals who have had tow episodes have a 70% chance of having a third, and individuals who have had three episodes have a 90% chance of having a fourth. About 5%-10% of individuals with Major Depressive Disorder, single Episode, subsequently develop a Manic Episode (i.e., develop Bipolar I Disorder). Major Depressive Episodes may end completely (in about two-thirds of cases), or only partially or not at all (in about one-third of cases). For individuals who have only partial remission, there is a greater likelihood of developing additional episodes and of continuing the pattern of partial interepisode recovery. The longitudinal course specifiers With Full Interepisode Recovery and Without Full Interepisode Recovery may therefore have prognostic value. A number of individuals have pre-existing Dysthymic Disorder prior to the onset of Major Depressive Disorder, single Episode. Some evidence suggests that these individuals are more likely to have additional Major Depressive Episodes, have poorer interepisode recovery, and may require additional acute-phase treatment and a longer period of continuing treatment to attain and maintain a more thorough and longer-lasting euthymic state. Follow-up naturalistic studies suggested that 1 year after the diagnosis of a major Depressive Episode, 40% of individuals still have symptoms that are sufficiently severe to meet criteria for a full Major Depressive Episode, roughly 20% continue to have some symptoms that no longer meet full criteria for a Major Depressive Episode (i.e., major Depressive Disorder, In Partial Remission), and 40% have no Mood Disorder. The severity of the initial Major Depressive Episode appears to predict persistence. Chronic general medical conditions are also a risk factor for more persistent episodes. Episodes of Major Depressive Disorder often follow a severe psychosocial stressor, such as the death of a loved one or divorce. Studies suggest that psychosocial events 9stressors) may play a more significant role in the precipitation of the first or second episodes of Major Depressive Disorder and may play less of a role in the onset of subsequent episodes. Chronic general medical conditions and Substance Dependence (particularly Alcohol or Cocaine Dependence) may contribute to the onset or exacerbation of Major Depressive Disorder. It is difficult to predict whether the first episode of a Major Depressive Disorder in a young person will ultimately evolve into a Bipolar Disorder. Some data suggest that the acute onset of severe depression, especially with psychotic features and psychomotor retardation, in a young person without prepubertal psychopathology is more likely to predict a bipolar disorder. A family history of Bipolar Disorder may also be suggestive of subsequent development of Bipolar Disorder.” p. 372-373
Diagnostic and statistical manual of mental disorders. 2000. 4th ed. Washington, D.C.: American Psychiatric Association.
________________ Major Depressive Disorder “Diagnostic Features The essential feature of Major Depressive Disorder is a clinical course that is characterized by one or more Major Depressive Episodes without a history of Manic, Mixed, or Hypomanic Episodes (Criteria A and C). Episodes of Substance-Induced Mood Disorder (due to the direct physiological effects of a drug of abuse, a medication, or toxin exposure) or of Mood Disorder Due to a General Medical Condition do not count toward a diagnosis of Major Depressive Disorder. In addition, the episodes must not be better accounted for by Schizoaffective Disorder and are not superimposed on Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified (Criterion B). The fourth digit in the diagnostic code for Major Depressive Disorder indicates whether it is a Single Episode (used only for first episodes) or Recurrent. It is sometimes difficult to distinguish between a single episode with waxing and waning symptoms and two separate episodes. For purposes of this manual, an episode is considered to have ended when the full criteria for eh Major Depressive Episode have not been met for at least 2 consecutive months. During this 2-month period, there is either complete resolution of symptoms or the presence of depressive symptoms that no longer meet the full criteria for a Major Depressive Episode (In Partial Remission). The fifth digit in the diagnostic code for Major Depressive Disorder indicates the current state of the disturbance. If the criteria for a Major Depressive Disorder are met, the severity of the episode is notes as Mild, Moderate, Severe Without Psychotic Features, or Severe With Psychotic Features. If the criteria for a Major Depressive Episode are not currently met, the fifth digit is used to indicate whether the disorder is In Partial Remission or In Full Remission. If Manic, Mixed, or Hypomanic Episodes develop in the course of Major Depressive Disorder, the diagnosis is changed to a Bipolar Disorder. However, if manic or hypomanic symptoms occur as a direct effect of antidepressant treatment, use of other medications, substance use, or toxin exposure, the diagnosis of Major Depressive Disorder remains appropriate and an addition diagnosis of Substance-induced Mood Disorder, With Manic features (or With Mixed Features), should be noted. Similarly, if manic or hypomanic symptoms occur as a direct effect of a general medical condition, the diagnosis of Major Depressive Disorder remains appropriate and an additional diagnosis of Mood Disorder Due to a General Medical Condition, With Manic Features (or With Mixed Features), should be noted.” p. 369 “Course Major Depressive Disorder may begin at any age, with an average age at onset in the mid-20s. Epidemiological data suggest that the age at onset is decreasing for those born more recently. The course of Major Depressive Disorder, Recurrent, is variable. Some people have isolated episodes that are separated by many years without any depressive symptoms, whereas others have clusters of episodes, and still others have increasingly frequent episodes as they grow older. Some evidence suggests that the periods of remission generally last longer early in the course of the disorder. The number of prior episodes predicts the likelihood of developing a subsequent Major Depressive Episode. At least 60% of individuals with Major Depresssive Disorder, Single Episode, can be expected to have a second episode. Individuals who have had tow episodes have a 70% chance of having a third, and individuals who have had three episodes have a 90% chance of having a fourth. About 5%-10% of individuals with Major Depressive Disorder, single Episode, subsequently develop a Manic Episode (i.e., develop Bipolar I Disorder). Major Depressive Episodes may end completely (in about two-thirds of cases), or only partially or not at all (in about one-third of cases). For individuals who have only partial remission, there is a greater likelihood of developing additional episodes and of continuing the pattern of partial interepisode recovery. The longitudinal course specifiers With Full Interepisode Recovery and Without Full Interepisode Recovery may therefore have prognostic value. A number of individuals have pre-existing Dysthymic Disorder prior to the onset of Major Depressive Disorder, single Episode. Some evidence suggests that these individuals are more likely to have additional Major Depressive Episodes, have poorer interepisode recovery, and may require additional acute-phase treatment and a longer period of continuing treatment to attain and maintain a more thorough and longer-lasting euthymic state. Follow-up naturalistic studies suggested that 1 year after the diagnosis of a major Depressive Episode, 40% of individuals still have symptoms that are sufficiently severe to meet criteria for a full Major Depressive Episode, roughly 20% continue to have some symptoms that no longer meet full criteria for a Major Depressive Episode (i.e., major Depressive Disorder, In Partial Remission), and 40% have no Mood Disorder. The severity of the initial Major Depressive Episode appears to predict persistence. Chronic general medical conditions are also a risk factor for more persistent episodes. Episodes of Major Depressive Disorder often follow a severe psychosocial stressor, such as the death of a loved one or divorce. Studies suggest that psychosocial events 9stressors) may play a more significant role in the precipitation of the first or second episodes of Major Depressive Disorder and may play less of a role in the onset of subsequent episodes. Chronic general medical conditions and Substance Dependence (particularly Alcohol or Cocaine Dependence) may contribute to the onset or exacerbation of Major Depressive Disorder. It is difficult to predict whether the first episode of a Major Depressive Disorder in a young person will ultimately evolve into a Bipolar Disorder. Some data suggest that the acute onset of severe depression, especially with psychotic features and psychomotor retardation, in a young person without prepubertal psychopathology is more likely to predict a bipolar disorder. A family history of Bipolar Disorder may also be suggestive of subsequent development of Bipolar Disorder.” p. 372-373 Diagnostic and statistical manual of mental disorders. 2000. 4th ed. Washington, D.C.: American Psychiatric Association. ________________ DID-PTSD-EMDR Dissociative Identity Disorder (DID) "The essential feature of Dissociative identity Disorder is the presence of two or more distinct identities or personality states (Criterion A) that recurrently take control of behavior (Criterion B). There is an inability to recall important personal information, the extent of which is too great to be explained by ordinary forgetfulness (Criterion C). The disturbance is not due tot eh direct physiological effects of a substance or a general medical condition (Condition D.). In children, the symptoms cannot be attributed to imaginary playmates or other fantasy play. Dissociative Identity Disorder reflects a failure to integrate various aspects of identity, memory, and consciousness. Each personality state may be experienced as if it has a distinct personal history, self-image, and identity, including a separate name. Usually there is a primary identity that carries the individual's given name and is passive, dependent, guilty, and depressed. The alternate identities frequently have different names and characteristics that contrast with the primary identity (e.g., are hostile, controlling, and self-destructive). Particular identities may emerge in specific circumstances and may differ in reported age and gender, vocabulary, general knowledge, or predominant affect. Alternate identities are experienced as taking control in sequence, ore at the expense of the other, and may deny knowledge of one another, be critical of one another, or appear to be in open conflict. Occasionally, one or more powerful identities allocate time to the others. Aggressive or hostile identities may at times interrupt activities or place the others in uncomfortable situations. Individuals with this disorder experience frequent gaps in memory for personal history, both remote and recent. The amnesia is frequently asymmetrical. The more passive identities tend to have more constricted memories, whereas the more hostile, controlling, or "protector" identities have more complete memories. An identity that is not in control may nonetheless gain access to consciousness by producing auditory or visual hallucinations (e.g., a voice giving instructions). Evidence of amnesia may be uncovered by reports from others who have witnessed behavior that is disavowed by the individual or by the individual's own discoveries (e.g., finding items of clothing at home that the individual cannot remember having bought). There may be loss of memory not only for recurrent periods of time, but also an overall loss of biographical memory for some extended period of childhood, adolescence, or even adulthood. Transitions among identities are often triggered by psychosocial stress. The time required to switch from one identity to another is usually a matter of seconds, but, less frequently, may b gradual. Behavior that may be frequently associated with identity switches include rapid blinking, facial changes, changes in voice or demeanor, or disruption in the individual's train of thoughts. The number of identities reported ranges from 2 to more than 100. Half of reported cases include the individuals with 10 or fewer identities." Diagnostic and Statistical Manual of Mental Disorders. 2000. 4th ed. Washington, D.C.: American Psychiatric Association. PTSD, DID, and EMDR Posttraumatic Stress Disorder "The essential feature of Posttraumatic Stress Disorder us the development of characteristic symptoms following exposure to an extreme traumatic stressor involving direct personal experience of an event that involves actual or threatened death or serious injury, or other threat to one's physical integrity; or witnessing an event that involves death, injury, or a threat to the physical integrity of another person; or learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate (Criteria A1). The person's response to the event must involve intense fear, helplessness, or horror (or in children, the response must involve disorganized or agitated behavior) (Criterion A2). The characteristic symptoms resulting from the exposure to the extreme trauma include persistent reexperiencing of the traumatic event (Criterion E), and the disturbance must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion F). Traumatic events that are experienced directly include, but are not limited to, military combat, violent personal assault (sexual assault, physical attack, robbery, mugging), being kidnapped, being taken hostage, terrorist attack, torture, incarceration as a prisoner of war or in a concentration camp, natural or manmade disasters, severe automobile accidents, or being diagnosed with a life-threatening illness. For children, sexually traumatic events may include developmentally inappropriate sexual experiences without threatened or actual violence or injury. Witnessed events include, but are not limited to, observing the serious injury or unnatural death of another person due to violent assault, accident, war, or disaster or unexpectedly witnessing a dead body or body parts. Events experienced by others that are learned about include, but are not limited to, violent personal assault, serious accident, or serious injury experienced y a family member or a close friend; learning about the sudden, unexpected death of a family member or a close friend; or learning that one's child has a life threatening disease. The disorder may be especially sever or long lasting when the stressor is of human design (e.g., torture, rape). the likelihood of developing this disorder may increase as the intensity of and physical proximity to the stressor increase. The traumatic event can be reexperienced in various ways. Commonly the person has recurrent and intrusive recollections of the event (Criterion B1) or recurrent distressing dreams during which the event can be replayed or otherwise represented (Criterion B2). In rare instances, the person experiences dissociative states that last from a few seconds to several hours, or even days, during which components of the event are relived and the person behaves as though experiencing the event at that moment (Criterion B3). These episodes, often referred to as "flashbacks," are typically brief but can be associated with prolonged distress and heightened arousal. Intense psychological distress (Criterion B4) or physiological reactivity (Criterion B5) often occurs when the person is exposed to triggering events that resemble or symbolize an aspect of the traumatic event (e.g., anniversaries of the traumatic event; cold, snowy weather or uniformed guards for survivors of death camps in cold climates; hot, humid weather for combat veterans of the South Pacific; entering any elevator for an woman who was reaped in an elevator). Stimuli associated with the trauma are persistently avoided. The person commonly makes deliberate efforts to avoid thoughts, feelings, or conversations about the traumatic event (Criterion C1) and to avoid activities, situations, or people who around recollections of it (Criterion C2). This avoidance of reminders may include amnesia for an important aspect of the traumatic event (Criterion C3). Diminished responsiveness to the external work, referred to as "psychic numbing" or "emotional anesthesia," usually begins soon after the traumatic event. The individual may complain of having markedly diminished interest or participation in previously enjoyed activities (Criterion C4), of feeling detached or estranged from other people (Criterion C5), or of having markedly reduced ability to feel emotions (especially those associated with intimacy, tenderness and sexuality) (Criterion C6). The individual may have a sense of a foreshortened future (e.g., not expecting to have a career, marriage, children, or a normal life span) (Criterion C7). The individual has persistent symptoms of anxiety or increased arousal that were not present before the trauma. these symptoms may include difficulty falling or staying asleep that may be to recurrent nightmares during which the traumatic event is relived (Criterion D1), hypervigilance (Criterion D4), and exaggerated startle response (Criterion D5). Some individuals report irritability or outburst of anger (Criterion D2) or difficulty concentrating or completing tasks (Criterion D3)."
EMDR Eye Movement Desensitization and Reprocessing "Eye Movement Desensitization and Reprocessing (EMDR)1 integrates elements of many effective psychotherapies in structured protocols that are designed to maximize treatment effects. These include psychodynamic, cognitive behavioral, interpersonal, experiential, and body-centered therapies2. EMDR is an information processing therapy and uses an eight phase approach. During EMDR1 the client attends to past and present experiences in brief sequential doses while simultaneously focusing on an external stimulus. Then the client is instructed to let new material become the focus of the next set of dual attention. This sequence of dual attention and personal association is repeated many times in the session. Eight Phases of Treatment The first phase is a history taking session during which the therapist assesses the client's readiness for EMDR and develops a treatment plan. Client and therapist identify possible targets for EMDR processing. These include recent distressing events, current situations that elicit emotional disturbance, related historical incidents, and the development of specific skills and behaviors that will be needed by the client in future situations. During the second phase of treatment, the therapist ensures that the client has adequate methods of handling emotional distress and good coping skills, and that the client is in a relatively stable state. If further stabilization is required, or if additional skills are needed, therapy focuses on providing these. The client is then able to use stress reducing techniques whenever necessary, during or between sessions. However, one goal is not to need these techniques once therapy is complete. In phase three through six, a target is identified and processed using EMDR procedures. These involve the client identifying the most vivid visual image related to the memory (if available), a negative belief about self, related emotions and body sensations. The client also identifies a preferred positive belief. The validity of the positive belief is rated, as is the intensity of the negative emotions. After this, the client is instructed to focus on the image, negative thought, and body sensations while simultaneously moving his/her eyes back and forth following the therapist's fingers as they move across his/her field of vision for 20-30 seconds or more, depending upon the need of the client. Athough eye movements are the most commonly used external stimulus, therapists often use auditory tones, tapping, or other types of tactile stimulation. The kind of dual attention and the length of each set is customized to the need of the client. The client is instructed to just notice whatever happens. After this, the clinician instructs the client to let his/her mind go blank and to notice whatever thought, feeling, image, memory, or sensation comes to mind. Depending upon the client's report the clinician will facilitate the next focus of attention. In most cases a client-directed association process is encouraged. This is repeated numerous times throughout the session. If the client becomes distressed or has difficulty with the process, the therapist follows established procedures to help the client resume processing. When the client reports no distress related to the targeted memory, the clinician asks him/her to think of the preferred positive belief that was identified at the beginning of the session, or a better one if it has emerged, and to focus on the incident, while simultaneously engaging in the eye movements. After several sets, clients generally report increased confidence in this positive belief. The therapist checks with the client regarding body sensations. If there are negative sensations, these are processed as above. If there are positive sensations, they are further enhanced. In phase seven, closure, the therapist asks the client to keep a journal during the week to document any related material that may arise and reminds the client of the self-calming activities that were mastered in phase two. The next session begins with phase eight, re-evaluation of the previous work, and of progress since the previous session. EMDR treatment ensures processing of all related historical events, current incidents that elicit distress, and future scenarios that will require different responses. The overall goal is produce the most comprehensive and profound treatment effects in the shortest period of time, while simultaneously maintaining a stable client within a balanced system. After EMDR processing, clients generally report that the emotional distress related to the memory has been eliminated, or greatly decreased, and that they have gained important cognitive insights. Importantly, these emotional and cognitive changes usually result in spontaneous behavioral and personal change, which are further enhanced with standard EMDR procedures." www.emdr.com
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NeuroBiology of Trauma
Hippocampus, Trauma and PTSD
Title: Hippocampal Volume and Memory Performance in a Community-Based Sample of Women With Posttraumatic Stress Disorder Secondary to Child Abuse. Author(s): Pederson, Cathy L., cpederson@wittenberg.edu, Biology Department, Wittenberg University, Springfield, OH, US; Maurer, Scott H., Biology Department, Wittenberg University, Springfield, OH, US; Kaminski, Patricia L., Psychology Department, University of North Texas, Denton, TX, US; Zander, Kelly A., Biology Department, Wittenberg University, Springfield, OH, US; Peters, Christina M., Biology Department, Wittenberg University, Springfield, OH, US; Stokes-Crowe, Linda A., Psychology Department, Wittenberg University, Springfield, OH, US; Osborn, Robin E., Radiology Department, Mercy Medical Center, Springfield, OH, US Address: Pederson, Cathy L., Biology Department, Wittenberg University, P.O. Box 720, Springfield, OH, US, 45501-0720, cpederson@wittenberg.edu Source: Journal of Traumatic Stress, Vol 17(1), Feb 2004. pp. 37-40. Journal URL: http://www.wkap.nl/journalhome.htm/0894-9867 Publisher: Netherlands: Kluwer Academic Publishers. Abstract: Childhood abuse is linked to posttraumatic stress disorder (PTSD), which follows abuse survivors into adulthood. This study identified the neuropsychological and neuromorphological sequelae of PTSD among prepubescently abused women. Right-handed women aged 20-40 years were placed into PTSD and abuse, abuse only, and normal control groups (n = 17 per group). Participants were screened for trauma history and psychiatric symptoms, demographically matched, and given neuropsychological tests and a magnetic resonance scan of their brain. Women with PTSD did not express significant deficits in memory performance or hippocampal volume when compared with the abuse and normal control groups. _____
Title: Attention, Learning, and Memory in Posttraumatic Stress Disorder. Author(s): Neylan, Thomas C., neylan@itsa.ucsf.edu, Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Lenoci, Maryanne, Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Rothlind, Johannes, Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Metzler, Thomas J., Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Schuff, Norbert, Magnetic Resonance Unit, San Francisco DVA Medical Center, San Francisco, CA, US; Du, An-Tao, Magnetic Resonance Unit, San Francisco DVA Medical Center, San Francisco, CA, US; Franklin, Kristin W., Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Weiss, Daniel S., Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Weiner, Michael W., Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US; Marmar, Charles R., Mental Health Service, San Francisco DVA Medical Center, San Francisco, CA, US Address: Neylan, Thomas C., PTSD Program, Psychiatry Service, VA Medical Center, 116P, 4150 Clement Street, San Francisco, CA, US, 94121, neylan@itsa.ucsf.edu Source: Journal of Traumatic Stress, Vol 17(1), Feb 2004. pp. 41-46. Abstract: This study compared attention and declarative memory in a sample of combat veterans with posttraumatic stress disorder (PTSD, n = 24) previously reported to have reduced concentrations of the hippocampal neuronal marker TV-acetyl aspartate (NAA), but similar hippocampal volume compared to veteran normal comparison participants (n = 23). Healthy, well-educated males with combat-related PTSD without current depression or recent alcohol/drug abuse did not perform differently on tests of attention, learning, and memory compared to normal comparison participants. Further, hippocampal volume, NAA, or NAA/Creatine ratios did not significantly correlate with any of the cognitive measures when adjustments for multiple comparisons were made. In this study, reduced hippocampal NAA did not appear to be associated with impaired declarative memory. _____
Title: Structural and functional brain changes in posttraumatic stress disorder. Author(s): Nutt, David J., david.j.nutt@bristol.ac.uk, Psychopharmacology Unit, University of Bristol, Bristol, United Kingdom; Malizia, Andrea L., Psychopharmacology Unit, University of Bristol, Bristol, United Kingdom Address: Nutt, David J., Psychopharmacology Unit, School of Medical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol, United Kingdom, BS1 3NY, david.j.nutt@bristol.ac.uk Source: Journal of Clinical Psychiatry, Vol 65(Suppl1), 2004. Special Issue: Update on posttraumatic stress disorder. pp. 11-17. Publisher: US: Physicians Postgraduate Press. Abstract: Posttraumatic stress disorder (PTSD) is a highly disabling condition that is associated with intrusive recollections of a traumatic event, hyperarousal, avoidance of clues associated with the trauma, and psychological numbing. The field of neuroimaging has made tremendous advances in the past decade and has contributed greatly to our understanding of the physiology of fear and the pathophysiology of PTSD. Neuroimaging studies have demonstrated significant neurobiologic changes in PTSD. There appear to be 3 areas of the brain that are different in patients with PTSD compared with those in control subjects: the hippocampus, the amygdala, and the medial frontal cortex. The amygdala appears to be hyperreactive to trauma-related stimuli. The hallmark symptoms of PTSD, including exaggerated startle response and flashbacks, may be related to a failure of higher brain regions (i.e., the hippocampus and the medial frontal cortex) to dampen the exaggerated symptoms of arousal and distress that are mediated through the amygdala in response to reminders of the traumatic event. The findings of structural and functional neuroimaging studies of PTSD are reviewed as they relate to our current understanding of the pathophysiology of this disorder. Conference: The International Consensus Group on Depression and Anxiety, 8th, Jul, 2002, Limerick, Ireland _____
Title: Tiagabine for posttraumatic stress disorder: A case series of 7 women. Author(s): Taylor, Fletcher B., tfletcher2@uswest.net, Rainier Associates, Tacoma, WA, US Address: Taylor, Fletcher B., Rainier Associates, 5909 Orchard West, Tacoma, WA, US, 98467, tfletcher2@uswest.net Source: Journal of Clinical Psychiatry, Vol 64(12), Dec 2003. pp. 1421-1425. Publisher: US: Physicians Postgraduate Press. Abstract: Posttraumatic stress disorder (PTSD) is often a chronic disorder, and, though 2 antidepressants are now approved by the U.S. Food and Drug Administration for its treatment, it often remains refractory to pharmacotherapy. The memory of traumatic events, by repeatedly stimulating the hippocampus and amygdala, may alter multiple biological systems, including gamma--aminobutyric acid (GABA) pathways, and eventually lead to the disorder. Tiagabine, a selective GABA reuptake inhibitor, was evaluated as a treatment for PTSD. Patients with DSM-IV PTSD who were stable on current medications and still symptomatic were eligible for inclusion in this open-label case series. The Clinical Global Impressions-Improvement scale and PTSD Checklist-Civilian Version (PCL-C) were used to evaluate changes in PTSD symptoms. Seven consecutive female patients were identified as eligible. Tiagabine markedly improved PTSD symptoms within 2 weeks for 6 of the 7 patients, and 6 patients were rated as "much improved" or "very much improved." These preliminary open-label findings suggest that the selective GABA reuptake inhibitor tiagabine may be a promising therapeutic option in the treatment of PTSD. _____
Title: Cortisol Levels Are Positively Correlated with Hippocampal N-Acetylaspartate. Author(s): Neylan, Thomas C., Mental Health Service, San Francisco Department of Veterans Affairs Medical Center, San Francisco, CA, US; Schuff, Norbert, Dept of Radiology, University of California, San Francisco, San Francisco, CA, US; Lenoci, Maryanne, Mental Health Service, San Francisco Department of Veterans Affairs Medical Center, San Francisco, CA, US; Yehuda, Rachel, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, US; Weiner, Michael W., Department of Psychiatry, University of California, San Francisco, San Francisco, CA, US; Marmar, Charles R., Mental Health Service, San Francisco Department of Veterans Affairs Medical Center, San Francisco, CA, US Address: Neylan, Thomas C., DVA Medical Center, PTSD Program 116P, 4150 Clement Street, San Francisco, CA, US, 94121 Source: Biological Psychiatry, Vol 54(10), Nov 2003. pp. 1118-1121. Publisher: United Kingdom: Elsevier Science. Abstract: This study examined the relationship of hypothalamic-pituitary-adrenal measures and hippocampal N-acetylaspartate (NAA) in posttraumatic stress disorder (PTSD) patients and control subjects. Eleven patients with combat-related PTSD and 11 control subjects were evaluated with magnetic resonance spectroscopy as well as by morning salivary cortisol samples before and after administration of low-dose dexamethasone (.5 mg). Left hippocampal NAA was strongly associated with both pre-dexamethasone cortisol levels (n = 22, r = .53, p = .013) and post-dexamethasone cortisol levels (n = 22, r = .63, p = .002). After accounting for clinical symptom severity and hippocampal volume, cortisol levels accounted for 21.9% of the variance (F = 5.6, p = .004) in left hippocampal NAA and 12.6% of the variance (F = 3.2, p = .035) in right hippocampal NAA. This study shows a positive relationship between cortisol levels and hippocampal NAA in subjects without hypercortisolemia. Within the range of values seen in our subjects, cortisol may have a trophic effect on the hippocampus. _____
Title: Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder. Author(s): Vermetten, Eric, Department of Psychiatry and Behavioral Sciences, Positron Emission Tomography Center/Nuclear Medicine, Emory University School of Medicine, Atlanta, GA, US; Vythilingam, Meena, Program for Mood and Anxiety Disorders, National Institute of Mental Health,, Bethesda, MD, US; Southwick, Steven M., Department of Psychiatry, Yale University School of Medicine, New Haven, CT, US; Charney, Dennis S., Program for Mood and Anxiety Disorders, National Institute of Mental Health,, Bethesda, MD, US; Bremner, J. Douglas, Department of Psychiatry and Behavioral Sciences, Positron Emission Tomography Center/Nuclear Medicine, Emory University School of Medicine, Atlanta, GA, US Address: Vermetten, Eric, Rudolf Magnus Institute of Neurosciences, Department of Psychiatry, University Medical Center, Internal mailbox B01206, Heidelberglaan 100, 3584 CX, Utrecht, Netherlands Source: Biological Psychiatry, Vol 54(7), Oct 2003. pp. 693-702. Publisher: United Kingdom: Elsevier Science. Abstract: Studies in patients with posttraumatic stress disorder (PTSD) found deficits in hippocampal-based declarative verbal memory and smaller hippocampal volume, as measured with magnetic resonance imaging (MRI). Recent preclinical evidence has shown that selective serotonin reuptake inhibitors promote neurogenesis and reverse the effects of stress on hippocampal atrophy. This study assessed the effects of long-term treatment with paroxetine on hippocampal volume and declarative memory performance in PTSD. Declarative memory was assessed with the Wechsler Memory Scale-Revised and Selective Reminding Test before and after 9-12 mos of treatment with paroxetine in PTSD. Hippocampal volume was measured with MRI. Of the 28 patients who started the protocol, 23 completed the full course of treatment and neuropsychological testing. Twenty patients were able to complete MRI imaging. Patients with PTSD showed a significant improvement In PTSD symptoms with treatment. Treatment resulted in significant improvements in verbal declarative memory and a 4.6% increase in mean hippocampal volume. These findings suggest that long-term treatment with paroxetine is associated with improvement of verbal declarative memory deficits and an increase in hippocampal volume in PTSD. _____
Title: Mood disorders and medical illness: Mood disorders and allostatic load. Author(s): McEwen, Bruce S., Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY, US Address: McEwen, Bruce S., The Rockefeller University, Box 165, 1230 York Avenue, New York, NY, US, 10021 Source: Biological Psychiatry , Vol 54(3), Aug 2003. pp. 200-207. Publisher: United Kingdom: Elsevier Science. Abstract: The brain controls both the physiologic and the behavioral coping responses to daily events and major stressors, and the nervous system is a target of the mediators of those responses through circulating hormones. The amygdala and hippocampus interpret what is stressful and regulate appropriate responses. The amygdala becomes hyperactive in posttraumatic stress disorder (PTSD) and depressive illness, and hypertrophy of amygdala nerve cells is reported after repeated stress in an animal model. The hippocampus expresses adrenal steroid receptors. It undergoes atrophy in several psychiatric disorders and responds to repeated stressors with decreased dendritic branching and reduction in number of neurons in the dentate gyrus. Stress promotes adaptation, but a perturbed diurnal rhythm or failed shutoff of mediators after stress leads over time, to allostatic load. Neural changes mirror the pattern in the cardiovascular, metabolic, and immune systems--short-term adaptation versus long-term damage. Allostatic load leads to impaired immunity, atherosclerosis, obesity, bone demineralisation, and atrophy of nerve cells in brain. Allostatic load is seen in major depressive illness and may also be expressed in other chronic anxiety disorders such as PTSD and should be documented. Conference: The Diagnosis and Treatment of Mood Disorders in the Medically Ill, Nov, 2002, Washington, DC, US Conference Note: Some of the material in this article was presented at the aforementioned conference sponsored by the Depression and Bipolar Support Alliance. _____
Title: Single-voxel proton MR spectroscopy of right versus left hippocampi in PTSD. Author(s): Menon, P. Mohanakrishnan, parekkat.mohanakrishnan@med.va.gov, U Cincinnati Medical Ctr, Cincinnati, OH, US; Nasrallah, Henry A., U Mississippi Medical Ctr, Dept of Psychiatry & Human Behavior, Jackson, MS, US; Lyons, Judith A., U Mississippi Medical Ctr, Dept of Psychiatry & Human Behavior, Jackson, MS, US; Scott, Mertis F., G.V. (Sonny) Montgomery VA Medical Ctr, Mental Health Service, Jackson, MS, US; Liberto, Vincent, U Mississippi Medical Ctr, Dept of Psychiatry & Human Behavior, Jackson, MS, US Address: Menon, P. Mohanakrishnan, U Cincinnati Medical Ctr, 231 Albert Sabin Way, Cincinnati, OH, US, 45267, parekkat.mohanakrishnan@med.va.gov Source: Psychiatry Research: Neuroimaging, Vol 123(2), Jun 2003. pp. 101-108. Publisher: United Kingdom: Elsevier Science. Abstract: Previous magnetic resonance (MR) volume imaging and proton MR spectroscopy studies have suggested a reduction in the hippocampal size and/or neuronal/axonal density in posttraumatic stress disorder (PTSD). The lack of agreement on the laterality of the hippocampal dysfunction prompted this study. A total of 20 veterans (18 men and two women) and one female non-veteran participated in this study conducted in accordance with approved human study protocols. Six of the male veterans and the female non-veteran were without PTSD. Vietnam veterans formed a large subset of the study subjects. Single-voxel proton MR spectra were obtained from the hippocampal region bilaterally on a clinical MR scanner operating at 1.5 T. Analysis of the proton MR spectra showed a decrease in hippocampal NAA/creatine ratio in PTSD subjects significantly higher on the left than the right for the entire study group, as well as for the Vietnam subset. It was concluded that the hippocampal dysfunction in PTSD is lateralized with the left side being more impaired than the right. _____
Title: MRI and PET study of deficits in hippocampal structure and function in women with childhood sexual abuse and posttraumatic stress disorder. Author(s): Bremner, J. Douglas, jdbremn@emory.edu; Vythilingam, Meena; Vermetten, Eric; Southwick, Steven M.; McGlashan, Thomas; Nazeer, Ahsan; Khan, Sarfraz; Vaccarino, L. Viola; Soufer, Robert; Garg, Pradeep K.; Ng, Chin K.; Staib, Lawrence H.; Duncan, James S.; Charney, Dennis S. Address: Bremner, J. Douglas, Emory Clinical Neuroscience Research Unit, 1256 Briarcliff Rd, Atlanta, GA, US, 30306, jdbremn@emory.edu Source: American Journal of Psychiatry, Vol 160(5), May 2003. pp. 924-932. Publisher: US: American Psychiatric Assn. Abstract: OBJECTIVE: Animal studies have suggested that early stress is associated with alterations in the hippocampus, a brain area that plays a critical role in learning and memory. The purpose of this study was to measure both hippocampal structure and function in women with and without early childhood sexual abuse and the diagnosis of posttraumatic stress disorder (PTSD). METHOD: Thirty-three women participated in this study, including women with early childhood sexual abuse and PTSD (N=10), women with abuse without PTSD (N=12), and women without abuse or PTSD (N=11). Hippocampal volume was measured with magnetic resonance imaging in all subjects, and hippocampal function during the performance of hippocampal-based verbal declarative memory tasks was measured by using positron emission tomography in abused women with and without PTSD. RESULTS: A failure of hippocampal activation and 16% smaller volume of the hippocampus were seen in women with abuse and PTSD compared to women with abuse without PTSD. Women with abuse and PTSD had a 19% smaller hippocampal volume relative to women without abuse or PTSD. CONCLUSIONS: These results are consistent with deficits in hippocampal function and structure in abuse-related PTSD. _____
Title: Neural correlates of declarative memory for emotionally valenced words in women with posttraumatic stress disorder related to early childhood sexual abuse. Author(s): Bremner, J. Douglas, Emory U School of Medicine, Emory Ctr for Positron Emission Tomography, Depts of Psychiatry & Behavioral Sciences & Radiology, Atlanta, GA, US; Vythilingam, Meena, National Inst of Mental Health, Mood & Anxiety Disorders Program, Bethesda, MD, US; Vermetten, Eric, Emory U School of Medicine, Emory Ctr for Positron Emission Tomography, Depts of Psychiatry & Behavioral Sciences & Radiology, Atlanta, GA, US; Southwick, Steven M., Yale U School of Medicine, Dept of Psychiatry, New Haven, CT, US; McGlashan, Thomas, Yale U School of Medicine, Dept of Psychiatry, New Haven, CT, US; Staib, Lawrence H., Yale U School of Medicine, Dept of Radiology, New Haven, CT, US; Soufer, Robert, Yale U School of Medicine, Dept of Medicine (Cardiology), New Haven, CT, US; Charney, Dennis S., National Inst of Mental Health, Mood & Anxiety Disorders Program, Bethesda, MD, US Address: Bremner, J. Douglas, Emory U-Emory West Campus, PET Ctr/Nuclear Medicine, Emory U Hosp, Room E154, 1256 Briarcliff Rd, Atlanta, GA, US, 30306 Source: Biological Psychiatry, Vol 53(10), May 2003. pp. 879-889. Publisher: United Kingdom: Elsevier Science. Abstract: This study assessed neural correlates of emotionally valenced declarative memory in 10 women with early childhood sexual abuse-related posttraumatic stress disorder (PTSD) and 11 controls. Ss underwent PET measurement of cerebral blood flow during a control condition and during retrieval of neutral and emotionally valenced word pairs. During retrieval of emotionally valenced word pairs, PTSD Ss had greater decreases in blood flow, including orbitofrontal cortex, anterior cingulate, and medial prefrontal cortex, left hippocampus, and fusiform gyrus/inferior temporal gyrus, with increased activation in posterior cingulate, left inferior parietal cortex, left middle frontal gyrus, and visual association and motor cortex. There were no differences in patterns of brain activation during retrieval of neutral word pairs between patients and controls. Findings are consistent with dysfunction of specific brain areas involved in memory and emotion in PTSD. Regions implicated in this study are similar to those from prior imaging studies in PTSD using trauma-specific stimuli for symptom provocation, adding further supportive evidence for a dysfunctional network of brain areas involved in memory in PTSD. _____
Title: Selectively reduced regional cortical volumes in post-traumatic stress disorder. Author(s): Rauch, Scott L., rauch@psych.mgh.harvard.edu, Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Shin, Lisa M., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Segal, Ethan, Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Pitman, Roger K., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Carson, Margaret A., VA Research Service and St. Anselm College, Manchester, NH, US; McMullin, Katherine , Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US Whalen, Paul J., Departments of Psychiatry and Psychology, University of Wisconsin, Madison, WI, US; Makris, Nikos, Center for Morphometric Analysis, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US Address: Rauch, Scott L., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 13th St., Bldg 149, CNY-9, Charlestown, MA, US, 02129, rauch@psych.mgh.harvard.edu Source: Neuroreport: For Rapid Communication of Neuroscience Research, Vol 14(7), May 2003. pp. 913-916. Abstract: Different subterritories of anterior cingulate cortex (ACC) and adjacent ventromedial frontal cortex have been shown to serve distinct functions. This scheme has influenced contemporary pathophysiologic models of psychiatric disorders. Prevailing neuro-circuitry models of post-traumatic stress disorder (PTSD) implicate dysfunction within pregenual ACC and subcallosal cortex(SC), as well as amygdala and hippocampus. In the current study, cortical parcellation of magnetic resonance imaging data was performed to test for volumetric differences in pregenual ACC and SC, between women with PTSD and trauma-exposed women without PTSD. The PTSD group exhibited selectively decreased pregenual ACC and SC volumes. These results are consistent with contemporary schemes regarding functional and structural dissection of frontal cortex, and suggest specific regional cortical pathology in PTSD. _____
Title: Biological Psychiatry: Erratum. Author(s): Fennema-Notestine, Christine, Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Stein, Murray B., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Kennedy, Colleen M., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Archibald, Sarah L., U California, Dept of Psychiatry, La Jolla, CA, US; Jernigan, Terry L., Veterans Affairs San Diego Healthcare System, San Diego, CA, US Address: Fennema-Notestine, Christine, U California, Dept of Psychiatry, 9500 Gilman Dr, La Jolla, CA, US, 92093-0985 Source: Biological Psychiatry, Vol 53(7), Apr 2003. pp. [np Publisher: United Kingdom: Elsevier Science. Abstract: Reports an error in the original article by C. Fennema-Notestine et al (Biological Psychiatry, 2002[Dec] Vol 52[11], 1089-1101). The incorrect journal volume 51 appears on the title page and subsequent pages in the article. (The following abstract of this article originally appeared in record 200211068-007.) Examined neuroanatomical morphometry in adult female victims of intimate partner violence (IPV) with and without posttraumatic stress disorder (PTSD). 17 nonvictimized comparison subjects and 22 victims of IPV, 11 with and 11 without PTSD, were studied. Using quantitative magnetic resonance imaging, three mesial temporal lobe areas were measured: hippocampus, amygdala, and parahippocampal gyrus. Relationships of morphometric measures to symptoms, abuse history, and neuropsychological function were examined. IPV subjects with PTSD did not demonstrate significant smaller hippocampal or other mesial temporal lobe volumes. Overall, IPV subjects had smaller supratentorial cranial vaults and smaller frontal and occipital gray matter volumes relative to nonvictimized comparison subjects. Supratentorial cranial vault volume was negatively correlated with severity of childhood physical abuse, but not with intimate partner violence or PTSD severity... _____
Title: A model of memory and arousal: Implications for posttraumatic stress disorder. Author(s): Lindsay, Dawn Louise , U Cincinnati, US Source: Dissertation Abstracts International: Section B: The Sciences & Engineering, Vol 63(8-B), Mar 2003. pp. 3926. Publisher: US: Univ Microfilms International. Abstract: Although Posttraumatic Stress Disorder (PTSD) is included among anxiety disorders in the diagnostic nomenclature, it also might be conceptualized as a disorder of memory processes. It has been suggested that under high levels of stress or emotional arousal, memories have the form of images and feelings rather than verbally mediated narrative, and that under these conditions an interaction occurs between the hippocampus and amygdala that mediates those memory phenomena. According to this model, at higher levels of intensity, the amygdala suppresses hippocampus functioning, and emotional memory processing is mediated by the amygdala. The model also assumes that the level at which the amygdala takes over memory functioning is potentially influenced and adjusted according to the individual experiences, including prior exposure to psychologically traumatic events. Demonstration of changes in performance on certain kinds of memory tasks may be one method of substantiating this increased sensitivity of the amygdala in trauma-exposed individuals. The von Restorff effect represents an appropriate behavioral measure with which to test the above notion. The von Restorff effect is described as the augmentation of recall of one distinct item, as well as decreased recall of proximate items, in an otherwise homogenous list of items, and has been found to be a robust effect across different types of stimuli. The major aim of this study was to evaluate several aspects of memory function in a sample of non-treatment seeking individuals who reported past exposure to traumatic events, utilizing the von Restorff effect. Another associated aim of the study was to investigate which psychiatric symptoms typically related to trauma exposure were related to memory function in individuals exposed to trauma. The rate of trauma exposure found in this sample was consistent with previous studies utilizing college-age samples that found rates of trauma exposure between 60 and 90%. The hypotheses were partially supported. These findings were interpreted in terms of the hypothesis of an interaction between hippocampus and amygdala function under conditions of emotional arousal and trauma exposure. _____
Title: Olfaction as a traumatic reminder in posttraumatic stress disorder: Case reports and review. Author(s): Vermetten, Eric, e.vermetten@azu.nl, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US; Bremner, J. Douglas, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US Address: Vermetten, Eric, Dept of Psychiatry, U Medical Ctr/Central Military Hosp-T2, Heidelberglaan 100, 3584 CX, Utrecht, Netherlands, e.vermetten@azu.nl Source: Journal of Clinical Psychiatry, Vol 64(2), Feb 2003. pp. 202-207. Publisher: US: Physicians Postgraduate Press. Abstract: Memory for odors that are associated with intense emotional experiences is often strongly engraved. Odors may be more closely connected to affect than other sensory experiences. They can serve as potent contextual cues for memory formation and emotional conditioning and can also serve as cues for olfactory flashbacks. Though trauma-related smells have long been noted by clinicians to be precipitants of traumatic memories in patients with posttraumatic stress disorder (PTSD), very few reports have been published that document this. The authors review olfactory memories and olfactory flashbacks by presenting 3 cases that illustrate the role of olfaction in PTSD. In these cases olfaction is either a precipitant of PTSD symptoms or an important component of reexperiencing. In PTSD, seemingly nonspecific cues have the potential to precipitate traumatic memories with strongemotional components. These conditioned responses in PTSD are hypothesized to be mediated by specific brain areas, i.e., amygdala, hippocampus, and orbitofrontal cortex. Questions about smells as a traumatic reminder should be part of the routine assessment of intrusive memories in PTSD. Smells may also have the potential to provide cues to exposure situations in therapy or to facilitate de novo conditioning. _____
Title: Relationship between distressing cancer-related recollections and hippocampal volume in cancer survivors. Author(s): Nakano, Tomohito; Wenner, Marcus; Inagaki, Masatoshi; Kugaya, Akira; Akechi, Tatsuo; Matsuoka, Yutaka; Sugahara, Yuriko; Imoto, Shigeru; Murakami, Koji; Uchitomi, Yosuke, National Cancer Ctr Research Inst East, Psycho-Oncology Div, Chiba, Japan Address: Uchitomi, Yosuke, National Cancer Ctr Research Inst East, Psycho-Oncology Div, 6-5-1 Kashiwanoha, Kashiwa, Chiba, Japan, 277-8577, yuchitom@east.ncc.go.jp Source: American Journal of Psychiatry, Vol 159(12), Dec 2002. pp. 2087-2093. Publisher: US: American Psychiatric Assn. Abstract: Distressing cancer-related recollections are frequently reported by cancer survivors. Smaller hippocampal volume has been observed in stress-related neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD) and major depression. The aim of this study was to determine whether there is a similar association between distressing cancer-related recollections and hippocampal volume. 67 women (aged 18-55 yrs) who had had breast cancer surgery 3 or more years earlier and had no history of PTSD or major depression before the cancer were evaluated with a semistructured interview to determine whether they had a history of distressing cancer-related recollections. Hippocampal volume was measured by three-dimensional magnetic resonance imaging, and memory function was assessed by the Wechsler Memory Scale-Revised. The volume of the left hippocampus was significantly smaller (5%) in the 28 subjects with a history of distressing cancer-related recollections than in the 39 without any such history. There were no significant differences in delayed memory or percentage retention. However, significantly worse immediate visual memory, but not verbal memory, was observed in the subjects with a history of distressing cancer-related recollections. _____
Title: Brain morphometry in female victims of intimate partner violence with and without posttraumatic stress disorder. Author(s): Fennema-Notestine, Christine, Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Stein, Murray B., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Kennedy, Colleen M., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Archibald, Sarah L., U California, Dept of Psychiatry, La Jolla, CA, US; Jernigan, Terry L. , Veterans Affairs San Diego Healthcare System, San Diego, CA, US Address: Fennema-Notestine, Christine, U California, Dept of Psychiatry, 9500 Gilman Dr, La Jolla, CA, US, 92093-0985 Source: Biological Psychiatry, Vol 52(11), Dec 2002. pp. 1089-1101. Publisher: Elsevier Science. Abstract: Examined neuroanatomical morphometry in adult female victims of intimate partner violence (IPV) with and without posttraumatic stress disorder (PTSD). 17 nonvictimized comparison subjects and 22 victims of IPV, 11 with and 11 without PTSD, were studied. Using quantitative magnetic resonance imaging, three mesial temporal lobe areas were measured: hippocampus, amygdala, and parahippocampal gyrus. Relationships of morphometric measures to symptoms, abuse history, and neuropsychologicalfunctio were examined. IPV subjects with PTSD did not demonstrate significant smaller hippocampal or other mesial temporal lobe volumes. Overall, IPV subjects had smaller supratentorial cranial vaults and smaller frontal and occipital gray matter volumes relative to nonvictimized comparison subjects. Supratentorial cranial vault volume was negatively correlated with severity of childhood physical abuse, but not with intimate partner violence or PTSD severity. These findings are inconsistent with prior reports of smaller hippocampal volumes in patients with PTSD. Rather, the findings point to cerebral abnormalities that may reflect the influence of early trauma on neurodevelopmental processes or denote brain morphometric characteristics of persons at increased risk for serious psychosocial adversity. _____
Title: Posttraumatski Stresni Poremecaj i Suicidalnost. Translated Title: Posttraumatic stress disorder and suicidality. Author(s): Kosanovic-Rajacic, Biljana, biljana@nef.hr, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Zagreb, Croatia; Begic, Drazen, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Zagreb, Croatia Address: Kosanovic-Rajacic, Biljana, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Kispaticeva 12, Hrvatska, 10000, Zagreb, Croatia, biljana@nef.hr Source: Socijalna Psihijatrija, Vol 30(4), Dec 2002. pp. 216-222. Publisher: Croatia: Croatian Psychiatric Society. Abstract: Posttraumatic stress disorder (PTSD) is a complex nosological psychiatric entity involving the psychological impact of a severe trauma in the context of neurobiological and social risk factors. Many recent researches show an increased suicide risk in PTSD patients. Combat veterans, refugees, victims of imprisonment, physical and sexual violence, and disasters were included in the researches. Even individuals with subthreshold symptoms who do not meet full criteria for the disorder suffer from significant impairment, including increased suicidal ideations. Assessment of suicide risk, adequate psychopharmacology, psychotherapy and social support may significantly reduce suicidal behavior in affected patients. Utilizing increasingly sophisticated brain imaging techniques, three neuroanatomical regions that are thought to be involved in PTSD are: amygdala, medial prefrontal cortex, and hippocampus. Concerning the genesis of PTSD, psychodynamic models central to understanding of this disorder are cognitive-behavioral and psychoanalytical approaches. _____
Title: Chicken, eggs and hippocampal atrophy. Author(s): Sapolsky, Robert M., Stanford U, Depts of Biological Sciences, Neurology & Neurological Sciences, Stanford, CA, US Source: Nature Neuroscience, Vol 5(11), Nov 2002. pp. 1111-1113. Publisher: US: Nature Publishing Group. Abstract: Examined the relationship between hippocampus size and trauma. Subjects (Ss) comprised 40 pairs of identical twins in which a single member experienced combat in Vietnam; 42% of those in combat developed posttraumatic stress disorder (PTSD). Collected data included hippocampus size. Results show that those Ss diagnosed with PTSD exhibited smaller hippocampi, with more severe PTSD symptoms associated with smaller size. However, those Ss not experiencing combat also displayed small hippocampi. The hippocampal volumes of non-combat and combat Ss were equally predictive of the severity of combat Ss' PTSD symptoms. More severe combat trauma was not associated with a smaller hippocampus. It is concluded that a small hippocampus preceded exposure to combat, and increased vulnerability to PTSD. Findings suggest that a small hippocampus may be a predisposing risk factor for PTSD, but not an extraordinarily strong one. _____
Title: Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Author(s): Gilbertson, Mark W., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Shenton, Martha E., Harvard Medical School, Dept of Psychiatry, Boston, MA, US; Ciszewski, Aleksandra, Brigham & Women's Hosp, Dept of Radiology, Boston, MA, US; Kasai, Kiyoto, Brigham & Women's Hosp, Dept of Radiology, Boston, MA, US; Lasko, Natasha B., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Orr, Scott P., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Pitman, Roger K., Harvard Medical School, Dept of Psychiatry, Boston, MA, US Address: Gilbertson, Mark W., Veterans Administration Medical Ctr, Research Service, 718 Smyth Road, Manchester, NH, US, 03104, mark.gilbertson@med.va.gov Source: Nature Neuroscience, Vol 5(11), Nov 2002. pp. 1242-1247. Publisher: US: Nature Publishing Group. Abstract: Examined the relationship between posttraumatic stress disorder (PTSD) and hippocampal volume in human males. Hippocampal MRI data were recorded concerning 17 monozygotic twin pairs (mean ages 51.8 and 53.1 yrs), 1 of whom had experienced combat in Vietnam. Results show the hippocampal volume of combat-experienced Ss was smaller in those with more severe PTSD symptoms. Non-combat subjects (Ss) also exhibited smaller hippocampal volume. Combat severity was not related to total hippocampal volume. It is concluded that smaller hippocampi in PTSD represents a pre-existing condition, rather than the neurotoxic product of trauma. _____
Title: Proton magnetic resonance spectroscopy of the hippocampus and occipital white matter in PTSD: Preliminary results. Author(s): Villarreal, Gerardo, gerardo.villarreal@med.va.gov, PTSD Clinic, Veterans Administration Hosp, Albuquerque, NM, US; Petropoulos, Helen, Clinical & Magnetic Resonance Research Ctr, U New Mexico, Albuquerque, NM, US; Hamilton, Derek A., Dept of Psychology, U New Mexico, Albuquerque, NM, US; Rowland, Laura M., Dept of Psychology, U New Mexico, Albuquerque, NM, US; Horan, William P., Dept of Psychiatry & Biobehavioral Sciences, U California, Los Angeles, CA, US; Griego, Jacqueline A., Inst of Cognitive Science, U Osnabrueck, Osnabrueck, Germany; Moreshead, Margaret, Dept of Psychology, U New Mexico, Albuquerque, NM, US; Hart, Blaine L., U Hosp, Albuquerue, NM, US; Brooks, William M., Clinical & Magnetic Resonance Research Ctr, Albuquerque, NM, US Address: Villarreal, Gerardo, VAMC, Psychiatry 116A, 1501 San Pedro Dr SE, Albuquerque, NM, US, 87108, gerardo.villarreal@med.va.gov Source: Canadian Journal of Psychiatry, Vol 47(7), Sep 2002. pp. 666-670. Publisher: Canada: Canadian Psychiatric Assn. Abstract: Previous proton magnetic resonance spectroscopy (-sup-1H-MRS) studies in posttraumatic stress disorder (PTSD) report decreased hippocampal N-acetylaspartate (NAA), an indicator of neuronal integrity. However, other areas of the brain need to be explored. This study examined the specificity of hippocampal NAA concentration changes in PTSD by also examining a control region, the occipital white matter (OWM). Eight PTSD patients (mean age 43.35 yrs) underwent single-voxel -sup-1H-MRS of the hippocampi and bilateral OWM. Absolute neurometabolite concentrations were determined. Results show trends toward reduced left hippocampal NAA and creatine were found in PTSD Ss compared with healthy control Ss. PTSD Ss also had reduced bilateral OWM creatine. It is concluded that findings replicate previous MRS studies and are consistent with decreased hippocampal neuronal integrity without effects in the OWM. _____
Title: Neuroimaging findings in post-traumatic stress. Author(s): Hull, Alastair M., U Aberdeen, Dept of Mental Health & Aberdeen Ctr for Trauma Research, Aberdeen, United Kingdom Address: Hull, Alastair M., Royal Cornhill Hosp, Aberdeen Ctr for Trauma Research, Bennachie, Aberdeen, United Kingdom, alhul@aol.com Source: British Journal of Psychiatry, Vol 181(2), Aug 2002. pp. 102-110. Publisher: England: Royal Coll of Psychiatrists. Abstract: Findings from neuroimaging studies complement our understanding of the wide-ranging neurobiological changes in trauma survivors who develop post-traumatic stress disorder (PTSD). This review aims to determine whether neuroimaging studies had identified structural and functional changes specific to PTSD. A review of all functional and structural neuroimaging studies of subjects with PTSD was carried out. Studies were identified using general medical and specific traumatic stress databases and paper searches of current contents and other secondary sources. The most replicated structural finding is hippocampal volume reduction, which may limit the proper evaluation and categorization of experience. Replicated localized functional changes include increased activation of the amygdala after symptom provocation (which may reflect its role in emotional memory) and and decreased activity of Broca's area at the same time (which may explain the difficulty patients have in labeling their experiences. _____
Title: Reduced hippocampal volume and total white matter volume in posttraumatic stress disorder. Author(s): Villarreal, Gerardo, U New Mexico School of Medicine, Dept of Psychiatry, Albuquerque, NM, US; Hamilton, Derek A., U New Mexico School of Medicine, Dept of Psychology, Albuquerque, NM, US; Petropoulos, Helen, U New Mexico School of Medicine, Clinical & Magnetic Resonance Research Ctr, Albuquerque, NM, US; Driscoll, Ira, U New Mexico School of Medicine, Dept of Psychology, Albuquerque, NM, US; Rowland, Laura M., U New Mexico School of Medicine, Dept of Psychology, Albuquerque, NM, US; Griego, Jaqueline A., U New Mexico School of Medicine, Dept of Psychology, Albuquerque, NM, US; Kodituwakku, Piyadasa W., U New Mexico School of Medicine, Dept of Psychiatry, Albuquerque, NM, US; Hart, Blaine L., U New Mexico School of Medicine, Dept of Radiology, Albuquerque, NM, US; Escalona, Rodrigo, U New Mexico School of Medicine, Dept of Psychiatry, Albuquerque, NM, US; Brooks, William M., U New Mexico School of Medicine, Dept of Neurosciences, Albuquerque, NM, US Address: Villarreal, Gerardo, VA Medical Ctr--Psychiatry, PTSD Clinic (116G), 1501 San Pedro Drive SE, Albuquerque, NM, US, 87108 Source: Biological Psychiatry, Vol 52(2), Jul 2002. pp. 119-125. Publisher: US: Elsevier Science. Abstract: Assessed hippocampal and whole brain volume in civilian posttraumatic stress disorder (PTSD). 12 subjects with PTSD and 10 control subjects (all aged 36-57 yrs) underwent brain MRI. Hippocampal volumes were visually quantified using a computerized volumetric program. Whole-brain volumes were obtained with automated k-means-based segmentation. No differences were found in intracranial volumes. Subjects with PTSD had higher cerebrospinal fluid (CSF)/intracranial volume ratios and lower white matter/intracranial volume ratios, consistent with generalized white matter (WM) atrophy. The effect of age on CSF/intracranial volume was more pronounced in the PTSD group. Subjects with PTSD had smaller absolute and normalized bilateral hippocampal volumes. These differences persisted after adjusting for lifetime weeks of alcohol intoxication. PTSD and depression scores correlated negatively with left hippocampal volume, but PTSD scores were a better predictor of hippocampal volumes. _____
Title: Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? Author(s): Elzinga, B. M., U Amsterdam, Dept of Clinical Psychology, Amsterdam, Netherlands; Bremner, J. D., Emory U School of Medicine, Dept of Psychiatry, Emory Ctr for Positron Emission Tomography, Atlanta, GA, US Address: Elzinga, B. M., U Amsterdam, Dept of Clinical Psychology, Roetersstraat 15, 1018 WB, Amsterdam, Netherlands, kp_elzinga@macmail.psy.uva.nl Source: Journal of Affective Disorders, Vol 70(1), Jun 2002. pp. 1-17. Publisher: Netherlands: Elsevier Science Publishers BV. Abstract: A model for PTSD as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD patients is reviewed in relation to 3 brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. _____
Title: Temporal lobe structural lesion in a case of posttraumatic stress disorder. Author(s): Seedat, Soraya, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; van der Westhuizen, Stephan, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; Matthey, Marius, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; Stein, Dan J., U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa Source: Journal of Neuropsychiatry & Clinical Neurosciences , Vol 14(2), Spr 2002. pp. 240-241. Publisher: US: American Psychiatric Press. Abstract: Few studies have documented gross structural abnormalities in posttraumatic stress disorder (PTSD). Of particular interest in the few studies of this kind is the finding of reduced hippocampal volume in PTSD, and a question that arises is whether hippocampal injury is an outcome of the disorder or is a preexisting vulnerability to its development. The author reports briefly the highlights of magnetic resonance imaging (MRI) findings of mesial temporal sclerosis (MTS) in a 16-yr-old female with chronic, treatment-resistant PTSD following being raped by her grandfather at age 6 yrs. Treatments included drug therapy and cognitive behavior therapy. MRI findings included mesial temporal sclerosis, right hippocampal atrophy and amygdala asymmetry. In some cases of PTSD, psychological trauma predates neuronal changes, but in other cases, underlying neuronal dysfunction may predispose the development of PTSD. The question of a relationship between MTS and PTSD cannot be answered by the data at hand. Nevertheless, this case demonstrates a possible link between gross neurological lesions, more subtle impairments, and PTSD. _____
Title: Neurocognitive functioning in posttraumatic stress disorder. Author(s): Horner, Michael David, Ralph H. Johnson Dept of Veterans Affairs Medical Ctr, Mental Health Service, Charleston, NC, US; Hamner, Mark B., Ralph H. Johnson Dept of Veterans Affairs Medical Ctr, Mental Health Service, Charleston, NC, US Address: Horner, Michael David, Ralph H. Johnson VA Medical Ctr, Mental Health Service (116), 109 Bee St, Charleston, NC, US, 29401, hornermd@musc.edu Source: Neuropsychology Review, Vol 12(1), Mar 2002. pp. 15-30. Publisher: US: Kluwer Academic. Abstract: Reviews the literature (published 1988-1998) on performance on standard neuropsychological tests among individuals with posttraumatic stress disorder (PTSD), both combat- and noncombat-related PTSD. Of 19 studies, 16 reported impairment of attention or immediate memory (or both); however, most of these studies included PTSD patients with significant psychiatric comorbidity, so that the extent to which the observed deficits are specifically attributable to PTSD remains unclear. Other potential confounds, including medical illness, substance abuse, and motivational factors, further preclude definitive conclusions at present. Results of structural and functional neuroimaging studies of PTSD are also summarized. Two studies have reported correlations between hippocampal volume and cognitive findings in PTSD patients. Functional studies have also indicated specific findings in limbic regions, although the relationship of these results to neuropsychological performance remains to be explored. _____
Title: Circuits and systems in stress: II. Applications to neurobiology and treatment in posttraumatic stress disorder. Author(s): Vermetten, Eric, Emory U School of Medicine, Dept of Psychiatry, Atlanta, GA, US; Bremner, J. Douglas, Emory U School of Medicine, Dept of Psychiatry, Atlanta, GA, US Address: Vermetten, Eric, Emory U School of Medicine/Atlanta VAMC, Emory Clinical Neurosciences Research Unit, 1256 Briarcliff Rd NE, Atlanta, GA, US, 30306, evermet@emory.edu Source: Depression & Anxiety, Vol 16(1), 2002. pp. 14-38. Publisher: US: John Wiley & Sons. Abstract: This paper follows the preclinical work on the effects of stress on neurobiological and neuroendocrine systems and provides a comprehensive working model for understanding the pathophysiology of posttraumatic stress disorder (PTSD). Studies of the neurobiology of PTSD in clinical populations are reviewed. Specific brain areas that play an important role in a variety of types of memory are also preferentially affected by stress, including hippocampus, amygdala, medial prefrontal cortex, and cingulate. This review indicates the involvement of these brain systems in the stress response, and in learning and memory. Affected systems in the neural circuitry of PTSD are reviewed (e.g., hypothalamic-pituitary-adrenal axis, catecholaminergic and serotonergic systems, endogenous benzodiazepines, neuro-immunological alterations) as well as changes found with structural and functional neuroimaging methods. Converging evidence has emphasized the role of early-life trauma in the development of PTSD and other trauma-related disorders. Current and new targets for systems that play a role in the neural circuitry of PTSD are discussed. This material provides a basis for understanding the psychopathology of stress-related disorders, in particular PTSD. _____
Title: Circuits and systems in stress. I. Preclinical studies. Author(s): Vermetten, Eric, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US; Bremner, J. Douglas, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US Address: Vermetten, Eric, Emory U School of Medicine/Atlanta VAMC, Emory Clinical Neurosciences Research Unit, 1256 Briarcliff Rd NE, Atlanta, GA, US, 30306, evermet@emory.edu Source: Depression & Anxiety, Vol 15(3), 2002. pp. 126-147. Publisher: US: John Wiley & Sons. Abstract: This paper reviews the preclinical literature related to the effects of stress on neurobiological and neuroendocrine systems. Preclinical studies of stress provide a comprehensive model for understanding neurobiological alterations in posttraumatic stress disorder (PTSD). The pathophysiology of stress reflects longstanding changes in biological stress response systems and in systems involved in stress responsivity, learning, and memory. The neural circuitry involved includes systems mediating hypothalamic-pituitary-adrenal (HPA) axis, norepinephrine (locus coeruleus), and benzodiazepine, serotonergic, dopaminergic, neuropeptide, and central amino acid systems. These systems interact with brain structures involved in memory, including hippocampus, amygdala, and prefrontal cortex. Stress responses are of vital importance in living organisms; however excessive and/or repeated stress can lead to long-lasting alterations in these circuits and systems involved in stress responsiveness. Intensity and duration of the stressor, and timing of the stressor in life, have strong impact in this respect. _____
Title: Cortisol and imaginal exposure in posstraumatic stress disorder: A case report. Author(s): Otte, Christian, otte@uke.uni-hamburg.de, University Hosp Hamburg-Eppendorf, Dept of Psychiatry & Psychotherapy, Hamburg, Germany; Arlt, Josef, University Hosp Hamburg-Eppendorf, Dept of Psychiatry & Psychotherapy, Hamburg, Germany; Wiedemann, Klaus, University Hosp Hamburg-Eppendorf, Dept of Psychiatry & Psychotherapy, Hamburg, Germany; Kellner, Michael, University Hosp Hamburg-Eppendorf, Dept of Psychiatry & Psychotherapy, Hamburg, Germany Address: Otte, Christian, Dept of Psychiatry & Psychotherapy, U of Hamburg, Martinistrasse 52, 20246, Hamburg, Germany, otte@uke.uni-hamburg.de Source: German Journal of Psychiatry, Vol 5(3), 2002. pp. 75-77. Publisher: Germany: German Journal of Psychiatry. Abstract: Imaginal exposure is closely associated with hippocampal processing of traumatic memory. The hippocampus is a target for glucocorticoids which influence memory retrieval and stress response. Glucocorticoid secretion in response to imaginal exposure has not been investigated. We measured subjective distress and salivary cortisol during the 1st and the 20th exposure session in a female patient (aged 45 yrs) with PTSD. Despite considerable arousal and anxiety, cortisol did not increase during the first exposure. During the 20th exposure there was a marked reduction of distress, although cortisol values did not differ from exposure 1. The response of glucocorticoids to imaginal exposure and mechanisms of the lacking cortisol response need further research. _____
Title: EMDR: A putative neurobiological mechanism of action. Author(s): Stickgold, Robert, Harvard Medical School, Dept of Psychiatry, Boston, MA, US Address: Stickgold, Robert, Harvard Medical School, Dept of Psychiatry, 74 Fernwood Rd, Boston, MA, US, 02115, rstickgold@hms.harvard.edu Source: Journal of Clinical Psychology, Vol 58(1), Jan 2002. pp. 61-75. Publisher: US: John Wiley & Sons. Abstract: Notes that F. Shapiro, in her original description of eye movement desensitization and reprocessing therapy (EMDR), proposed that its directed eye movements mimic the saccades of rapid eye movement sleep (REM), but provided no clear explanation of how such mimicry might lead to clinical improvement. This paper revisits her original proposal and presents a complete model for how EMDR could lead to specific improvement in PTSD and related conditions. It is proposed that the repetitive redirecting of attention in EMDR induces a neurobiological state, similar to that of REM sleep, which is optimally configured to support the cortical integration of traumatic memories into general semantic networks. It is suggested that this integration can then lead to a reduction in the strength of hippocampally mediated episodic memories of the traumatic event as well as the memories' associated, amygdala-dependent, negative affect. Experimental data in support of this model are reviewed and possible tests of the model are suggested. _____
Title: Memory impairments following chronic stress? A critical review. Author(s): Jelicic, Marko , U Maastricht, Maastricht Brain & Behaviour Inst, Maastricht, Netherlands; Bonke, Benno Address: Jelicic, Marko, U Maastricht, Maastricht Brain & Behaviour Inst, Neuropsychology & Biopsychology Section, PO Box 616, 6200 MD, Maastricht, Netherlands Source: European Journal of Psychiatry, Vol 15(4), Oct-Dec 2001. pp. 225-232. Publisher: Spain: European Journal of Psychiatry. Abstract: Does chronic stress lead to memory impairments? Several authors hypothesized that elevated levels of glucocorticosteroids, released in the blood during sustained stress, cause damage to the hippocampus--a brain area involved in episodic memory. The authors reviewed evidence for impaired memory performance due to chronic stress and found that glucocorticoid excess as a result of Cushing's syndrome, atypical aging, or use of synthetic corticosteroids such as prednisone is associated with hippocampal atrophy and memory dysfunction. However, studies showing reduced memory performance after acute stress suffer from methodological shortcomings. In addition, attributing memory impairments and reduced hippocampal volume in trauma survivors suffering from posttraumatic stress disorder to the effects of sustained stress appears to be problematic. The authors promote longitudinal research into glucocorticoids and memory functioning in individuals with stressful professions. This could yield more information about the possibly deleterious effects of stress on memory. _____
Title: Longitudinal MRI study of hippocampal volume in trauma survivors with PTSD. Author(s): Bonne, Omer, Hadassah U Hosp, Dept of Psychiatry, Jerusalem, Israel; Brandes, Dalia; Gilboa, Asaf; Gomori, J. Moshe; Shenton, Martha E.; Pitman, Roger K.; Shalev, Arieh Y. Source: American Journal of Psychiatry, Vol 158(8), Aug 2001. pp. 1248-1251. Publisher: US: American Psychiatric Assn. Abstract: The authors prospectively explored whether a reduction in the volume of the hippocampus occurs in recent trauma survivors who develop posttraumatic stress disorder (PTSD). 37 survivors of traumatic events (mean age 33.7 yrs) were assessed within a week of the traumatic event and 6 mo later. The assessment included magnetic resonance imaging (MRI) of the brain (including 124 coronal slices of 1.5-mm thickness), psychometric testing, and structured clinical interviews. The Clinician-Administered PTSD Scale conferred PTSD diagnoses at 6 mo. Results show that 10 Ss (27%) had PTSD at 6 mo. The Ss with PTSD did not differ from those without PTSD in hippocampal volume (right or left) at 1 wk or 6 mo. There was no reduction in hippocampal volume in the PTSD subjects between 1 wk and 6 mo. The authors conclude that smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 mo of expressing the disorder. This brain abnormality might occur in individuals with chronic or complicated PTSD. _____
Title: A pilot longitudinal study of hippocampal volumes in pediatric maltreatment-related posttraumatic stress disorder. Author(s): De Bellis, Michael D., U Pittsburgh Medical Ctr, Developmental Traumatology Neuroimaging Lab, Western Psychiatric Inst & Clinic, Pittsburgh, PA, US; Hall, Julie; Boring, Amy M.; Frustaci, Karin; Moritz, Grace Source: Biological Psychiatry, Vol 50(4), Aug 2001. pp. 305-309. Publisher: US: Elsevier Science. Abstract: Adult posttraumatic stress disorder (PTSD) is associated with decreased hippocampal volumes; however, decreased hippocampal volumes were not seen in pediatric maltreatment-related PTSD. The authors examined hippocampal volumes longitudinally to determine if a history of childhood traumatic stress alters hippocampal growth during puberty. Magnetic resonance imaging was used to measure temporal lobes, amygdala, and hippocampal volumes in nine prepubertal maltreated subjects with pediatric maltreatment-related PTSD and nine sociodemographically matched healthy nonmaltreated yoked control subjects at baseline and after at least 2 years follow-up (during the later stages of pubertal development) using identical equipment and measurement methodology. Temporal lobe, amygdala and hippocampal volumes did not differ between groups at baseline, follow-up, or across time. Whereas these data are from a small sample, the results do not support hippocampal changes in pediatric maltreatment-related PTSD. _____
Title: Biological markers and diagnostic accuracy in the genetics of posttraumatic stress disorder. Author(s): Radant, Allen, Puget Sound Health Care System, Mental Health Service, Seattle, WA, US; Tsuang, Debby; Peskind, Elaine R.; McFall, Miles; Raskind, Wendy Source: Psychiatry Research, Vol 102(3), Jul 2001. pp. 203-215. Publisher: US: Elsevier Scientific. Abstract: Family and twin studies suggest a substantial genetic contribution to the etiology of posttraumatic stress disorder (PTSD). Identification of the nature of this genetic contribution should enhance understanding of the pathophysiology of PTSD and suggest improved therapeutic strategies for its treatment. However, a broadly defined phenotype, specific requirement for an environmental exposure and high frequency of comorbid psychiatric illness all complicate genetic studies of PTSD. It is likely that genetic heterogeneity, incomplete penetrance, pleiotropy and the involvement of more than one gene all constitute formidable obstacles to the genetic analysis of PTSD. One way to circumvent these problems is to perform genetic analysis of traits associated with PTSD, rather than PTSD itself, an approach that has been fruitful for other diseases with complex modes of inheritance. Hypothalamic-pituitary-adrenal axis hypofunction, physiologic markers of increased arousal, and increased acoustic startle response are all potential PTSD-associated traits that might be susceptible to genetic analysis, however, the capacity of these traits to distinguish PTSD from non-PTSD patients and their familial pattern must be better defined before they can be employed in genetic studies. _____
Title: Hippocampal damage mediated by corticosteroids--A neuropsychiatric research challenge. Author(s): Hoeschl, Cyril, Prague Psychiatric Ctr, Praha, Czech Republic; Hajek, Tomas , Prague Psychiatric Ctr, Praha, Czech Republic Address: Hoeschl, Cyril, Prague Psychaitric Ctr, Ustavni 91, 18103, Praha, Czech Republic, hoschl@pcp.lf3.cuni.cz Source: European Archives of Psychiatry & Clinical Neuroscience, Vol 251(Suppl2), 2001. Special Issue: From measurement to clinical outcome: Festschrift in honour of Per Bech on the occasion of his 60th birthday. pp. 81-88. Publisher: Germany: Springer-Verlag. Abstract: There is increasing evidence that cortiosteroids damage the hippocampus in rodents and in primates. Hippocampal atrophy induced by corticosteroids may play an important role in the pathogenesis of a range of neuropsychiatric disorders. Hippocampus is necessary for short-term memory consolidation and PA axis regulation. Signs of hippocampal damage (HPA dysregulation in combination with memory impairment) are found in affective disorders, Alzheimer's disease and in posttraumatic stress disorder. MRI volumetry reveals reduced hippocampal volume in these diseases. Evidence supporting the "glucocorticoid hypothesis" of psychiatric disorders is reviewed in the first part of the paper. Unresolved questions concerning temporary aspects of neurodegeneration, causality, reversibility, type of damage, factors increasing hippocampal vulnerability, and both pharmacological (CRH antagonists, antiglucocorticoid drugs, GABA-ergic, serotonergic, glutamatergic agents) and non-pharmacologial (psychotherapy) treatment approaches are discussed in the second part. _____
Title: Hippocampal damage mediated by corticosteroids--A neuropsychiatric research challenge. Author(s): Hoeschl, Cyril, Prague Psychiatric Centre, Czech Republic; Hajek, Tomas Source: European Archives of Psychiatry & Clinical Neuroscience, Vol 251(8), 2001. pp. II81-II88. Publisher: Germany: Springer-Verlag. Abstract: There is an increasing evidence that corticosteroids damage the hippocampus in rodents and in primates. Hippocampal atrophy induced by corticosteroids may play an important role in the pathogenesis of a range of neuropsychiatric disorders. The hippocampus is necessary for short-term memory consolidation and hypothalamo-pituitary-adrenal (HPA) axis regulation. Signs of hippocampal damage (HPA dysregulation in combination with memory impairment) are found in affective disorders, Alzheimer's disease and in posttraumatic stress disorder. MRI volumetry reveals reduced hippocampal volume in these diseases. Evidence supporting the "glucocorticoid hypothesis" of psychiatric disorders is reviewed in the first part of the paper. Unresolved questions concerning temporary aspects of neurodegeneration, causality, reversibility, type of damage, factors increasing hippocampal vulnerability, and both pharmacological (CRH antagonists, antiglucocorticoid drugs, GABA-ergic, serotonergic, glutamatergic agents) and non-pharmacological (psychotherapy) treatment approaches are discussed in the second part. _____
Title: Hypotheses and controversies related to effects of stress on the hippocampus: An argument for stress-induced damage to the hippocampus in patients with posttraumatic stress disorder. Author(s): Bremner, J. Douglas, Yale U, School of Medicine, Dept of Diagnostic Radiology & Psychiatry, New Haven, CT, US Source: Hippocampus, Vol 11(2), 2001. pp. 75-81. Publisher: US: Wiley Liss. Abstract: Reviews literature supporting the theory that stress-induced neurological damage underlies symptoms of posttraumatic stress disorder (PTSD). Animal studies have shown that stress can lead to hippocampal damage, and human PTSD studies have suggested that stress and PTSD development are associated with hippocampal atrophy and associated memory deficits. Evidence suggests that effects are PTSD-specific, and not the result of nonspecific stress exposure effects or other confounding factors such as alcohol or drug abuse. Stress-induced glucocorticoid release and other factors may be involved. _____
Title: Commentary on PTSD discussion. Author(s): McEwen, Bruce S., Rockefeller U, Harold & Margaret Hatch Lab of Neuroendocrinology, New York, NY, US Source: Hippocampus, Vol 11(2), 2001. pp. 82-84. Publisher: US: Wiley Liss. Abstract: Comments on articles by R. Pitman (2001), J. D. Bremner, and R. Yehuda concerning the possible role of hippocampal atrophy in posttraumatic stress disorder (PTSD). There are 4 uncertainties concerning the role of hippocampal atrophy in PTSD, including: (1) the nature of neuroanatomical changes leading to a smaller hippocampus; (2) the life history of this reduced volume; (3) the importance of glucocorticoids in hippocampus atrophy processes; and (4) the hypothalamic pituitary adrenal (HPA) axis status in PTSD. Imaging technique improvements, twin studies, early childhood abuse-neglect studies, longitudinal hippocampal volume studies, and wider PTSD HPA activity sampling are needed to resolve these issues. _____
Title: Are glucocortoids responsible for putative hippocampal damage in PTSD? How and when to decide. Author(s): Yehuda, Rachel, Mount Sinai School of Medicine, Dept of Psychiatry, New York, NY, US Source: Hippocampus, Vol 11(2), 2001. pp. 85-89. Publisher: US: Wiley Liss. Abstract: Comments on the article of J. D. Bremner, which concludes that stress induces hippocampal damage in patients with posttraumatic stress disorder (PTSD). It is possible to find explanations for hippocampal atrophy in PTSD that is consistent with neuroendocrine data. Glucocorticoid receptor responsiveness, not glucocorticoid toxicity, might be responsible for hippocampal atrophy in PTSD. _____
Title: Atrophy of the hippocampus in posttraumatic stress disorder: How and when? Author(s): Sapolsky, Robert M., Stanford U, Dept of Biological Sciences & Dept of Neurology, Stanford, CA, US Source: Hippocampus, Vol 11(2), 2001. pp. 90-91. Publisher: US: Wiley Liss. Abstract: Provides an introduction for and comments on the articles of J. D. Bremner, R. Pitman (2001), and R. Yehuda concerning the possible role of hippocampal atrophy in posttraumatic stress disorder (PTSD). These authors were asked to focus on the timing of hippocampal atrophy and the role of an excess of glucocorticoids in its mediation. _____
Title: A biological model for delayed recall of childhood abuse. Author(s): Bremner, J. Douglas, Va Connecticut Healthcare System, New Haven, CT, US Source: Journal of Aggression, Maltreatment & Trauma, Vol 4(2), 2001. pp. 165-183. Publisher: US: Haworth Press. Abstract: There is currently scientific controversy related to the validity of delayed recall of memories of childhood abuse. posttraumatic stress disorder (PTSD) is a possible consequence of childhood abuse. Changes in brain structures and systems mediating memory offer a possible explanation for delayed recall of childhood abuse in patients with abuse-related PTSD. Brain areas affected by traumatic stress are involved in memory and the modulation of emotion and include the hippocampus and medial prefrontal cortex. Stress also results in acute and chronic changes in neurochemical systems, including cortisol and norepinephrine, that strengthens or weakens the laying down of memory traces. Patients with PTSD have alterations in a broad range of memory functions, including insertions, deletions and distortions. PTSD patients also show changes in structure and function in brain regions mediating memory, including the hippocampus and medial prefrontal cortex, as well as in brain chemical systems involved in the stress response that influence the laying down and retrieval of memories, including cortisol and norepinephrine. The effects of stress on the brain highlight the importance of considering PTSD in research on memory that is generalized to questions about the delayed recall of childhood abuse. _____
Title: The neurobiology of stress: From serendipity to clinical relevance. Author(s): McEwen, Bruce S., Rockefeller U, Harold & Margaret Miliken Hatch Lab of Neuroendocrinology, New York, NY, US Source: Brain Research, Vol 886(1-2), Dec 2000. pp. 172-189. Publisher: Netherlands: Elsevier Science. Abstract: Discusses the protective and damaging effects of hormones and other physiological agents that mediate the effects of stress on the body as they relate to the immune system and brain. Two new terms, allostasis and allostatic load, which are intended to supplement and clarify the meanings of stress and homeostasis, are presented. For the immune system, acute stress enhances immune function whereas chronic stress suppresses it. These effects can be beneficial for some types of immune responses and deleterious for others. For the brain, acute stress enhances the memory of events that are potentially threatening to the organism. Chronic stress causes adaptive plasticity in the brain. A comparison of the effects of experimenter-applied stressors and psychosocial stressors show that what animals do to each other is often more potent than what experimenters do to them. The brain is resilient and capable of adaptive plasticity. Stress-induced structural changes in brain regions such as the hippocampus have clinical ramifications for disorders such as depression, posttraumatic stress disorder (PTSD), and individual differences in the aging process. Conference: Brain Research Interactive Symposium., 3rd, Nov, 2000, New Orleans, LA, US _____
Title: Information processing and PTSD: A review of the empirical literature. Author(s): Buckley, Todd C., National Ctr for PTSD, VA Boston Healthcare System, Boston, MA, US; Blanchard, Edward B.; Neill, W. Trammell Source: Clinical Psychology Review, Vol 20(8), Nov 2000. pp. 1041-1065. Publisher: US: Elsevier Science/Pergamon. Abstract: Reviews a series of studies that have utilized information-processing paradigms with posttraumatic stress disorder (PTSD) populations. The authors suggest that pretrauma measures of intelligence (IQ) are predictive of the development of PTSD symptoms following trauma. It is noted that there is also evidence of impaired performance on standardized tests of memory (independent of IQ) in PTSD populations. PTSD populations were found to exhibit deficits in memory function that may be due to hippocampus damage secondary to excessive neuroendocrine responses to conditioned stimuli. In addition, individuals with PTSD evince an attentional bias towards trauma-related stimuli at postrecognition stages of information processing. The review also concludes that there is insufficient evidence to either support, or reject, the theoretical proposition that PTSD patients are sensitive to global valence effects at the earliest stages of information processing relative to traumatized non-PTSD populations. Finally, the authors argue that there is some evidence to suggest that the processes associated with autobiographical memory in PTSD populations are similar to those seen in depression. The implications of these findings for the behavioral and cognitive treatment of PTSD are discussed. _____
Title: Glucocorticoids and hippocampal atrophy in neuropsychiatric disorders. Author(s): Sapolsky, Robert M. , Stanford U, Dept of Biological Sciences, Stanford, CA, US Source: Archives of General Psychiatry, Vol 57(10), Oct 2000. pp. 925-935. Publisher: US: American Medical Assn. Abstract: Reviews the possibility that glucocorticoids (GCs) have adverse morphological effects in humans with Cushing syndrome, depression, or posttraumatic stress disorder (PTSD); specifically, these disorders all seem to involve a volume loss in the hippocampus. The author begins with a brief overview of hippocampal anatomy and function. Studies involving hippocampal atrophy in the 3 neuropsychiatric disorders are examined. The author addresses whether these effects are lateralized, how much anatomical specificity there is to hippocampal atrophy, whether hippocampal atrophy has functional consequences, when hippocampal volume loss occurs, the likely cellular mechanisms underlying the hippocampal atrophy, and whether GCs are the damaging agents. It is concluded that these disorders are somewhat selective with atrophy of the hippocampus. _____
Title: Psihobioloske osnove akutnog stresnog poremecaja i posttraumatskog stresnog poremecaja. Translated Title: The psychobiology of acute stress disorder and posttraumatic stress disorder. Author(s): Kuljic, Blagoje, Inst of Neuropsychiatric Diseases "Dr. Lza Lazarevic", Belgrade, Croatia Source: Psihijatrija Danas, Vol 32(2-3), 2000. pp. 73-93. Publisher: Yugoslavia: Instituta Za Mentalno Zdravlje. Abstract: Discusses the psychological and biological theories used in studying the psychobiology of acute stress disorder and posttraumatic stress disorder (PTSD). Acute stress disorder and PTSD are defined as disorders directly caused by stressors. Traumatized people form a defense mechanism to protect themselves from intrusive elements related to trauma. If this does not occur, PTSD develops. The following negative biological and neuroanatomic consequences of PTSD are discussed: elevation of adrenaline, noradrenaline, serotonin, and testosterone levels; reduction of cortisol level; elevation of serum free T3, total T3, and total T4 levels; and decrease in hippocampal volume. _____
Title: Neural correlates of memories of childhood sexual abuse in women with and without posttraumatic stress disorder. Author(s): Bremner, J. Douglas, Yale U, School of Medicine, VA PET Ctr-VA Connecticut Healthcare System, New Haven, CT, US; Narayan, Meena; Staib, Lawrence H.; Southwick, Steven M.; McGlashan, Thomas; Charney, Dennis S. Source: American Journal of Psychiatry, Vol 156(11), Nov 1999. pp. 1787-1795. Publisher: US: American Psychiatric Assn. Abstract: Measured neural correlates of childhood sexual abuse (CSA) memories in 22 women with and without the diagnosis of posttraumatic stress disorder (PTSD). Ss underwent injection of [-sup-1-sup-5O]H-sub-2O, followed by positron emission tomography imaging of the brain while listening to neutral and traumatic (personalized CSA events) scripts. Memories of CSA were associated with greater increases in blood flow in portions of anterior prefrontal cortex, posterior cingulate, and motor cortex in Ss with PTSD than in Ss without PTSD. CSA memories were associated with alterations in blood flow in medial prefrontal cortex, with decreased blood flow in subcallosal gyrus, and a failure of activation in anterior cingulate. There was also decreased blood flow in right hippocampus, fusiform/inferior temporal gyrus, supramarginal gyrus, and visual association cortex in Ss with vs. without PTSD. These findings implicate dysfunction of medial prefrontal cortex (subcallosal gyrus and anterior cingulate), hippocampus, and visual association cortex in pathological memories of CSA in women with PTSD. Increased activation in posterior cingulate and motor cortex was seen in women with PTSD. Dysfunction in these brain areas may underlie PTSD symptoms provoked by traumatic reminders in Ss with PTSD. _____
Title: Does stress damage the brain? Author(s): Bremner, J. Douglas, Yale Psychiatric Inst, New Haven, CT, US Source: Biological Psychiatry, Vol 45(7), Apr 1999. pp. 797-805. Publisher: US: Elsevier Science. Abstract: Presents a review of research addressing the effects of stress on the brain. Studies in animals showed that stress results in damage to the hippocampus, a brain area involved in learning and memory, with associated memory deficits. The mechanism involves glucocorticoids and possibly serotonin acting through excitatory amino acids to mediate hippocampal atrophy. Patients with posttraumatic stress disorder (PTSD) from Vietnam combat and childhood abuse had deficits on neuropsychological measures that have been validated as probes of hippocampal function. In addition, magnetic resonance imaging (MRI) showed reduction in volume of the hippocampus in both combat veterans and victims of childhood abuse. In combat veterans, hippocampal volume reduction was correlated with deficits in verbal memory on neuropsychological testing. These studies introduce the possibility that experiences in the form of traumatic stressors can have long-term effects on the structure and function of the brain. _____
Title: Do glucocorticoids have adverse effects on brain function? Author(s): Keenan, P. A., Harper Hosp, Dept of Psychiatry & Behavioral Neurosciences, Detroit, MI, US; Kuhn, T. W. Source: CNS Drugs, Vol 11(4), Apr 1999. pp. 245-251. Publisher: New Zealand: Adis International. Abstract: Reviews literature on the potential adverse effects of glucocorticoids on the brain, particularly the hippocampus. The effect is most likely to be indirect and in response to either endogenously or exogenously induced hypercortisolaemia. While the stress response is clearly adaptive and therapeutic doses of synthetic glucocorticoids treat many medical disorders effectively, both corticosterone injections and prolonged stress in rodents can result in changes in glucocorticoid receptor levels, altered hippocampal dendritic morphology, and impaired spatial memory. It is suggested that patients with posttraumatic stress disorder (PTSD) or Cushing's syndrome have decreased hippocampal volume and memory impairment. Of particular clinical relevance is a memory decline that accompanies standard doses of corticosteroids. It is concluded that the risk of memory impairment should be carefully considered before initiating treatment with glucocorticoids and their use should be considered in the differential diagnosis of memory loss. _____
Title: MRI volume of the amygdala: A reliable method allowing separation from the hippocampal formation. Author(s): Convit, Antonio, New York U, School of Medicine, Dept of Psychiatry, Aging & Dementia Research Ctr, Neuroimaging Lab, New York, NY, US; McHugh, Pauline; Wolf, Oliver T.; de Leon, Mony J.' Bobinski, Maciek; De Santi, Susan; Roche, Alexandra; Tsui, Wai Source: Psychiatry Research: Neuroimaging, Vol 90(2), Apr 1999. pp. 113-123. Publisher: Ireland: Elsevier Scientific Publishers Ireland. Abstract: Describes the development of a method for the magnetic resonance imaging (MRI)-based in vivo measurement of the amygdala (AMG) volume which allows a better separation of the AMG from the adjoining hippocampal formation. In 9 normal male 30-52 yr olds, 3-dimensional spoiled gradient recalled acquisition, 1.3-mm thick, T1 weighted sagittal MR images and created electronically linked reformatted images in the coronal and axial planes were obtained. On the original sagittal and the reformatted axial planes, the boundaries between the AMG and the hippocampus and the AMG and the hippocampo-amygdala transition area were delineated. Those markings were then projected onto the coronal plane, where the other boundaries of the AMG are more easily seen. Using these markings as a guide and utilizing extra-amygdalar coronal landmarks for the anterior end, the whole AMG on the coronal plane was outlined and its volume determined. It was observed that 45% of the coronal slices that contained AMG also contained some hippocampus. The AMG measurement had high test-retest reliability. The ability to reliably and validly measure the AMG in vivo may facilitate the study of psychiatric disorders, such as posttraumatic stress disorder (PTSD), anxiety disorders, and schizophrenia. _____
Title: The neurobiology of posttraumatic stress disorder: An integration of animal and human research. Author(s): Bremner, J. Douglas, Yale U, School of Medicine, New Haven, CT, US; Southwick, Steven M.; Charney, Dennis S. Source: Saigh, Philip A. (Ed); Bremner, J. Douglas (Ed); 1999. Posttraumatic stress disorder: A comprehensive text. Needham Heights, MA, US: Allyn & Bacon. pp. 103-143 Abstract: This chapter reviews findings from animal studies demonstrating alterations in brain function and structure following exposure to stress. First, the use of animal models for the study of stress is reviewed. Then, findings from animal studies related to stress-induced alterations in norepinephrine, corticotropin releasing factor (CRF)/hypothalamic-pituitary-adrenal (HPA) axis, endogenous benzodiazepine, dopamine, endogenous opiate, and serotonin function is examined. Evidence for the involvement of brain regions involved in memory and emotion, including hippocampus and amygdala, in the detrimental effects of stress is reviewed. Studies which have begun to replicate these findings in human populations of posttraumatic stress disorder (PTSD) patients is outlined. Extrapolations are made from findings in biological studies to the clinical presentation of patients with PTSD. _____
Title: The effects of stress on memory and the hippocampus throughout the life cycle: Implications for childhood development and aging. Author(s): Bremner, J. Douglas, Yale Psychiatric Inst, New Haven, CT, US; Narayan, Meena Source: Development & Psychopathology, Vol 10(4), Fal 1998. Special Issue: Risk, trauma, and memory. pp. 871-885. Publisher: US: Cambridge Univ Press. Abstract: Studies in animals showing hippocampal atrophy and associated memory deficits in stress and aging have implications for stress and aging in humans. Clinical studies in traumatized human populations with posttraumatic stress disorder (PTSD) have replicated studies in animals, showing reduction in volume of the hippocampus measured with magnetic resonance imaging and associated memory deficits. Trauma at different stages of development (early childhood abuse versus trauma in later life due to combat) may influence the nature of memory deficits and hippocampal atrophy. Studies in aging human subjects are consistent with animal studies, although future research is needed in this area. The similarities between biological findings related to cortisol and the hippocampus in stress and aging in both animal and human studies raises the question of whether PTSD can be seen as a form of accelerated aging. Evidence that stress affects the hippocampus and the capacity for learning has broad implications for public health policy, underlying the need for additional resources in this important area and a reexamination of our understanding of factors influencing academic achievement. _____
Hippocampus and Trauma
Title: Hippocampal Volume and Memory Performance in a Community-Based Sample of Women With Posttraumatic Stress Disorder Secondary to Child Abuse. Author(s): Pederson, Cathy L., cpederson@wittenberg.edu, Biology Department, Wittenberg University, Springfield, OH, US; Maurer, Scott H., Biology Department, Wittenberg University, Springfield, OH, US; Kaminski, Patricia L., Psychology Department, University of North Texas, Denton, TX, US; Zander, Kelly A., Biology Department, Wittenberg University, Springfield, OH, US; Peters, Christina M., Biology Department, Wittenberg University, Springfield, OH, US; Stokes-Crowe, Linda A., Psychology Department, Wittenberg University, Springfield, OH, US; Osborn, Robin E., Radiology Department, Mercy Medical Center, Springfield, OH, US Address: Pederson, Cathy L., Biology Department, Wittenberg University, P.O. Box 720, Springfield, OH, US, 45501-0720, cpederson@wittenberg.edu Source: Journal of Traumatic Stress, Vol 17(1), Feb 2004. pp. 37-40. Publisher: Netherlands: Kluwer Academic Publishers. Abstract: Childhood abuse is linked to posttraumatic stress disorder (PTSD), which follows abuse survivors into adulthood. This study identified the neuropsychological and neuromorphological sequelae of PTSD among prepubescently abused women. Right-handed women aged 20-40 years were placed into PTSD and abuse, abuse only, and normal control groups (n = 17 per group). Participants were screened for trauma history and psychiatric symptoms, demographically matched, and given neuropsychological tests and a magnetic resonance scan of their brain. Women with PTSD did not express significant deficits in memory performance or hippocampal volume when compared with the abuse and normal control groups. _____
Title: Structural and functional brain changes in posttraumatic stress disorder. Author(s): Nutt, David J., david.j.nutt@bristol.ac.uk, Psychopharmacology Unit, University of Bristol, Bristol, United Kingdom; Malizia, Andrea L., Psychopharmacology Unit, University of Bristol, Bristol, United Kingdom Address: Nutt, David J., Psychopharmacology Unit, School of Medical Sciences, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol, United Kingdom, BS1 3NY, david.j.nutt@bristol.ac.uk Source: Journal of Clinical Psychiatry, Vol 65(Suppl1), 2004. Special Issue: Update on posttraumatic stress disorder. pp. 11-17. Publisher: US: Physicians Postgraduate Press. Abstract: Posttraumatic stress disorder (PTSD) is a highly disabling condition that is associated with intrusive recollections of a traumatic event, hyperarousal, avoidance of clues associated with the trauma, and psychological numbing. The field of neuroimaging has made tremendous advances in the past decade and has contributed greatly to our understanding of the physiology of fear and the pathophysiology of PTSD. Neuroimaging studies have demonstrated significant neurobiologic changes in PTSD. There appear to be 3 areas of the brain that are different in patients with PTSD compared with those in control subjects: the hippocampus, the amygdala, and the medial frontal cortex. The amygdala appears to be hyperreactive to trauma-related stimuli. The hallmark symptoms of PTSD, including exaggerated startle response and flashbacks, may be related to a failure of higher brain regions (i.e., the hippocampus and the medial frontal cortex) to dampen the exaggerated symptoms of arousal and distress that are mediated through the amygdala in response to reminders of the traumatic event. The findings of structural and functional neuroimaging studies of PTSD are reviewed as they relate to our current understanding of the pathophysiology of this disorder. Conference: The International Consensus Group on Depression and Anxiety, 8th, Jul, 2002, Limerick, Ireland _____
Title: Neural correlates of declarative memory for emotionally valenced words in women with posttraumatic stress disorder related to early childhood sexual abuse. Author(s): Bremner, J. Douglas, Emory U School of Medicine, Emory Ctr for Positron Emission Tomography, Depts of Psychiatry & Behavioral Sciences & Radiology, Atlanta, GA, US; Vythilingam, Meena, National Inst of Mental Health, Mood & Anxiety Disorders Program, Bethesda, MD, US; Vermetten, Eric, Emory U School of Medicine, Emory Ctr for Positron Emission Tomography, Depts of Psychiatry & Behavioral Sciences & Radiology, Atlanta, GA, US; Southwick, Steven M., Yale U School of Medicine, Dept of Psychiatry, New Haven, CT, US; McGlashan, Thomas, Yale U School of Medicine, Dept of Psychiatry, New Haven, CT, US; Staib, Lawrence H., Yale U School of Medicine, Dept of Radiology, New Haven, CT, US; Soufer, Robert, Yale U School of Medicine, Dept of Medicine (Cardiology), New Haven, CT, US; Charney, Dennis S., National Inst of Mental Health, Mood & Anxiety Disorders Program, Bethesda, MD, US Address: Bremner, J. Douglas, Emory U-Emory West Campus, PET Ctr/Nuclear Medicine, Emory U Hosp, Room E154, 1256 Briarcliff Rd, Atlanta, GA, US, 30306 Source: Biological Psychiatry, Vol 53(10), May 2003. pp. 879-889. Publisher: United Kingdom: Elsevier Science. Abstract: This study assessed neural correlates of emotionally valenced declarative memory in 10 women with early childhood sexual abuse-related posttraumatic stress disorder (PTSD) and 11 controls. Ss underwent PET measurement of cerebral blood flow during a control condition and during retrieval of neutral and emotionally valenced word pairs. During retrieval of emotionally valenced word pairs, PTSD Ss had greater decreases in blood flow, including orbitofrontal cortex, anterior cingulate, and medial prefrontal cortex, left hippocampus, and fusiform gyrus/inferior temporal gyrus, with increased activation in posterior cingulate, left inferior parietal cortex, left middle frontal gyrus, and visual association and motor cortex. There were no differences in patterns of brain activation during retrieval of neutral word pairs between patients and controls. Findings are consistent with dysfunction of specific brain areas involved in memory and emotion in PTSD. Regions implicated in this study are similar to those from prior imaging studies in PTSD using trauma-specific stimuli for symptom provocation, adding further supportive evidence for a dysfunctional network of brain areas involved in memory in PTSD. _____
Title: Selectively reduced regional cortical volumes in post-traumatic stress disorder. Author(s): Rauch, Scott L., rauch@psych.mgh.harvard.edu, Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Shin, Lisa M., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Segal, Ethan, Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Pitman, Roger K., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Carson, Margaret A., VA Research Service and St. Anselm College, Manchester, NH, US; McMullin, Katherine, Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US; Whalen, Paul J., Departments of Psychiatry and Psychology, University of Wisconsin, Madison, WI, US; Makris, Nikos, Center for Morphometric Analysis, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, US Address: Rauch, Scott L., Psychiatric Neuroimaging Research Group, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 13th St., Bldg 149, CNY-9, Charlestown, MA, US, 02129, rauch@psych.mgh.harvard.edu Source: Neuroreport: For Rapid Communication of Neuroscience Research, Vol 14(7), May 2003. pp. 913-916. Publisher: US: Lippincott Williams & Wilkins. Abstract: Different subterritories of anterior cingulate cortex (ACC) and adjacent ventromedial frontal cortex have been shown to serve distinct functions. This scheme has influenced contemporary pathophysiologic models of psychiatric disorders. Prevailing neuro-circuitry models of post-traumatic stress disorder (PTSD) implicate dysfunction within pregenual ACC and subcallosal cortex(SC), as well as amygdala and hippocampus. In the current study, cortical parcellation of magnetic resonance imaging data was performed to test for volumetric differences in pregenual ACC and SC, between women with PTSD and trauma-exposed women without PTSD. The PTSD group exhibited selectively decreased pregenual ACC and SC volumes. These results are consistent with contemporary schemes regarding functional and structural dissection of frontal cortex, and suggest specific regional cortical pathology in PTSD. _____
Title: A model of memory and arousal: Implications for posttraumatic stress disorder. Author(s): Lindsay, Dawn Louise, U Cincinnati, US Source: Dissertation Abstracts International: Section B: The Sciences & Engineering, Vol 63(8-B), Mar 2003. pp. 3926. Publisher: US: Univ Microfilms International. Abstract: Although Posttraumatic Stress Disorder (PTSD) is included among anxiety disorders in the diagnostic nomenclature, it also might be conceptualized as a disorder of memory processes. It has been suggested that under high levels of stress or emotional arousal, memories have the form of images and feelings rather than verbally mediated narrative, and that under these conditions an interaction occurs between the hippocampus and amygdala that mediates those memory phenomena. According to this model, at higher levels of intensity, the amygdala suppresses hippocampus functioning, and emotional memory processing is mediated by the amygdala. The model also assumes that the level at which the amygdala takes over memory functioning is potentially influenced and adjusted according to the individual experiences, including prior exposure to psychologically traumatic events. Demonstration of changes in performance on certain kinds of memory tasks may be one method of substantiating this increased sensitivity of the amygdala in trauma-exposed individuals. The von Restorff effect represents an appropriate behavioral measure with which to test the above notion. The von Restorff effect is described as the augmentation of recall of one distinct item, as well as decreased recall of proximate items, in an otherwise homogenous list of items, and has been found to be a robust effect across different types of stimuli. The major aim of this study was to evaluate several aspects of memory function in a sample of non-treatment seeking individuals who reported past exposure to traumatic events, utilizing the von Restorff effect. Another associated aim of the study was to investigate which psychiatric symptoms typically related to trauma exposure were related to memory function in individuals exposed to trauma. The rate of trauma exposure found in this sample was consistent with previous studies utilizing college-age samples that found rates of trauma exposure between 60 and 90%. The hypotheses were partially supported. These findings were interpreted in terms of the hypothesis of an interaction between hippocampus and amygdala function under conditions of emotional arousal and trauma exposure. _____
Title: Olfaction as a traumatic reminder in posttraumatic stress disorder: Case reports and review. Author(s): Vermetten, Eric, e.vermetten@azu.nl, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US; Bremner, J. Douglas, Emory U School of Medicine, Dept of Psychiatry & Behavioral Sciences, Atlanta, GA, US Address: Vermetten, Eric, Dept of Psychiatry, U Medical Ctr/Central Military Hosp-T2, Heidelberglaan 100, 3584 CX, Utrecht, Netherlands, e.vermetten@azu.nl Source: Journal of Clinical Psychiatry, Vol 64(2), Feb 2003. pp. 202-207. Publisher: US: Physicians Postgraduate Press. Abstract: Memory for odors that are associated with intense emotional experiences is often strongly engraved. Odors may be more closely connected to affect than other sensory experiences. They can serve as potent contextual cues for memory formation and emotional conditioning and can also serve as cues for olfactory flashbacks. Though trauma-related smells have long been noted by clinicians to be precipitants of traumatic memories in patients with posttraumatic stress disorder (PTSD), very few reports have been published that document this. The authors review olfactory memories and olfactory flashbacks by presenting 3 cases that illustrate the role of olfaction in PTSD. In these cases olfaction is either a precipitant of PTSD symptoms or an important component of reexperiencing. In PTSD, seemingly nonspecific cues have the potential to precipitate traumatic memories with strong emotional components. These conditioned responses in PTSD are hypothesized to be mediated by specific brain areas, i.e., amygdala, hippocampus, and orbitofrontal cortex. Questions about smells as a traumatic reminder should be part of the routine assessment of intrusive memories in PTSD. Smells may also have the potential to provide cues to exposure situations in therapy or to facilitate de novo conditioning. _____
Title: The action of mexidol on the state of conditioned reflex activity after traumatic brain lesions. Author(s): Mering, T. A., Science Research Institute of the Brain, Russian Academy of Medical Sciences, Moscow, Russia Source: Neuroscience & Behavioral Physiology, Vol 33(2), Feb 2003. pp. 133-138. Publisher: Netherlands: Kluwer Academic Publishers. Abstract: It is demonstrated that even partial damage to the hippocampus is accompanied by impairments to counting time intervals lasting several months (1200-1500 presentations) without alteration of other complex conditioned reflex responses. After treatment with mexidol, which has a wide spectrum of actions, particularly antioxidant, antihypoxic, and antistress, rats showed a normal process of acquisition of a conditioned reflex to time. Unlike animals of the control group, there was no prolonged period during which there was complete impairment of the mechanism for counting time intervals. Thanks to significant improvements in autonomic processes and emotional-motivational responses, experiments could use a large number of conditioned stimuli. For example, after brain trauma mexidol strengthened compensatory-restorative processes: animals showed accelerated recovery of impaired functions, with decreases in the rate of retrograde degeneration of brain areas directly connected to the damaged parts, phenomena such as Monakow diaschisis were not observed, and so on. _____
Title: Childhood trauma associated with smaller hippocampal volume in women with major depression. Author(s): Vythilingam, Meena, NIMH, Mood & Anxiety Disorders Program, Bethesda, MD, US; Heim, Christine; Newport, Jeffrey; Miller, Andrew H.; Anderson, Eric; Bronen, Richard; Brummer, Marijn; Staib, Lawrence; Vermetten, Eric; Charney, Dennis S.; Nemeroff, Charles B.; Bremner, J. Douglas Address: Vythilingam, Meena, NIMH, Mood & Anxiety Disorders Program, 15K North Dr, Room 111, MSC 2670, Bethesda, MD, US, 20892-2670, meena.vythi@nih.gov Source: American Journal of Psychiatry, Vol 159(12), Dec 2002. pp. 2072-2080. Abstract: The volumes of the hippocampus and of control brain regions were measured in depressed women with and without childhood abuse and in healthy nonabused comparison subjects. Study participants were 32 women with current unipolar major depressive disorder--21 with a history of prepubertal physical and/or sexual abuse and 11 without a history of prepubertal abuse--and 14 healthy nonabused female volunteers. The volumes of the whole hippocampus, temporal lobe, and whole brain were measured on coronal MRI scans by a single rater who was blind to the subjects' diagnoses. The depressed subjects with childhood abuse had an 18% smaller mean left hippocampal volume than the nonabused depressed subjects and a 15% smaller mean left hippocampal volume than the healthy subjects. Right hippocampal volume was similar across the three groups. The right and left hippocampal volumes in the depressed women without abuse were similar to those in the healthy subjects. _____
Title: Brain morphometry in female victims of intimate partner violence with and without posttraumatic stress disorder. Author(s): Fennema-Notestine, Christine, Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Stein, Murray B., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Kennedy, Colleen M., Veterans Affairs San Diego Healthcare System, San Diego, CA, US; Archibald, Sarah L., U California, Dept of Psychiatry, La Jolla, CA, US; Jernigan, Terry L., Veterans Affairs San Diego Healthcare System, San Diego, CA, US Address: Fennema-Notestine, Christine, U California, Dept of Psychiatry, 9500 Gilman Dr, La Jolla, CA, US, 92093-0985 Source: Biological Psychiatry, Vol 52(11), Dec 2002. pp. 1089-1101. Publisher: Elsevier Science. Abstract: Examined neuroanatomical morphometry in adult female victims of intimate partner violence (IPV) with and without posttraumatic stress disorder (PTSD). 17 nonvictimized comparison subjects and 22 victims of IPV, 11 with and 11 without PTSD, were studied. Using quantitative magnetic resonance imaging, three mesial temporal lobe areas were measured: hippocampus, amygdala, and parahippocampal gyrus. Relationships of morphometric measures to symptoms, abuse history, and neuropsychologicalfunctio were examined. IPV subjects with PTSD did not demonstrate significant smaller hippocampal or other mesial temporal lobe volumes. Overall, IPV subjects had smaller supratentorial cranial vaults and smaller frontal and occipital gray matter volumes relative to nonvictimized comparison subjects. Supratentorial cranial vault volume was negatively correlated with severity of childhood physical abuse, but not with intimate partner violence or PTSD severity. These findings are inconsistent with prior reports of smaller hippocampal volumes in patients with PTSD. Rather, the findings point to cerebral abnormalities that may reflect the influence of early trauma on neurodevelopmental processes or denote brain morphometric characteristics of persons at increased risk for serious psychosocial adversity. _____
Title: Posttraumatski Stresni Poremecaj i Suicidalnost. Translated Title: Posttraumatic stress disorder and suicidality. Author(s): Kosanovic-Rajacic, Biljana, biljana@nef.hr, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Zagreb, Croatia; Begic, Drazen, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Zagreb, Croatia Address: Kosanovic-Rajacic, Biljana, Klinika za psihijatriju, Klinicki bolnicki centar Zagreb, Kispaticeva 12, Hrvatska, 10000, Zagreb, Croatia, biljana@nef.hr Source: Socijalna Psihijatrija, Vol 30(4), Dec 2002. pp. 216-222. Publisher: Croatia: Croatian Psychiatric Society. Abstract: Posttraumatic stress disorder (PTSD) is a complex nosological psychiatric entity involving the psychological impact of a severe trauma in the context of neurobiological and social risk factors. Many recent researches show an increased suicide risk in PTSD patients. Combat veterans, refugees, victims of imprisonment, physical and sexual violence, and disasters were included in the researches. Even individuals with subthreshold symptoms who do not meet full criteria for the disorder suffer from significant impairment, including increased suicidal ideations. Assessment of suicide risk, adequate psychopharmacology, psychotherapy and social support may significantly reduce suicidal behavior in affected patients. Utilizing increasingly sophisticated brain imaging techniques, three neuroanatomical regions that are thought to be involved in PTSD are: amygdala, medial prefrontal cortex, and hippocampus. Concerning the genesis of PTSD, psychodynamic models central to understanding of this disorder are cognitive-behavioral and psychoanalytical approaches. _____
Title: Chicken, eggs and hippocampal atrophy. Author(s): Sapolsky, Robert M., Stanford U, Depts of Biological Sciences, Neurology & Neurological Sciences, Stanford, CA, US Source: Nature Neuroscience, Vol 5(11), Nov 2002. pp. 1111-1113. Publisher: US: Nature Publishing Group. Abstract: Examined the relationship between hippocampus size and trauma. Subjects (Ss) comprised 40 pairs of identical twins in which a single member experienced combat in Vietnam; 42% of those in combat developed posttraumatic stress disorder (PTSD). Collected data included hippocampus size. Results show that those Ss diagnosed with PTSD exhibited smaller hippocampi, with more severe PTSD symptoms associated with smaller size. However, those Ss not experiencing combat also displayed small hippocampi. The hippocampal volumes of non-combat and combat Ss were equally predictive of the severity of combat Ss' PTSD symptoms. More severe combat trauma was not associated with a smaller hippocampus. It is concluded that a small hippocampus preceded exposure to combat, and increased vulnerability to PTSD. Findings suggest that a small hippocampus may be a predisposing risk factor for PTSD, but not an extraordinarily strong one. _____
Title: Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Author(s): Gilbertson, Mark W., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Shenton, Martha E., Harvard Medical School, Dept of Psychiatry, Boston, MA, US; Ciszewski, Aleksandra, Brigham & Women's Hosp, Dept of Radiology, Boston, MA, US; Kasai, Kiyoto, Brigham & Women's Hosp, Dept of Radiology, Boston, MA, US; Lasko, Natasha B., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Orr, Scott P., Veterans Administration Medical Ctr, Research Service, Manchester, NH, US; Pitman, Roger K., Harvard Medical School, Dept of Psychiatry, Boston, MA, US Address: Gilbertson, Mark W., Veterans Administration Medical Ctr, Research Service, 718 Smyth Road, Manchester, NH, US, 03104, mark.gilbertson@med.va.gov Source: Nature Neuroscience, Vol 5(11), Nov 2002. pp. 1242-1247. Publisher: US: Nature Publishing Group. Abstract: Examined the relationship between posttraumatic stress disorder (PTSD) and hippocampal volume in human males. Hippocampal MRI data were recorded concerning 17 monozygotic twin pairs (mean ages 51.8 and 53.1 yrs), 1 of whom had experienced combat in Vietnam. Results show the hippocampal volume of combat-experienced Ss was smaller in those with more severe PTSD symptoms. Non-combat subjects (Ss) also exhibited smaller hippocampal volume. Combat severity was not related to total hippocampal volume. It is concluded that smaller hippocampi in PTSD represents a pre-existing condition, rather than the neurotoxic product of trauma. _____
Title: Studies of hormone action in the hippocampal formation: Possible relevance to depression and diabetes. Author(s): McEwen, Bruce S., Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US; Magarinos, Ana Maria, Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US; Reagan, Lawrence P., Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US Source: Journal of Psychosomatic Research, Vol 53(4), Oct 2002. Special Issue: Depression and mental disorders and diabetes, renal disease, and obesity and nutritional disorders. pp. 883-890. Publisher: US: Elsevier Science. Abstract: Reviews the plasticity and vulnerability of the hippocampus (HIP), which is involved in learning and memory, as well as in the control of autonomic and vegetative functions. Discussed are its role in the regulation of glucose homeostasis, and the need of HIP neurons for glucose because of their high metabolic activity. The HIP is also vulnerable to damage by stroke and head trauma, susceptible to damage during aging and repeated stress, and sensitive to the effects of diabetes. A summary of recent work in the authors' laboratory and related work using citations, in part, from Medline. In addition to its vulnerability, the HIP's plasticity and adaptability makes it capable of structural reorganization, including remodeling of dendrites and neurogenesis of dentate gyrus granule neurons in response to repeated stress. Animal models of Type 1 diabetes show accelerated remodeling of dendrites; Type 2 diabetes remains to be studied in this regard. This is relevant to major depressive illness, in which a progressive atrophy of the HIP is reported and is accompanied by impairment of cognitive function in those subjects with HIP shrinkage. HIP atrophy in depression and in diabetes may reflect damage or plasticity involving structural reorganization that is potentially treatable. _____
Title: Neuroimaging findings in post-traumatic stress. Author(s): Hull, Alastair M., U Aberdeen, Dept of Mental Health & Aberdeen Ctr for Trauma Research, Aberdeen, United Kingdom Address: Hull, Alastair M., Royal Cornhill Hosp, Aberdeen Ctr for Trauma Research, Bennachie, Aberdeen, United Kingdom, alhul@aol.com Source: British Journal of Psychiatry, Vol 181(2), Aug 2002. pp. 102-110. Publisher: England: Royal Coll of Psychiatrists. Abstract: Findings from neuroimaging studies complement our understanding of the wide-ranging neurobiological changes in trauma survivors who develop post-traumatic stress disorder (PTSD). This review aims to determine whether neuroimaging studies had identified structural and functional changes specific to PTSD. A review of all functional and structural neuroimaging studies of subjects with PTSD was carried out. Studies were identified using general medical and specific traumatic stress databases and paper searches of current contents and other secondary sources. The most replicated structural finding is hippocampal volume reduction, which may limit the proper evaluation and categorization of experience. Replicated localized functional changes include increased activation of the amygdala after symptom provocation (which may reflect its role in emotional memory) and and decreased activity of Broca's area at the same time (which may explain the difficulty patients have in labelling their experiences. _____
Title: Structural plasticity and tianeptine: Cellular and molecular targets. Author(s): McEwen, B. S., Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US; Magarinos, A. M., Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US; Reagan, L. P., Rockefeller U, Harold & Margaret Milliken Hatch Lab of Neuroendocrinology, New York, NY, US Address: McEwen, B. S., Rockefeller U, Box 165, 1230 York Avenue, New York, NY, US, 10021, mcewen@rockvax.rockefeller.edu Source: European Psychiatry, Vol 17(Suppl3), Jul 2002. pp. 318s-330s. Publisher: France: Editions Scientifiques Elsevier. Abstract: Examines the molecular and cellular targets of action of tianeptine in relation to its role influencing structural plasticity of the hippocampus. Animal model studies have shown that the hippocampus is a particularly sensitive/vulnerable brain region that responds to stress/stress hormones. Stress suppresses neurogenesis of dentate gyrus granule neurons, and repeated stress causes remodeling of dendrites in the CA3 region, a region that is particularly important in memory processing. Both forms of structural remodeling of the hippocampus are mediated by adrenal steroids working in concert with excitatory amino acids (EAA) and N-methyl-D-aspartate (NMDA) receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures, head trauma, and ischemia, and alterations of calcium homeostasis that accompany age-related cognitive impairment. Tianeptine (tianeptine) is an effective antidepressant that prevents and even reverses the actions of stress and glucocorticoids on dendritic remodeling in an animal model of chronic stress. This review summarizes findings on neurochemical targets of adrenal steroid actions that may explain their role in the remodeling process. Conference: A new pharmacology of depression: the concept of synaptic plasticity., Oct, 2002, ECNP Barcelona, Barcelona, Spain _____
Title: Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? Author(s): Elzinga, B. M., U Amsterdam, Dept of Clinical Psychology, Amsterdam, Netherlands; Bremner, J. D., Emory U School of Medicine, Dept of Psychiatry, Emory Ctr for Positron Emission Tomography, Atlanta, GA, US Address: Elzinga, B. M., U Amsterdam, Dept of Clinical Psychology, Roetersstraat 15, 1018 WB, Amsterdam, Netherlands, kp_elzinga@macmail.psy.uva.nl Source: Journal of Affective Disorders, Vol 70(1), Jun 2002. pp. 1-17. Publisher: Netherlands: Elsevier Science Publishers BV. Abstract: A model for PTSD as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD patients is reviewed in relation to 3 brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. _____
Title: Temporal lobe structural lesion in a case of posttraumatic stress disorder. Author(s): Seedat, Soraya, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; van der Westhuizen, Stephan, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; Matthey, Marius, U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa; Stein, Dan J., U Stellenbosch, Dept of Psychiatry, Cape Town, South Africa Source: Journal of Neuropsychiatry & Clinical Neurosciences, Vol 14(2), Spr 2002. pp. 240-241. Publisher: US: American Psychiatric Press. Abstract: Few studies have documented gross structural abnormalities in posttraumatic stress disorder (PTSD). Of particular interest in the few studies of this kind is the finding of reduced hippocampal volume in PTSD, and a question that arises is whether hippocampal injury is an outcome of the disorder or is a preexisting vulnerability to its development. The author reports briefly the highlights of magnetic resonance imaging (MRI) findings of mesial temporal sclerosis (MTS) in a 16-yr-old female with chronic, treatment-resistant PTSD following being raped by her grandfather at age 6 yrs. Treatments included drug therapy and cognitive behavior therapy. MRI findings included mesial temporal sclerosis, right hippocampal atrophy and amygdala asymmetry. In some cases of PTSD, psychological trauma predates neuronal changes, but in other cases, underlying neuronal dysfunction may predispose the development of PTSD. The question of a relationship between MTS and PTSD cannot be answered by the data at hand. Nevertheless, this case demonstrates a possible link between gross neurological lesions, more subtle impairments, and PTSD. _____
Title: Circuits and systems in stress: II. Applications to neurobiology and treatment in posttraumatic stress disorder. Author(s): Vermetten, Eric, Emory U School of Medicine, Dept of Psychiatry, Atlanta, GA, US; Bremner, J. Douglas, Emory U School of Medicine, Dept of Psychiatry, Atlanta, GA, US Address: Vermetten, Eric, Emory U School of Medicine/Atlanta VAMC, Emory Clinical Neurosciences Research Unit, 1256 Briarcliff Rd NE, Atlanta, GA, US, 30306, evermet@emory.edu Source: Depression & Anxiety , Vol 16(1), 2002. pp. 14-38. Publisher: US: John Wiley & Sons. Abstract: This paper follows the preclinical work on the effects of stress on neurobiological and neuroendocrine systems and provides a comprehensive working model for understanding the pathophysiology of posttraumatic stress disorder (PTSD). Studies of the neurobiology of PTSD in clinical populations are reviewed. Specific brain areas that play an important role in a variety of types of memory are also preferentially affected by stress, including hippocampus, amygdala, medial prefrontal cortex, and cingulate. This review indicates the involvement of these brain systems in the stress response, and in learning and memory. Affected systems in the neural circuitry of PTSD are reviewed (e.g., hypothalamic-pituitary-adrenal axis, catecholaminergic and serotonergic systems, endogenous benzodiazepines, neuro-immunological alterations) as well as changes found with structural and functional neuroimaging methods. Converging evidence has emphasized the role of early-life trauma in the development of PTSD and other trauma-related disorders. Current and new targets for systems that play a role in the neural circuitry of PTSD are discussed. This material provides a basis for understanding the psychopathology of stress-related disorders, in particular PTSD. _____
Title: Zur Rolle von Sprache und Korper bel der Integration traumatischer Erfahrungen. Translated Title: Neurobiological correlates of traumatic experiences. Author(s): Huther, Gerald, ghuether@gwde.de Address: Huther, Gerald, Klinik und Poliklinik fur Psychiatrie und Psychotherapie, Von-Siebold-Str. 5, 37075, Gottingen, Germany, ghuether@gwde.de Source: Experimentelle und Klinische Hypnose , Vol 18(1-2), 2002. pp. 8-22. Publisher: Germany: dgvt-Verlag. Abstract: Traumatic experiences elicit an uncontrollable activation of stress-sensitive cortico-limbic neuronal networks and neuroendocrine circuits. The overshooting excitation in conjunction with strong and long-lasting activation of the HPA-System and cortisol secretion causes a destabilization of established neuronal circuitry (dendritic degeneration, synaptic regression) in brain regions with high cortisol receptor density and glutamatergic input (e.g. the hippocampus). Under these conditions,most victims of a trauma switch back into a pattern of "behavioral emergency reactions" (freezing, panic, stereotypes) and a (variety of self-protective, defensive response-patterns (dissociation, depersonalization, derealization). The more the neuronal and synaptic connections involved in the generation of these defense responses become facilitated and stabilized, the more automatized the response. It is difficult under these conditions to acquire novel, more complex (frontocortical) patterns of coping, especially for children. More detrimental to the internal organization of the brain than the actually experienced trauma is the subjectively felt loss or destruction of security-providing resources (psychosocial support, self-image, competence, faith and belief). _____
Title: Long-term hyperexcitability in the hippocampus after experimental head trauma. Author(s): Santhakumar, Vijayalakshmi, U California, Dept of Anatomy & Neurobiology, Irvine, CA, US; Ratzliff, Anna D. H.; Jeng, Jade; Toth, Zsolt; Soltesz, Ivan Source: Annals of Neurology, Vol 50(6), Dec 2001. pp. 708-717. Publisher: US: Wiley Liss. Abstract: Examined the effects of head trauma on early and long-term limbic hyperexcitability in the hippocampus of rats. Ss were subjected to fluid percussion injury (FPI) on the intact dura. Some Ss were administered bicuculline or the ionotropic glutamate receptor antagonists 2-amino-5-phosphovaleric acid (APV) and 6- cyano-7-nitroquinoxaline-2,3-dione (CNQX). Results show low-frequency, single-shock stimulation of the perforant path revealed an early granule cell hyperexcitability in head-injured Ss that returned to control levels 1 mo subsequently, even following bicuculline administration. However, there was a persistent decrease in threshold to induction of seizure-like electrical activity in response to high-frequency tetanic stimulation in the hippocampus following head injury. Both early- and long-term mossy fiber sprouting were observed at low to moderate levels in the dentate gyrus of Ss that experienced FPI. There was a long-lasting increase in the frequency of spontaneous inhibitory postsynaptic currents in dentate granule cells following FPI. Both APV and CNQX decreased the spontaneous inhibitory postsynaptic current frequency. It is concluded that a single episode of experimental closed head trauma induces long-lasting alterations in the hippocampus. _____
Title: Memory impairments following chronic stress? A critical review. Author(s): Jelicic, Marko, U Maastricht, Maastricht Brain & Behaviour Inst, Maastricht, Netherlands; Bonke, Benno Address: Jelicic, Marko, U Maastricht, Maastricht Brain & Behaviour Inst, Neuropsychology & Biopsychology Section, PO Box 616, 6200 MD, Maastricht, Netherlands Source: European Journal of Psychiatry, Vol 15(4), Oct-Dec 2001. pp. 225-232. Publisher: Spain: European Journal of Psychiatry. Abstract: Does chronic stress lead to memory impairments? Several authors hypothesized that elevated levels of glucocorticosteroids, released in the blood during sustained stress, cause damage to the hippocampus--a brain area involved in episodic memory. The authors reviewed evidence for impaired memory performance due to chronic stress and found that glucocorticoid excess as a result of Cushing's syndrome, atypical aging, or use of synthetic corticosteroids such as prednisone is associated with hippocampal atrophy and memory dysfunction. However, studies showing reduced memory performance after acute stress suffer from methodological shortcomings. In addition, attributing memory impairments and reduced hippocampal volume in trauma survivors suffering from posttraumatic stress disorder to the effects of sustained stress appears to be problematic. The authors promote longitudinal research into glucocorticoids and memory functioning in individuals with stressful professions. This could yield more information about the possibly deleterious effects of stress on memory. _____
Title: Capture of a novel protein synthesis-dependent component of long-term depression. Author(s): Kauderer, Beth Susan, Columbia U., US Source: Dissertation Abstracts International: Section B: The Sciences & Engineering, Vol 62(3-B), Sep 2001. pp. 1250. Publisher: US: Univ Microfilms International. Abstract: Hippocampal based behavioral memories are divisible into short and long term phases, with the long term phase requiring the synthesis of new proteins for its persistence. Similar phases have also been encountered in hippocampal based forms of synaptic plasticity, such as long term potentiation (LTP), which involves an enhancement of synaptic strength. By contrast, it is less clear whether long term depression (LTD), an activity-dependent weakening of synaptic strength, can be divisible into phases of expression. I studied LTD at CA3-CA1 synapses in hippocampal organotypic slice cultures. The slice culture preparation offered a very stable system in which to study LTD as the cultures have a chance to recover, over the course of a week, from the trauma to their cut processes. An analysis of LTD in the cultures showed that the LTD was persistent, homosynaptic, synapse-specific, NMDA-dependent and could be reversed by LTP. In addition, the LTD observed was found to be more substantial than that observed in acute slices, making it an optimal preparation in which to analyze whether LTD, like behavioral memory and LTP, could be divisible into phases of expression. My findings revealed that LTD was also not a unitary event but a complex, multi-phase process. Using both electrical stimulation and various inhibitors, I was able to distinguish two components of LTD: a long-lasting late phase and a transient, early phase. A prolonged stimulus consisting of 900 stimuli spaced at 1 Hz for 15 minutes induced a protein synthesis-dependent late phase of LTD (L-LTD). By contrast, a shorter train consisting of the same 900 stimuli massed at 5 Hz for 3 minutes produced a short-lasting LTD (E-LTD). Phases of LTD were also distinguished with the protein synthesis inhibitors, anisomycin and emetine, and with the transcriptional inhibitor, actinomycin D. The short-lasting 5-Hz E-LTD was similar in its time course to the early phase of 1-Hz L-LTD that was unmasked by inhibitors of protein synthesis. Furthermore, I observed the phenomenon of capture of LTD. L-LTD produced at one input was captured by E-LTD produced at another input. The shorter 5-Hz stimulus or the prolonged 1-Hz stimulus in the presence of protein synthesis inhibitors were each transformed into a stable and enduring late phase of depression when the prolonged stimulus was applied to another input in the same population of neurons. _____
Title: Longitudinal MRI study of hippocampal volume in trauma survivors with PTSD. Author(s): Bonne, Omer, Hadassah U Hosp, Dept of Psychiatry, Jerusalem, Israel; Brandes, Dalia; Gilboa, Asaf; Gomori, J. Moshe; Shenton, Martha E.; Pitman, Roger K.; Shalev, Arieh Y. Source: American Journal of Psychiatry, Vol 158(8), Aug 2001. pp. 1248-1251. Publisher: US: American Psychiatric Assn. Abstract: The authors prospectively explored whether a reduction in the volume of the hippocampus occurs in recent trauma survivors who develop posttraumatic stress disorder (PTSD). 37 survivors of traumatic events (mean age 33.7 yrs) were assessed within a week of the traumatic event and 6 mo later. The assessment included magnetic resonance imaging (MRI) of the brain (including 124 coronal slices of 1.5-mm thickness), psychometric testing, and structured clinical interviews. The Clinician-Administered PTSD Scale conferred PTSD diagnoses at 6 mo. Results show that 10 Ss (27%) had PTSD at 6 mo. The Ss with PTSD did not differ from those without PTSD in hippocampal volume (right or left) at 1 wk or 6 mo. There was no reduction in hippocampal volume in the PTSD subjects between 1 wk and 6 mo. The authors conclude that smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 mo of expressing the disorder. This brain abnormality might occur in individuals with chronic or complicated PTSD. _____
Title: Stress and development: Behavioral and biological consequences. Author(s): Bremner, J. Douglas, Emory U School of Medicine, Atlanta, GA, US; Vermetten, Eric Source: Development & Psychopathology , Vol 13(3), Sum 2001. Special Issue: Stress and development: Biological and psychological consequences. pp. 473-489. Publisher: US: Cambridge Univ Press. Abstract: Childhood abuse is an important public health problem; however, little is known about the effects of abuse on the brain and neurobiological development. This article reviews the behavioral and biological consequences of childhood abuse and places them in a developmental context. Animal studies show that both positive and negative events early in life can influence neurobiological development in unique ways. Early stressors such as maternal separation result in lasting effects on stress-responsive neurobiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic systems. These studies also implicate a brain area involved in learning and memory, the hippocampus, in the long-term consequences of early stress. Clinical studies of patients with a history of abuse also implicate dysfunction in the HPA axis and the noradrenergic and hippocampal systems; however, there are multiple questions related to chronicity of stress, developmental epoch at the time of the stressor, presence of stress-related psychiatric disorders including posttraumatic stress disorder and depression, and psychological factors mediating the response to trauma that need to be addressed in this field of research. _____
Title: Severe amnesia in epilepsy: Causes, anatomopsychological considerations, and treatment. Author(s): Guerreiro, Carlos A. M., McGill U, Dept of Neurology & Neurosurgery, Montreal Neurological Inst & Hosp, Montreal, PQ, Canada; Jones-Gotman, Marilyn, McGill U, Dept of Neurology & Neurosurgery, Montreal Neurological Inst & Hosp, Montreal, PQ, Canada; Andermann, Frederick, McGill U, Dept of Neurology & Neurosurgery, Montreal Neurological Inst & Hosp, Montreal, PQ, Canada; Bastos, Alexandre, McGill U, Dept of Neurology & Neurosurgery, Montreal Neurological Inst & Hosp, Montreal, PQ, Canada; Cendes, Fernando, McGill U, Dept of Neurology & Neurosurgery, Montreal Neurological Inst & Hosp, Montreal, PQ, Canada Address: Jones-Gotman, Marilyn, Montreal Neurological Inst, 3801 University Street, Montreal, PQ, Canada, H3A 2B4, mjg@ego.psych.mcgill.ca Source: Epilepsy & Behavior, Vol 2(3,Part1), Jun 2001. pp. 224-246. Publisher: US: Academic Press. Abstract: This article reports five patients (aged 25-52 yrs) with pronounced memory loss who had extensive neuropsychological and electroencephalographic testing. magnetic resonance imaging (MRI) was also performed in four of the patients, MRI volumetric measurements of amygdala and hippocampal formation in three, and measurements of entorhinal cortex in two. The amnesia occurred after head trauma in one patient, following encephalitis in one, after partial status epilepticus in two, and after unilateral surgical resection in a woman with bilateral lesions. On the basis of these studies it was impossible to distinguish the role of recurrent temporal lobe epileptic seizures as distinct from underlying lesions in the genesis and course of memory loss. The authors reviewed the anatomical substrate, neuropsychological, and other investigations and the etiological factors leading to the amnesia in these patients, together with current concepts regarding possible causes of such severe memory dysfunction. In patients with this degree of memory deficit, temporal resection in an attempt to control seizures did not lead to a measurable increase in memory problems. It also, however, did not bring about worthwhile improvement in seizure control. _____
Title: Child sexual abuse and its impact on children's reading ability. Author(s): Wiggins, Karen Sue , Capella U., US Source: Dissertation Abstracts International Section A: Humanities & Social Sciences, Vol 61(10-A), May 2001. pp. 3942. Publisher: US: University Microfilms International. Abstract: Child sexual abuse has been prevalent in our society since the Roman Empire. Child sexual abuse has increased dramatically in numbers, and societal laws have not been able to maintain a pace adequate to arrest this problem. Research has indicated that sexual abuse affects the emotional, physical, and psychosocial aspects of a child's life, but there is a lack of information concerning the impact of this abuse on the victim's learning ability, especially in the area of reading comprehension. Studies conducted with adults indicate learning difficulties do exist in some of the cases. Few studies have focused primarily on abused children due to various factors such as confidentiality issues, small subject samples, grouping of abuses into one category, and inadequate test administration. The research conducted reveals that trauma can result in a loss of hippocampal volume. The hippocampus is the center of complex memory capability focusing on events, facts, and verbal material. All of these are essential elements in the reading process. A decrease in hippocampal volume can deter the acquisition of reading skills necessary to comprehend at one's appropriate grade level. This researcher used a quantitative design and had the Wide Range Achievement Test-3 (WRAT-3) administered to a controlled group of nonabused children and a group of abused children. Test results indicated on this sample that child sexual abuse did not have a significant impact on reading ability as reported by the WRAT-3. _____
Title: A biological model for delayed recall of childhood abuse. Author(s): Bremner, J. Douglas, Va Connecticut Healthcare System, New Haven, CT, US Source: Journal of Aggression, Maltreatment & Trauma, Vol 4(2), 2001. pp. 165-183. Publisher: US: Haworth Press. Abstract: There is currently scientific controversy related to the validity of delayed recall of memories of childhood abuse. posttraumatic stress disorder (PTSD) is a possible consequence of childhood abuse. Changes in brain structures and systems mediating memory offer a possible explanation for delayed recall of childhood abuse in patients with abuse-related PTSD. Brain areas affected by traumatic stress are involved in memory and the modulation of emotion and include the hippocampus and medial prefrontal cortex. Stress also results in acute and chronic changes in neurochemical systems, including cortisol and norepinephrine, that strengthens or weakens the laying down of memory traces. Patients with PTSD have alterations in a broad range of memory functions, including insertions, deletions and distortions. PTSD patients also show changes in structure and function in brain regions mediating memory, including the hippocampus and medial prefrontal cortex, as well as in brain chemical systems involved in the stress response that influence the laying down and retrieval of memories, including cortisol and norepinephrine. The effects of stress on the brain highlight the importance of considering PTSD in research on memory that is generalized to questions about the delayed recall of childhood abuse. _____
Title: Plasticity of the hippocampus: Adaptation to chronic stress and allostatic load. Author(s): McEwen, Bruce S., Rockefeller U, Lab of Neuroendocrinology, New York, NY, US Source: Sorg, Barbara A. (Ed); Bell, Iris R. (Ed); 2001. The role of neural plasticity in chemical intolerance. Annals of the New York Academy of Sciences, vol. 933. New York, NY, US: New York Academy of Sciences. pp. 265-277 Abstract: Discusses the capacity of the hippocampus (HC) to change structurally and functionally as a result of chronic restraint and psychosocial stress. The HC is important for declarative, spatial, and contextual memory and is implicated in the perception of chronic pain. The HC formation is vulnerable to damage from seizures, ischemia, and head trauma and is particularly sensitive to the effects of adrenal glucocorticoids secreted during the diurnal rhythm and chronic stress. Adrenal steroids typically have adaptive effects in the short run, but promote pathophysiology when there is either repeated stress or dysregulation of the HPA axis. Adrenal steroids display both protective and damaging effects on the HC. The HC also displays structural plasticity, involving ongoing neurogenesis of the dentate gyrus, synaptogenesis under control of estrogens in the CA1 region, and dendritic remodeling caused by repeated stress or elevated levels of exogenous glucocorticoids in the CA3 region. The author's working hypothesis is that structural plasticity in response to repeated tress starts out as an adaptive and protective response, but ends us as damage if the imbalance in the regulation of the key mediators is not resolved. _____
Title: Differential effects of stress on hippocampal and amygdaloid LTP: Insight into the neurobiology of traumatic memories. Author(s): Diamond, David M., U South Florida, Depts of Psychology, Tampa, FL, US; Park, Collin R.; Puls, Michael J.; Rose, Gregory M. Source: Hoelscher, Christian (Ed); 2001. Neuronal mechanisms of memory formation: Concepts of long-term potentiation and beyond. New York, NY, US: Cambridge University Press. pp. 379-403 Abstract: This chapter begins with a brief discussion of the complexity of the long-term potentiation (LTP)-memory debate. The authors suggest that the notion of LTP as a unitary 'memory encoding device' is too simplistic to survive rigorous experimentation and debate. However, while there are difficulties in making the direct connection between LTP and memory, the authors have not abandoned the proposition that LTP studies can enhance an understanding of the physiology of memory. The primary focus of this chapter is to incorporate studies on LTP, memory, and stress into a synthesis on the dynamics of emotional memory storage in the hippocampus and amygdala. The work is based on the idea that the induction or blockade of LTP can serve as a 'diagnostic' measure of how stress affects information processing by different brain structures. The synthesis provides a novel perspective on why the characteristics of nonemotional memories differ from the pathologically intense, and fragmented, characteristics of traumatic memories. _____
Title: Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. Author(s): Driessen, Martin, Luebeck School of Medicine, Dept of Psychiatry, Luebeck, Germany; Herrmann, Joerg; Stahl, Kerstin; Zwaan, Martin; Meier, Szilvia; Hill, Andreas; Osterheider, Marita; Petersen, Dirk Source: Archives of General Psychiatry, Vol 57(12), Dec 2000. pp. 1115-1122. Publisher: US: American Medical Assn. Abstract: Examined volumes of the hippocampus and the amygdala, neuropsychological functioning, and history of childhood traumatization in 21 female patients (aged 21-40 yrs) with borderline personality disorder (BPD). The authors analyzed the interrelationships between volumes and neuropsychological functioning, as well as between measured volumes and the extent of childhood experiences. Ss completed the Structured Clinical Interview for DSM-IV Personality Disorders, neuropsychological test batteries, and the Childhood Trauma Questionnaire. magnetic resonance imaging (MRI) scans and MRI-based volumetric measurements were performed. Results show volumes of the hippocampus in the BPD group nearly 16% smaller than those of the healthy control Ss even when controlling for brain volume. Similar, but less pronounced results were found with regard to the amygdala, with volumes nearly 8% smaller. The hypothesis of stress- or trauma-induced volume reductions in BPD (at least those of the hippocampus) can only in part be supported by the negative correlations between volumes of the hippocampus and the extent and duration of self-reported traumatic experiences, because these correlations were found only with regard to the whole sample but not when the BPD and the healthy groups were analyzed separately. _____
Title: Information processing and PTSD: A review of the empirical literature. Author(s): Buckley, Todd C., National Ctr for PTSD, VA Boston Healthcare System, Boston, MA, US; Blanchard, Edward B.; Neill, W. Trammell Source: Clinical Psychology Review, Vol 20(8), Nov 2000. pp. 1041-1065. Publisher: US: Elsevier Science/Pergamon. Abstract: Reviews a series of studies that have utilized information-processing paradigms with posttraumatic stress disorder (PTSD) populations. The authors suggest that pretrauma measures of intelligence (IQ) are predictive of the development of PTSD symptoms following trauma. It is noted that there is also evidence of impaired performance on standardized tests of memory (independent of IQ) in PTSD populations. PTSD populations were found to exhibit deficits in memory function that may be due to hippocampus damage secondary to excessive neuroendocrine responses to conditioned stimuli. In addition, individuals with PTSD evince an attentional bias towards trauma-related stimuli at postrecognition stages of information processing. The review also concludes that there is insufficient evidence to either support, or reject, the theoretical proposition that PTSD patients are sensitive to global valence effects at the earliest stages of information processing relative to traumatized non-PTSD populations. Finally, the authors argue that there is some evidence to suggest that the processes associated with autobiographical memory in PTSD populations are similar to those seen in depression. The implications of these findings for the behavioral and cognitive treatment of PTSD are discussed. _____
Title: Short-term behavioral and electrophysiological consequences of underwater trauma. Author(s): Wang, Jian, U Haifa, Dept of Psychology, Haifa, Israel; Akirav, Irit; Richter-Levin, Gal Source: Physiology & Behavior, Vol 70(3-4), Aug-Sep 2000. pp. 327-332. Publisher: US: Elsevier Science. Abstract: Notes that a relationship between behaviorally induced stress and hippocampal plasticity has been reported in studies in which the induction of long term potentiation (LTP) in the hippocampus of rats was inhibited following behavioral stressors. This study assessed whether this trauma, like other models of stress, would reduce the probability of inducing synaptic plasticity in the hippocampus. The possible correlation between the effects of the trauma on neural plasticity and spatial performance was examined. Two groups of adult male Sprague-Dawley rats were trained for 8 days on a spatial memory task in the water maze. At the end of training, 1 group was held underwater for 30 sec, and a 2nd group was given 1 min to swim. A 3rd group of naive animals was included to dissociate the effects of the trauma and possible effects of the training itself. Results show the traumatized rats showed impaired performance in a spatial learning task in the water maze 20 min after the trauma and a reduced level of dentate gyrus LTP 40 min after high-frequency stimulation to the perforant path. A positive correlation between the behavioral performance and hippocampal plasticity was also found. _____
Title: Psihobioloske osnove akutnog stresnog poremecaja i posttraumatskog stresnog poremecaja. Translated Title: The psychobiology of acute stress disorder and posttraumatic stress disorder. Author(s): Kuljic, Blagoje, Inst of Neuropsychiatric Diseases "Dr. Lza Lazarevic", Belgrade, Croatia Source: Psihijatrija Danas, Vol 32(2-3), 2000. pp. 73-93. Publisher: Yugoslavia: Instituta Za Mentalno Zdravlje. Abstract: Discusses the psychological and biological theories used in studying the psychobiology of acute stress disorder and posttraumatic stress disorder (PTSD). Acute stress disorder and PTSD are defined as disorders directly caused by stressors. Traumatized people fo |
