|
|
|
|
 |
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.
_______________________
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
|
|
NeuroBiology of Trauma
Hypothalamus and PTSD
Translated Title: Serum cortisol level and DST result of patients with (PTSD) after Tangshan earthquake. Author(s): Zhang, Ben, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Xu, Guangming, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Ma, Wenyou , Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Sun, Hexian, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Liu, Xiouhua, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Sun, Taiqi, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Yu, Zhenjian, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Miao, Liling, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China; Niou, Junhong, Mental Health Ctr of Kailuan Limited Liability Corporation, Tangshan, China Source: Chinese Mental Health Journal , Vol 16(12), Dec 2002. pp. 817-821. Publisher: China: Chinese Mental Health. Abstract: Explored the change of the hypothalamus-pituitary-adrenal (HPA) axis in patients with post-traumatic stress disorder (PTSD) after the 1979 Earthquake in Tangshan, China. 35 patients with PTSD (mean age 52 yrs) and 33 normal subjects (mean age 52 yrs) were examined with a serum cortisol level measurement and dexamethasone suppression test (DST). The results show that there was no significant difference in the levels of serum cortisol between PTSD patients and normal Ss and there was no significant difference in the basal levels of serum cortisol between males and females. In the DST, after taking the same doses (0.75 mg) of dexamethasone, the PTSD group exhibited a significantly lower serum cortisol level and significantly higher suppression effect rate than the control subjects group. Whereas males and females in each group showed no significant difference on basal serum level and the serum level after taking dexamethasone, and on the rate of suppression effect. The study concludes that patients with PTSD have increased sensitivity to DST, but such sensitivity has no gender difference. _____
Title: Psychoneuroendocrinological contributions to the etiology of depression, posttraumatic stress disorder, and stress-related bodily disorders: The role of the hypothalamus-pituitary-adrenal axis. Author(s): Ehlert, Ulrike, U Zurich, Dept of Clinical Psychology, Zurich, Switzerland; Gaab, Jens; Heinrichs, Markus Source: Biological Psychology , Vol 57(1-3), Jul-Aug 2001. pp. 141-152. Publisher: Netherlands: Elsevier Science. Abstract: Following the assumption that stressors play an important part in the etiology and maintenance of psychiatric disorders, it is necessary to evaluate parameters reflecting stress-related physiological reactions. Results from these examinations may help to deepen the insight into the etiology of psychiatric disorders and to elucidate diagnostic uncertainties. One of the best-known stress-related endocrine reactions is the hormonal release of the hypothalamic-pituitary-adrenal (HPA) axis. Dysregulations of this axis are associated with several psychiatric disorders. Profound hyperactivity of the HPA-axis has been found in melancholic depression, alcoholism, and eating disorders. In contrast, posttraumatic stress disorder (PTSD), stress-related bodily disorders like idiopathic pain syndromes, and chronic fatigue syndrome seem to be associated with diminished HPA activity (lowered activity of the adrenal gland). Hypotheses referring to (a) the psychophysiological meaning and (b) the development of these alterations are discussed. _____
Title: Reward deficicency syndrome: A biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors. Author(s): Blum, Kenneth, U North Texas, Dept of Biological Sciences, Denton, TX, US; Braverman, Eric R.; Holder, Jay M.; Lubar, Joel F.; Monastra, Vincent J.; Miller, David; Lubar, Judith O.; Chen, Thomas J. H.; Comings, David E. Source: Journal of Psychoactive Drugs, Vol 32Suppl), Nov 2000. pp. 1-68. Publisher: US: Haight-Ashbury Publications. Abstract: "The reward cascade" is the release of serotonin, which in turn at the hypothalamus stimulates enkephalin, which in turn inhibits gamma-aminobutyric acid (GABA) at the substantia nigra, which in turn fine tunes the amount of dopamine (DA) released at the nucleus accumbens or "reward site." When DA is released into the synapse, it stimulates a number of DA receptors which results in increased feelings of well-being and stress reduction. It is suggested that when there is a dysfunction in the brain reward cascade, especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. The lack of D-sub-2 receptors causes individuals to have a high risk of multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, attention deficit hyperactivity disorder (ADHD), Tourette's syndrome, autism, chronic violence, posttraumatic stress disorder (PTSD), schizoid/avoidant cluster, conduct disorder, and antisocial behavior. _____
Title: Biology of posttraumatic stress disorder. Author(s): Yehuda, Rachel, Mt Sinai School of Medicine, Psychiatry Dept, Traumatic Stress Studies Program, New York, NY, US Source: Journal of Clinical Psychiatry, Vol 61(Suppl7), 2000. Special Issue: New strategies for the treatment of posttraumatic stress disorder. pp. 14-21. Publisher: US: Physicians Postgraduate Press. Abstract: An understanding of the biological basis of posttraumatic stress disorder (PTSD) requires an examination of the underlying neurobiology of fear and the factors that might contribute to an unsuccessful termination of the fear response in some individuals. Several factors may lead to an inadequate termination of a stress response, and the failure to contain the biological alterations initiated by stress may have long-term adverse consequences. In particular, a prolonged continuation of biological responses following stress may lead to an inappropriate pairing of the traumatic memory with distress and may then initiate a cascade of secondary biological alterations. The roles played by the amygdala, its projection to the lateral hypothalamus and then to the rostral ventral medulla, and the initiation of sympathetic nervous system (and catecholamine) responses are discussed. Projections from the central amygdala to the bed nucleus of the stria terminalis and the initiation of the hypothalamic-pituitary-adrenal axis response are also examined. _____
Title: Induction of corticotropin-releasing hormone gene expression by glucocorticoids: Implication for understanding the states of fear and anxiety and allostatic load. Author(s): Schulkin, Jay, Georgetown U, Dept of Physiology & Biophysics, Washington, DC, US; Gold, Philip W.; McEwen, Bruce S. Source: Psychoneuroendocrinology, Vol 23(3), Apr 1998. pp. 219-243. Publisher: US: Elsevier Science Ltd/Pergamon. Abstract: Summarizes the evidence that glucocorticoids have differential effects on corticotropin-releasing hormone (CRH) expression in the forebrain. Evidence supports the idea of 2 distinct CRH systems in the brain: one which is constrained by glucocorticoids and the other which is not. It is this latter system that includes 2 primary sites (central nucleus of the amygdala and the lateral bed nucleus of the stria terminalis) in which the regulation of CRH gene expression can be disassociated from that of the paraventricular nucleus of the hypothalamus. It is this other system that we think is linked to fear and anxiety and to clinical syndromes (excessively shy fearful children, melancholic depression, posttraumatic stress disorder [PTSD] and self-administration of psychotropic drugs). The excess glucocorticoids and CRH, and the state of anticipatory anxiety, contribute to allostatic load, a new term that refers to the wear and tear on the body and brain arising from attempts to adapt to adversity. _____
Title: Neural circuits and mechanisms of post-traumatic stress disorder. Author(s): Charney, Dennis S., Yale U, School of Medicine, Dept of Psychiatry, New Haven, CT, US; Deutch, Ariel Y.; Southwick, Steven M.; Krystal, John H. Source: Friedman, Matthew J. (Ed); Charney, Dennis S. (Ed); et al; 1995. Neurobiological and clinical consequences of stress: From normal adaptation to post-traumatic stress disorder. Philadelphia, PA, US: Lippincott Williams & Wilkins Publishers. pp. 271-287 Abstract: [discusses] functional neuroanatomy that can account for the spectrum of symptoms associated with posttraumatic stress disorder (PTSD) / preclinical and clinical investigations provide strong evidence for linking several brain structures to the signs and symptoms of anxiety and fear associated with trauma / chief among these are amygdala, locus coeruleus, hippocampus, hypothalamus, thalamus, periaqueductal gray, and orbitofrontal cortex / [review] the neuroanatomy, neurochemistry, and neural mechanisms relevant to the role these brain structures play in anxiety and fear / [discuss] the implications of these findings for a better understanding of the pathophysiology and treatment of PTSD _____
Title: The psychoneuroendocrinology of functional hypothalamic amenorrhea. Author(s): Berga, Sarah L. , U Pittsburgh School of Medicine, PA, US; Girton, Lyda G. Source: Psychiatric Clinics of North America , Vol 12(1), Mar 1989. pp. 105-116. Publisher: US: WB Saunders. Abstract: Women with functional hypothalamic amenorrhea display multiple neuroendocrine aberrations suggestive of altered central neurotransmission. The role of antecedent stress as an explanation for both the neurochemical changes and the dysfunctional behavior of these women is examined by utilizing concepts provided by the animal model of inescapable shock and the human condition of posttraumatic stress disorder (PTSD). _____ Hypothalamus and Trauma
Title: The relationship between circadian rhythmicity and vasoactive intestinal polypeptide in the suprachiasmatic nucleus of congenitally anophthalmic mice. Author(s): Laemle, Lois K., UMDNJ New Jersey Medical School, Dept of Anatomy, Cell Biology & Injury Sciences, Newark, NJ, US; Ottenweller, John E. Address: Laemle, Lois K., UMDNJ New Jersey Medical School, Dept of Anatomy, Cell Biology & Injury Sciences, 185 South Orange Avenue, Newark, NJ, US, 07103, laemlelb@umdnj.edu Source: Brain Research, Vol 917(1), Oct 2001. pp. 105-111. Publisher: Netherlands: Elsevier Science. Abstract: To date, the search for the clock component that is both necessary and sufficient for generation of circadian rhythms has relied primarily on experimental interventions such as lesions and transplantation of fetal suprachiasmatic nuclei (SCN). While these approaches have been fruitful, lesions disrupt adjacent host tissue and fiber pathways, and donor tissue is likewise subject to trauma during harvest and transplantation. The current investigation has used congenitally anophthalmic (eyeless) mice to ask whether vasoactive intestinal polypeptide immunoreactive (VIP)-IR SCN neurons are necessary and sufficient for generation of circadian rhythms. In this animal model, arrhythmic mice occur naturally, together with their rhythmic littermates. The researchers have combined recording of wheel-running activity with light microscopic immunocytochemistry for VIP and cytoarchitectural analysis of the SCN in rhythmic vs arrhythmic anophthalmic mice. These data provide the first definitive evidence that the presence of VIP neurons in the SCN is not sufficient for generation of circadian locomotor rhythms. _____
Title: Stress-induced sensitization of CRH-ir but not P-CREB-ir responsivity in the rat central nervous system. Author(s): Bruijnzeel, Adrie W., U Medical Ctr, Div of Pharmacology & Anatomy, Rudolf Magnus Inst of Neurosciences, Utrecht, Netherlands; Stam, Rianne; Compaan, Josje C.; Wiegant, Victor M. Address: Bruijnzeel, Adrie W., Division of Pharmacology and Anatomy, Rudolf Magnus Institute of Neurosciences, University Medical Center, P.O. Box 85060, 3508 AB, Utrecht, Netherlands, a.w.bruijnzeel@med.uu.nl Source: Brain Research, Vol 908(2), Jul 2001. pp. 187-196. Publisher: Netherlands: Elsevier Science. Abstract: Investigated the long-term effects in male rats of a traumatic event on brain corticotropin-releasing hormone immunoreactivity (CRH-ir) and phospho-cyclic adenosine monophosphate response element binding protein-immunoreactivity (P-CREB-ir). Ss underwent foot shocks; 2 wks subsequently, behavior was recorded as Ss received an electrified prod in the home cage. Results show no basal differences in brain CRH-ir and P-CREB-ir levels between Ss receiving only preshocks and control Ss. However, preshocked Ss exposed to the electrified prod exhibited significant increases in CRH-ir in the paraventricular nucleus of the hypothalamus (PNH) and the median eminence and the central amygdala. Prod exposure increased the number of P-CREB-ir neurons in the PNH and the locus ceruleus, but the preshock experience did not affect this response. In another experiment, plasma hormone levels were measured 14 days after the foot shocks. Results show that the preshock experience sensitized shock prod-induced responses concerning adreno-corticotropin hormone and corticosterone. No behavioral differences were observed. It is concluded that long-term stress-induced changes in neuropeptide dynamics of CRH-ir neurons play a role in long-term stress-induced neuroendocrine sensitization. _____
Title: Biology of posttraumatic stress disorder. Author(s): Yehuda, Rachel, Mt Sinai School of Medicine, Psychiatry Dept, Traumatic Stress Studies Program, New York, NY, US Source: Journal of Clinical Psychiatry, Vol 61(Suppl7), 2000. Special Issue: New strategies for the treatment of posttraumatic stress disorder. pp. 14-21. Publisher: US: Physicians Postgraduate Press. Abstract: An understanding of the biological basis of posttraumatic stress disorder (PTSD) requires an examination of the underlying neurobiology of fear and the factors that might contribute to an unsuccessful termination of the fear response in some individuals. Several factors may lead to an inadequate termination of a stress response, and the failure to contain the biological alterations initiated by stress may have long-term adverse consequences. In particular, a prolonged continuation of biological responses following stress may lead to an inappropriate pairing of the traumatic memory with distress and may then initiate a cascade of secondary biological alterations. The roles played by the amygdala, its projection to the lateral hypothalamus and then to the rostral ventral medulla, and the initiation of sympathetic nervous system (and catecholamine) responses are discussed. Projections from the central amygdala to the bed nucleus of the stria terminalis and the initiation of the hypothalamic-pituitary-adrenal axis response are also examined. _____
Title: A variant of the Kleine-Levin syndrome following head trauma. Author(s): Kostic, Vladimir S., Clinical Ctr of Serbia, Inst of Neurology, Belgrade, Yugoslavia; Stefanova, E.; Svetel, M.; Kozic, D. Source: Behavioural Neurology , Vol 11(2), 1998. pp. 105-108. Publisher: Netherlands: IOS Press. Abstract: A 19-yr-old man developed the Kleine-Levin syndrome 3 wks after head trauma and subsequent neurosurgical evacuation of a right-sided, fronto-temporal epidural hematoma. The expression of periodic episodes was observed for hypersomnolence and, to a lesser degree, for behavioral disturbances, while the hyperphagia was constantly present during a period of 1.5 yrs. These clinical features were associated with the focal, right-sided hypothalamic lesion and ipsilateral posttraurnatic parenchymal temporal lobe damage on NMR imaging. _____
Title: Lesion of hypothalamic paraventricular nucleus and maternal aggressive behavior in female rats. Author(s): Consiglio, Angelica R., Federal U of Rio Grande do Sul, Dept of Physiology, Porto Alegre, Brazil; Lucion, Aldo B. Source: Physiology & Behavior, Vol 59(4-5), Apr-May 1996. pp. 591-596. Publisher: US: Elsevier Science. Abstract: 36 lactating female rats were randomly divided among 3 groups that received (1) no surgery, (2) a sham lesion, or (3) bilateral lesions of the hypothalamic paraventricular nucleus (PVN). Maternal aggressive behavior was recorded by introducing a strange male in the territory of the female and her offspring, on the 5th, 7th, and 9th days postpartum. Lesioning was performed on the 5th day postpartum. The results show that the PVN lesion reduced the frequency and duration of attacks on the intruder. In addition, the lesion caused reduced weight gain in the pups compared to pups of the sham lesion group. Findings suggest that the PVN participates in the modulation of maternal aggression in rats. A possible role of oxytocin in that behavior is discussed. _____
Title: Neural circuits and mechanisms of post-traumatic stress disorder. Author(s): Charney, Dennis S., Yale U, School of Medicine, Dept of Psychiatry, New Haven, CT, US; Deutch, Ariel Y.; Southwick, Steven M.; Krystal, John H. Source: Friedman, Matthew J. (Ed); Charney, Dennis S. (Ed); et al; 1995. Neurobiological and clinical consequences of stress: From normal adaptation to post-traumatic stress disorder. Philadelphia, PA, US: Lippincott Williams & Wilkins Publishers. pp. 271-287 Abstract: [discusses] functional neuroanatomy that can account for the spectrum of symptoms associated with posttraumatic stress disorder (PTSD) / preclinical and clinical investigations provide strong evidence for linking several brain structures to the signs and symptoms of anxiety and fear associated with trauma / chief among these are amygdala, locus coeruleus, hippocampus, hypothalamus, thalamus, periaqueductal gray, and orbitofrontal cortex / [review] the neuroanatomy, neurochemistry, and neural mechanisms relevant to the role these brain structures play in anxiety and fear / [discuss] the implications of these findings for a better understanding of the pathophysiology and treatment of PTSD _____
Title: Aphagic and adipsic effects of interleukin-1. Author(s): Chance, William T., U Cincinnati Medical Ctr, Dept of Surgery, OH, US; Fischer, Josef E. Source: Brain Research, Vol 568(1-2), Dec 1991. pp. 261-264. Publisher: Netherlands: Elsevier Science. Abstract: Assessed the feeding and drinking responses of 24 male schedule-fed rats following intrahypothalamic treatment with interleukin-1a (IL-1a) or saline. Intake of rat chow and water was reduced 4 and 8 hrs after the injection of IL-1a. Although core body temperature was also elevated significantly for at least 4 hrs by the administration of this cytokine, resting energy expenditure was not altered. Results suggest that IL-1a may be involved in the reduction of feeding associated with trauma, infection, or cancer by inducing early satiety. Additionally, hyperthermia associated with the injection of IL-1a appears to be maintained by decreased heat dissipation rather than by increased thermogenesis. _____
Title: The behavioural effects of intrahypothalamic multistage versus single injections of 6-hydroxydopamine. Author(s): Willis, Gregory L. , Monash U Prince Henry's Hosp, Dept of Psychological Medicine, Melbourne, Australia; Smith, Graeme C. Source: Brain Research , Vol 245(2), Aug 1982. pp. 345-352. Publisher: Netherlands: Elsevier Science. Abstract: Assessed the effects of 6-hydroxydopamine (6-OHDA) on consummatory and motor behavior in 13 male Sprague-Dawley rats. 16 mug of 6-OHDA were injected bilaterally into the lateral hypothalamus of Ss in either a single injection or in a series of multistage injections over 75 days. While the single injection produced behavioral deficits typical of those observed following catecholamine depletion of the forebrain, the behavior of Ss injected incrementally with the same dose was indistinguishable from that of controls. Fluorescent histochemical assessment revealed that Ss in the multistage injection group, the behaviorally unimpaired, suffered more severe depletion of forebrain catecholamines than those in the single-stage injection group. Accumulation of amines proximal to the site of drug injection was extensive only in Ss displaying behavioral deficits, that is, the group with the lesser amount of forebrain catecholamine depletion. It is suggested that the severity of deficits in consummatory and motor behavior occurring after hypothalamic trauma is determined by a lesion's effectiveness in producing amine accumulation rather than catecholamine depletion. (32 ref) _____
Title: Gastric pathology produced by hypothalamic lesions in rats. Author(s): Lindholm, Ernes, Arizona State U; et al. Source: Physiology & Behavior, Vol 14(2), Feb 1975. pp. 165-169. Publisher: US: Elsevier Science. Abstract: 32 male albino Holtzman rats made aphagic and adipsic by damage to the lateral hypothalamus developed gastric lesions and lost body weight excessively over a 4-day period. Control observations of 20 sham-operated and 32 unoperated Ss indicate that these effects cannot be accounted for by food and water deprivation or by operative trauma. The possibility that gastric lesions may contribute to aphagia or anorexia is discussed. (29 ref) _____
Translated Title: The effect of cholinotropic substances, introduced into the hypothalamus, on the course of traumatic shock. Author(s): Denisenko, P. P. , Leningrad Medical Hygiene Inst., USSR; Dolgushina, A. T. Source: Farmakologiya i Toksikologiya, Vol. 35(6), Nov 1972. pp. 657-660. Publisher: Russia: Folium Publishing Co. Abstract: Studied the effects of benactyzine (10 micrograms); hemicholine (5 micrograms); pediphen (50 micrograms); nivaline (10 micrograms); nicotine (5 and 10 micrograms); arecoline (acetylcholine) (10 micrograms); and sovcain (5 and 10 micrograms), introduced bilaterally into the anterior and posterior hypothalamus of a total of 69 rabbits, during traumatic shock, given 10 min after the introduction of the substances (4 hrs in the case of hemicholine). The shock consisted of an initial 50 blows with a soft cloth, followed after 1 hr by further blows, until the pressure in the main carotid artery dropped to a predetermined level. The change in sensitivity of the Ss under the effects of the drugs was measured according to the change in the number of blows which led to a reduction of the S's blood pressure to the fixed level. Benactyzine and hemicholine raised, while arecoline reduced, the resistance of the Ss to the trauma. Pediphen introduced into the dorsal hypothalamus increased the life span of the Ss. Results suggest that the cholinergic systems of the hypothalamus play a part in the transmission of painful stimuli and that there is a dependence of the duration of traumatic shock on the functional state of the cholinoreactive systems. (English summary) _____
Translated Title: On the role of negative and positive emotional states in cholesterol level and blood pressure changes. Author(s): Yastrebtsova, N. L., Cardiological Research Inst., Moscow, USSR; Simutenko, L. V. Source: Doklady Akademii Nauk SSSR, Vol. 201(4), 1971. pp. 1001-1003. Abstract: In acutely and chronically prepared dogs microelectrodes were lowered into the ventromedial nucleus of the hypothalamus to create negative emotional states and into the lateral hypothalamic region to create positive emotional states. Chronic tests began 1-2 wk. after the operation. The Ss' blood cholesterol and blood pressure levels were measured. The insertion of the electrodes by itself produced a measurable response that lasted 2-3 wk. The response was not that of a postoperational trauma, since it varied as a function of the brain site involved. Blood pressure and cholesterol level increased if the site was related to negative emotional states. These measures decreased if the site was involved in positive emotion. Similar results were obtained with electrical stimulation of these brain sites. In comparison with control experiments in which cholesterol changes did not exceed 3%, stimulation in the emotional brain sites yielded changes in base-line level from 10-50%. It is hypothesized that arteriosclerosis and high blood pressure may be possibly caused by the same mechanism, namely a disorder in the subcortical structures involved in the control of vegetative functions under conditions of stress. _____
Title: The neurosecretory system in white rats during experimental shock. Author(s): Kopaczyk, Franciszek, Medical Academy, Poznan, Poland; Kowalski, Ewaryst; Pawlaczyk, Jerzy Source: Polish Endocrinology , Vol. 21(2), 1970. pp. 131-140. Abstract: Studied the neurosecretory nuclei of the supraoptic part of the hypothalamus and posterior lobe of the hypophysis in the course of experimental shock induced by burns. Ss were 56 sexually mature male white rats. Thermal trauma 1st caused disappearance of neurosecretion from the cells of the supraoptic and paraventricular nuclei, and its accumulation in the neurohypophysis. On the 3rd day of the experiment, degeneration of some of the neurocytes in both nuclei and decreased content of neurosecretion in the posterior lobe of the hypophysis were observed. (27 ref.) _____
Translated Title: On a clinical complex of precocious puberty, acromegaliform macrosomia with obesity and severe retardation through corticohypothalamic encephalopathy of an obstetrical nature in an adolescent girl. Author(s): Schachter, M., Comite de l'Enfance Deficiente, Marseille, France Source: Rivista di Neurobiologia , 14(1), 1968. pp. 3-15. Publisher: Italy: Ospedale Neuropsichiatrico Provenciale. Abstract: Describes a female S who, at age 10.9 yr. had the somatic and sexual development of a 15 yr. old, and at age 15, that of an adult woman. In sharp contrast was the S's oligophrenic and infantile behavior that made her totally dependent on her mother. The diagnosis, based on clinical observations since age 10, was corticohypothalamic pseudoendocrinological syndromes of a significant encephalopathic nature (obstetric trauma and neonatal anoxia). (French & English summaries) _____
Title: A contribution to the etiology, therapy, and prophylaxis of schizophrenia; a psychosomatic study. Author(s): Steinfeld, Julius I., Forest Sanitarium, Des Plaines, Ill. Source: 1953. Oxford, England: Forest Press. 31 pp. Abstract: The malfunctioning of the hypothalamus, produced from vegetative-somatic trauma in infancy, produces the psychotic process. Stimulation of the vegetative-somatic system through a combination of shock therapy and starvation diet enables the patient to relive the original trauma. This type of treatment results in "clinical restoration" and a resetting of the hypothalamic regulatory functions. Eleven case histories are included. 33 references. _____
Title: Non-schizophrenic catatonic states. Author(s): Herman, M.; Harpham, D.; Rosenblum, M. Source: New York State Journal of Medicine , 42, 1942. pp. 624-627. Publisher: US: Medical Society of the State of New York. Abstract: The authors report 12 cases of catatonia, identical with that of schizophrenia, in syphilis of the nervous system epilepsy, head trauma, and toxic psychoses. Cases of catatonia can be grouped into 3 categories: those in which cortical damage predominates; those in which psychologic factors predominate; those with marked hypothalamic symptoms. Theoretically and by experimental results catatonia is apparently a neurologic phenomenon, the mechanism of which resides in the posterior part of the hypothalamus. The neocortex controls this mechanism through the factors of organic brain disease and psychological influences. The relative importance of psychological factors in schizophrenic catatonia is still undetermined. Cerebral control may also be disturbed by hypothalamic lesions which cut off the lower centers from cortical influences. The clouded sensorium found in organic brain disease differentiates the catatonia of these cases from that of schizophrenia. _____ Hypothalamus and Trauma
Title: The relationship between circadian rhythmicity and vasoactive intestinal polypeptide in the suprachiasmatic nucleus of congenitally anophthalmic mice. Author(s): Laemle, Lois K., UMDNJ New Jersey Medical School, Dept of Anatomy, Cell Biology & Injury Sciences, Newark, NJ, US; Ottenweller, John E. Address: Laemle, Lois K., UMDNJ New Jersey Medical School, Dept of Anatomy, Cell Biology & Injury Sciences, 185 South Orange Avenue, Newark, NJ, US, 07103, laemlelb@umdnj.edu Source: Brain Research, Vol 917(1), Oct 2001. pp. 105-111. Publisher: Netherlands: Elsevier Science. Abstract: To date, the search for the clock component that is both necessary and sufficient for generation of circadian rhythms has relied primarily on experimental interventions such as lesions and transplantation of fetal suprachiasmatic nuclei (SCN). While these approaches have been fruitful, lesions disrupt adjacent host tissue and fiber pathways, and donor tissue is likewise subject to trauma during harvest and transplantation. The current investigation has used congenitally anophthalmic (eyeless) mice to ask whether vasoactive intestinal polypeptide immunoreactive (VIP)-IR SCN neurons are necessary and sufficient for generation of circadian rhythms. In this animal model, arrhythmic mice occur naturally, together with their rhythmic littermates. The researchers have combined recording of wheel-running activity with light microscopic immunocytochemistry for VIP and cytoarchitectural analysis of the SCN in rhythmic vs arrhythmic anophthalmic mice. These data provide the first definitive evidence that the presence of VIP neurons in the SCN is not sufficient for generation of circadian locomotor rhythms. _____
Title: Stress-induced sensitization of CRH-ir but not P-CREB-ir responsivity in the rat central nervous system. Author(s): Bruijnzeel, Adrie W., U Medical Ctr, Div of Pharmacology & Anatomy, Rudolf Magnus Inst of Neurosciences, Utrecht, Netherlands; Stam, Rianne; Compaan, Josje C.; Wiegant, Victor M. Address: Bruijnzeel, Adrie W., Division of Pharmacology and Anatomy, Rudolf Magnus Institute of Neurosciences, University Medical Center, P.O. Box 85060, 3508 AB, Utrecht, Netherlands, a.w.bruijnzeel@med.uu.nl Source: Brain Research, Vol 908(2), Jul 2001. pp. 187-196. Publisher: Netherlands: Elsevier Science. Abstract: Investigated the long-term effects in male rats of a traumatic event on brain corticotropin-releasing hormone immunoreactivity (CRH-ir) and phospho-cyclic adenosine monophosphate response element binding protein-immunoreactivity (P-CREB-ir). Ss underwent foot shocks; 2 wks subsequently, behavior was recorded as Ss received an electrified prod in the home cage. Results show no basal differences in brain CRH-ir and P-CREB-ir levels between Ss receiving only preshocks and control Ss. However, preshocked Ss exposed to the electrified prod exhibited significant increases in CRH-ir in the paraventricular nucleus of the hypothalamus (PNH) and the median eminence and the central amygdala. Prod exposure increased the number of P-CREB-ir neurons in the PNH and the locus ceruleus, but the preshock experience did not affect this response. In another experiment, plasma hormone levels were measured 14 days after the foot shocks. Results show that the preshock experience sensitized shock prod-induced responses concerning adreno-corticotropin hormone and corticosterone. No behavioral differences were observed. It is concluded that long-term stress-induced changes in neuropeptide dynamics of CRH-ir neurons play a role in long-term stress-induced neuroendocrine sensitization. _____
Title: Biology of posttraumatic stress disorder. Author(s): Yehuda, Rachel, Mt Sinai School of Medicine, Psychiatry Dept, Traumatic Stress Studies Program, New York, NY, US Source: Journal of Clinical Psychiatry, Vol 61(Suppl7), 2000. Special Issue: New strategies for the treatment of posttraumatic stress disorder. pp. 14-21. Publisher: US: Physicians Postgraduate Press. Abstract: An understanding of the biological basis of posttraumatic stress disorder (PTSD) requires an examination of the underlying neurobiology of fear and the factors that might contribute to an unsuccessful termination of the fear response in some individuals. Several factors may lead to an inadequate termination of a stress response, and the failure to contain the biological alterations initiated by stress may have long-term adverse consequences. In particular, a prolonged continuation of biological responses following stress may lead to an inappropriate pairing of the traumatic memory with distress and may then initiate a cascade of secondary biological alterations. The roles played by the amygdala, its projection to the lateral hypothalamus and then to the rostral ventral medulla, and the initiation of sympathetic nervous system (and catecholamine) responses are discussed. Projections from the central amygdala to the bed nucleus of the stria terminalis and the initiation of the hypothalamic-pituitary-adrenal axis response are also examined. _____
Title: A variant of the Kleine-Levin syndrome following head trauma. Author(s): Kostic, Vladimir S., Clinical Ctr of Serbia, Inst of Neurology, Belgrade, Yugoslavia; Stefanova, E.; Svetel, M.; Kozic, D. Source: Behavioural Neurology , Vol 11(2), 1998. pp. 105-108. Publisher: Netherlands: IOS Press. Abstract: A 19-yr-old man developed the Kleine-Levin syndrome 3 wks after head trauma and subsequent neurosurgical evacuation of a right-sided, fronto-temporal epidural hematoma. The expression of periodic episodes was observed for hypersomnolence and, to a lesser degree, for behavioral disturbances, while the hyperphagia was constantly present during a period of 1.5 yrs. These clinical features were associated with the focal, right-sided hypothalamic lesion and ipsilateral posttraurnatic parenchymal temporal lobe damage on NMR imaging. _____
Title: Lesion of hypothalamic paraventricular nucleus and maternal aggressive behavior in female rats. Author(s): Consiglio, Angelica R., Federal U of Rio Grande do Sul, Dept of Physiology, Porto Alegre, Brazil; Lucion, Aldo B. Source: Physiology & Behavior, Vol 59(4-5), Apr-May 1996. pp. 591-596. Publisher: US: Elsevier Science. Abstract: 36 lactating female rats were randomly divided among 3 groups that received (1) no surgery, (2) a sham lesion, or (3) bilateral lesions of the hypothalamic paraventricular nucleus (PVN). Maternal aggressive behavior was recorded by introducing a strange male in the territory of the female and her offspring, on the 5th, 7th, and 9th days postpartum. Lesioning was performed on the 5th day postpartum. The results show that the PVN lesion reduced the frequency and duration of attacks on the intruder. In addition, the lesion caused reduced weight gain in the pups compared to pups of the sham lesion group. Findings suggest that the PVN participates in the modulation of maternal aggression in rats. A possible role of oxytocin in that behavior is discussed. _____
Title: Neural circuits and mechanisms of post-traumatic stress disorder. Author(s): Charney, Dennis S., Yale U, School of Medicine, Dept of Psychiatry, New Haven, CT, US; Deutch, Ariel Y.; Southwick, Steven M.; Krystal, John H. Source: Friedman, Matthew J. (Ed); Charney, Dennis S. (Ed); et al; 1995. Neurobiological and clinical consequences of stress: From normal adaptation to post-traumatic stress disorder. Philadelphia, PA, US: Lippincott Williams & Wilkins Publishers. pp. 271-287 Abstract: [discusses] functional neuroanatomy that can account for the spectrum of symptoms associated with posttraumatic stress disorder (PTSD) / preclinical and clinical investigations provide strong evidence for linking several brain structures to the signs and symptoms of anxiety and fear associated with trauma / chief among these are amygdala, locus coeruleus, hippocampus, hypothalamus, thalamus, periaqueductal gray, and orbitofrontal cortex / [review] the neuroanatomy, neurochemistry, and neural mechanisms relevant to the role these brain structures play in anxiety and fear / [discuss] the implications of these findings for a better understanding of the pathophysiology and treatment of PTSD _____
Title: Aphagic and adipsic effects of interleukin-1. Author(s): Chance, William T., U Cincinnati Medical Ctr, Dept of Surgery, OH, US; Fischer, Josef E. Source: Brain Research, Vol 568(1-2), Dec 1991. pp. 261-264. Publisher: Netherlands: Elsevier Science. Abstract: Assessed the feeding and drinking responses of 24 male schedule-fed rats following intrahypothalamic treatment with interleukin-1a (IL-1a) or saline. Intake of rat chow and water was reduced 4 and 8 hrs after the injection of IL-1a. Although core body temperature was also elevated significantly for at least 4 hrs by the administration of this cytokine, resting energy expenditure was not altered. Results suggest that IL-1a may be involved in the reduction of feeding associated with trauma, infection, or cancer by inducing early satiety. Additionally, hyperthermia associated with the injection of IL-1a appears to be maintained by decreased heat dissipation rather than by increased thermogenesis. _____
Title: The behavioural effects of intrahypothalamic multistage versus single injections of 6-hydroxydopamine. Author(s): Willis, Gregory L. , Monash U Prince Henry's Hosp, Dept of Psychological Medicine, Melbourne, Australia; Smith, Graeme C. Source: Brain Research , Vol 245(2), Aug 1982. pp. 345-352. Publisher: Netherlands: Elsevier Science. Abstract: Assessed the effects of 6-hydroxydopamine (6-OHDA) on consummatory and motor behavior in 13 male Sprague-Dawley rats. 16 mug of 6-OHDA were injected bilaterally into the lateral hypothalamus of Ss in either a single injection or in a series of multistage injections over 75 days. While the single injection produced behavioral deficits typical of those observed following catecholamine depletion of the forebrain, the behavior of Ss injected incrementally with the same dose was indistinguishable from that of controls. Fluorescent histochemical assessment revealed that Ss in the multistage injection group, the behaviorally unimpaired, suffered more severe depletion of forebrain catecholamines than those in the single-stage injection group. Accumulation of amines proximal to the site of drug injection was extensive only in Ss displaying behavioral deficits, that is, the group with the lesser amount of forebrain catecholamine depletion. It is suggested that the severity of deficits in consummatory and motor behavior occurring after hypothalamic trauma is determined by a lesion's effectiveness in producing amine accumulation rather than catecholamine depletion. (32 ref) _____
Title: Gastric pathology produced by hypothalamic lesions in rats. Author(s): Lindholm, Ernes, Arizona State U; et al. Source: Physiology & Behavior, Vol 14(2), Feb 1975. pp. 165-169. Publisher: US: Elsevier Science. Abstract: 32 male albino Holtzman rats made aphagic and adipsic by damage to the lateral hypothalamus developed gastric lesions and lost body weight excessively over a 4-day period. Control observations of 20 sham-operated and 32 unoperated Ss indicate that these effects cannot be accounted for by food and water deprivation or by operative trauma. The possibility that gastric lesions may contribute to aphagia or anorexia is discussed. (29 ref) _____
Translated Title: The effect of cholinotropic substances, introduced into the hypothalamus, on the course of traumatic shock. Author(s): Denisenko, P. P. , Leningrad Medical Hygiene Inst., USSR; Dolgushina, A. T. Source: Farmakologiya i Toksikologiya, Vol. 35(6), Nov 1972. pp. 657-660. Publisher: Russia: Folium Publishing Co. Abstract: Studied the effects of benactyzine (10 micrograms); hemicholine (5 micrograms); pediphen (50 micrograms); nivaline (10 micrograms); nicotine (5 and 10 micrograms); arecoline (acetylcholine) (10 micrograms); and sovcain (5 and 10 micrograms), introduced bilaterally into the anterior and posterior hypothalamus of a total of 69 rabbits, during traumatic shock, given 10 min after the introduction of the substances (4 hrs in the case of hemicholine). The shock consisted of an initial 50 blows with a soft cloth, followed after 1 hr by further blows, until the pressure in the main carotid artery dropped to a predetermined level. The change in sensitivity of the Ss under the effects of the drugs was measured according to the change in the number of blows which led to a reduction of the S's blood pressure to the fixed level. Benactyzine and hemicholine raised, while arecoline reduced, the resistance of the Ss to the trauma. Pediphen introduced into the dorsal hypothalamus increased the life span of the Ss. Results suggest that the cholinergic systems of the hypothalamus play a part in the transmission of painful stimuli and that there is a dependence of the duration of traumatic shock on the functional state of the cholinoreactive systems. (English summary) _____
Translated Title: On the role of negative and positive emotional states in cholesterol level and blood pressure changes. Author(s): Yastrebtsova, N. L., Cardiological Research Inst., Moscow, USSR; Simutenko, L. V. Source: Doklady Akademii Nauk SSSR, Vol. 201(4), 1971. pp. 1001-1003. Abstract: In acutely and chronically prepared dogs microelectrodes were lowered into the ventromedial nucleus of the hypothalamus to create negative emotional states and into the lateral hypothalamic region to create positive emotional states. Chronic tests began 1-2 wk. after the operation. The Ss' blood cholesterol and blood pressure levels were measured. The insertion of the electrodes by itself produced a measurable response that lasted 2-3 wk. The response was not that of a postoperational trauma, since it varied as a function of the brain site involved. Blood pressure and cholesterol level increased if the site was related to negative emotional states. These measures decreased if the site was involved in positive emotion. Similar results were obtained with electrical stimulation of these brain sites. In comparison with control experiments in which cholesterol changes did not exceed 3%, stimulation in the emotional brain sites yielded changes in base-line level from 10-50%. It is hypothesized that arteriosclerosis and high blood pressure may be possibly caused by the same mechanism, namely a disorder in the subcortical structures involved in the control of vegetative functions under conditions of stress. _____
Title: The neurosecretory system in white rats during experimental shock. Author(s): Kopaczyk, Franciszek, Medical Academy, Poznan, Poland; Kowalski, Ewaryst; Pawlaczyk, Jerzy Source: Polish Endocrinology , Vol. 21(2), 1970. pp. 131-140. Abstract: Studied the neurosecretory nuclei of the supraoptic part of the hypothalamus and posterior lobe of the hypophysis in the course of experimental shock induced by burns. Ss were 56 sexually mature male white rats. Thermal trauma 1st caused disappearance of neurosecretion from the cells of the supraoptic and paraventricular nuclei, and its accumulation in the neurohypophysis. On the 3rd day of the experiment, degeneration of some of the neurocytes in both nuclei and decreased content of neurosecretion in the posterior lobe of the hypophysis were observed. (27 ref.) _____
Translated Title: On a clinical complex of precocious puberty, acromegaliform macrosomia with obesity and severe retardation through corticohypothalamic encephalopathy of an obstetrical nature in an adolescent girl. Author(s): Schachter, M., Comite de l'Enfance Deficiente, Marseille, France Source: Rivista di Neurobiologia , 14(1), 1968. pp. 3-15. Publisher: Italy: Ospedale Neuropsichiatrico Provenciale. Abstract: Describes a female S who, at age 10.9 yr. had the somatic and sexual development of a 15 yr. old, and at age 15, that of an adult woman. In sharp contrast was the S's oligophrenic and infantile behavior that made her totally dependent on her mother. The diagnosis, based on clinical observations since age 10, was corticohypothalamic pseudoendocrinological syndromes of a significant encephalopathic nature (obstetric trauma and neonatal anoxia). (French & English summaries) _____
Title: A contribution to the etiology, therapy, and prophylaxis of schizophrenia; a psychosomatic study. Author(s): Steinfeld, Julius I., Forest Sanitarium, Des Plaines, Ill. Source: 1953. Oxford, England: Forest Press. 31 pp. Abstract: The malfunctioning of the hypothalamus, produced from vegetative-somatic trauma in infancy, produces the psychotic process. Stimulation of the vegetative-somatic system through a combination of shock therapy and starvation diet enables the patient to relive the original trauma. This type of treatment results in "clinical restoration" and a resetting of the hypothalamic regulatory functions. Eleven case histories are included. 33 references. _____
Title: Non-schizophrenic catatonic states. Author(s): Herman, M.; Harpham, D.; Rosenblum, M. Source: New York State Journal of Medicine , 42, 1942. pp. 624-627. Publisher: US: Medical Society of the State of New York. Abstract: The authors report 12 cases of catatonia, identical with that of schizophrenia, in syphilis of the nervous system epilepsy, head trauma, and toxic psychoses. Cases of catatonia can be grouped into 3 categories: those in which cortical damage predominates; those in which psychologic factors predominate; those with marked hypothalamic symptoms. Theoretically and by experimental results catatonia is apparently a neurologic phenomenon, the mechanism of which resides in the posterior part of the hypothalamus. The neocortex controls this mechanism through the factors of organic brain disease and psychological influences. The relative importance of psychological factors in schizophrenic catatonia is still undetermined. Cerebral control may also be disturbed by hypothalamic lesions which cut off the lower centers from cortical influences. The clouded sensorium found in organic brain disease differentiates the catatonia of these cases from that of schizophrenia.
|
