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Bipolar Disorder and PTSD
Affect Regulation-Self Esteem-Expecting Best-Preparing for Worst
Bipolar Disorder and Trauma
Bipolar Disorder DSM-IV
Bipolar I Disorder
Bipolar II Disorder
Cingulate Gyrus and Trauma
Circadiam Rhythm and PTSD
Circadian Rhythm and REM Behavior Disorder
Circadian Rhythm and Sleepwalking
Circadian Rhythm and Trauma
Circadian Rhythm DSM-IV
Corpus Callosum and PTSD
Cortisol and Dissociation
Cortisol and Trauma
Dissociation and Affect Dysregulation
Fornix and Trauma
Hippocampus Trauma and PTSD
Hypothalamus and PTSD
Limbic System and Trauma
MRI and Trauma
Neocortex and Trauma
NeuroImaging and DID
NeuroImaging and Trauma
NMRI and PTSD
Prefrontal Lobe and Trauma
ADHD and PTSD
ADHD and EMDR
ADHD and Dissociation
ADHD and DID
ADHD and Trauma
Affect Regulation
Attachment and Relational Trauma II
Affect Development and Attachment
Affect Regulation: Mentalization and the Development of the Self
Attachment and Affect Development
AffectDysregulation and Dissociation
Affect Dysregulation and Disorders of the Self
Affect Regulation and Attachment
Affect Dysregulation and Disorders of the Self
Affect Regulation and Attachment I
Affect Regulation and Attachment II
Affect Dysregulation
Affect Regulation and PTSD
Affect Regulation and Binge Drinking
Affect Regulation in Married Styles
Affect Regulation and Trauma
Affect Regulation-Delayed memories of Childhood
Affect Regulation-Mentalization and Development of The Self
Affect Regulaqtion-Recurrent Abortiona in Bulimics
Affect Regulation-Social Context on Childrens Affect Regulation
Affect Regulation-the Development of Psychopathology
Amygdala and Fear
Amygdala and PTSD
Aspergers Disorder and Adolescence
Aspergers Disorder and Childhood
Aspergers Disorder and Development
Aspergers Disorder and Infancy
Aspergers Disorder DSM-IV
Basal Ganglia and PTSD
Basal Ganglia and Trauma
Bipolar Disorder and DID
Sleepwalking and Trauma
Sleepwalking and PTSD
Sleep Disorders and PTSD
Sleep Disorders and Trauma
Sleep Disorders DSM-IV-R
Circadian Rhythm DSMIV-R
Sleep Terror Disorder
Self-Mutilization and Trauma
Self-Mutilization and Resilience
Self-Mutilization and PTSD
Self-Mutilization and DID
Human Stress Continuum

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


side active view


underside surface view


underside active view

Functions

  • sets the emotional tone of the mind

  • filters external events through internal states (emotional coloring)

  • tags events as internally important

  • stores highly charged emotional memories

  • modulates motivation

  • controls appetite and sleep cycles

  • promotes bonding

  • directly processes the sense of smell

  • modulates libido

Problems

  • moodiness, irritability, clinical depression

  • increased negative thinking

  • perceive events in a negative way

  • decreased motivation

  • flood of negative emotions

  • appetite and sleep problems

  • decreased or increased sexual responsiveness

  • social isolation

The Basal Ganglia System


left side active view


underside active view

Functions

  • integrates feeling and movement

  • shifts and smoothes fine motor behavior

  • suppression of unwanted motor behaviors

  • sets the body's idle or anxiety level

  • enhances motivation

  • pleasure/ecstasy

Problems

  • anxiety, nervousness

  • panic attacks

  • physical sensations of anxiety

  • tendency to predict the worst

  • conflict avoidance

  • Gilles de la Tourette's Syndrome/tics

  • muscle tension, soreness

  • tremors

  • fine motor problems

  • headaches

  • low or excessive motivation

The Prefrontal Cortex


dorsal lateral prefrontal cortex
outside view


inferior orbital prefrontal cortex
outside view


side surface view
dorsal lateral prefrontal area


inferior orbital prefrontal area
inside view


underside surface view
inferior orbital prefrontal area


top-down surface view
dorsal lateral prefrontal area

Functions

  • attention span

  • perseverance

  • judgment

  • impulse control

  • organization

  • self-monitoring and supervision

  • problem solving

  • critical thinking

  • forward thinking

  • learning from experience

  • ability to feel and express emotions

  • influences the limbic system

  • empathy

Problems

  • short attention span

  • distractibility

  • lack of perseverance

  • impulse control problems

  • hyperactivity

  • chronic lateness, poor time management

  • disorganization

  • procrastination

  • unavailability of emotions

  • misperceptions

  • poor judgement

  • trouble learning from experience

  • short term memory problems

  • social and test anxiety

The Cingulate Gyrus


inside side view


side active view


active top-down view


active front-on view

  • allows shifting of attention

  • cognitive flexibility

  • adaptability

  • helps the mind move from idea to idea

  • gives the ability to see options

  • helps you go with the flow

  • cooperation

Problems

  • worrying

  • holds onto hurts from the past

  • stuck on thoughts (obsessions)

  • stuck on behaviors (compulsions)

  • oppositional behavior, argumentative

  • uncooperative, tendency to say no

  • addictive behaviors (alcohol or drug abuse, eating disorders, chronic pain)

  • cognitive inflexibility

  • obsessive compulsive disorder

  • OCD spectrum disorders

  • eating disorders, road rage

The Temporal Lobes


side view


side surface view


underside surface view


active side view

Functions

Dominant Side (usually the left)

  • understanding and processing language

  • intermediate term memory

  • long term memory

  • auditory learning

  • retrieval of words

  • complex memories

  • visual and auditory processing

  • emotional stability

Problems

Dominant Temporal Lobe

  • aggression, internally or externally driven

  • dark or violent thoughts

  • sensitivity to slights, mild paranoia

  • word finding problems

  • auditory processing problems

  • reading difficulties

  • emotional instability

Non-dominant Side (usually the right)

  • recognizing facial expression

  • decoding vocal intonation

  • rhythm

  • music

  • visual learning

  • difficulty recognizing facial expression

  • difficulty decoding vocal intonation

  • implicated in social skill struggles


Either/Both Temporal Lobe Problems

  • memory problems, amnesia

  • headaches or abdominal pain without a clear explanation

  • anxiety or fear for no particular reason

  • abnormal sensory perceptions, visual or auditory distortions

  • feelings of déjà vu or jamais vu

  • periods of spaciness or confusion

  • religious or moral preoccupation

  • hypergraphia, excessive writing

  • seizures

 

 

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

 1Shapiro, F. (2001). Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols and Procedures (2nd ed.). New York: Guilford Press.

2Shapiro, F. (2002). EMDR as an Integrative Psychotherapy Approach: Experts of Diverse Orientations Explore the Paradigm Prism. Washington, DC: American Psychological Association Books.

 

 

 

 

NeuroBiology of Trauma

 

Basal Ganglia and Trauma

Title: Interactions between aging and cortical cholinergic deafferentation on attention.
Author(s)/Editor(s): Burk, Joshua A.; Herzog, Christopher D.;
Porter, M. Christine; Sarter, Martin
Author Affiliation: Ohio State U, Dept of Psychology, Columbus, OH, US Ohio State U, Dept of Psychology, Columbus, OH, US Ohio State U, Dept of Psychology, Columbus, OH, US
Source/Citation: Neurobiology of Aging; Vol 23(3) May-Jun 2002, US: Elsevier Science; 2002, 467-477
Abstract/Review/Citation: Pre-existing trauma to basal forebrain corticopetal cholinergic neurons has been hypothesized to render this system vulnerable to age-related processes. The present longitudinal study assessed the
interactions between the effects of partial cortical cholinergic
deafferentation and aging on sustained attention performance. After pre-surgical training, male rats were given sham-surgery or bilateral infusions of the immunotoxin 192 IgG-saporin into the basal forebrain. The lesion was intended to yield a limited loss of cortical cholinergic inputs and thus to produce minor immediate effects on sustained attention performance.  All animals were tested continuously until age 36 mo. The attentional performance of lesioned and sham-lesioned animals did not dissociate until age 31 mo, when the lesioned animals exhibited an impairment in overall sustained attention performance. Importantly, this impairment interacted with the effects of time-on-task, and thus reflected a specific impairment in attentional processes. These results support the notion that pre-existing damage to the basal forebrain corticopetal cholinergic neurons yields age-related impairments in the attentional capabilities that depend on the integrity of this neuronal system.
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Title: Attention deficit disorder: A neuropsychoanalytic sketch.
Author(s)/Editor(s): Levin, Fred M.
Source/Citation: Psychoanalytic Inquiry: Special Issue: Self-regulation: Issues of attention and attachment.; Vol 22(3) 2002, US: Analytic Press; 2002, 336-354
Abstract/Review/Citation: Presents a neuropsychoanalytic sketch of attention deficit disorder (ADD). ADD is defined in terms of its core symptoms, then discussed from the perspective of etiology, pathenogenesis, diagnosis, differential diagnosis, and treatment. The author also attempts to describe
the patient's inner experiences and begin to map these onto the external perspective of what is happening psychologically and neurologically inside the patient's brain. A number of speculations are created regarding the role of the executive control network (ECN), particularly that of the basal ganglia,
cerebellum, anterior cingulate, and those parts of the ECN that are responsible for such things as cognitive shifting between low-level routine information processing modes and those used for high-level processing applicable for sensitive or complex analysis. The effects of trauma on the tagging of memories are also considered. Research by several other authors that integrates the mind and brain is discussed with reference to cognitive and personality disordering in ADD.
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Title: Unilateral lesions of the globus pallidus: Report of four patients presenting with focal or segmental dystonia.
Author(s)/Editor(s): Muenchau, A.; Mathen, D.; Cox, T.;
Quinn, N. P.; Marsden, C. D.; Bhatia, K. P.
Source/Citation: Journal of Neurology, Neurosurgery & Psychiatry; Vol 69(4) Oct 2000, England: BMJ Publishing Group; 2000, 494-498
Abstract/Review/Citation: Examined clinical features in 4 cases of patients with unilateral lesions of the globus pallidus (GP), on the basis of physiology of the basal ganglia. Three patients presented with contralateral dystonia largely confined to 1 arm (1 case) and 1 leg (2 cases). One patient had
predominant contralateral hemiparkinsonism manifested mainly as micrographia and mild dystonia in 1 arm. The cause of the lesions was unknown in 2 patients. In the other 2 cases, symptoms had developed after head trauma and after anoxia. All lesions involved the internal segment of the GP. Two
patients, including the patient with hemiparkinsonism, had additional involvement of the external segment of the GP. In literature reports on 26 patients with bilateral lesions restricted to the GP, only 2 with unilateral lesions were found. The patients with bilateral pallidal lesions manifested with dystonia, parkinsonism, or abulia. One patient with unilateral GP lesions
had contralateral hemidystonia, the other contralateral arm tremor. It is concluded that these cases emphasize the importance of the GP, particularly its internal segment, in the pathophysiology of dystonia.
========================================

Title: Advancing from the ventral striatum to the extended amygdala:  Implications for neuropsychiatry and drug use:  In honor of Lennart Heimer.
Author(s)/Editor(s): McGinty, Jacqueline F.
Source/Citation: New York, NY, US: New York Academy of Sciences; 1999, (xv, 835) Annals of the New York Academy of Sciences, Vol. 877.
Abstract/Review/Citation: This conference on the ventral striatum and the extended amygdala brought together basic and clinical investigators to explore the relationships among the anatomy, neurochemistry, and function of the basal forebrain systems implicated in neuropsychiatric and addictive disorders.
Notes/Comments:  Introduction by Jacqueline F. McGinty The concept of the ventral striatopallidal system and extended amygdala Jose S. de Olmos and Lennart Heimer                 Part I. Functional organization of the ventral striatopallidal system The concept of the ventral striatum in nonhuman primates Suzanne N. Haber and Nikolaus R. McFarland
Convergence and segregation of ventral striatal inputs and outputs Henk J. Gorenewegen, Christopher I. Wright, Arno V. J. Beijer and Pieter Voorn Involvement of the pallidal-thalamocortical circuit in adaptive behavior Peter W. Kalivas, Lynn Churchill and Anastasia Romanides Functional specificity of ventral striatal compartments in appetitive behaviors Ann E. Kelley Mesolimbic neuronal activity across behavioral states Donald J. Woodward, Jing-Yu Chang, Patricia Janak, Alexy Azarov and Kristin Anstrom                                              Part II. Modulation of ventral striatopallidal compartments Functional-anatomical implications of the nucleus accumbens core and shell subterritories Daniel S. Zahm Regulation of neurotransmitter interactions in the ventral striatum Jacqueline F. McGinty The synaptic framework for chemical signaling in nucleus accumbens G. E. Meridith Modulation of cell firing in the nucleus accumbens Patricio
O'Donnell, Jennifer Greene, Nina Pabello, Barbara L. Lewis and Anthony A. Grace Opioid modulation of ventral pallidal inputs T. Celeste Napier and Igor Mitrovic Cross-species studies of sensorimotor gating of the startle reflex Neal R. Swederdlow, David L. Braff and Mark A. Geyer                                      Part III. Organization and functions of the extended amygdala The intrinsic organization of the central extended amygdala Martin D. Cassell, Lorin J. Freedman and Changjun Shi The medial extended amygdala in male reproductive behavior: A node in the mammalian social behavior network Sarah Winans Newman The extended amygdala and salt appetite Alan Kim Johnson, Jose de Olmos, Cinthia V. Pastuskovas, Andrea ZM. Zardett-Smith and Laura Vivas The extended amygdala: Are the central nucleus of the amygdala and the bed nucleus of the stria terminalis differentially involved in fear versus anxiety? Michael David and Changjun Shi Brain and sexual behavior Knut Larsson and Sven Ahlenius                                             Part IV: Interactions of the extended amygdala with other brain regions Cortical afferents to the extended amygdala Alexander J. McDonald, Sara J. Shammah-Lagnado, Changjun Shi and Michael Davis The basal forebrain corticopetal system revisited L. Zaborszky, K. Pang, J. Somogyi, Z. Nadasky and I. Kallo Basal forebrain afferent projections modulating  cortical acetylcholine, attention, and implications for neuropsychiatric disorders Martin Sarter, John P. Bruno and Janita Turchi Prefrontal cortical networks related to visceral function and mood Joseph L. Price Functions of the amygdala and related forebrain areas in attention and cognition Michela Gallagher and Geoffrey Schoenbaum Associative processes in addiction and reward: The role of amygdala-ventral striatal subsystems Barry J. Everitt, John A. Parkinson, Mary C. Olmstead, Mercedes
Arroyo, Patricia Robledo and Trevor W. Robbins Functional and anatomical relationships among the amygdala, basal forebrain, ventral striatum, and cortex: An integrative discussion Thackery S. Gray Part V. Implications for drug abuse The role of the striatopallidal and extended amygdala systems in
drug addiction George F. Koob Drug addiction as a disorder of associative learning: Role of nucleus accumbens shell/extended amygdala dopamine G. di Chiara, G. Tanda, V. Bassareo, F. Pontieri, E. Acquas, S. Fenu, C. Cadoni and E. Carboni The bed nucleus of the stria terminalis: A target site for noradrenergic actions in opiate withdrawal Gary Ashton-Jones, Jill M. Delfs, Jonathan Druhan and Yan Zhu The role of dopamine, dynorphin, and CART systems in the ventral striatum and amygdala in cocaine abuse Yasmin L. Hurd, Pernilla Svensson and Marjan Ponten D-sub-3 dopamine and kappa opioid receptor
alterations in human brain of cocaine-overdose victims Deborah C. Mash and Julie K. Staley Functional magnetic resonance imaging of brain reward circuitry in the human Hans C. Breiter and Bruce R. Rosen                                                      Part VI. Implications for neuropsychiatry Epilepsy, schizophrenia, and the extended amygdala Janice R. Stevens Mesolimbic activity associated with psychosis in schizophrenia: Symptom-specific PET studies Jane Epstein, Emily Stern and
David Silversweig Ventromedial temporal lobe pathology in dementia, brain trauma, and schizophrenia Gary W. Van Hoesen, Jean C. Augustinack and Sarah J. Redman D-sub-3 receptors and the actions of neuroleptics in the ventral
striatopallidal systems of schizophrenics Jeffrey N. Joyce and Eugenia V. Gurevich Prefrontal cortical-amygdalar metabolism in major depression Wayne C. Drevets On some clinical implications of the ventral striatum and the extended amygdala: Investigations of aggression Michael R. Trimble and Ludger Tebartz Van Elst                                                    VII. Poster papers Index of contributors neuroanatomy &
neurochemistry & function of basal forebrain & ventral striatum & extended amygdala & relation to neuropsychiatric & addictive disorders Conference Proceedings/Symposia
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Title: Parkinson's syndrome after closed head injury: A single case report.
Author(s)/Editor(s): Doder, M.; Jahanshahi, M.; Turjanski, N.; Moseley, I. F.; Lees, A. J.
Source/Citation: Journal of Neurology, Neurosurgery & Psychiatry; Vol 66(3) Mar 1999, England: BMJ Publishing Group; 1999, 380-385
Abstract/Review/Citation: A 36 year old man, who sustained a skull fracture in 1984, was unconscious for 24 hours, and developed signs of Parkinson's syndrome 6 weeks after the injury. When assessed in 1995, neuroimaging
disclosed a cerebral infarction due to trauma involving the left caudate and lenticular nucleus. Parkinson's syndrome was predominantly right sided, slowly progressive, and unresponsive to levodopa therapy. Reaction time tests showed slowness of movement initiation and execution with both hands, particularly
the right. Recording of movement related cortical potentials suggested bilateral deficits in movement preparation. Neuropsychological assessment disclosed no evidence of major deficits on tests assessing executive function or working memory, with the exception of selective impairments on the Stroop and on a test of self ordered random number sequences. There was evidence of abulia. The results are discussed in relation to previous literature on basal ganglia lesions and the effects of damage to different points of the
frontostriatal circuits.
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Title: Posttraumatic obsessive-compulsive disorder: A three-factor model.
Author(s)/Editor(s): Dinn, Wayne M.; Harris, Catherine L.;
Raynard, Richard C.
Source/Citation: Psychiatry: Interpersonal & Biological Processes: Special Issue: Trauma: Memory, avoidance, and biopsychosocial regulators.; Vol 62(4) Win 1999, US: Guilford Publications; 1999, 313-324
Abstract/Review/Citation: Presented a 3-factor causal model of obsessive-compulsive disorder (OCD), which posits that exposure to long-term traumatic stress generates an inordinate degree of anxiety during the psychological development of the premorbid OCD child. In response to these
conditions the child evolves a distinct cognitive style characterized by exaggerated threat appraisal and magical beliefs, and experiences alterations in brain metabolism. An entire functional brain system (a basal ganglia-orbitofrontal circuit) enters into a state of enhanced responsiveness
following exposure to protracted threat. Over time the threshold for stimulation is dramatically lowered, resulting in a hypersensitivity to cues that signify potential harm. Individuals adapt to this hypersensitivity through a variety of strategies, which constitute OCD. It is concluded that the biological abnormalities associated with OCD represent a dynamic
biopsychosocial process in which repeated trauma renders a discrete neural circuit unusually responsive to threat-related stimuli.
========================================

Title: Secondary tic disorders.
Author(s)/Editor(s): Kumar, Rajeeve; Lang, Anthony E.
Source/Citation: Neurologic Clinics; Vol 15(2) May 1997, US: W.B. Saunders & Co.; 1997, 309-331
Abstract/Review/Citation: Reviews the literature on the putative relationship between a variety of neurologic and neuropsychotic disorders, which have been reported in association with tics. These disorders include head and peripheral trauma, encephalitis, rheumatic fever, stroke, metabolic and toxic encephalopathies, inherited neurodegenerative diseases, dystonia, chromosomal disorders, inborn errors of metabolism, mental retardation, neuropsychiatric disorders, and psychogenic disorders. Tics also may be increased or exacerbated by drugs affecting a variety of neurotransmitter systems. Recognition and study of these secondary tic disorders may further the understanding of basal ganglia physiology and the pathogenesis of Tourette
syndrome.
========================================

Title: Neuropsychiatry, neuropsychology, and clinical neuroscience:  Emotion, evolution, cognition, language, memory, brain damage, and abnormal behavior (2nd ed.).
Author(s)/Editor(s): Joseph, Rhawn
Source/Citation: Baltimore, MD, US: Williams & Wilkins Co; 1996, (xxv, 864)
Abstract/Review/Citation: This book is written for clinicians, neuroscientists, practitioners of neuropsychiatry, neuropsychology, and behavioral neurology, and philosophers and neuroanatomists of the mind. It has been my intent
throughout to present a multidisciplinary synthesis of facts, theories, and research findings about what is known, debated, established, and theorized regarding the functional neuroanatomy of the brain.
Notes/Comments:  Preface Acknowledgments Brain plates Section I: Evolution The evolution of the brain: The neuron,
nerve net, limbic system, brainstem, midbrain, basal ganglia, and telencephalon Paleo-neurology and the evolution of the human mind and brain: The frontal and inferior parietal lobes, sex differences, language, tool technology, and the Cro-Magnon/Neanderthal wars                                          Section II: The cerebral hemispheres The right cerebral hemisphere: Emotion, language, music, visual-spatial skills, confabulation, body image, dreams, and social-emotional
intelligence The left cerebral hemisphere: Language, aphasia, apraxia, alexia agraphia, psychosis, the evolution of reading and writing, and the origin of thought                         Section III: The limbic system The limbic system: Sex, emotion, emotional intelligence, pheromones, sexual differentiation, attention, memory, the pleasure principle, and primary process The hippocampus, amygdala, memory, and amnesia: Synaptic potentiation and cognitive and emotional neural networks Limbic language, social-emotional intelligence, development, and attachment: Amygdala, septal nuclei, cingulate gyrus, maternal language, sex differences, emotional deprivation, contact comfort, and limbic love The limbic system and the soul: Evolution and the neuroanatomy of religious experience                                                             Section IV: The brainstem and basal ganglia Caudate, putamen, globus pallidus, amygdala, and limbic striatum: Parkinson's disease, Alzheimer's disease, psychosis,
catatonia, obsessive-compulsions, and disorders of movement The brainstem, midbrain, DA, 5HT, NE, cranial nerves, and cerebellum: Motor programming, arousal, psychosis, coma, sleep and dreaming, sleep disorders, vocalization, and emotion Section V: The lobes of the brain The frontal lobes: Arousal,
attention, perseveration, personality, catatonia, memory, aphasia, melodic speech, confabulation, schizophrenia, movement disorders, and the alien hand The parietal lobes: The body image and hand in visual space, apraxia,
Gerstmann's syndrome, neglect, denial, and the evolution of geometry and math The occipital lobes: Vision, blind sight, hallucinations, visual agnosias The temporal lobes: Language, auditory, visual, emotional, and memory functioning,
form and face recognition, aphasia, epilepsy, and psychosis Section VI: The neuroanatomy of psychotic and emotional disorders The neuropsychology of repression: Hemispheric laterality, positive versus negative emotions, corpus
callosum immaturity, the frontal lobes, trauma, contextual cues, and recovered memories The neuroanatomy and neurophysiology and dissociation, repression, and traumatic stress: The amygdala, hippocampus, and disconnection
Neuroanatomy of psychosis: Depression, mania, hysteria, obsessive-compulsions, hallucinations, schizophrenia      Section VII: Neuroanatomy and pathophysiology of head injury, stroke, neoplasm, and abnormal development Neuroanatomy of normal and abnormal cerebral development: Neuronal migration errors, congenital defects, neural plasticity, environmental influences, trauma, abuse, psychosis Cerebral and cranial trauma: Neuroanatomy and pathophysiology of mild, moderate, and severe brain injury Stroke and cerebral-vascular disease
Cerebral neoplasms References Index abnormal behavior & disorders & other issues in neuropsychiatry & neuropsychology & clinical neurosciences of brain, professional textbook
========================================

Title: Depression in neurologic diseases.
Author(s)/Editor(s): Cummings, Jeffrey L.
Source/Citation: Psychiatric Annals; Vol 24(10) Oct 1994, US: SLACK Incorporated; 1994, 525-531
Abstract/Review/Citation: Reviews the definition of depression and the challenges to the recognition of depression in neurological diseases (NDs).  Focal brain disorders (stroke, trauma, tumors, epilepsy, and multiple sclerosis) with depression are described. The occurrence of depression in
basal ganglia and other subcortical disorders (Parkinson's disease, Huntington's disease, Wilson's disease, and HIV-related diseases) are presented, and the interface between depression and dementia is discussed. The most efficacious treatments of depression in the setting of NDs are noted.
Principles relating depressed mood to brain dysfunction are summarized.
========================================

Title: Neuropsychology, neuropsychiatry, and behavioral neurology.
Author(s)/Editor(s): Joseph, Rhawn
Source/Citation: New York, NY, US: Plenum Press; 1990, (xxix, 383) Critical issues in neuropsychology.
Abstract/Review/Citation: This book is written for the clinician, students, and practitioners of neuropsychology, neuropsychiatry, and behavioral neurology.  It has been my intent throughout to present a synthesis of ideas and research
findings.  Nevertheless, many of the books in the neurosciences treat psychiatry, neurology, and neuropsychology as if they were separate and mutually exclusive fields. It is my belief that these areas of study are in
fact one and the same. I think it is important to realize that what appears to be a "manic" disorder may in fact be a manifestation of right frontal lobe disease, or that the patient who suddenly develops "schizophrenia" may instead have suffered a stroke involving the basal ganglia or left temporal lobe. I believe it is also important to recognize not only that diverse symptoms may be indicative of localized dysfunction but also how specific abnormalities can be secondary to
disconnection syndromes, disinhibition, epileptic disturbances, and/or tumors, strokes, head injury, and diffuse physiological changes. To understand and recognize these problems it is necessary to have at least some knowledge of neuroanatomy and the manner in which various nuclei and brain regions
interact. These are just some of the issues detailed in the pages that follow.
Notes/Comments:  Brain plates The right cerebral hemisphere: Emotion, music, visual-spatial skills, body image,
dreams, and awareness Left hemisphere overview Consciousness, awareness, memory, and dreaming The left cerebral hemisphere: Aphasia, alexia, agraphia, agnosia, apraxia, language, and thought Egocentric and linguistic thought The development of language and thought Egocentric speech Disorders of language Alexia and agraphia Language and temporal-sequential motor control The limbic system: Emotion, laterality, and unconscious mind Affective origins: Olfaction and somesthesis Hypothalamus Amygdala Hippocampus The primary process Septal nuclei The frontal lobes: Neuropsychiatry, neuropsychology, and behavioral neurology Motor regions of the frontal lobes The posterior frontal convexity The orbital frontal lobes and inferior convexity Lateral-frontal cortical monitoring Personality and behavioral alterations secondary to frontal injury The right and left frontal lobes The parietal lobes Parietal topography The primary somesthetic receiving areas The somesthetic association area Area 7 and the superior-posterior parietal lobule Lesions and laterality The inferior parietal lobule Apraxia Gerstmann's syndrome Attention and neglect Delusional denial The occipital lobe Precortical visual analysis Striate cortex: Area 17
Association areas 18 and 19 Cortical blindness Visual agnosia Prosopagnosia Simultanagnosia Impaired color recognition The temporal lobes Temporal topography Auditory functioning Auditory association area Middle temporal lobe Inferior temporal lobe Memory Hallucinations Temporal lobe (partial complex)
seizures Schizophrenia Cerebral and cranial trauma: Anatomy and pathophysiology of mild, moderate, and severe head injury The meninges The skull Skull injuries Hematomas Herniation Contusions Coup and contrecoup contusions Rotation and shearing forces Diffuse axonal injury Hypoxia and blood flow Coma and consciousness Mortality Vegetative states Memory
Personality and emotional alterations Recovery Epilepsy Concussion and mild head injuries Postconcussion syndrome Premorbid characteristics Stroke and cerebrovascular disease Cerebral infarction Functional anatomy of the heart and arterial distribution The blood supply of the brain Cerebrovascular
disease Atherosclerosis Cerebral ischemia Thrombosis Embolism Transient ischemic attacks Lacunar strokes Multi-infarct dementia Heart disease, myocardial infarction, and cardiac surgery Hemorrhage Hypertension Aneurysms, AVMs, tumors, amyloid angiopathy Localized hemorrhagic symptoms Hemorrhages and strokes: Arterial syndromes Recovery and mortality Cerebral neoplasms Tumor development: Genetics Establishment and growth of a tumor Neoplasms and symptoms associated with tumor formation Focal syndromes and neoplasms Astrocytoma and glioblastoma multiforme Lymphomas, sarcomas, neuroblastomas, cysts Unilateral tumors and bilateral dysfunction Herniation Prognosis Index
========================================

Title: Functional effects of fetal striatal transplants.
Author(s)/Editor(s): Norman, Andrew B.; Lehman, Michael N.; Sanberg, Paul R.
Source/Citation: Brain Research Bulletin: Special Issue: Spinal cord_ecent work on trauma and recovery; Vol 22(1) Jan 1989, US: Elsevier Science Inc; 1989, 163-172
Abstract/Review/Citation: Reviews studies that demonstrate how fetal striatal transplants into excitotoxin-lesioned adult striatum in rats can elicit changes in behavior. The review includes research on (1) the effects of striatal transplants on lesion-produced behavioral deficits in locomotor
activity, rewarded alternation, and sensory motor tasks; (2) the pharmacological properties of striatal transplants; (3) neuroanatomical correlates of behavioral recovery; and (4) adrenal medullary grafts as possible mechanisms of action.
========================================

Title: Aphasia: a problem in differential diagnosis and re-education.
Author(s)/Editor(s): Meyers, R.
Source/Citation: Quarterly Journal of Speech; 23 1937, US: Speech Communication Assn.; 1937, 357-377
Abstract/Review/Citation: A five-fold classification of speech disorders is presented, taking account of etiology as well as locus of the disease process. Manifestations of speech disturbance are accordingly due to (1) aberrations of
personality, (2) developmental anomalies and other disease processes in the peripheral mechanisms involved in speech, (3) disease processes in the segmental mechanisms involved in speech, (4) disease processes in the subcortical coordinating mechanisms represented by the cerebellum and basal
ganglia, and (5) disease processes in the highest integrating mechanisms represented by the cerebral hemispheres and cortex. "The term aphasia should be reserved for disturbances of speech which are manifested only as a disability of formulating and communicating the arbitrary social symbols of
perceptual patterns." Various etiologic factors may underlie aphasia, e.g., brain trauma, pathological process of the cerebral blood vessels, brain tumors, infections of the brain, degenerative brain diseases, allergic cerebral edema, pre- and post-convulsive seizure states. Cases are cited to show that recent evidence makes untenable the various theories of the
localization of language functions in brain centers. Moreover, psychological considerations are corroborated by clinical evidence in throwing doubt on the existence of "pure" aphasias of the various alleged types. On the basis of the preceding analysis of aphasias resting upon organic etiology, the author summarizes an appropriate sequence of procedures for the speech re-education of the aphasic.

Record #1.
Source: PsycINFO
Search Query: kw: basal ganglia and traumatic stress (1 of 4)

Title: Serotonin and anxiety: Current models.
Author(s)/Editor(s): Stein, Dan J.
  Stahl, Stephen
Paper Number: 20001129
Source/Citation: International Clinical Psychopharmacology: Special Issue:
  Selective serotonin reuptake inhibitors in the anxiety disorders.; Vol
  15(Suppl2) Aug 2000, US: Lippincott Williams & Wilkins; 2000, S1-S6
Description/Edition Info.: Journal Article; 250
Abstract/Review/Citation: Reviews models of serotonin in anxiety disorders and
  emphasizes the clinical advantages of the serotonin reuptake inhibitors
  (SSRIs) in these conditions. Models of serotonin in anxiety disorders include:
  (1) a 'see-saw' model; (2) an 'amygdala model'; and (3) a 'basal ganglia
  model'. The authors maintain that, while any simplistic schema in this complex
  area must fail, these various models have some heuristic value for the
  clinician. From a clinical perspective, the availability of the SSRIs has
  proved a significant step forward in the treatment of the anxiety disorders
  such as panic disorder, obsessive-compulsive disorder, post-traumatic stress
  disorder, and social anxiety disorder (social phobia); these agents offer
  several advantages over previously existing pharmacotherapeutic alternatives
  such as the benzodiazepines and tricyclic antidepressants. (PsycINFO Database
  Record (c) 2000 APA, all rights reserved)
Subject Descriptors: Anxiety Disorders
  Drug Therapy
  Psychopharmacology
  Serotonin
  Serotonin Reuptake Inhibitors
  Models
  Clinical Psychopharmacology--3340
Notes/Comments: Print (Paper) Human 10 clinical advantages of selective
  serotonin reuptake inhibitors & models of serotonin in anxiety disorders
  Conference Proceedings/Symposia 0600
ISSN: 0268-1315
Vendor Numbers: 2000-16380-008
========================================
Record #2.
Source: PsycINFO
Search Query: kw: basal ganglia and traumatic stress (2 of 4)

Title: Posttraumatic obsessive-compulsive disorder: A three-factor model.
Author(s)/Editor(s): Dinn, Wayne M.
  Harris, Catherine L.
  Raynard, Richard C.
Paper Number: 20000401
Source/Citation: Psychiatry: Interpersonal & Biological Processes: Special
  Issue: Trauma: Memory, avoidance, and biopsychosocial regulators.; Vol 62(4)
  Win 1999, US: Guilford Publications; 1999, 313-324
Description/Edition Info.: Journal Article; 250
Abstract/Review/Citation: Presented a 3-factor causal model of
  obsessive-compulsive disorder (OCD), which posits that exposure to long-term
  traumatic stress generates an inordinate degree of anxiety during the
  psychological development of the premorbid OCD child. In response to these
  conditions the child evolves a distinct cognitive style characterized by
  exaggerated threat appraisal and magical beliefs, and experiences alterations
  in brain metabolism. An entire functional brain system (a basal
  ganglia-orbitofrontal circuit) enters into a state of enhanced responsiveness
  following exposure to protracted threat. Over time the threshold for
  stimulation is dramatically lowered, resulting in a hypersensitivity to cues
  that signify potential harm. Individuals adapt to this hypersensitivity
  through a variety of strategies, which constitute OCD. It is concluded that
  the biological abnormalities associated with OCD represent a dynamic
  biopsychosocial process in which repeated trauma renders a discrete neural
  circuit unusually responsive to threat-related stimuli. (PsycINFO Database
  Record (c) 2000 APA, all rights reserved)
Subject Descriptors: Cognitive Processes
  Models
  Obsessive Compulsive Disorder
  Premorbidity
  Psychological Stress
  Childhood Development
  Frontal Lobe
  Neuroses & Anxiety Disorders--3215
Notes/Comments: Print (Paper) Human 10 traumatic stress & impairments in
  information processing & orbitofrontal dysfunction in 3-factor model of
  obsessive-compulsive disorder  Empirical Study 0800
ISSN: 0033-2747
Vendor Numbers: 2000-13805-003
========================================
Record #3.
Source: PsycINFO
Search Query: kw: basal ganglia and traumatic stress (3 of 4)

Title: Neuropsychiatry, neuropsychology, and clinical neuroscience:  Emotion,
  evolution, cognition, language, memory, brain damage, and abnormal behavior
  (2nd ed.).
Author(s)/Editor(s): Joseph, Rhawn
Paper Number: 19970301
Source/Citation: Baltimore, MD, US: Williams & Wilkins Co; 1996, (xxv, 864)
Description/Edition Info.: Authored Book; 120
Abstract/Review/Citation: This book is written for clinicians, neuroscientists,
  practitioners of neuropsychiatry, neuropsychology, and behavioral neurology,
  and philosophers and neuroanatomists of the mind. It has been my intent
  throughout to present a multidisciplinary synthesis of facts, theories, and
  research findings about what is known, debated, established, and theorized
  regarding the functional neuroanatomy of the brain. (PsycINFO Database Record
  (c) 2000 APA, all rights reserved)
Subject Descriptors: Brain
  Brain Disorders
  Mental Disorders
  Neuropsychiatry
  Neuropsychology
  Basal Ganglia
  Brain Stem
  Limbic System
  Neuroanatomy
  Psychophysiology
  Neurological Disorders & Brain Damage--3297
  Physiological Psychology & Neuroscience--2500
Class. Code/Usage: Psychology: Professional & Research PS
Notes/Comments: Print (Paper) Human 10 (Abbreviated) Preface Acknowledgments
  Brain plates Section I: Evolution The evolution of the brain: The neuron,
  nerve net, limbic system, brainstem, midbrain, basal ganglia, and
  telencephalon Paleo-neurology and the evolution of the human mind and brain:
  The frontal and inferior parietal lobes, sex differences, language, tool
  technology, and the Cro-Magnon/Neanderthal wars Section II: The cerebral
  hemispheres The right cerebral hemisphere: Emotion, language, music,
  visual-spatial skills, confabulation, body image, dreams, and social-emotional
  intelligence The left cerebral hemisphere: Language, aphasia, apraxia, alexia
  agraphia, psychosis, the evolution of reading and writing, and the origin of
  thought Section III: The limbic system The limbic system: Sex, emotion,
  emotional intelligence, pheromones, sexual differentiation, attention, memory,
  the pleasure principle, and primary process The hippocampus, amygdala, memory,
  and amnesia: Synaptic potentiation and cognitive and emotional neural networks
  Limbic language, social-emotional intelligence, development, and attachment:
  Amygdala, septal nuclei, cingulate gyrus, maternal language, sex differences,
  emotional deprivation, contact comfort, and limbic love The limbic system and
  the soul: Evolution and the neuroanatomy of religious experience Section IV:
  The brainstem and basal ganglia Caudate, putamen, globus pallidus, amygdala,
  and limbic striatum: Parkinson's disease, Alzheimer's disease, psychosis,
  catatonia, obsessive-compulsions, and disorders of movement The brainstem,
  midbrain, DA, 5HT, NE, cranial nerves, and cerebellum: Motor programming,
  arousal, psychosis, coma, sleep and dreaming, sleep disorders, vocalization,
  and emotion Section V: The lobes of the brain The frontal lobes: Arousal,
  attention, perseveration, personality, catatonia, memory, aphasia, melodic
  speech, confabulation, schizophrenia, movement disorders, and the alien hand
  The parietal lobes: The body image and hand in visual space, apraxia,
  Gerstmann's syndrome, neglect, denial, and the evolution of geometry and math
  The occipital lobes: Vision, blind sight, hallucinations, visual agnosias The
  temporal lobes: Language, auditory, visual, emotional, and memory functioning,
  form and face recognition, aphasia, epilepsy, and psychosis Section VI: The
  neuroanatomy of psychotic and emotional disorders The neuropsychology of
  repression: Hemispheric laterality, positive versus negative emotions, corpus
  callosum immaturity, the frontal lobes, trauma, contextual cues, and recovered
  memories The neuroanatomy and neurophysiology and dissociation, repression,
  and traumatic stress: The amygdala, hippocampus, and disconnection
  Neuroanatomy of psychosis: Depression, mania, hysteria, obsessive-compulsions,
  hallucinations, schizophrenia Section VII: Neuroanatomy and pathophysiology of
  head injury, stroke, neoplasm, and abnormal development Neuroanatomy of normal
  and abnormal cerebral development: Neuronal migration errors, congenital
  defects, neural plasticity, environmental influences, trauma, abuse, psychosis
  Cerebral and cranial trauma: Neuroanatomy and pathophysiology of mild,
  moderate, and severe brain injury Stroke and cerebral-vascular disease
  Cerebral neoplasms References Index abnormal behavior & disorders &
  other issues in neuropsychiatry & neuropsychology & clinical
  neurosciences of brain, professional textbook Textbook 4100
ISBN: 0-683-04485-0
Vendor Numbers: 1996-98545-000
========================================
Record #4.
Source: PsycINFO
Search Query: kw: basal ganglia and traumatic stress (4 of 4)

Title: Neuroscience year:  Supplement 3 to the "Encyclopedia of
  Neuroscience."
Author(s)/Editor(s): Smith, Barry H.
  Adelman, George
Paper Number: 19970101
Source/Citation: Cambridge, MA, US: Birkhaeuser; 1993, (xiii, 190)
Description/Edition Info.: Edited Book; 140
Abstract/Review/Citation: [This supplement, as part of the "Encyclopedia of
  Neuroscience," includes:] (1) developing topics in neuroscience that were
  not covered as separate entries in the ["Encyclopedia"] or were only
  briefly covered in other related articles . . . (2) newly emerging topics that
  were not covered in the "Encyclopedia" and that are associated with
  possible research breakthroughs . . . and (3) updates of topics in which there
  have been significant developments.  /// The "Encyclopedia" surveys
  the physical-chemical-electrical substrates, the anatomical-biological
  structures, the physiological-neurological transductive mechanisms, and the
  behavioral-psychological outcome of all this interactive processing--the full
  spectrum of body and mind activities, from vegetative functions and motor
  activities to higher brain function.  /// The articles are written for a wide
  audience--professional neuroscientists and their students as well as a broad
  range of professionals and students from other scientific areas who want
  brief, ready-reference access to the field. (PsycINFO Database Record (c) 2000
  APA, all rights reserved)
Subject Descriptors: Neurosciences
  Physiological Psychology & Neuroscience--2500
Class. Code/Usage: Psychology: Professional & Research PS
Notes/Comments: Print (Paper) Human 10 Agrin Uel Jackson McMahan Alzheimer's
  disease, pharmacologic therapy Michel J. Calache, Ezio Giacobini and Robert E.
  Becker Angelman syndrome Jill Clayton-Smith Attention deficit hyperactivity
  disorder Louise S. Kiessling Basal Ganglia, anatomy and circuitry Michael D.
  Crutcher and Garrett E. Alexander Basal ganglia, models of function: Normal
  and disease Thomas Wichmann and Mahlon R. DeLong Bell's palsy David Sternman
  and David M. Simpson Blindsight, residual vision Lawrence Weiskrantz Brain
  grafts, genetic engineering Jasodhara Ray and Fred H. Gage Cachexia and tumor
  necrosis factor Ilene L. Bernstein Cerebellum, messenger molecules Andrew M.
  Batchelor and John Garthwaite Conscious experience, neural basis Benjamin
  Libet Conus venom neuropeptides Lourdes J. Cruz and Baldomero M. Olivera
  Depression, childhood, and treatment Alan E. Kazdin Drosophila, genes and
  behavior Jeffrey C. Hall Dystonia-parkinsonism syndrome, X-linked (XDP) Ulrich
  Mueller Dystrophin and Duchenne muscular dystrophy Hart G. W. Lidov and Louis
  M. Kunkel Extracellular matrix, laminin and integrins Michael J. Ignatius
  Facial expression and emotion Erika L. Rosenberg and Paul Ekman Fragile X
  syndrome W. Ted Brown and Edmund C. Jenkins Gelsolin Bertrand Y. Tuan and
  David J. Kwiatkowski Gilles de la Tourette Syndrome and self-injurious
  behavior Mary M. Robertson Glial growth factors Hideo Kimura Glucose-sensitive
  potassium channels Sylvie Zini, Valerie Crepel and Yehezkel Ben-Ari G-proteins
  and neuronal signal transduction Mark R. Brann Hair cells, sensory
  transduction David P. Corey Hepatic encephalopathy Anthony S. Basile Herpes
  simplex virus and its use in neuroscience research Julie K. Andersen and
  Xandra O. Breakefield Hyperkalemic periodic paralysis Bertrand Fontaine, James
  F. Gusella and Robert H. Brown, Jr. Induced rhythms, oscillations, in the
  brain Theodore H. Bullock Long-term depression (LTD) Masao Ito Malignant
  tumors of brain and head, boron neutron capture treatment William H. Sweet
  Marijuana receptor gene, cloning and characterization Lisa A. Matsuda Mental
  imagery Stephen M. Kosslyn and Lisa A. Shin Neuropsychiatry Richard M. Restak
  The NO hypothesis P. Read Montague Nociceptors, novel classes Stephen McMahon
  and Martin Koltzenburg Obsessive-compulsive disorder, neurobiology of Thomas
  R. Insel Olivopontocerebellar atrophy Sid Gilman Pain as learning Clifford J.
  Woolf Pain receptors (peripheral) and chronic pain Daniel F. B. Bossut and
  Edward R. Perl Panic disorder, psychobiology Andrew W. Goddard and Dennis S.
  Charney Paraneoplastic disorders Jerome B. Posner Parkinsonism, effects of
  lesions of the subthalamic nucleus Hagai Bergman, Thomas Wichmann and Mahlon
  R. DeLong Polyamines in the nervous system Michel Baudry and Imad Najm
  Post-Traumatic Stress Disorder (PTSD), psychobiology Dennis S. Charney, Steven
  M. Southwick and John H. Krystal Prader-Willi syndrome Joan H. M. Knoll,
  Joseph Wagstaff and Marc Lalande Prosopagnosia Daniel Tranel and Antonio R.
  Damasio Prostaglandins in the CNS: Arachidonic acid Leonhard S. Wolfe Protein
  phosphorylation and neuronal modulation Irwin B. Levitan Pseudotumor cerebri
  Thomas H. Milhorat Reading disorders, nonaphasic, and their treatment Josef
  Zihl Serotonin (5-hydroxytryptamine) receptor subtypes: Clinical relevance
  Stephen J. Peroutka Signal transduction in neurons by phospholipid breakdown
  products Jan Krzystof Blusztajn and Barbara E. Slack Sudden infant death
  syndrome (SIDS): A neural perspective Laurence Edward Becker Taste
  transduction Stephen D. Roper Transcranial sonography N. Venketasubramanian
  and J. P. Mohr Tremor Rodger J. Elble Vertigo Joseph G. Feghali Viscerosensory
  functions Gyoergy Adam Volume (extrasynaptic) transmission Paul Bach-y-Rita
  Wilson's disease Dominique Muller and Joseph A. Ghika Zebrins: Compartment
  markers in the cerebellum Richard Hawkes Zoster and postherpetic neuralgia
  Anne A. Gershon Index research in neurosciences, encyclopedia Reference
  Material 7000
ISBN: 0-8176-3592-0
Vendor Numbers: 1993-99007-000

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