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Circadian Rhythm and Trauma
Developmental NeuroBiology and DID
Developmental NeuroBiology and Dissociation
Developmental NeuroBiology and EMDR
Fornix and Trauma
Hippocampus Trauma and PTSD
Hypothalamus and PTSD
Developmental NeuroBiology and PTSD
Limbic System and Trauma
NeuroImaging and DID
Prefrontal Lobe and Trauma
NMRI and PTSD
NeuroImaging and Trauma
Neocortex and Trauma
MRI and Trauma
Dissociation and Affect Dysregulation
Developmental Traumatology
Developmental NeuroBiology and Trauma
Corpus Callosum and PTSD
Circadian Rhythm and Sleepwalking
Circadian Rhythm and REM Behavior Disorder
Cingulate Gyrus and Trauma
Circadiam Rhythm and PTSD
Circadian Rhythm DSM-IV
Cortisol and Dissociation
Cortisol and Trauma
Bipolar II Disorder
Bipolar I Disorder
Bipolar Disorder DSM-IV
BiPolar Disorder and Trauma
Bipolar Disorder and PTSD
Bipolar Disorder and DID
Basal Ganglia and Trauma
Basal Ganglia and PTSD
Aspergers Disorder DSM-IV
Aspergers Disorder and Infancy
Aspergers Disorder and Development
Aspergers Disorder and Childhood
Aspergers Disorder and Adolescence
Amygdala and PTSD
Amygdala and Fear
Affect Regulation-the Development of Psychopathology
Affect Regulation-Social Context on Childrens Affect Regulation
Affect Regulaqtion-Recurrent Abortiona in Bulimics
Affect Regulation-Mentalization and Development of The Self
Affect Regulation-Delayed memories of Childhood
Affect Regulation and Trauma
Affect Regulation and PTSD
Affect Dysregulation and Disorders of the Self
Affect Regulation and Attachment
ADHD and Trauma
Affect Dysregulation and Disorders of the Self
AffectDysregulation and Dissociation
Affect Regulation

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

 

Limbic System and Trauma

  

Title: Age of abuse onset and its relationship to autonomic arousal in Borderline Personality Disorder.

Author(s)/Editor(s): Kozel, Jennifer Jane

Source/Citation: Dissertation Abstracts International: Section B: The Sciences & Engineering; Vol 61(7-B) Feb 2001, US: Univ Microfilms International; 2001, 3849

Abstract/Review/Citation: Childhood abuse is considered an important etiological factor in the development of Borderline Personality Disorder (BPD). Compared with women who suffer from other personality disorders, women with BPD are more likely to have experienced a combination of verbal, physical, and sexual abuse and are more likely to have been abused by multiple individuals. In adult humans who have been diagnosed with BPD and who have a history of childhood trauma, irregular EEG patterns have been found. These patterns are suggestive of dysregulation of the limbic structures and a lower threshold for autonomic nervous system reactivity. It has also been shown that the severity of abuse and age of abuse onset predicts many of the problematic behaviors that are common to BPD. This study examined the differential impact of childhood trauma, including age of onset and severity of trauma, on

individuals with (n = 28) or without (n = 31) Borderline Personality Disorder (BPD, as defined by the SCID-II). A combination of self-report measures and physiological measures were used to address several specific hypothesis regarding the proposed effects of childhood trauma.  The findings showed an

inverse relationship between age of abuse onset and electrodermographic reactivity to high and low intensity pictorial slides. The results also showed that those who were abused at either the earliest ages (0 to 6 years

old) or at the later ages (13 to 18) rated their physiological responses to slides of varying levels of arousal/excitability more strongly than did those who reported abuse onset between 7 to 12 years old. Other findings showed that persons diagnosed with BPD produced physiological measures of skin conductance

that were indicative of greater autonomic arousal than did nonclinical controls. These findings suggest that persons who have a diagnosis of BPD and histories of childhood traumatization have altered autonomic functioning and lowered thresholds for limbic system reactivity.  ========================================

 

Title: Low cortisol and a flattening of expected daytime rhythm: Potential indices of risk in human development. .

Author(s)/Editor(s): Gunnar, Megan R.; Vazquez, Delia M.

Source/Citation: Development & Psychopathology: Special Issue: Stress and development: Biological and psychological consequences.; Vol 13(3) Sum 2001, US: Cambridge Univ; 2001, 515-538

Abstract/Review/Citation: Since the work of H. Selye, stress has been associated with increased activity of the limbic-hypothalamic-pituitary-adrenocortical (LHPA) axis. Recently, a number of studies in adults have shown that this neuroendocrine axis may be hyporesponsive in a number of stress-related states. Termed hypocortisolism (HPT), the paradoxical suppression of the LHPA axis under conditions of trauma and prolonged stress presently challenges basic concepts in stress research. Adverse conditions that produce elevated cortisol levels early in life are hypothesized to contribute to the development of HPT in adulthood. However, as reviewed in this paper, HPT also may be a common phenomenon early in human childhood. The authors argue that

developmental studies are needed that help explicate the origins of low cortisol and to determine whether the development of HPT is preceded by periods of frequent or chronic activation of the LHPA axis. They also argue that developmental researchers who incorporate measures of salivary cortisol into their studies of at-risk populations need to be aware of the HPT phenomenon. Lastly, they note that evidence of low cortisol under adverse early life conditions in humans adds to the importance of understanding the

implications of HPT for health and development.  ========================================

 

Title: Environmental illness:  Myth and reality.

Author(s)/Editor(s): Staudenmayer, Herman

Seller: Private Practice

Source/Citation: Boca Raton, FL, US: CRC Press, Inc; 1999, (376)

Abstract/Review/Citation: Several hundred individuals who believed they were suffering from environmental illness have been evaluated or treated by the author since the 1970s. He believed the symptoms harming his patients actually had psychophysiological origins--based more in fear of a hostile world than any suspected toxins contained in the environment. This book defines environmental illness in easily understood terms, reviews the lack of scientific evidence to support toxicogenic theories, outlines alternatives to toxicogenic explanations for symptoms attributed to low-level chemical

sensitivities, explains the symptoms of multiple chemical sensitivities from a physiological viewpoint, addresses psychosocial influences contributing to the belief of environmental illness, and discusses psychiatric diagnosis and

treatment.

Notes/Comments:  What is "environmental illness"? Toxicogenic theory Unsubstantiated diagnoses and treatments

Studies supporting the psychogenic theory Assessment of the toxicogenic research program Psychogenic theory Placebo and somatization Learned sensitivity The stress-response Panic attacks and anxiety disorders Trauma and post-traumatic stress disorder The limbic system and trauma Personality

disorders Iatrogenic illness: Exploitation and harm Treatment Politics Future directions Appendix A. A methodology of scientific research programs Appendix B. Court rulings unfavorable to environmental illness Glossary References

Index psychosomatic origins of alleged environmental illness

========================================

 

Title: The body keeps the score: Memory and the evolving psychobiology of posttraumatic stress.

Author(s)/Editor(s): van der Kolk, Bessel A.

Source/Citation: Essential papers on posttraumatic stress disorder., New York, NY, US: New York University Press; 1999, (vii, 548), 301-326 Essential papers in psychoanalysis.

Source editor(s): Horowitz, Mardi J. (Ed)

Abstract/Review/Citation: Contemporary research on the biology of posttraumatic stress disorder (PTSD) suggests that there are persistent and profound alterations in stress hormone secretion and memory processing in Ss with PTSD.  This article reviews PTSD symptomatology, psychophysiology, and hormonal stress responses. Also reviewed is how differences in developmental level may influence the psychobiological effects of trauma. The relationship between trauma and memory is discussed, as well as the role of the limbic system in that relationship. Finally, the use of psychopharmacological agents in the treatment of PTSD is reviewed.  ========================================

 

Title: Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: A PET investigation.

Author(s)/Editor(s): Shin, Lisa M.; McNally, Richard J.; Kosslyn, Stephen M.; Thompson, William L.; Rauch, Scott L.; Alpert, Nathaniel M.; Metzger, Linda J.; Lasko, Natasha B.; Orr, Scott P.; Pitman, Roger K.

Source/Citation: American Journal of Psychiatry; Vol 156(4) Apr 1999, US: American Psychiatric Assn; 1999, 575-584

Abstract/Review/Citation: Positron emission tomography (PET) was used to measure regional cerebral blood flow (rCBF) in 16 women (aged 19-54 yrs) with histories of childhood sexual abuse: 8 with posttraumatic stress disorder (PTSD) and 8 without PTSD. In separate script-driven imagery conditions, Ss

recalled and imagined traumatic and neutral autobiographical events. In the traumatic condition vs the neutral control conditions, both groups exhibited rCBF increases in orbitofrontal cortex and anterior temporal poles; these increases were greater in the PTSD group. The comparison group exhibited rCBF increases in insular cortex and anterior cingulate gyrus; increases in anterior cingulate gyrus were greater in the comparison group than in the PTSD group. Regional CBF decreases in bilateral anterior frontal regions were greater in the PTSD group, and only the PTSD group exhibited rCBF decreases in left inferior frontal gyrus.

========================================

 

Title: Mindbody healing in hypnosis: Immediate-early genes and the deep psychobiology of psychotherapy.

Author(s)/Editor(s): Rossi, Ernest Lawrence

Source/Citation: Japanese Journal of Hypnosis; Vol 43(1) 1998, Japan: Japanese Society of Hypnosis; 1998, 1-10

Abstract/Review/Citation: Describes the 4 major levels of communication between mind and genes as the scientific basis of psychotherapy and holistic healing in the new millennium. This new model of mind-body communication involves (1) the mindbrain and the limbic-hypothalamic-pituitary system, (2) immediate early genes in psychobiological adaptation, (3) new protein synthesis in stress, trauma, and healing, and (4) messenger molecules and state-dependent memory. The proposed psychobiological approach to holistic medicine is

consistent with much of the classical theory of psychoanalysis and psychosomatic medicine and with the modern neuroscience of memory and learning at the cellular-genetic level.  ========================================

 

Title: Is posttraumatic stress disorder an overlearned survival response? An evolutionary-learning hypothesis.

Author(s)/Editor(s): Silove, Derrick

Source/Citation: Psychiatry: Interpersonal & Biological Processes; Vol 61(2) Sum 1998, US: Guilford Publications; 1998, 181-190

Abstract/Review/Citation: Hypothesizes that a primitive learning center in the limbic system rehearses traumatic memories immediately following exposure to trauma, thus inducing durable memories of the sources of novel threat. It is

postulated that the mechanism developed during early evolution when, in the absence of cognitive mechanisms, automatic learning following single exposure to novel threat would have conferred survival value on the species. With the evolution of the brain, a second cortical pathway developed for the cognitive processing of trauma memories. It is possible that synchrony between the two phylogenetically distinct pathways may be lost in vulnerable individuals under conditions of extreme stress resulting in failure of cortical inhibition of

limbic trauma rehearsal mechanisms. A mismatch between archaic biological mechanisms and novel cues in the modern environment also may play a role in triggering traumatic memories and associated fight and flight reactions. The intrusive phenomena of posttraumatic stress disorder (PTSD) thus may reflect an overlearned survival response in those in whom the putative limbic rehearsal mechanism evades cortical control. The heuristic value and limitations of such an evolutionary-learning theory are discussed.  ========================================

 

Title: EEG measures of subjects with idiopathic chemical sensitivity: A test of the sensitization model.

Author(s)/Editor(s): Fernandez, Mercedes

Source/Citation: Dissertation Abstracts International: Section B: The Sciences & Engineering; Vol 59(4-B) Oct 1998, US: Univ. Microfilms International; 1998, 1904

Abstract/Review/Citation: This study tested the sensitization model proposed by Bell, Miller & Schwartz (1992) to study multiple chemical sensitivity (MCS). The sensitization models indicates that a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways and future less intense trauma or stimuli, in the same or different modality, can elicit an amplified response. Three groups of subjects were tested: (1) women who reported chemical sensitivity; (2) sexually abused women without chemical

sensitivity; and (3) healthy woman without chemical sensitivity nor sexual abuse history. All subjects were exposed to odorant and nonodorant control stimuli once a week for three weeks. Electroencephalographic (EEG) activity was recorded while subjects sniffed the odorant and control stimuli. Based on the sensitization model, it was hypothesized that subjects who reported chemical sensitivity as well as subjects who reported a history of sexual abuse would show increases in the amplitude spectrum in the alpha frequency band across experimental sessions during exposure to odorant stimuli. Additionally, it was hypothesized that the healthy control subjects would show

little or no changes over time. As predicted, the chemically sensitive and the sexually abused groups showed sensitization across experimental sessions. Additionally, the healthy control subjects showed habituation across experimental sessions. These findings indicate that individuals with chemical sensitivity show evidence of sensitization and that sensitization is not

specific to MCS.  ========================================

 

Title: Preliminary evidence for abnormal cortical development in physically and sexually abused children using EEG coherence and MRI.

Author(s)/Editor(s): Teicher, Martin H.; Ito, Yutaka; Glod, Carol A.; Andersen, Susan L.; et al

Source/Citation: Psychobiology of posttraumatic stress disorder., New York, NY, US: New York Academy of Sciences; 1997, (xv, 550), 160-175 Annals of the New York Academy of Sciences, Vol. 821.

Source editor(s): Yehuda, Rachel (Ed)

Abstract/Review/Citation: Physical or sexual abuse during childhood has been associated with the development of an array of psychiatric disorders including multiple personality disorder, borderline personality disorder, and refractory

psychosis. Childhood physical abuse may also sensitize patients to the later development of posttraumatic stress disorder (PTSD). We postulated that early deprivation or abuse could result in neurobiological abnormalities responsible for subsequent psychiatric disorders. We hypothesized that early childhood abuse or trauma could affect the development of the cerebral cortex and limbic system. The research presented examines the developmental effects of physical and sexual abuse in children, adolescents, and adults abused in childhood.

========================================

 

Title: Victim-to-perpetrator process: Effect of trauma on incarcerated adult male sex offenders.

Author(s)/Editor(s): Hulnick, Marjory Joan

Source/Citation: Dissertation Abstracts International Section A: Humanities & Social Sciences; Vol 57(9-A) Mar 1997, US: University Microfilms International; 1997, 3826

Abstract/Review/Citation: Trauma before age 16, and its relationship to adult perpetration were investigated in 69 incarcerated adult male sex offenders (primarily pedophiles and rapists), and a comparison group of 46 employed working-class adult males. Physical, sexual, emotional, family, and general

trauma were expected to predict perpetration. Hypothesized as mediators of the victim-to-perpetrator process were psychobiological sequelae of trauma, namely Posttraumatic Stress Disorder (PTSD), dissociation, central nervous

(limbic) system dysregulation (CNS), and anger-rage. Substance abuse disinhibitors, buffers such as help with traumatization, and protective and resilience factors were anticipated modifiers. Supporting the study model and hypotheses, negative outcome was predicted by the absence of buffers, and presence of trauma, its sequelae, and disinhibitors. Incarcerated offenders experienced more childhood trauma on all dimensions, higher levels of anger-rage, and greater PTSD, dissociative, and CNS symptomatology. They received less help with traumatization, had fewer protective and resiliency traits, and engaged in more antisocial and non-sexual criminal acts as both juveniles and adults. Chance results were unlikely, since significance levels ranged from p <01 to p =.01. Predictive of antisocial and non-sexual criminal behavior were: anger-rage, PTSD, general abuse, and absence of sexual abuse, accounting for 43% and 50% of the variance on juvenile and adult levels respectively. These adult behaviors were highly correlated with earlier acts as juveniles.  Anger-rage initially was the most important predictor of felon (versus

non-felon) group membership, but was replaced subsequently by PTSD, emotional abuse, substance abuse, and absence of protective and resilience factors, accounting for 51%. The presence of sexual abuse and absence of family dysfunction were responsible for 21% of the shared variance in offender

subgroups, pedophile versus rapist. Limbic system dysregulation, anger-rage, dissociation, physical abuse, and absence of both family dysfunction and protective and resiliency traits accounted for 53% of the PTSD variance. Though not causal, results were consistent with the concept that childhood trauma and adult perpetration are strongly associated.  ========================================

 

Title: The body keeps score:  Approaches to the psychobiology of posttraumatic stress disorder.

Author(s)/Editor(s): van der Kolk, Bessel A.

Source/Citation: Traumatic stress:  The effects of overwhelming experience on mind, body, and society., New York, NY, US: The Guilford Press; 1996, (xxv, 596), 214-241

Source editor(s): van der Kolk, Bessel A. (Ed)

Abstract/Review/Citation: examines the biology of posttraumatic stress disorder (PTSD) including both hormonal and autonomic nervous dimensions / topics covered include the unusual patterns of cortisol, norepinephrine, and dopamine

metabolite excretion; the role of the serotonergic and opioid systems; and receptor modification by processes such as kindling / examines the involvement of central pathways involved in the integration of perception, memory, and arousal, as well as the impact of these central pathways on patterns of

information processing in PTSD general background: the interrelated systems of the brain / the psychobiological symptomology of PTSD [physiological arousal, loss of emotions as signals] / psychophysiological effects of trauma [conditioned responses to specific stimuli, hyperarousal to intense but

neutral stimuli] / neurohormonal effects of trauma [background: neurohormones and their roles in the stress response, specific neuroendocrine abnormalities in PTSD] / developmental level affects the psychobiological effects of trauma [trauma, neurohormones, and memory consolidation] / trauma and the central nervous system [background: structures and functions of the limbic system, "emotional memory may be forever," specific limbic system abnormalities in PTSD, lateralization]  ========================================

 

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) 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.

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: Neuroanatomy and neurotransmitter function in panic disorder.

Author(s)/Editor(s): Gorman, Jack M.; Papp, Laszlo A.; Coplan, Jeremy D.

Source/Citation: Anxiety as symptom and signal., Hillsdale, US: Analytic Press, Inc; 1995, (x, 182), 39-56

Source editor(s): Roose, Steven P. (Ed)

Abstract/Review/Citation: presents our most current thinking on brain function in panic disorder / [contend] that anxiety disorders represent an exquisite interplay of both higher and lower brain function / higher brain function, located in the frontal cortex, mediates cognition and complex associate

learning / lower brain function, located in the brain stem and limbic cortex of the brain, mediates visceral function such as heart rate and respiration as well as memory / what, in our opinion, is often labelled psychological really represents cortically mediated events, and what is often labelled biological

represents brain stem--and limbic lobe--mediated events / a comprehensive theory of panic disorder, therefore, should include careful reference to both / neuroanatomical hypothesis / ventilatory function in panic / noradrenergic hyperactivity in panic / serotonergic involvement in panic / role of genes and

environmental trauma  ========================================

 

Title: The affective dimension of pain: A model.

Author(s)/Editor(s): Chapman, C. Richard

Source/Citation: Pain and the brain:  From nociception to cognition., New York, NY, US: Raven Press; 1995, (xix, 584), 283-301 Advances in pain research and therapy, Vol. 22.

Source editor(s): Bromm, Burkhart (Ed)

Abstract/Review/Citation: offer a model to account for the affective dimension of pain / propose that tissue trauma: (a) excites both spinoreticular and spinothalamic pathways; (b) generates concomitant affective and sensory processes that subserve complementary adaptive functions; and (c) activates

predominantly noradrenergic limbic structures to produce the affective dimension of pain; and that (d) the hypothalamically-mediated stress response is an important feature of pain and a mechanism of its emotional dimension / emotion, its functions, and its expressions / basis for the emotional dimension of pain [nociception and central noradrenergic processing, the locus

coeruleus and the dorsal noradrenergic bundle, ventral noradrenergic bundle and the hypothalamo-pituitary-adrenocortical (HPA) axis] / pain and stress

========================================

 

Title: Information processing of trauma.

Author(s)/Editor(s): Hartman, Carol R.; Burgess, Ann W.

Source/Citation: Child Abuse & Neglect: Special Issue: Clinical recognition of sexually abused children; Vol 17(1) Jan-Feb 1993, US: Elsevier Science Inc; 1993, 47-58

Abstract/Review/Citation: Presents a neuropsychosocial model of information processing of trauma that emphasizes the limbic system as being the primary system for coding incoming information. This encoding relates to the process of memory retrieval and recall. The neurobiological basis of the altered

alarm/dissociative process during and post sexual trauma impedes the development of information processing essential for the discerning of intentionality, personal responsibility (blame), sense of control over events, and trust in others. Once this imbalance occurs, the child is restricted in developing cognitive schema to deal with interpersonal intimacy. This, in turn, results in secondary patterns of aggression and/or avoidance. Necessary inhibition and discrimination are altered, and there is a collapsing of categories that indicate danger. (French & Spanish abstracts)  ========================================

 

Title: Biological response to psychic trauma.

Author(s)/Editor(s): van der Kolk, Bessel A.; Saporta, Jose

Source/Citation: International handbook of traumatic stress syndromes., New York, NY, US: Plenum Press; 1993, (xxxiii, 1011), 25-33 The Plenum series on stress and coping.

Source editor(s): Wilson, John Preston (Ed)

Abstract/Review/Citation: the biological response to trauma is examined / present a detailed analysis of the rapidly growing literature on the psychobiology of posttraumatic stress disorder (PTSD) / review the attempts to understand a trauma's impact on neurological functioning / [examine] the core symptomatology of PTSD and then summarize the literature on the neural structures (e.g., limbic system, locus coeruleus) which play specific and general roles in the production of symptom manifestation / the following neural subsystems and behavioral phenomena are analyzed and then placed into a

comprehensive and integrated summary: autonomic hyperreactivity and intrusive reexperiencing, numbing of responsiveness, developmental levels and the effects of trauma, the limbic system, noradrenergic and serotonergic pathways, endogenous opioid system, and the role of the locus coeruleus and related structures  ========================================

 

Title: Psychosocial consequences of epilepsy.

Author(s)/Editor(s): Vermeulen, Jan; Canger, Raphael

Source/Citation: Quantitative assessment in epilepsy care., New York, NY, US: Plenum Press; 1993, (viii, 214), 145-153 NATO ASI series. Series A: Life sciences, Vol. 255.

Source editor(s): Meinardi, Harry (Ed)

Abstract/Review/Citation: there is abundant evidence that people with epilepsy, as a group, have more psychological and social problems than normal people / the topics reviewed here represent problem areas on which considerable debate

has centred / they are: developmental problems, personality traits, aggression, sexual dysfunction, psychiatric illness and general SES in epilepsy / various emotional and personality correlates of epilepsy represent more than simply an understandable psychological reaction to the emotional trauma of physical, social, or cognitive disability / neurophysiological-neurochemical mechanisms, particularly those reflecting

limbic system dysfunction, may be involved as well / both approaches to psychosocial problems in epilepsy will be considered  ========================================

 

Title: A reinterpretation of memorative functions of the limbic system.

Author(s)/Editor(s): MacLean, Paul D.

Source/Citation: Contemporary neuropsychology and the legacy of Luria., Hillsdale, NJ, US: Lawrence Erlbaum Associates, Inc; 1990, (xi, 287), 127-154 Institute for research in behavioral neuroscience.

Source editor(s): Goldberg, Elkhonon (Ed)

Abstract/Review/Citation: [discusses anterograde amnesia, a condition resulting in a patient's inability to recall ongoing experiences subsequent to some disease, trauma, or other affliction] / clinico-pathological correlations / hippocampal formation / the amnestic syndrome in animals / similarity to the

amnesia of ictal automatisms / electrophysiological and anatomical data

========================================

 

Title: Psychobiological factors in violent behavior.

Author(s)/Editor(s): Kutzer, Dennis J.

Source/Citation: Violent behavior, Vol. 1:  Assessment & intervention., Costa Mesa, CA, US: PMA Publishing Corp; 1990, (xii, 339), 27-44

Source editor(s): Hertzberg, Leonard J. (Ed)

Abstract/Review/Citation: limbic system / organic pathology associated with violent behavior / head trauma / alcohol / drugs of abuse / idiosyncratic reactions and side effects of prescribed medications / anoxia and hypoxemia / electrolyte disturbances / endocrine disorders / genetic and developmental

disorders / epilepsy / the dyscontrol syndrome / space-occupying lesions / infections / the dementias / cerebral vascular disease / functional disorders associated with violent behavior / affective disorders / schizophrenia / character disorders  ========================================

 

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: Infanticide in Limbic (?) Psychotic Trigger Reaction in a man with Jacksonian and petit mal (?) seizures: "Kindling" by traumatic experiences.

Author(s)/Editor(s): Pontius, Anneliese A.

Source/Citation: Psychological Reports; Vol 67(3, Pt 1) Dec 1990, US: Psychological Reports; 1990, 935-945

Abstract/Review/Citation: Describes a case in which a crying infant girl was hit fatally by her devoted father while he was off anticonvulsants prescribed for Jacksonian and petit mal seizures with "porencephalic cyst involving motor cortex and limbic system." The S was a White married man in his late 20s in whom crying revived traumatic memories of frequently repeated ("kindling") experiences of his mother crying when hit by his father, in turn sometimes hit by S while helping the mother. Hitting also had been helpful (cognitive mismatch between helpful and harmful hitting) during the victim's accidental choking 11 days earlier. Symptoms of the well remembered, unmotivated infanticide included flat affect, olfactory and command hallucinations, and delusions of grandeur. The author proposes that this is a case of limbic (?) psychotic trigger reaction.  ========================================

 

Title: Coma and the etiology of violence: II.

Author(s)/Editor(s): Bell, Carl C.

Source/Citation: Journal of the National Medical Association; Vol 79(1) Jan 1987, US: National Medical Association; 1987, 79-85

Abstract/Review/Citation: Reviews the literature on clinical surveys of violent individuals and studies of the clinical treatment of violence. Animal studies and research into posttraumatic anger and violence, tumors and lesions of the limbic system, temporal lobe epilepsy, episodic dyscontrol syndrome, and clinical treatment of violence indicate that central nervous system (CNS) factors are involved in some instances of violent behavior. Consistent findings indicate that lower socioeconomic groups are more predisposed to brain injury from trauma, and several studies have indicated that this problem particularly affects the Black community. It is concluded that investigations of the relationship between the CNS and violence are, therefore, imperative for the Black community.  ========================================

 

Title: Illness behavior and psychosocial correlates of cancer.

Author(s)/Editor(s): Haney, C. Allen

Source/Citation: Social Science & Medicine; Vol 11(4) Mar 1977, United Kingdom: Elsevier Science Ltd.; 1977, 223-228

Abstract/Review/Citation: A recurrent theme in the literature on cancer concerns various psychosocial precursors of the disease. These factors have ranged from those which focus on the personality of the individual to those associated

with various life events such as death of a loved one or divorce. Numerous explanations and interpretations have been offered to account for these findings. It has been asserted that these factors operate through their influence on such processes and mechanisms as the limbic system, endocrine system, hormone levels, or the CNS. The explanation offered in the present paper, however, is that these events can determine the extent to which one attends to his/her body and the nature of an individual's illness behavior, that is, the ways in which the individual perceives, evaluates, and acts on

bodily messages and sensations. (37 ref)  ========================================

 

Title: Neurological factors in violent behavior (the dyscontrol syndrome).

Author(s)/Editor(s): Elliott, Frank A.

Source/Citation: Bulletin of the American Academy of Psychiatry & the Law; Vol 4(4) 1976, US: American Academy of Psychiatry & the Law; 1976, 297-315

Abstract/Review/Citation: As part of a 1976 symposium on violence in families, the effect of neurological diseases is discussed, especially the organic dysfunction syndrome (ODS), whose most dangerous symptom is the attack of explosive anger for trivial causes. The ODS is described on the basis of 70 cases observed over a 5-yr period (25 females, 45 males, aged 14-68, chiefly from the middle and upper classes). The prevalence of ODS is not known, but it is probably much underreported. Several studies indicate that it is usually the product of a damaged limbic system. Its etiology is discussed in detail. Males are more subject to ODS than females at all ages, and adolescents and young adults more than older people. Some patients have exhibited temper tantrums from infancy on; others show the symptoms only after later injury or illness. Causes discussed include head trauma, minimal brain dysfunction, epilepsy, brain tumor, infections, cerebral vascular disease, other neurological diseases, and endocrine and metabolic disorders. Diagnostic aids are specified. Management of the case and treatment of the patient are discussed, particularly the use of specific drugs. (81 ref)  ========================================

 

Title: Memory disturbances caused by focal brain lesions.

Author(s)/Editor(s): Luriya, A. R.

Source/Citation: Voprosy Psychologii; Vol. 19(4) Jul 1973, Russia: Voprosy Psikhologii; 1973, 109-117

Abstract/Review/Citation: Presents a review of observations on the nature of memory disturbances in cerebral trauma made by the author and his coworkers. Both deep and superficial lesions increase the susceptibility of memory traces to inhibition, except in cases of left temporal lobe and left

parieto-temporal-occipital lobe lesions, in which simultaneous weakening of memory traces is also observed. The nature of (a) weakly pronounced memory disturbances caused by slight lesions in the limbic system; (b) massive general memory disturbances caused by deep tumors along the midline that interfere with the functioning of the Papez circle; (c) partial, modality-specific memory disturbances caused by focal lesions on the surface of the lobes; (d) disturbances caused by lesions in the frontal lobes; and (e) system-specific memory disturbances is discussed. Connections between memory

phenomena and those of consciousness and cognitive processes are pointed out, and the complexity of the structure of memory processes is stressed.

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