Neuro(bio-)psychology and trauma studies

Excellent PTSD Site

2010-04-10T14:55:00.001-07:00

Neuropsychology: Self-Test on TBI - KEY

2010-03-18T12:10:00.000-07:00

Traumatic Brain Injury Peter Brown
Neuropsychological Disorders

Quiz Answer Key

1. b. MVAs account for over 50% of TBI – includes vehicle v. vehicle, vehicle v. bike,
vehicle v. pedestrian injuries.

2. c. It is important to work in concert with the multidisciplinary treatment team and
triangulate data via various assessment instruments, neuroimaging, individual/family reports, and observations, taking all available information into account.

3. a. Somatic (dizziness), cognitive (memory), and emotional/behavioral (irritability)
symptoms are all present in mTBI, though to a lesser degree and typically without LOC – and oftentimes are missed due to subclinical presentation. However, research demonstrates that detrimental effects occur in athletes such as football players and boxers over time (See also Zilmer, et al., 2008).

4. c. Severity of TBI is classified by based on admission Glasgow Coma Score, duration
of unconsciousness and post-traumatic amnesia and any focal neurological findings. The “Severe” TBI diagnosis includes a GCS < 9; more than 6 hrs coma; PTA > 24 hrs, so the answer of of GCS of 3, LOC of 34 hrs, and PTA of one week meets these criteria.

5. d. DAI is associated with coma and poor outcome and often accompanies mTBI. The
shifting and shearing in DAI is the signature of this injury and contributes to a poorer prognosis.

Neuropsychology: Self-Test on Traumatic Brain Injury Presentation

2010-03-18T12:08:00.000-07:00

Traumatic Brain Injury Peter Brown
Neuropsychological Disorders

Quiz - Circle the best answer.

1. What is the leading cause of TBI in the US?

a. Gunshot wounds (GSW)
b. Motor/Moving Vehicle Accident (MVA)
c. High diving and boxing
d. Concussion grenades and IEDs

2. How can a Neuropsychologist best diagnose TBI?

a. S/he can’t. Best to wait for the MRI.
b. Perform a HRB.
c. Utilize various measures, especially the GCS and WAIS-III DS in concert with other
reports of the treatment team.
d. Ask the patient, his/her family members, and the Neurologist.

3. What are some signs and/or symptoms of CHI/m(mild)TBI/concussion?

a. Dizziness, no or very brief loss of consciousness (LOC), irritability, and vague
memory problems
b. Psychosis, mania, and vomiting
c. Retrograde Amnesia (RA), Loss of Consciousness for 35 minutes, and Post
Concussion Syndrome (PCS)
d. Fluid/Bleeding from the ears and nose, nystagmus, and noise sensitivity.

4. Which of the following must be included in the diagnosis of severe TBI?

a. Coma, LOC for 1.5 hours, with a history of TBI
b. Age greater than 5, brief LOC, and dysphagia
c. Glasgow Coma Scale of 3, LOC of 34 hours, with PTA of one week
d. Presence of low levels of S-100B Protein in labs

5. Diffuse Axonal Injury is associated with which of the following?

a. Good outcome, though with PCC/PCS (Post Concussion Complaints/Syndrome)
b. Higher hospital costs
c. Moderate to Severe TBI
d. Coma and poor outcome

Traumatic Brain Injury

2010-03-18T10:20:00.000-07:00

Traumatic Brain Injury Peter Brown
Neurological Disorder

TBI Terminology

• TBI involves an alteration of consciousness, including Loss of Consciousness (LOC),
amnesia both Retrograde (RA) and Posttraumatic (PTA), and coma (Lezak, et al, 2004).
• Primary injuries: Closed Head Injuries (CHI)/blunt head injuries; Penetrating Head
Injuries (PHI)/open head injuries; Sometimes also refer to stroke and anoxia (Lezak, et al., 2004)
• Considered the “signature injury” among US military personnel involved in combat in
Iraq and Afghanistan due to Improvised Explosive Devices and the improvements made in personal body armoring (Kevlar helmets and body armor) which increase polytraumatic survival rates (McCrea, et al., 2008)
• Coup and contracoup injuries + Secondary Injury Syndrome (SIS)
• Diffuse Axonal Injuries (DAI) - very prevalent in mild (m)TBI/Concussions
• Epidural Hematomas EDH, Subdural Hematomas SDH, and Intracerebral Hematomas
ICH - even Delayed Traumatic Intracerebral Hematomas DTICH
• Swelling, elevated Intracranial Pressure (ICP), hypoxia, ischemia, hyperemia,
hydrocephalus, herniation, and edema are the secondary injuries in CHI, alongside the biochemical cascades - glutamate, calcium and sodium ionic influx, mitochondrial dysfunction (see also Lezak, et al., 2004)

Signs and symptoms of TBI

• Three general categories:
– Somatic (i.e., headache, sleep problems, fatigue, seizures)
– Cognitive (i.e., attention, memory, processing speed)
– Emotion/behavioral (i.e., depression, anxiety, mania, psychosis
- the last two are rare (French, et al., 2008, p. 1006)
• Signs and symptoms of neurological impairment caused by focal TBI depend on which
structures are damaged.
• Other common symptoms include: nervousness, disinhibition, impulsiveness,
inappropriate laughter, irritability, diplopia, difficulty concentrating or thinking, aphasia, dysphagia, dizziness, incoordination of movements, lightheadedness, loss of balance, difficulty walking or sitting, loss of memory, muscle stiffness and/or spasms, sleep difficulties (more or less sleep than pre-injury), slurred and/or slowed speech, tingling, numbness, pain, vertigo, weakness in one or more limbs, facial muscles, or on an entire side of the body (see also www.neurologychannel.com/tbi)

Course

• Symptom progression proceeds typically from coma, to post-traumatic amnesia (PTA),
to the recovery phase (http://www.neurologychannel.com/tbi/symptoms-progression.shtml) - though Lezak, et al. (2004) warns against the usage of the word “recovery” as any alteration of mental status and/or accompanying LOC will not necessarily result in premorbid levels of functioning (see also p. 162).
• A substantial group of patients develop post-concussional complaints (PCC) or Post-
concussional Syndrome (PCS) if symptoms persist 3 months post injury (McCrea, et al., 2008, p. 20). There is little information on the effectiveness of various methods suggested for reducing the frequency of PCC. (De Kruijk, et al., 2001).
• Retrograde amnesia (RA) frequently accompanies PTA (Lezak, et al., 2004, p. 161).

Course - Penetrating Head Injury

• PHI: behavioral and cognitive impairments that are localized to the area of injury,
accompanied by impairments of attention, concentration, memory, and mental slowing with focal effects more pronounced than diffuse ones.
• Rapid gains in first 1-2 years especially in cognitive impairment such as language and
constructional disorders while sensory defects can remain permanently (blind spots, etc.)
• Epilepsy and other seizure disorders are highly correlated which can increase ICP
Course - Closed Head Injury
• Diffuse damage compromises mental speed, attention, cognitive efficiency, and when
severe - high level conceptualization and reasoning.
• Pts complain of confusion, perplexity, irritability, fatigue, and reduced ability - often
attributing the cause as memory problems
• Anosmia, diplopia, photophobia, tinnitus, and hyperacusis are prominent sensory issues
• Acceptable functioning to permanent disability possible
• See also Lezak, 2004.

Diagnostic criteria

• Based on admission Glasgow coma score, duration of unconsciousness and post-
traumatic amnesia and any focal neurological findings
• Severe (GCS < 9; more than 6 hrs coma; PTA > 24 hrs), moderate (GCS 9-12; no longer
than 6 hrs coma; PTA > 1 hr) or mild (GCS > 12; less than 20 min coma; PTA < 1 hr) (see also Lezak, et al., 2004).
• Most traumatic brain injuries are classified as mild traumatic brain injury (MTBI).
Headache, nausea and dizziness are frequent symptoms after MTBI and may continue for weeks to months after the trauma. MTBI may also be complicated by intracranial injuries. Experimental animal models and post-mortem studies have shown axonal damage and dysfunction in MTBI. This damage is mostly localized in the frontal lobes. Serum S-100 and NSE have been reported to be markers for the severity of brain damage. In the literature, indications for radiodiagnostic evaluation following MTBI have been the subject of debate. Radiographs of the skull are used to exclude skull fractures, but are not useful for an evaluation of brain injury. Computed tomography of the brain seems to be the best way to exclude the development of relevant intracranial lesions. (De Kruijk, et al., 2001)
• There is significant debate in the field around the course and duration, even existence of
mTBI. This becomes especially complex with the comorbidity of personality factors, PTSD, and a host of other correlated factors including compensation seeking, etc.
• Course ranges from no recovery, to appreciable improvement between 1-12 months,
before the TBI enters the chronic category. PCS thought to account for chronicity. (see also Lezak, et al., 2004)

Demographic and risk factors

• TBI occurs twice as often in men as in women. Lower SES, unemployment, and lower
educational levels also correlate (Lezak, 2004, p. 159).
• Populations at a higher risk include the following:
– Individuals between the ages of 15 and 24 years -- the military is a particularly
vulnerable group (Clement, et al., 2003, p. 1025)
– Individuals age 75 and older
• Half of all traumatic brain injuries involve alcohol use, either by the victim or the person
causing the injury.
• Children age five and younger are also at a higher-than-average risk. According to the
National Pediatric Trauma Registry, more than 30,000 children are permanently disabled each year as a result of brain injuries. The greatest risk occurs from midafternoon to early evening, and during weekends and the summer months. Children are especially at risk after school. Nearly half (42.6%) of all children's injuries occur in roads, 34.3% occur at home and 6.6% occur in recreation areas.
• Other risk factors include boxing and other impact sports, premorbid personality, and
repeat instances of TBI
• See also http://www.neurologychannel.com/patient-information-tbi/index.shtml

Incidence and prevalence (Civilian)
• Very wide variability in the statistics, and the fact that mTBI, often not reported,
incidence ranges from 100-700:100,000 (function of severity and Diagnosis). Additionally, there is no one central statistical data collection center for TBI.
• According to the Centers for Disease Control and Prevention (CDC), approximately 1.4
million people suffer TBI each year in the United States and about 50,000 people die from the injury. Estimates of the number of people who have survived a TBI range from 2.5 million to 6.5 million. The range is broad because mild TBI often goes unreported. (see also http://www.neurologychannel.com/tbi/index.shtml)
• The cost of traumatic brain injuries in the United States is estimated at $48.3 billion
annually: $31.7 billion in hospitalization costs and another $16.6 billion in costs associated with fatalities. The CDC estimates the total cost of acute care and rehabilitation for TBI victims in the United States is $9 billion to $10 billion per year, not including indirect costs to families and society (e.g., lost earnings, work time, and productivity for family members, caregivers, and employers, or the costs associated with providing social services).It is estimated that over a lifetime, it can cost between $600,000 and $1,875,000 to care for a survivor of severe TBI. (see also http://www.neurologychannel.com/tbi/index.shtml)

Etiology and risk factors

• The three most common causes of TBI are the following:
– Motor vehicle, bicycle, or vehicle-pedestrian mishaps (more than 50%)
– Falls (approximately 25%)
– Violence (nearly 20%)
• Vehicle-related injuries involve people of all ages. Falls are most common among the
elderly and the very young. Alcohol and medication use are common contributing factors in falls.
• Gunshot wounds account for a small proportion of TBIs (10%), but a high percentage of
related fatalities (44%). Nine out of ten people who incur TBI from a firearm die.
• Domestic abuse (including shaken baby syndrome) and sports injuries are common
causes of TBI. Approximately 3% of all hospitalizations for TBI are incurred while playing sports. Most sports-related TBI are relatively minor and therefore go unreported. (see also Lezak, et al., 2004, and http://www.neurologychannel.com/tbi/causes.shtml)

Lab and imaging findings

• Blood and serum markers (protein S-100B marks neuronal/glial damage)
• CT (in the ER - view bleeds, fractures, foreign bodies, etc.)
• EEG, QEEG, and transcranial Doppler can be used
• Evoked potential studies
• MRI (more sensitive than CT, even to DAI)
• Angiography - detect blood vessel Dx; (see also Lezak, et al., 2004)

Neurolawyers have long dreamed of an "objective" test that could conclusively establish the existence of brain injury in cases of mild to moderate TBI where CT scans, MRI's and EEG's are negative or inconclusive the vast majority of the time. Too many brain injured individuals have been denied the compensation they deserve by insurance adjusters or juries who where unwilling to accept the diagnosis of brain injury based on "subjective" reports of impairment or neuropsychological testing. In recent years a new technology has evolved which holds promise of establishing an objective test for the presence of brain injury. That technology is Positron Emission Tomography, otherwise known as PET scanning… [t]here is a rapidly growing body of peer reviewed literature about the use of PET in the diagnosis and management of patients with a wide variety of disorders. A Medline search revealed numerous journal articles describing the use of PET and SPECT in the diagnosis of TBI. The vast majority of the literature supports the premise that PET is a useful diagnostic tool in the diagnosis of TBI…Based on the volume of current literature and the number of investigators studying the use of PET in the diagnosis of brain injury it appears that the clinical use of PET is rapidly gaining general acceptance within the medical community. The use of PET for the diagnosis of mild TBI has not yet gained widespread clinical acceptance [emphasis added], in part due to the limited availability of PET equipment and resultant high cost of PET scans. Health insurers are likely to deny benefits for PET scans in cases involving mild TBI based on claims it is "experimental.” Any attorney seeking the admission of PET scans following head trauma should be familiar with the Practice Statement on PET adopted by the American Academy of Neurology (Neurology, February 1991, Vol. 41:163-167). According to the Practice Statement, "The role of PET in the evaluation of head trauma has not been established." Given the age of the Practice Statement (it was adopted May 5, 1990), its conclusions are of questionable current value. However, defense counsel will surely cite the Practice Statement as evidence PET is not reliable in the diagnosis of brain injury. Hopefully, the Academy will revisit its position on PET and head trauma in the near future as much research on the subject has accumulated in the last 9 years. (see also Charles G. Monnett III and associates, 2009, http://www.carolinalaw.com/CM/Articles/article-scientific-evidence.asp)

Neuroanatomy and neurochemistry of TBI

• Highly dependent upon site of injury; diffusion, and CHI v. PHI
• Focal injuries often exacerbate systemic disorders and also include symptoms of diffuse
damage
• Can distinguish focal injuries via lateralization of symptoms
• Generally, the more rapid the onset (as in instantaneous trauma + sequelae over a longer
duration), the more widespread the effects
• Post trauma release of cytotoxins (glutamate cascade), reduction in cerebral circulation,
depressed metabolism, diaschisis (depression of activity in area around focal injury), and apoptosis (auto cell death)
• See also Lezak, et al., 2004

Common neuropsychological instruments used in diagnosis

• GCS, GOAT, Glasgow Outcome Scale, Disability Rating Scale, tests of orientation and
PTA, simple cog tests, WAIS-III (especially the very sensitive Digit Symbol subtest; Processing Speed Index)
• Rancho Los Amigos scale (Levels of cognitive functioning); Assessment of Individuals
with Cognitive Impairment (sensitive to ABD); San Diego Neuropsychological Test Battery (4 WAIS-III tests, 4 expanded HRB tests); (Lezak, et al., 2004)
• Can use children’s scales when severe TBI
• Use of testability scales, in rehab and other settings
• Military Acute Concussion Evaluation (MACE) and Standard Assessment
of Concussion (SAC) (McCrea, et al. 2008)
• Repeatable Battery for the Assessment of Neuropsychological Status (RBANS); Pt
interview; family/witness interview; record review; (French, et al., 2008)
• California Verbal Learning Test (CVLT); Controlled Oral Fluency Test (COWAT);
Wisconsin Card Sorting Test (WCST); Map Planning Test, Mazes Test; Paced Auditory Addition Test (PASAT); American New Adult Reading Test (ANART); (Drake, et al., 2000)

Neuropsychological profile – consider that…

• Many moderate and severe TBI patients achieve average levels on Wechsler and
Halsted-Reitan batteries yet continue to suffer frontal apathy, memory deficits, severely slowed thinking, and mental tracking ability (Lezak, 2004) “[G]lobal intelligence is relatively unaffected…speed of information processing is particularly vulnerable to brain injury” (Clement, et al., 2003, p. 1028)
• “[S]table verbal skills are most resistant to brain injury, followed by nonverbal reasoning
and visuospatial ability, and then working memory with speed of information processing being the most vulnerable…” (Clement, et al., 2003)
• Insufficient or inappropriate behavioral examinations of TBI can lead to unjust social
and legal decisions concerning employability and competency and confuse family members, adding to financial burdens and distress (see also Lezak, et al., 2004, pp. 186-7).

Neuropsychological Profile of TBI by domain
• Orientation
– O x 3/4 (purpose) (time and place especially susceptible), GCS/GOAT, can all be
– impaired due to coma and/or PTA
• Sensation/perception
– Impaired dependent on location/diffusion of injury; see also Visuospatial for
visual perception
– Auditory impairment contralaterally
– Skin writing - especially in DAI patients can be impaired
– Olfactory impairment possible, and indicator of likelihood of future employment
problems
• Attention
– Impaired, especially in decreased process speed and correlated with memory impairment (e.g., DS, WAIS-III, and modified Stroop tests; also TMT-A/B and Map in TEA); Sentence repetition impaired in DAI pts; see also Lezak, et al. 2004)
– Attention/concentration deficits very sensitively measured by Seashore Rhythm
Test in determining severity of TBI

• Motor
– Wide variability - especially as measured by drawing tests - CFT, etc.
– Planning deficits in Porteus Maze tests (all displayed psychosocial deficits as well)
• Visuospatial
– JLO short form shows some impairment; some visual form disturbance in acute TBI samples on the VFD; some visual organization impairment with Gollin Figures; perseveration and misidentification on Overlapping Figures Test
• Language skills
– Impaired; Aphasia especially as measured by CADL-2; Mill Hill Vocab scores
decreased;
– Fluency impaired especially correlated with length of coma and PTA, and
presence of DAI
• Memory
– (DS), STM impairment; RA/PTA impairments; occasionally, the only marker of
TBI is in impaired outcomes on working memory (e.g. Digits Backward, N-Back, and LN-Sequencing; see also Lezak, p. 356-63)
– WMS in examining associate learning and verbal memory, which can be
impaired
– Free and cued recall in PAL subtests (WMS) (especially correlated to enlarged
ventricles, duration of coma, and surgical repair of left hemispheric subarachnoid hemorrhage.
– In Story recall, TBI pts show good primacy and recency effects, though tend to
remember the middle sections poorly; CFT recall is impaired, especially after time delay
– Prospective memory impaired in severe TBI
• Abstract reasoning/conceptualization
– Impaired (usually in moderate to severe TBI), though variably, as illustrated in
WAIS-III Comprehension subtest - low scores indicating social competence impairment and functional independence predictor, post-rehab
– Sentence arrangement test shows impaired sequential reasoning (verbal)
– In moderate to severe (acute phase) TBI pts, Picture Completion subtest showed
depressed scores, especially in DAI
– Picture Arrangement is the second most sensitive in TBI (after DS)
– Arithmetic tends to be abnormally low in acute TBI patients
– Design Fluency tests reveal impaired output volume and
variability/inventiveness, as well as rule-breaking, perseveration, and less novel designs
• Emotional/psychological distress
– Tinker Toy Test reveals sensitivity to impaired psychosocial functioning,
including poor empathy, judgment, and absent mindedness; good measure of executive functioning
– As revealed in Rorschach testing, TBI pts show impaired ability to cope with
feelings and emotional situations and show poor social skills, with impoverished responses in making decisions, personality defects, and impaired social/relational abilities
– TBI pts show MCMI-III elevations on Anxiety, Dysthymia, Somatoform,
Narcissistic, Anti-social-Aggressive, and Passive-Aggressive scales, regardless of amount of time since injury or severity of TBI
– MMPI-2 Scale 4 (Pd) often most elevated, especially in males
– TBI patients show interesting progression on Sickness Impact Profile (SIP) over
periods of time since injury: most significantly impaired scales are psychosocial, body care and movement, ambulation home management, past times and recreation, mobility, and work
– SCL-90-R shows elevations in O-C and SOM scales

Psychiatric comorbidity

• Sequelae of TBI include
– Behavioral problems
– Depression and anxiety
– Emotional disturbances, distress, and fatigue
– Impaired empathy
– PTSD
– Obsessive/Compulsive features
– Social isolation
– Axis II increases (severe TBI), especially BPD, APD, Paranoid PD, OCPD, NPD

Functional impact

• TBI impairs: attention, conceptual ability, constructional ability, executive functioning
• Contributes to forgetting, inconsistency, memory deficits, learning issues, perceptual
issues, deleterious orientation, personality and reasoning, and mental processing (especially speed)
• Headaches, dizziness, fatigue, mental efficiency, motor dysfunction, motor slowing,
reaction time, and self-perception
• TBI significantly impacts activities of daily living, family, litigation, psychosocial
problems, and social withdrawal.
• TBI often results in death and loss/bereavement issues and can be financially crippling.

CONTROVERSY

• TBI litigation and damage assessment
– Does the neuropsychiatric impact have correspondence with medical evidence
and is it quantifiable?
– Does medical documentation substantiate a focal neuropsychological finding?
– Is there an existing image product that substantiates the above? (Granacher,
2008)
– Do you notice any problems here?
Acute Treatment of TBI

• Golden hour haste (ABC), assessment in ER, stabilization, ICU, intubation/ventilation,
iV fluids, polytrauma management
• Neurosurgery - craniotomy, catheterization/shunt placement, mass lesions,
suction/removal of hematomas, debridement in PHI, and decompressive craniectomy (primary DC) to address hematomas and control high ICP
• Pharmacotherapy - including norepinephrine, BZs, sedatives, analgesics, paralytic
agents, hypertonic saline to maintain ICP, diuretics,

• Subacute/Chronic Rehabilitation (Neurological, Neuropsychological, psychotherapeutic,
speech, physical, occupational, recreational therapies, etc.)
• See also Wikipedia and Zillmer, et al., 2008, pp. 390-398

Rehabilitation of TBI

• The Neuropsychologist considers the following factors when evaluating influences on
recovery from TBI:
– Location and extent of damage
– Duration of time since injury
– Age (wrt brain plasticity)
– Premorbid intellectual level
– Premorbid personality characteristics
– Premorbid functional level
– Medical health
– Emotional health
– Support system
– Type of treatment
• Encouraging is the fact that theories of rehabilitation take into account the abilities of the
brain to heal via plasticity, substitution, diaschisis, restitution, sprouting, and denervation supersensitivity.
• See also Zilmer, et al., 2008, pp. 388-398.

Prognosis

• Permanent disability approaches 10% in mTBI, 66% in moderate, and 100% in severe
injuries
• mTBI has a good clinical outcome, although a substantial group of patients develop post-
concussional complaints (PCC). There is little information on the effectiveness of various methods suggested for reducing the frequency of PCC. (De Kruijk, et al., 2001)
• Lezak maintains that once LOC or alteration of consciousness occurs, there is no
recovery possible. Though this does not preclude adaptation and compensation for deficits, nor rehabilitory learning (if not impaired)
• Prognosis differs depending on the lesion type. Subarachnoid hemorrhage approximately
doubles mortality. Subdural hematoma is associated with worse outcome and increased mortality, while people with epidural hematoma are expected to have a good outcome if they receive surgery quickly. Diffuse axonal injury is often associated with coma and poor outcome. (Wikipedia)

Organizations

• APA, especially Divisions 6 (Behavioral Neuroscience and
Comparative) 22 (Rehabilitation Psychology) and 40 (Clinical Neuropsychology)
• American Academy of Clinical Neuropsychology (AACN)
• National Academy of Neuropsychology
• Defense and Veterans Brain Injury Center (DVBIC), Walter Reed
– Working Group on the Acute Management of Mild Traumatic Brain
Injury in Military Operational Settings
• Various online TBI fora
• American Congress of Rehabilitation Medicine (ACRM)
• Centers for Disease Control (CDC)
• World Health Organization (WHO)
• Brain Injury Association of America
• The Ian Tillman Foundation (encouraging safety gear)
• The Neurotrauma Registry (www.neure.com)
• Local BI Support Groups
• Journal of Rehabilitation (TBI and Polytrauma special issue)

References and further reading

Bryant, R. A. (2008). Disentangling mild traumatic brain injury and stress reactions. New
England Journal of Medicine, 358(5), 525-527.
Clement, P. F., & Kennedy, J. E. (2003). Wechsler adult intelligence scale-third edition
characteristics of a military traumatic brain injury sample. Military Medicine, 168(12), 1025-1028.
Drake, A. I., Gray, N., Yoder, S., Pramuka, M., & Llewellyn, M. (2000). Factors
predicting return to work following mild traumatic brain injury: A discriminant analysis. Journal of Head Trauma Rehabilitation. Special Issue: Defense and Veterans Head Injury Program, 15(5), 1103-1112.
French, L. M., & Parkinson, G. W. (2008). Assessing and treating veterans with
traumatic brain injury. Journal of Clinical Psychology, 64(8), 1004-1013.
Granacher, R. (2008). Traumatic brain injury: Methods for clinical and forensic
neuropsychiatric assessment, 2nd Ed. Boca Raton, FL: CRC.
Hoge, C. W., McGurk, D., Thomas, J., Cox, A. L., Engel, C. C., & Castro, C. A. (2008).
Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal of Medicine, 358(5), 453-463.
De Kruijk, J., Twijnstra A., Leffers, P. (2001). Diagnostic criteria and differential
diagnosis of mild traumatic brain injury. Brain injury, 15, 2, 99-106.
Lezak, M., Howieson, D., Loring, D. (2004). Neuropsychological Assessment, 4th ed.
New York: Oxford University Press.
McCrea, M., Pliskin, N., Barth, J., Cox, D., Fink, J., French, L., et al. (2008). Official
position of the military TBI task force on the role of neuropsychology and rehabilitation psychology in the evaluation, management, and research of military veterans with traumatic brain injury. Clinical Neuropsychologist, 22(1), 10-26.
Ryan, M. A. K., Lloyd, D. W., Conlin, A. M. S., Gumbs, G. R., & Keenan, H. T. (2008).
Evaluating the epidemiology of inflicted traumatic brain injury in infants of U.S. military families. American Journal of Preventive Medicine, 34(4), S143-S147.
Taber, K. H., Warden, D. L., & Hurley, R. A. (2008). Blast-related traumatic brain injury:
What is known?, 75.
Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of Neuropsychology, 2nd
ed. Belmont, CA: Thomson Wadsworth.

Psychohistorical and ontological crisis mindmap

2010-01-24T16:11:00.000-08:00

Coming out of a horse sized K-hole: Ketamine's antagonist action at NMDA receptors and impacts of D1 upregulation in dlPFC

2009-12-06T20:06:00.000-08:00

One class of addictive drugs called dissociatives include such drugs as dextromethorphan (DXM), phencyclidine (PCP), and ketamine (K). Ketamine, commonly used in both veterinary and human medicine (high dose) as an anesthetic, is also used recreationally (typically in lower, subanesthetic doses), bringing on feelings of derealization, euphoria, dissociation, depersonalization, hallucinations, spiritual mind trips, etc., and is often used at dance events and parties. More specifically, “[k]etamine is a noncompetitive antagonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor” usually administered by intramuscular injection (IM) (Narendran, R., Frankle, W., Keefe, R., Gil, R., et al., 2005, p. 2352; action at the NMDA receptor as an indirect antagonist - Carlson, 2010, p. 615). Loose translation of the previous is that ketamine interferes with glutamate transmission at the NMDA receptor (not unlike alcohol, that also acts on GABA(A) receptors – Carlson, 2010, p. 631).

Perhaps not surprisingly, ketamine is linked to memory impairments, as the NMDA receptors are involved in long-term potentiation, implicit in learning (Carlson, 2010, p. 447). However, the long term effects of chronic ketamine use remain largely unknown (Narendran, 2005, p. 2352), while commonly thought to include K-pains – due to deterioration of the bladder, cognitive impairments – including memory, and neural network dysfunctions of various sorts (dearborization, etc. – see also common encyclopedic entries, ketamine was first synthesized in 1962 and is easily researched; see also RxList.com or Wikipedia.com).

Interestingly, the study I reviewed attempted to substantiate effects of chronic NMDA antagonist users (of ketamine) on the dorsolateral prefrontal cortex (dlPFC) because of earlier findings from “animal data indicated that the dorsolateral prefrontal cortex dopamine projections were especially vulnerable to repeated NMDA antagonist administration” (Narendran, et al., 2005, p. 2357). The study found that “D1 (dopaminergic) receptor availability was significantly up-regulated [“a compensatory increase in the sensitivity of receptors” (Carlson, 2010, p. 631); here, in correlation with the number of vials used per week] in chronic ketamine users… relative to comparison subjects … [and that] [n]o significant differences were noted in other cortical, limbic, or striatal regions” (Narendran, et al., 2005, p. 2357). While the authors did not, much to their surprise, find any cognitive deficits in users, it was made explicit that the typical user (who was not admitted to the study due to various psychiatric comorbidities, including polysubstance abuse), “even in the absence of cognitive deficits… repeated ketamine exposure… [is] associated with signs of disruptions of a critical component of cognition, the prefrontal dopamine system” (p. 2357).

In sum, the authors found that more research was needed, despite the evidence of neurotoxicity in animal models, as to the toxicity in humans (2005). They clearly stated, however that “the repeated use of ketamine for recreational purposes affects prefrontal dopaminergic transmission, a system critically involved in working memory and executive function [and might damage brain neurotransmission generally]” (p. 2358).

This study is a good one because of the link between exogenous substances, the dlPFC and receptor sites, with such illnesses as schizophrenia. Schizophrenia is characterized by an imbalance in dopamine transmission, especially at the D1 receptors (DA deficit; cognitive impairment) and the D2 receptors (DA excess; psychosis) (p. 2358). The authors provided the following link: “[t]he fact that chronic ketamine users and patients with schizophrenia exhibit the same endophenotypic trait (up-regulated D1 receptor expression in the dorsolateral prefrontal cortex) supports the hypothesis that in schizophrenia, this alteration might be secondary to NMDA dysfunction” (p. 2358). In fact, many researchers have long since established the link between DA agonists like cocaine and amphetamine, that also cause positive symptoms of schizophrenia (hallucinations, delusions, etc.), as well as PCP (angel dust) and ketamine (Special K or Vitamin K), as capable of causing positive, negative (poverty of speech, anhedonia, etc.), and cognitive symptoms (attentional problems, deficits in learning and memory, poor problem solving, etc.) of schizophrenia and therefore study the effects of these drugs with the hope of curing schizophrenia (Carlson, 2010, pp. 557, 567)

While not formally addressed in the article reviewed, is withdrawal from ketamine. I looked up information from a drug treatment center that described both the physiological and psychological processes involved. Since ketamine involves both psychological and physical effects, withdrawal is both a physical and mental process. The person undergoing the process should be kept under close supervision, due to the strength of the psychological addiction. While displacement away from the sources of drugs are a good tactic for the person in withdrawal, along with psychotherapy and behavior modification, another aspect of ketamine withdrawal, which is best addressed in a professional setting, is the physical side of ketamine withdrawal. The user more often than not has neglected their own physical well-being and often needs the help of nutritionists and physicians. (see also http://www.ketamine-effects.com/ketamine-withdrawal.htm)

Prolonged use has been associated with physical and psychological addiction. In the majority of individuals who frequently use ketamine, tolerance does develop to these effects, thus requiring the addicts to consume higher doses.

Although ketamine does not give rise to physical dependence like that seen with morphine, heroin or alcohol, it is associated with a powerful psychological addiction - like that seen with cocaine. Because of its ability to produce intense, vivid psychedelic effects it is frequently abused. The psychedelic effects and out of body experiences have been primary reasons why the drug is abused.

In conclusion, ketamine addiction, like all addiction begins with the acceptance of a problem by the individual. Many drug rehabilitation and treatment facilities are available for ketamine treatment. There are no antidotes to ketamine and the majority of therapy is psychotherapeutic. (see also http://www.addictionsearch.com/treatment_articles/article/ketamine-addiction-abuse-and-withdrawal_23.html)

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Narendran, R., Frankle, W., Keefe, R., Gil, R., et al. (2005). Altered Prefrontal Dopaminergic Function in Chronic Recreational Ketamine Users. The American Journal of Psychiatry, 162(12), 2352-9. doi: 942933491.

Biopsychologically Informed Treatment of Trauma

2009-12-06T19:34:00.000-08:00

Biopsychologically Informed Treatment of Trauma
by
Peter A. Brown, MA

California Institute of Integral Studies
Clinical Psychology
School of Professional Psychology

Biopsychologically Informed Treatment of Trauma

In much of the literature there are ongoing debates surrounding etiology of subcortical abnormalities in Post Traumatic Stress Disorder (PTSD)/trauma, with two prominent hypotheses: the predisposition hypothesis, and the so-called neurotoxicity hypothesis. In my recent paper, I reviewed these two hypotheses and some of the literature in this subfield of biopsychotraumatology and found that both are likely operative (reminiscent of the nature-nurture debate) (Brown, 2009). That said, and with a long-term goal of specialization in neuropsychotraumatology in mind, this paper covers the biopsychologically informed treatment of trauma used in the field today.

The person suffering from PTSD is likely to have a dysfunctional hippocampus that does not distinguish a safe context from a dangerous one, thereby triggering amygdalic-emotional response (see also Carlson, 2010, p. 607). This subcortical process follows the ‘low road’ in amygdalic connectivity parlance, bypassing the (ventro-)medial prefrontal cortex ((v-)mPFC – especially the Anterior Cingulate Cortex – ACC) which is unable to inhibit these triggers (or is itself impaired); the amygdala is highly connected, both ascending to cortical structures like the vmPFC or ACC and descending to other (sub-)pontine structures (including the spinal cord) (Zillmer, Spiers, & Culbertson, 2008, p. 150). Treatment, therefore, would need to address the subcortical, bottom-up processing ‘road’ and not only the top-down, cortical, cognitive ‘road’.

Interestingly enough, the sine qua non of the psychotraumatology specialty is cognitive-behavioral therapy, a high road therapy. Certainly, other treatments, such as pharmacotherapies are viable options, alongside integrative high and low road therapies. In this paper, I review a brief sampling from literatures related to pharmacotherapies and integrative methods, leaving those that focus on cognitive methods to future articles. I think that both pharmacotherapies and integrative therapies are vital to effective treatment, and maintain that biopsychologically informed treatments can help (even if simply to help researchers ask the right questions) to ameliorate efforts in the biopsychotherapeutically oriented treatment programs and research streams currently active today.

Literal wounds to the brain

One current article I reviewed argued for the re-medicalization of the PTSD construct in order to help fight against pathologization and stigmatization of PTSD and victims of trauma Nash, Silva, & Litz, 2009). In fact, the authors pointed out the deliberate decision to stigmatize ‘shell shock’ so as to prevent desertion during the world wars: “stigma was attached to mental health labels intentionally as a deterrent to stress-casualty epidemics” (p. 794). This re-neurologization of the modern research paradigm is revitalizing the work of Pierre Janet, a contemporary of Freud, who dealt with dissociation’s (theoretical) effects on brain function at the beginning of the 20th century (p. 792). In fact, the most recent studies indicate that severe stress can literally injure the brain and calls for this paradigm shift in thinking about traumatic stress (p. 792). While much of the rhetoric of the writing in the field, and of the article reviewed, (discussing etiological mechanisms) dovetails with the CBT literature, interesting conclusions merit attention, especially in the
extinction of fear-based conditioning… mediated by the medial prefrontal cortex, and social cue recognition… mediated by the orbitofrontal cortex, in addition to the hippocampus and amygdala…[and the ACC, a] brain center essential for the inhibition of situationally inappropriate or irrelevant thoughts and emotions, as well as for the situation specific regulation of autonomic arousal, including pulse and blood pressure. (p. 792)

What the authors fail to mention are the treatment modalities toward which they allude: behavioral modification (‘extinction’ etc., along the lines of classical conditioning), socially based therapies (milieu, systems, etc.), and biofeedback oriented psychoeducation (relaxation, mindfulness, guided imagery, hypnosis, etc.). They call for treatments that include remedying “deficits in memory…extinction of fear-based learning, [gaining] authority over one’s own emotions and thoughts, and the regulation of autonomic arousal” (p. 792).

The most valuable contribution of the article was articulation of the position that the suffering and impairment of those who suffer from PTSD, (especially soldiers, sailors, airmen, and marines),
are not due to their own failure or weakness, any more than any other physical wound would be. …this conception can provide a framework for more effective primary and secondary prevention programs in the military and other community settings, as have been adopted recently by the Navy and Marine Corps. By lessening the barriers to early recognition, the stress injury model may also promote more effective and targeted early interventions, such as those based on cognitive-behavioral therapy. (pp. 793-4)

Pharmacotherapeutic Treatment of Trauma

In light of what researchers know of the excitotoxicity of glutamatergic cascades, (as seen in Traumatic Brain Injury, depression, etc.) and along the lines of the excitotoxic hypothesis of PTSD (see also Brown, 2009), combined with the typical high-road focus of CBT oriented research and therapies, the field needs and fortunately uses medications as a growing, primary treatment modality. For example, phenytoin/Dilantin is an anticonvulsant used in epilepsy treatment that seems to modulate glutamatergic transmission, and was recently studied as to the cognitive and neurophysiologic impacts in PTSD patients (Bremner, et al., 2005, p. 159). The authors found that “[p]henytoin treatment resulted in a significant 6% increase in right brain volume … [and] [i]ncreased hippocampal volume was correlated with reductions in symptom severity” (p. 159). The mechanistic postulate is phenytoin antagonizes glutamate excitation and blocks the effect at the NMDA receptor (p. 163). Noting that the right side was ameliorated over the left, the authors called attention to the well-known contribution of the right brain to emotion and non-verbal cognitive processes, over and above that of the left side (p. 163).

The most important aspect of this study was the demonstration that medications used in neuropsychiatric treatments actually had effects on the very physiology of the brain itself (p. 163). This line of research, and that of other pharmacotherapies, such as propranolol (see also Pitman, et al., 2004, pp. 241-2) and paroxetine (one year SSRI treatment yielding a 5% increase in hippocampal volume and a 35% improvement in verbal declarative memory function in PTSD patients; Vermetten as cited in Bremner, et al., 2005, p. 160) are some of the most promising research that I reviewed, considering the biopsychological focus in the treatment of trauma.

Biopsychologically Focused Psychopharmacological Treatment

Another area of vital importance to the traumatology specialty is memory. It is commonly known that the amygdala influences the aroused encoding and consolidation of memory and that the extreme arousal of trauma leads to persistent memory traces (McCleery & Harvey, 2004, p. 487). While traumatically consolidated memories are stubbornly resistant to treatment, “the strength of memory for a learned task can be modified (either weakened or enhanced) by treatments, including drugs and hormones (adrenaline, glucocorticoids, …[though] the longer the gap… [before] treatment, the less effective the modification (McGaugh as cited in McCleery & Harvey, 2004, p. 488). This line of research suggests the modification by hormonal means can act on the activation of adrenergic and muscarinic cholinergic receptors in the basolateral nucleus of the amygdala (BLA), thereby leading to alternative interventions on those areas of the brain involved in traumatic memory (McCleery & Harvey, 2004, p. 488).

Another interesting approach is in the use of centrally acting noradrenergic beta-(receptor antagonists)blockers in order to inhibit the emotional enhancement of memory (p. 488); I think of prazosin/Minipress, a similar drug, though it acts on alpha-1-receptors and is typically used off-label for PTSD related nightmares in both veterans and civilians (Singh, personal communication, 2008; see also Friedman, Davidson, & Stein, 2009, who suggest the aforementioned, as well as alpha-2-receptor agonists like clonidine and guanfacine, p. 564). Contrariwise, yohimbine stimulates noradrenergic enhancement of memory (McCleery & Harvey, 2004, p. 488). Both these are interesting in examining the best course of treatment (considering a conservative approach) matched to the individual and the context – naturally fraught with problems. The undergirding is that when a memory is invoked and made labile, it may be acted upon and before reconsolidation, alteration can occur. In fact, “there is preliminary evidence … that a beta blocker administered soon after a traumatic event may reduce the strength of fear conditioning” (Pitman as cited in McCleery & Harvey, 2004, p. 488). Other methods under investigation include disruption of the conditioned fear response in rats by inhibiting protein synthesis after reactivating the memory (McCleery & Harvey, 2004, p. 489). However, the authors also point out that “[t]here is still little direct evidence for the reconsolidation hypothesis in humans” (p. 489), which naturally limit externalization of these findings.

I find it very interesting that the field seems to contradict itself in many areas, for example, that of the role of arousal in trauma and in trauma treatment:
in a positive psychosocial context … [arousal in response to traumatic events] forms an essential part of the mechanism of adaptation. Initial memories of a traumatic event will inevitably be distressing and, as described above, successful psychological adjustment seems to involve the incorporation of both increased factual detail and more positive interpretations … into declarative memory. This therapeutic processing… will also be promoted by arousal…[and] the success of exposure treatment is greater when there is a higher degree of arousal during treatment …with the possible exception of extremely high levels. The addition to exposure treatment of interventions specifically designed to reduce anxiety/arousal… has not been found to improve outcome. (p. 492)

Many studies note that using a more neurobiological consideration of the role of arousal and how pharmacotherapies might be helpful, for example in drastically reducing arousal states and promoting amnesia after trauma: psychotherapy plus beta blockers to reduce the strength of memories, beta blockers plus exposure therapy, and even administering beta blockers as soon as possible post-trauma (p. 492), similar to the proposed use of propranolol (Pitman, et al., 2004). However, the authors warn that while these drugs may be helpful in preventing overconsolidation of traumatic memory traces, they could also prevent incorporation of safety information, thus preventing timely recovery (McCleery & Harvey, 2004, p. 487). So for people who might even recover well (which it is still very difficult to completely determine propensity for PTSD development, “drug treatments are likely to be of benefit only if targeted very carefully at high risk individuals, whom it may not be possible to identify accurately in the acute phase” (p. 493) might be harmed by hasty use of beta blockers (or propranolol, or benzodiazepines - BZs - that induce anterograde amnesia in the BLA) (p. 488; see also Friedman, Davidson, & Stein, 2009, who maintain that BZs are contraindicated for PTSD monotherapy, p. 566).

In conclusion to the section on pharmacotherapies, due to the fact that trauma survivors need a robust cortisol response in order to contain sympathetic arousal, and that those with highest risk for development of PTSD typically do not show one, it is promising to consider that the use of “stress-level hydrocortisone treatment… was associated with a reduction in PTSD symptoms” (McCleery & Harvey, 2004, p. 493). However, this
preventative strategy…given the continuing uncertainty about the status of the HPA axis in PTSD patients and the fact that acute cortisol administration has been found to enhance emotional memory, this strategy too cannot be regarded as being without risk of harm. (p. 493)

Note that the brain might be damaged due to psychological distress by action of “stress-induced disturbance of the hypothalamic-pituitary-adrenal axis” (Sapolsky as cited in Schmahl, et al., 2009, p. 294), glucocorticoids, and glutamate active in the limbic system (see also Carlson, 2010; Zillmer, et al., 2008), but the exactness of the predispositional versus the neurotoxic etiologies of chronic PTSD is still debated (see also Brown, 2009).

Integrative Treatment Approach: EMDR

So, because of the difficulties in targeting those at risk for development of PTSD in the acute phase (and even the risk of harming them) with pharmacologic intervention, and that “[t]op-down approaches… do not process the episodic memories or resolve physiological hyperarousal” (Solomon & Heide, 2005, p. 56), what is the best treatment approach?

It is clear that people will, even after years of therapy, come into contact with events that ‘trigger’ them physiologically, and that their response is not of a logical, top-down, high-road, cortical nature, especially of the sort that therapies like CBT target (p. 56). In contrast,
[b]iologically informed therapy focuses on processing …[e]pisodic memories [that] are … transferred from the limbic system to the neocortex and filed away along with other narrative memories. Biologically informed therapy includes bottom-up processing, which focuses on what is going on in the body. This approach helps clients connect with their bodies and with their feelings. It facilitates their learning to tolerate intense feelings and to release emotion appropriately. Survivors learn to calm their physiology. (p. 57)

Eye Movement Desensitization and Reprocessing (EMDR) therapy involves visual, tactile, and auditory (even proprioceptive) stimuli that alternately stimulate the left and right hemispheres (p. 58). Some say “repetitive redirecting of attention [especially through eye movement] in EMDR induces a REM sleep-like state… that facilitates the activation of episodic memories…[which] are processed and integrated into neural networks in the neocortex as semantic (narrative) memory” (p. 58). This therapy is proving to increase
bilateral activity in the…[ACC, a] part of the brain that modulates the limbic system and helps us distinguish real from perceived (but not real) threat. The increase …[in ACC] activity suggests a decrease in hypervigilance… [there was also an] increase in prefrontal lobe metabolism, suggesting greater ability to make sense of incoming sensory stimulation. (p. 58)

Conclusions

It is clear that both high road and low road therapies must work together, alongside those underpinning hypotheses (neurotoxic v. predisposition) in order to develop innovative applications in prevention and treatment of PTSD and base them on biopsychological bases. Perhaps in a foreshadowing of what is still yet to come, Sapolsky (2002) suggests that, should the neurotoxicity hypothesis stand, the field needs to develop a kind of post-traumatic golden hour of response along with antidote to the cascade of glucocorticoids and glutamate in the brain (p. 1113; not unlike the propranolol preventative treatments - Pitman, et al., 2004, pp. 241-2).

As I mentioned elsewhere, single case findings from researchers treating PTSD patients with EMDR for 90 minutes per week for 8 weeks, show that this therapy increased total baseline hippocampal volume by some 11% (Letizia, 2007, pp. 475-6). I imagine that through ongoing studies such as these, in combination with various other methods of treatment, will give the field more questions to consider to the age-old human problem of suffering and its alleviation. The integrative application of biopsychology is indeed a powerful force in this change.

References

Bremner, J., Mletzko, T., Welter, S., Quinn, S., Williams, C., Brummer, M., … Nemeroff, C. (2005). Effects of phenytoin on memory, cognition and brain structure in post-traumatic stress disorder: A pilot study. Journal of Psychopharmacology, 19(2), 159-165. doi:10.1177/0269881105048996

Brown, P. (2009, November 14). Traumatic predisposition or neurotoxicity: Examining hippocampal volume and PTSD. [Web log post]. Retrieved from http://peterallenbrown.blogspot.com/2009/11/traumatic-predisposition-or.html

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Friedman, M., Davidson, J., & Stein, D. (2009). Psychopharmacotherapy for adults. In E. Foa, T. Keane, M. Friedman & J. Cohen (Eds.), Effective treatments for PTSD: Practice guidelines from the international society for traumatic stress studies (2nd ed.). (pp. 269-278). New York, NY, US: Guilford Press.

Letizia, B., Andrea, F., & Paolo, C. (2007). Neuroanatomical changes after eye movement desensitization and reprocessing (EMDR) treatment in posttraumatic stress disorder. The Journal of Neuropsychiatry and Clinical Neurosciences, 19(4), 475-476. doi:10.1176/appi.neuropsych.19.4.475

McCleery, J., & Harvey, A. (2004). Integration of psychological and biological approaches to trauma memory: Implications for pharmacological prevention of PTSD. Journal of Traumatic Stress, 17(6), 485-496. doi:10.1007/s10960-004-5797-5

Nash, W., Silva, C., & Litz, B. (2009). The historic origins of military and veteran mental health stigma and the stress injury model as a means to reduce it. Psychiatric Annals, 39(8), 789-794. doi:10.3928/00485713-20090728-05

Pitman, R., Sanders, K., Zusman, R., Healy, A., Cheema, F., Lasko, N. … Orr, S. (2004). Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Curr Psychiatry Rep., 6(4), 241-2.

Sapolsky, R. (2002). Chicken, eggs and hippocampal atrophy. Nature Neuroscience, 5(11), 1111-1113. doi:10.1038/nn1102-1111

Schmahl, C., Berne, K., Krause, A., Kleindienst, N., Valerius, G., Vermetten, E., & Bohus, M. (2009). Hippocampus and amygdala volumes in patients with borderline personality disorder with or without posttraumatic stress disorder. Journal of Psychiatry & Neuroscience, 34(4), 289-295.

Solomon, E., & Heide, K. (2005). The biology of trauma: Implications for treatment. Journal of Interpersonal Violence. Special 20th Anniversary Issue, 20(1), 51-60. doi:10.1177/0886260504268119

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

The Synaptic Button and Drug Action

2009-12-02T10:50:00.001-08:00

The synapse of the terminal button, both pre- and post-synaptically (that is, from transmitting to receiving button) are also effected by a mechanism called hyperpolarization of the dendritic autoreceptors where they are activated by neurotransmitter or antagonist drug action (that binds to and blocks the receptors) thereby reducing the rate of firing of the neuron, effectively acting as an antagonist (Carlson, 2010, p. 113). Certainly, drugs that block the autoreceptors antagonistically, reduce the effect of hyperpolarization (which is regulatory by nature) and thereby work as agonists (reducing this regulatory effect) (p. 113).

Drugs can affect synaptic transmission in a variety of ways. Carlson (2010) mentions at least 11 ways, ranging from drugs serving as precursor agonists (like L-Dopa on dopamine), inhibits synthesis of neurotransmitter antagonist (like PCPA on serotonin), prevents storage of neurotransmitter in vesicles as antagonist (reserpine on monoamines), stimulates release of neurotransmitter as agonist (spider venom on acetylcholine-ACh), inhibits release of neurotransmitter as antagonist (toxin on ACh), stimulates postsynaptic receptors as agonists (nicotine and muscarine on ACh), and naturally several others like blocks as antagonists, blocks or stimulates autoreceptors, blocks reuptake as agonists, or inactivates as agonists that which is transmitted synaptically. Certainly, the two basic forms of these are agonists and antagonists (drugs that are facilitating versus inhibiting postsynaptic effects) (p. 111).

Drug reactivity in tolerance and sensitization are both similar and different (compensatory mechanisms v. direction of effect). Drug reactions are similar in these two phenomena because drugs follow a dose-response curve that reciprocates larger drug effects with increase doses, up to a maximum effect, where dose increases no longer produce drug reactivity, and increase prevalence of side effects and risk (p. 107). Drug effects that diminish with repeated dosage are called tolerance; and effects that increase are called sensitization (p. 108). Drug tolerance effects are the bane of illicit drug users (think heroine), in that the brain works to maintain optimal levels of functioning at all times and with repeated (and increasing) doses of exogenous substances, the brain produces opposite reactions to compensate (hence the opposite withdrawal symptoms upon substance stop) (p. 109). Further, the sites where the substances bind become less sensitive to the drug as it is used more frequently and the receptors actually decrease in number, also knows as a compensatory mechanism (similar to the decrease in effectiveness of coupling, another compensatory mechanism) (p. 109). In contrast to tolerance mechanisms, sensitization is more rare (p. 109). Because sensitization causes ever-larger drug effects, compensatory mechanisms direct regulatory efforts away from physiologic processes, as in respiratory depressive effects of barbiturates or opiates that show sensitization (especially in combination) versus their euphoric and/or analgesic properties that show tolerance effects (p. 109).

References
Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Social psychology tangent - Anomie or Cradle to Flag-Draped Grave: Social Constructivism and War

2009-11-28T22:46:00.000-08:00

Running head: SOCIAL CONSTRUCTIVISM AND WAR

Anomie or Cradle to Flag-Draped Grave: Social Constructivism and War

Peter A. Brown

Professor Dr. Benjamin Tong
Social Psychology, Fall 2009

Author Note

Peter A. Brown, MA; California Institute of Integral Studies, School of Professional Psychology, Clinical Psychology Doctoral Program; 1453 Mission St., San Francisco, CA 94103; telephone: (415) 575-6100 x 6453.

Anomie or Cradle to Flag-Draped Grave: Social Constructivism and War

The innocent American is the violent American –
which is usually how other nations perceive us.
-- James Hillman, (2004, p. 133)

Abstract
Background: Social psychologists have long studied violence, war, groups, hate and anger, power, and rules that people live by and how people can both decry war in all its forms and devastate whole societies when self-serving views are threatened.

Aims: This paper endeavors to present contemporary and historical evidence on the nature of the relationship between war and social constructivism and offer an integrative synthesis of findings.

Method: This synthesis follows what Torraco (2005) called an “integrative literature review.” In this sense, each article is integrated in order to generate innovations in this area of research and practice.

Results: The results are clear that war is both amenable to social constructivism and impervious to it, while always embedded in a biosocial matrix that uses its self-construction in order to raise consciousness of itself.

Conclusions: A conclusion of this study is the implication for evidence-based practice in healing the wounds of war – that is, an applied understanding of social constructivism as vital in therapeutic settings.

Keywords: social constructivism, war, social psychology

Table of Contents

Social Constructivism & War, Defined 3
Personal Perspective and Positioning Epoche 4
Living Questions and Method: An Exploration 5
From Rush to Mao: “Turn it 20,000 degrees and let’s start over.” 6
Integrated discussion of research: Will the dualists please approach 9
War as embedded in the social matrix: Co-constructed, burned-in – embodied violence 10
War’s Construction-of-Society-through-Destructive-Means Prize 17
Herr Dr. Mengele please report to the lab, the gentlemen from the thought police are here to see you: Constructing warring societies 20
Conclusion 24
References 27

O Lord our God,
help us
to tear their soldiers
to bloody shreds
with our shells;
help us
to cover their smiling fields
with the pale forms
of their patriotic dead;
help us
to drown the thunder
of the guns
with the shrieks
of their wounded
writhing in pain;
help us
to lay waste
their humble homes
with a hurricane of fire;

-- Mark Twain, from The War Prayer, 1923 (Hillman, 2004, p. 201)

Anomie or Cradle to Flag-Draped Grave: Social Constructivism and War

“Why did millions of people begin to kill one another? Who told them to do it? It would seem that it was clear to each of them that this could not benefit any of them, but would be worse for them all…the causes were innumerable and…not one of them deserves to be called the cause.” For Tolstoy war was governed by something like a collective force beyond individual human will.

The task, then, is to imagine the nature of this collective force. War’s terrifying prospect brings us to a crucial moment in the history of the mind, a moment when imagination becomes the method of choice, and the sympathetic psychologizing learned in a century of consulting rooms takes precedence over the outdated privileging of scientific objectivity. (Hillman, 2004, p. 7)

The above quotation from Tolstoy with commentary by James Hillman illustrates a commonly held fact: alongside a failure of imagination, culture and the society’s attitudes toward violence are primary factors in its spread (Elbert, Rockstroh, Kolassa, Schauer, & Neuner, 2006, p. 342). At the individual-as-embedded-in-culture level, one study found that between “34% to 45% of the interstate…serial killer activity could be accounted for by dimensions of local culture, with higher rates of violence being found in states supporting game hunting, military training, and a local culture supporting punitive violence” (DeFronzo & Prochnow as cited in Elbert, 2006, et al., p. 342). In any society, these are crimes and are outlawed; with war, at least of the traditional and historical variety, with thousands if not millions of combatants, wars and armed conflicts seem to have slipped through institutionalized ‘loop-holes’ (Elchenroth, 2006, pp. 907-8). After the bloodbaths in Rwanda and Yugoslavia, and
[a]s a reaction to the threat for the respect of fundamental rights caused by periods of armed conflict and by the breakdown of national institutions, there have been repeated efforts from the international community resulting in the growing institutionalization of international humanitarian law, which is supposed to compensate for the legal loophole generated by armed conflicts, by defining the principles of a minimal and irreducible law. (pp. 907-8)

However, does this push cover the seeming escalation of the “new wars” of organized violence? These new wars are state sponsored - harassment, torture, terrorism – and over 90% of these are intra-state conflicts, civil wars, and actions by rebel armies (using irregular forces, affiliations to different groups – ethnic, religious, etc., targeting civilians – over 80% of the casualties of new wars are civilians, and due to economic factors, including use of foreign resources to fund them) (Elbert, et al., 2006, pp. 343-4).

Naturally, there are consequences of these wars at both the individual and collective levels. Prevalence rates for trauma spectrum disorders – that is, disorders that incapacitate - range from 20% to as much as 60% (p. 344). These figures effectively wipe out communities and their abilities to recover from war, and produce secondary effects on the population such as domestic violence, intimate partner violence, transmission of trauma, further warring, and fosters a cycle of violence in whole regions and continents (most poignant in Africa) (pp. 344-5). These devastating effects have been referred to as “societal trauma” (p. 345).

Social Constructivism & War, Defined

This paper examines the relationship between war and social constructivism. Social constructivism is a critical theory that emphasizes a socially constructed view of reality by those involved; either emically – as insiders – within a context of time and place and supplanting a more positivist search for universal truth, or a more etically oriented – that is, ‘objective’ and outsider - perspective (Miller, Kulkarni, & Kushner, 2006, pp. 412-3). Emically, this paper eschews a positivist stance - despite the flavor and structure of an ‘integrative literature review’ as a legitimate, scientific method – in favor of a more pluralistic and constructive, postmodern view.

The late Dr. Sue Mansfield, Professor Emerita at Claremont McKenna College (Claremont, CA), who died in 2002, defines war as:

a particular type of institutionalized aggression in which social pressure is used to force individuals to kill other people they may not even hate or fear [or know]…[and] through which a group of individuals attempts to satisfy its needs by destructuring and imposing its will on another group. (Mansfield & Keen, 1982, p. 382)

Naturally, war might also be considered a state of anomie, where lawlessness prevails. On the other hand, war can also be constructed and used by societies. War is socially constructed in that it is fought over a differing construal of reality, truth, or belief. It is also far beyond that which a society can collectively understand, as it typically destroys societies. There are rules of war, war propaganda, war crimes, illegal wars, ethical wars, and total wars. There are honors in war, war hawks, societies or brotherhoods of war, war trophies, winning over hearts and minds, ethnic cleansings, truth and reconciliations committees, war crimes tribunals, holocausts, genocides, fratricides, and any number of destructive and counter-destructive acts of war and reactions to war. War confuses, enrages, and changes everything in its path.

Personal Perspective and Positioning Epoche

As a former Regular Army Captain, combat veteran, military academy graduate (USMA-West Point, Class of 1996, graduate [Cullum] number 53,003), I have some firsthand knowledge of rules of war, if captured was to be held to Category III of the Geneva Conventions (that is, a ranking system that also provides for pay to prisoners of war; Cat., III is for warrant officers and those commissioned officers below the rank of Major, who holds Cat. IV), the conduct of war, and the feel of war – that unmistakable pungency, the electricity and fear in the air; the sweat and the heat, the roar. I have shipped youth home in metal boxes and have helped put them in the ground; both close colleagues and strangers. I have luckily survived and can report that my hands are clean, though I fear much has rubbed off on me. I have had the opportunity to study the great wars, the strategists and generals, the participants, and battlefields. Despite this, in the wake of what is being called “The Fort Hood Massacre,” I am left shaking my head. Perhaps at the aggrandized and glorious end of the war-spectrum, “[a] wartime perception of reality has a "mythic" quality,” (Social construction of war, 2003). War has a particular salience in my work; that about sums it up.

Living Questions and Method: An Exploration

Social psychology has long sought to understand the problem of human suffering, especially with regards to Aronsonian categorization of the field: conformity, mass communication/propaganda/persuasion, cognition, self-justification, aggression, prejudice, loving/sensitivity, and science – perhaps boiling down to social influence that people have over others (Aronson, 2009, pp. v and 6). Perhaps then, this study is best suited to asking further questions in lieu of providing quasi-positivist ‘reality-as-it-really-is’ answers, exploring instead: “what are factors at play in influencing people’s relationship to war?” or “how does social constructivism relate to war and thereby influence people?” or “does social constructivism capture the manifold valences of war?” With these questions in mind, I aim to explore some of the relevant literature, while integrating material from authors in the fields of social psychology, neuropsychology and neuroscience, philosophy, anthropology, traumatology, and even some practitioners of psychotherapy. While this may seem like a vast area of research, the exploration serves as performatively oriented social construction of war, by way of dialogical argument.

Perhaps, too, it is important to mention that this study is by no means an exhaustive review of the literature, nor does it attempt to solve the dilemma of war, offer a groundbreaking theory, or cover every angle. Rather, my curiosity in the area of intersection between social constructivism and war piqued my interest sufficiently to design the present study according to a hybridization of what Torracco (2005) calls an integrative review of the literature, compellingly relevant to the study of social constructivism.

The method of literature review was to search using a common database. Some interesting studies turn up in the research and peer-reviewed literature, albeit largely in philosophic, qualitative, or case study format. In a search of one database (PsychInfo), I found 13 articles, 2 of which were brief reviews of much larger works, and 7 of which were suitable for inclusion in this paper based on keyword criteria, availability, and dated after 9/11(/2001) (keywords: social constructivism, war, violence, combat, trauma, construction, constructionism, constructivism and variants by thesaurus and combined search options).

From Rush to Mao: “Turn it 20,000 degrees and let’s start over.”

The rationale for this review of social constructivism and war, especially in terms of social psychological methods and their application, is my ongoing research into the nature of epistemic concerns in the research and treatment of combat veterans. These epistemic concerns, really a critique of whole, socially constructed, dogmatic paradigms of scientific hegemony, are not unlike religious belief systems where the diversity of others’ views are largely neglected, dismissed, and sometime, outright destroyed through violent means. This is not to say that scientific domination is the responsible culprit for wars in the world today, rather, that it is in the very beliefs themselves that power brokers use to maintain an intolerance of diversity.
Take for example, James Hillman’s book A Terrible Love of War, where he cogently argues that the Judeo-Christian ethic, as purveyor of monotheistic, patriarchal belief systems, is, at its root, a violent system that elicits warmaking (2004). Hillman wasn’t alone in his condemnation of the Judeo-Christian monistic and violent belief system, either. Perhaps Dr. Hillman knew Sue Mansfield who said: “Christian culture is at once more pacifistic in its intent and more violent in its action than any other culture that has existed” (Mansfield & Keen, 1982, p. 385). Hillman notes that

[w]ar presents theological dilemmas about the nature and intention of a one and only almighty God whose goodness and mercy are exalted by the three great monotheistic religions. By definition this God has the greatest power; there is nothing he cannot do – that is what omnipotence means. So why does he not put a stop to war? … Either he can’t stop war or he doesn’t want to. The first rebuts his claim to almightiness and the second implies that he likes war, or at least by not stopping it, he sustains it” (Hillman, 2004, p. 187).

It is perhaps clear that Hillman, a post-Jungian, founder of archetypal psychology, and a veteran of World War II himself (he was a corpsman in a hospital treating some of the more grisly injuries of the war), sees tolerance and belief as core splits that precipitate war:

[b]ecause a monotheistic psychology must be dedicated to unity, its psychopathology is intolerance of difference. Hence the issue of toleration has plagued theological thinkers for ages, leading to schisms and more schisms. As long as you hold that your god is the perfect supreme deity, all other gods will be lesser. There are no several truths, no other roads to the Kingdom. …Moreover, as long as the others, the lesser, continue to practice their precepts and believe in a different god (or a slight variation in the nature of your god), they exhibit in their very existence a denial of the complete truth of your god. It is a necessity of your truth and your faith to war against them, because no matter how quietly they live or how far away their territories, their existence places in essential doubt the foundations of your belief in your god [or politics, or money, or epistemological ground, or philosophy…and provides ample opportunity to fight ever more strongly for the cause of defending the faith, nation, etc.]. (Hillman, 2004, p. 183)

Social psychologists aren’t only complaining; they are also involved in researching the attempted control of war, through social justice efforts. One article I reviewed presented evidence to substantiate four major research programs in thinking about justice and war: 1) social justice is constructed and embedded in the same frame as the viewer – that is, people see it in their own terms (especially involving the fundamental attribution error (Jones & Nisbett as cited in Hatfield & Rapson, 2005, p. 173), 2) people define social justice to serve themselves (especially in primatology and in entitlement, neurobiology, etc.) 3) authority, power, and peer pressure have tremendous influence on how people treat each other, (Milgram, Zimbardo, et al.) and 4) emotions determine social justice views and how people treat each other (emotional contagion, basic biopsychology and neurophysiology, and research showing that people, when angry and frustrated will take it out on scapegoats – witness the holocaust, Stalin’s and Mao-Tse-Tung’s purges) (Hatfield & Rapson, 2005, pp. 172-4). Perhaps the best example of these is an excerpt from the infamous Rush Limbaugh, commenting on “his angry and nationalistic reaction to hearing of the American’s torture of the Abu Ghraib Prison prisoners in Baghdad, Iraq, and the subsequent killing of an American hostage [by beheading]” (p. 174) quoted here at length:

They’re the ones who are sick..[.] They’re the ones who are perverted. They’re the ones who are dangerous. They’re the ones who are subhuman. They’re the ones who are human debris, not the United States of America and not our soldiers and not our prison guards… [On Nick Berg’s beheading:] I thought I saw a couple smiles through the mouth holes in the mask, and at that instant I wanted to call George Bush and say, “Level the place. Turn it 20,000 degrees and let’s start over. …They don’t deserve to live. They don’t deserve sympathy. They don’t deserve understanding. They don’t deserve compassion. They don’t deserve traditional justice… To hell with rights and all this stuff. I wanted to be in the charge leading into that room to wipe ‘em out. (p. 174)

Integrated discussion of research: Will the dualists please approach

Several articles provide good material for the present study and raise several issues for consideration. For simplicity of presentation, the following indicate several positions in what I consider to be a debate for a positive correlation between social constructivism and war, and its counterpoints and alternatives. I will discuss each in turn, and synopsize with a brief conclusion.

War as embedded in the social matrix: Co-constructed, burned-in – embodied violence

In an attempt to understand war, look up the social construction of war in a Google search, and find striking headlines such as: “Females seem to find war to be an aphrodisiac…War makes people feel so alive… War: Comprehending Its Mystique and Its Madness…Letting out the (war) dogs…War is a force that gives us meaning…” and others. Indeed,

during wartime, notions of good and evil become black and white--it's us vs. them; the future of history hangs in the balance … the enemy acts out of a will-to-power, whereas we act out of self-defense, benevolence and a commitment to the fight; since the enemy is evil and untruthful, communication is impossible--only force will settle the conflict; the same actions are good when we do them, evil when the enemy does them; we are concerned only about outcomes, not causes of the conflict; and citizens who take umbrage with these perceptions of reality are considered traitors. (Utne as cited in Social construction of war, 2003)

In familial terms, Schore (2003) cites “why interpersonal deprivations and failures in the earliest stages of human development serve as a primordial matrix for a personality that is at high risk for violence” (Schore, 2003, p. 107) and that “experiences in infancy which result in the child’s inability to regulate strong emotions are too often the overlooked source of violence in children and adults” (Brazelton as cited in Schore, 2003, p. 107).

Even from the very beginnings, paternal abuse and neglect, indeed, any disruption in so-called natural biorhythms of man and infant or woman and infant, results in early imprinting of corticolimbic (especially right hemisphere) structures that are in a developmentally vital phase (first 2 years of life) (Schore, 2003, p. 130). Especially in cases of repetitive early abuse or neglect, it is in

this spatiotemporal imprinting of terror, rage, and dissociation [as the caregiver is also abuser, therefore the infant has no where to go for comfort except dissociative mechanisms which become ever more sophisticated and organized] is a primary mechanism for the intergenerational transmission of violence. (p. 130)

Clearly, then, violence begets violence, and very often this happens in the man-infant relationship, where little boys first learn modulation of fear and aggression (p. 130). Witness, too, the presence of seemingly innocuous exemplar of violence in movies and on TV, providing “all kinds of evidence to the effect that violent solutions to conflict and frustrations are not only predominant but also valued” (Aronson, 2008, p. 296). These formative experiences and reinforcements affect our neurophysiology, as we shall see.

Indeed, in postnatal development of the frontal lobes, especially the ventro-medial prefrontal cortex (vmPFC, and its role in limbic modulation of affectual triggers, ‘high-road’ inhibition) (see also Carlson, 2010; Zillmer, Spiers, & Culbertson, 2008) and orbitofrontal cortex (OFC) where traumatic or neglectful early attachment relationships lead to the aforementioned imprinting and ‘in-burning’, the amygdalic response to environmental stimuli is not regulated by the frontal brain structures, thereby leaving the person vulnerable to aggressive dysregulation and attacks of rage (pp. 134-6).

This begs the question, are biopsychological correlates of behavior not also embedded in a socially constructed reality? In a sense, the body is embedded, insofar as the cycle of transmission of aggression and violence has biological correlates to behavior, and certainly in that ‘parenting’ practices are socialized. Further, “the body may symbolize a society, and the dangers that threaten a society can be compared with the dangers threatening the body…rituals [therefore] work upon the body politic through the symbolic medium of the physical body (Douglas as cited in Sigurdson, 2007, p. 246).

Okay, but how does the biopsychological undermine or support the idea that war is socially constructed? Another way at approaching this question is through co-constructive (the confluence of genetic-biological and external, sociocultural systems) approaches (Elbert, et al., 2006, p. 327). So, is war a culturally determined expression of gene-potentiality (p. 327) and thereby an imposed, institutionalized “structure and function resulting from a history of genetic expression” (p. 327)? It certainly sounds plausible, though I might caveat this with allusion to the larger debate in the field of biopsychology and neuroscience, that of the post-traumatic neurotoxicity hypothesis versus the genetic predisposition hypothesis and refer the reader to an article I wrote available at: http://peterallenbrown.blogspot.com/2009/11/traumatic-predisposition-or.html . This gives ground for co-constructivist examination of how wars of terror and violence influence the brain, which individuals subsequently distribute to the society at large; the literature notes a

qualitative change in the way wars are waged and organized violence is exerted; in other words, a transformation in the culture of violence… [is at hand]. Moreover, scientific methods are available to study how traumatic stressors change individuals and communities so we can expect increasing knowledge about how social stressors and related learning conditions shape the structure and function of both the brain and the “societal mind,” including individual behavior and interactions on the community level. (p. 327)

Taking a bit of an implicit and inductive tact, Schore (2003) puts forth both the idea that biological correlates of neurological damage and relational trauma (abuse and neglect) contribute to “neurologically acquired sociopathy” (p. 137) (reminiscent of the legendary case of Phineas Gage – see also Zillmer, et al., 2008). The ideas of “hostile attributional biases” contribute to this line of thinking, in that it is believed that early onset antisocial boys (7-11) have these biases acutely activated as threats to the self, integrated in their “hostile world schema” (Dodge & Somberg as cited in Schore, 2003, p. 140). These are mechanisms of the cycle of violence, where the individual, embedded in community relationships, internalizes and structures himself or herself around and within the social matrix. It is clear from much of the research that people inculcate traumatic memories (amygdalic emotional learning) and that the collective memory trace (read: intergenerational transmission of trauma) precipitates violence through the aforementioned relational mechanism (see also Elchenroth, p. 910).

Therefore, it is my contention, and that of others - including Dr. Mansfield, that war as social construct starts in the arms of mother and father, really with the whole lineage of war and aggression. Even in pre-history, the institutionalization and reification of war follows distinct patterns of influence, literally, from cradle to grave (see also Mansfield & Keen, 1982, pp. 381 & 383). Even the reinforcement paradigms evolved from kings and rulers into the (patriarchal) family, supporting a feudal system of greed and materialist reward, using aggression and war as institutional purveyors of rage, discipline, and guilt (p. 383). This system eventually, and in terms of which Skinner might approve, became conditioned to equate goods with love, thereby awarding/reinforcing aggression with goods/booty, and finally making the extension (or stretch) that war is love (hence the elites diversified desires for goods – read: love - used aggression and war to satiate those desires) (see also Mansfield as cited in Keen, 1982, p. 384). Indeed, this reinforced (especially in the US) social matrix provides role models of violence as early as possible. Here, I feel moved to include a passage of some of the thoughts of Ron Roberts on this theme, as particularly salient and quoted here at length:

[c]onsiderable evidence exists that both the US and UK have nurtured the growth of extremist movements [even individual people] in areas of strategic interest (Ahmed as cited in Roberts, 2007, p. xi)…this ‘alternative’ narrative involves a profound reframing of the psychology that accompanies acculturation into Western society – in particular how and why people internalize the motives of Western governing elites [especially in regards to the obviously – at least as easily seen by those outside of the ‘West’ – aggressive, vindictive, and single-minded pursuit of energy, wealth and power]. … What does this tell us about our own psychology? … [Is the US actually preparing] citizens (children and adults alike) to not only accept the state’s actions but to assume benevolence in its intentions[?] … [Is this] a new postmodern variant of totalitarian rule fashioned by the security state [and propagated, executed, and controlled by complicit fields such as psychology] to safeguard elite interests at home and abroad, as well as the idea, unspeakable in our own media, that ‘we’, i.e. the… alliance of Britain, the US and Israel, do not want peace in the Middle East. Implanted deep in the American and British psyche is the product of a grand deception – the notion that we are continually exploring all means to bring peace, stability, justice, human rights and democracy to the world. The opposite fact appears more likely to be true: that all available avenues are followed to avoid peace, to wage war, to solicit evidence from torture and to antagonize people around the world toward position of hatred and violence…. This reality somehow survives outside of any critical scrutiny, even in the face of widespread skepticism about the motives of individual politicians. As the window on this hypocrisy opens ever wider, people in the West face the loss of the moral legitimacy of their culture in the wider world. … A common theme in this analysis is the power of social representations: of warfare, terrorism, and political action to shape our culture (a culture that has been engaged in military action abroad) and the actions of individuals within it. The theory of social representations makes possible a different kind of critique than that afforded by the experimental social psychology of the 1960s and 70s. It is not that the world of Stanley Milgram or Philip Zimbardo is no longer relevant to any understanding of the events unfolding in Iraq – particularly with respect to the commission of war crimes and torture at Abu Ghraib... but in the 2000s there is a need to look beyond these situationist accounts and direct our gaze at the wider culture within which the meaning of these actions are to be found – for actors and interpreters alike. (2007, pp. xi-xiii)

Foucault would approve and remind us that the roots are quite antique; the seekers of a perfect society (18th century) also sought a perfect militaire, with fundamental reference to “permanent coercions, not to fundamental rights, but to indefinitely progressive forms of training, not to the general will but to automatic docility (1979, p. 169).

Perhaps as a response to Roberts’ condemnation, albeit years prior and arguably a particularly insidious and backwardly subtle part of the rhetoric against which Roberts writes, an organization called the Psychologists for Social Responsibility (PSR), issued a statement that belies support of the very language that the PSR claims to decry. For example, the statement uses language such as in the urging of the UN to “thwart claims that the US has imperialist intentions in the Middle East…reverse the images of the US as a country that is unable to cooperate with other countries, threatens force when it doesn’t get its way, and breaks its word in international agreements,” (Washington, DC, US., 2003, p. 160) (perhaps this image is an honest account of US policy?). I might translate this statement as ‘help us help you move back into denial about our stance, give us peace as an to help us forget and repress’ about which Hillman also writes (peace as anesthetic of war and arguable cause of future wars; 2004). The tone of the PSR statement did not seem to help a struggling psychological field, in time of war, to frame its social responsibility as helping the populace to forget – ironic perhaps that it was published in a journal called Constructivism in the Human Sciences; how apropos.

War’s Construction-of-Society-through-Destructive-Means Prize

All I know is what they told me at command school. There are certain rules about a war.
Rule number one is ‘young men die.’ Rule number two is that ‘doctors can’t change rule number one.’

-- Colonel Blake, Commander, M*A*S*H (to Hawkeye, after his patient dies) (Humphreys, 2009, p. 716)

In setting up this debate, I earlier referenced so-called power brokers, promulgators of beliefs that maintain an intolerance of diversity. These power brokers might even be whole fields of study, like psychology where:

[i]t would be an act of supreme folly should we [psychologists] choose to ignore these global developments [referring to globalization, increasing economic disparities, induced climate changes, destruction of the biosphere, and the coming energy crisis consequent on the depletion of the planet’s natural resources…lead(ing) to further major conflict…(like) Iraq, Afghanistan and the ‘War on Terror’ (as)…manifestations of the end of the petroleum age, and the beginning of the battle for control of the world’s remaining energy reserves], hanging on desperately instead to an intellectually and morally bankrupt position which asserts the irrelevance of these things to psychology and psychologists. (Harper, Roberts, & Sloboda, 2007, pp. 222-3)

In fact, social psychologists of many camps, both the realistic-conflict- theorists and international-relations-thinkers (who generally favor power asymmetry hypotheses) in contrast to social-constructivists and social-identity-theorists (who favor shared identity-modulated threat perception) all have salient and important contributions in thinking about how people are likely to view powerful, threatening ‘others’ (Rousseau & Garcia-Retamero, 2007, p. 744). In one sense, this too is a construction of meaning used to understand warmaking. However, what these thinkers are finding, in their ‘hard-data’ experiments is that both power asymmetry and shared identity influence perception of threat in a systematic manner (p. 744). In fact, the authors of the study found, perhaps counterintuitively, that shared identity moderates the perception of power balance (high identity similarity equates to lower threat perception, which increases cooperation); naturally, as “shared identity decreases, the material balance of power becomes a more powerful predictor of threat perception” (p. 766). (The authors demonstrated these findings experimentally using a 2 x 2, between participant, design, including manipulation checks and an N=169.) This is important because the authors provide evidence for the systematic effect of ideas on threat perception – if a state needs an enemy, it may be easier to find one that is most dissimilar to blame – and history bristles with examples (any fascist dictatorship or hawkish state). Therefore, in shaping a (warring) society, there are factors both within (ideas and perceptions) and without (overt acts, etc.) – all taking place within ever-larger nested layers of a social matrix.

Are there any limits? Indeed, and it is perhaps vital to consider the confines of the social matrix, the ‘biosphere’, and how this ultimately shapes the construction of a social reality. These global challenges seem to demand the people of the world to regulate its population, with evolutionary forces and the survival of the fittest leading to wars of scarcity and competition for ever-dwindling resources.

Interestingly perhaps, is an article in the November “Awards Issue” of The American Psychologist – the flagship journal of the American Psychological Association – also recently presented at the APA’s annual conference in Toronto, Ontario, Canada, and for which the author, Dr. Keith Humphrey’s of the Palo Alto VA Health Care System, was awarded the “Award for Distinguished Early Career Contributions to Psychology in the Public Interest.” Dr. Humphreys’ article (2009) discusses the role of psychology in mental health provision of services to those affected by war, with special attention to “social problem definition,” (p. 713) which is how the psychology profession ‘reframes’ problems in such a way as to ensure ‘successful’ application of resources. This very interesting point is perhaps, on the surface - at least for Dr. Humphreys - simple, requisite, and obvious, though he states that

[t]he problem of problem definition often involves intense political struggle… because stakeholders appreciate that once a social problem is defined in a particular way certain policy responses seem more logical than others… In addition, a faulty problem definition can lead to the pursuit of a path that will never resolve the problem given infinite resources. (p. 714)

Curiously, this statement begs the question, that Dr. Humphreys cursorily addresses earlier in the article, that, ‘if a problem is really a problem, doesn’t that mean that by nature it is something about which is unknown, over which people struggle, for which resources allocated, and for whom there is some special interest?’ Interestingly, Dr. Humphreys’ earlier, brief reference was that one of his mentors referred to unsolvable problems as ‘facts’ and that was the rationale for altering the conceptualization of the problem. I might conjecture that the manipulation of problem definition is a means of social constructivism by power brokers who have the ability to alter reality such that their power remains dominant. This is a dark-side of post-modern thinking in that the shifting sands of thought, knowledge, and power, are easily changeable for those with resources to change social structures, laws, rules, and even language. This might be an appropriate time to introduce a historical view, from perhaps the most notoriously able reality-warping machines of all time, the Nazi Third Reich.

Herr Dr. Mengele please report to the lab, the gentlemen from the thought police are here to see you: Constructing warring societies

With regards to human experimentation and altered construction of reality of a particularly evil variety, a very interesting article I reviewed was on the neurosciences during Hitler’s Third Reich. According to Karenberg’s synopsis of the Nazi health policy, where “euthanasia, eugenics, and therapy were the three pillars…many researchers set ethical norms aside” (2006, p. 169). In a particularly poignant example of the brutality of man again man at war, and the power-broker’s ability to construct reality to support their own ends, these neuroscientists and psychiatrists in 1930s and ‘40s Nazi Germany began to find “interesting cases” in those who were treatment refractory/resistant or otherwise incurable and who also been first clinically observed and then murdered; who readily offered up – so to speak – their brains for histological examination (p. 169).

These diabolical social actors used science as social constructivist mechanism in time of war to further their scientific agendas. Parenthetically, and perhaps in acknowledgement and reparation of these horrors, many burials have taken place in recent years, complete with a German presidential apology in 2001 for “the suffering caused to the victims of these crimes in the name of science” (Markl as cited in Karenberg, 2006, p. 170). This reconstruction of the chaotic is revisited at the end of this section.

So, why examine a work such the Nazi example? The outrage and the imagery are atrocious and revelatory of the depths of human evil and the deliberate use of these depths to alter whole worldviews. I bring this work to illuminate the dangerousness of

state control from above instead of need-driven planning; the intertwining of science, the military and industry; dissolution of science and enlightenment; human experiments, some of them resulting in death…[s]hall we selectively define only a few of the historical periods…[?]…[or is society merely doomed to repeat history…shall I compare the NIH or NIMH to the Third Reich?]” (p. 170).

Perhaps these are far fetched, but Karenberg anticipated such a response. Quoting Shevell and Pfeiffer, Karenberg mentions that it is not adequate to simply state that the Nazi regime is a good example of what not to do (p. 171). Rather, he mentions several reasons why this is inadequate: 1) pure science in search of truth no longer exists and it is clear from examples such as these that there are political, financial, and social pressures that exert tremendous influence, 2) the Nazi example shows the medical fields the enduring conflict with ethical values (perhaps as a method of social control and constructivism in and out of war; see also the writings of Ken Pope against the APA for its lack of action against torture, www.kenpope.com) – “where and whenever the desire for scientific progress dominates and is made superior to all other moral values, that is where and when the ‘dark side’ of medicine will be found…” and 3) memory and history are fallible and prone to distortion (and/or manipulation or deliberate social construction (pp. 171-2). The images of the holocaust reverberate around Karenberg’s article, apropos to this present study.

While psychological research is perhaps different than the biological, for reasons more obviously owing to the physiology of the human body (which is also subject to the effects of social construction), there is, alas, ever a wound, psychic or bodily. These differences, between psychological and the biological, are perhaps encompassed in the fact that researchers seek out “subjects” (even the word choice, subject v. research participant, is revelatory) who do not always understand what is going on, data collection is self-serving in order to complete studies (itself a social construction), and there are “intense motivation[s] to gather data and other personal needs and agendas” (Koocher & Keith-Spiegel, 1998, p. 415). Certainly, the psychological and societal wound of the holocaust endures, even after the last brain specimen collected by euthanizing, self-serving, warped-constructivist, Nazi eugenicists, (and of the Nazi’s themselves,) have long since decomposed.

Before wrapping up this debate, I need to return to the point on reconstruction out of chaos and the German presidential apology. This last position is that of the very influential and institutionalized (read: constructed) upholders of the collective vulnerability worldview: the International Committee of the Red Cross (ICRC) and a long arm of international humanitarian law: the Geneva Conventions (GC). The GC turned 50 years old in 1999, and celebrated with a large survey of some 12000+ people of war torn lands on their thoughts about war (Elchenroth, 2006, p. 914). These people provided a surprising perspective, especially as masses of individuals who experienced tremendous vulnerability and a common fate whilst living in war zones (2006). From this study, and Elchenroth’s (2006) reanalysis of the data across cultures, it is clear that war causes people to experience great ambiguity especially with regards to their social norms and principles (pp. 911-2). In the context of uncertainty, the demand characteristics are for the community to modulate the tension (that is inherent in uncertain situations) of war, in order to reconstruct what has been de-constructed, made irrelevant, and that which has been destroyed (p. 912) – much as the German president attempted to do by apologizing these many years after the holocaust. That said, after whole communities, not just individual sufferers of war trauma, suffer systematic violence, they become objectified and their impacts are felt even beyond group boundaries and enter into every facet of life in the society, rendering all its populace vulnerable, which leads to a reshaping of belief systems, values, and meanings (p. 925), not to mention further propagation of violence, both interpersonally and societally – and here I return to the opening section of this paper and the data on both serial killers and intergenerational transmission of trauma. Even the humanitarian law itself is objectified as it is created contextually, in times of war, to protect those vulnerable to objectification (p. 925). The findings from this study, perhaps paradoxically, spell out that

within post-war societies, [individual] victims of war are less likely than their community fellows to adopt a legal perspective when judging war behavior…[which calls] into question claims that trials have some kind of therapeutic value and can provide a sense of closure to those most traumatized by war and mass atrocity…[alongside the finding that, at the collective level, it is] an important desire for seeing formal justice being held within those communities that have been the most strongly affected by collective war trauma, as a reaction to common experience of generalized vulnerability. (p. 926)

Conclusion

Interestingly, I find that as I reflect on this study, I notice that there seems to be an ever-expanding spider’s web of information and linkages to other fields, ideas, and approaches – in fact, I am starting to feel a kind of uncertainty about the material – a kind of desperation in the literature, now that I am moving toward conclusion. Foucault might have said, ‘bravo’ and echoed that

[t]he positivity of a [historical a priori] discourse…characterizes its unity throughout time, and well beyond individual œuvres, books, and texts. … Different œuvres, dispersed books, that whole mass of texts that belong to a single discursive formation – and so many authors who know or do not know one another, criticize one another, invalidate one another, pillage one another, meet without knowing it and obstinately intersect their unique discourses in a web of which they are not the masters, of which they cannot see the whole and of whose breadth they have a very inadequate idea… . (Foucault, 1972, p. 126)

Perhaps this entangled web of the de-construction of constructivism is what Kaisa Puhakka (2008) meant by the ‘post-modern malaise’. Perhaps it is that the field of psychology, with ever-greater range of methods and theory to choose from, loss of coherence and the accompanying uncertainty, and a new openness to alternative views – that the malaise sets in. Fortunately for us, Dr. Puhakka gives us an antidote in the form of transpersonal psychology (p. 6) – likely not without its own set of wars and issues. Perhaps the problematic is succinctly surmised by

a certain indeterminacy and inability to be fully captured by any theory or set of paradigmatic assumptions [which is] intrinsic to transpersonal psychology... This is because it is an inquiry that aspires to expand human consciousness beyond the ken of conceptual thought within which paradigms and their assumptions are forged… [It is within]…this postmodern predicament…[that the] isolation of people and fragmentation of the social fabric, in the ease with which ‘‘truth’’ has come to be equated with ‘‘opinion’’ or ‘‘feeling’’ and is used as a tool for manipulation by the media and in politics and advertising. (pp. 8-10)

While it is now clear that war is both embedded in the social matrix, and beyond it as well – especially in its destructive capacity – war is here to stay – part of humanity (one author reviewed suggested we adopt the homo hostilis moniker). Even how humanity goes about limiting war is yet another, ongoing war. Perhaps the splinter groups and anti-hawks will begin The War on ‘The War on Terror’. How will society construct this?

There is community in dying, and if your death belongs to others,
we are essentially not alone –
that is one of the great teachings of war.

-- James Hillman (2004, p. 153)

Ho ka he!
-- Lakota Native battle cry – translated it means, “Today is a good day to die.”

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Elbert, T., Rockstroh, B., Kolassa, I.-T., Schauer, M., Neuner, F. (2006). The Influence of organized violence and terror on brain and mind: A Co-constructivist perspective. in P. Baltes (Ed.), Lifespan development and the brain: The Perspective of biocultural co-constructivism, pp. 326-349. New York: Cambridge University Press.

Foucault, M. (1972). The Archeology of knowledge and the discourse on language. A. M. S. Smith (Trans.). New York: Pantheon Books.

Foucault, M. (1979). Discipline and punish: The Birth of the prison. A. Sheridan (Trans.). New York: Vintage Books.

Hatfield, E., & Rapson, R. L. (2005). Social justice and the clash of cultures. Psychological Inquiry, 16(4), 172-175. doi:10.1207/s15327965pli1604_06

Hillman, J. (2004). A Terrible love of war. New York: The Penguin Press.

Humphreys, K. (2009). Responding to the psychological impact of war on the Iraqi people and U.S. veterans: Mixing icing, praying for cake. The American Psychologist, 64(8), 712-23.

Karenberg, A. (2006). Neurosciences and the Third Reich: Introduction. Journal of the History of the Neurosciences, 15(3), 168-172. doi:10.1080/09647040600717181

Koocher, G. & Keith-Spiegel, P. (1998). Ethics in psychology: Professional standards and cases, 2nd ed. New York: Oxford University Press.

Mansfield, S., & Keen, S. (1982, June). War as ultimate therapy. Psychology Today. 380-387.

Miller, K., Kulkarni, M., Kushner, H. (2006). Beyond trauma-focused psychiatric epidemiology: Bridging research and practice with war-affected populations. American Journal of Orthopsychiatry, 76(4), 409-22. doi:10.1037/0002-9432.76.4.409

Psychologists for Social Responsibility, Washington, DC, US. (2003). Statement on the Iraq war. Constructivism in the Human Sciences, 8(1), 159-160.

Puhakka, K. (2008). Transpersonal perspective: An Antidote to the postmodern malaise. The Journal of Transpersonal Psychology, 40(1), 6-19.

Roberts, R. (2007). Introduction. in R. Roberts (Ed.), Just war: Psychology and terrorism. Ross-on-Wye, UK: PCCS Books.

Rousseau, D. L., & Garcia-Retamero, R. (2007). Identity, power, and threat perception: A cross-national experimental study. Journal of Conflict Resolution, 51(5), 744-771. doi:10.1177/0022002707304813

Sigurdson, O. (2007). The Christian body as a grotesque body. in J. Krois, M. Rosengren, A. Steidele, & D. Westerkamp (Eds.), Embodiment in cognition and culture. Amsterdam: John Benjamins Publishing.

Social construction of war. (2003, January 25). Book review: The Psychology of War by Lawrence LeShan. The Christian Century. Retrieved from http://findarticles.com/p/articles/mi_m1058/is_2_120/ai_97173987/

Toracco, R. (2005, September). Writing integrative literature reviews: Guidelines and examples. Human resource development review, 4(3), 356-367.

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Polymodality in hemispheric lateralization: Auditory, language, and music processing

2009-11-23T21:02:00.001-08:00

For this post, I will focus on verbal behavior and brain lateralization and link these to the latest research on music and hemispheric specialization. The auditory and language systems are inextricably linked because humans gained language via hearing, evolutionarily and developmentally (Zillmer, Spiers, & Culbertson, 2008, p. 215). In fact, it is in the study of people who have lost ability to speak or comprehend speech (aphasia), that researchers are able to discover such "neuropsychological… [anomalies such as] preserved singing capabilities in aphasic patients…[thus demonstrating] predominant involvement of the right hemisphere" (Sparing, Meister, Wienemann, Buelte, Staedtgen, & Boroojerdi, 2007, p. 322).

It is generally assumed that language functionality is located in the left hemisphere. The major language areas (and their functions) are Broca’s area (frontal operculum - speech production), Wernicke’s area (secondary auditory processing area - word recognition), arcuate fasiculus (connecting bundle allowing for thoughts to be translated into words) (Carlson, 2010, p. 499). These major speech areas, along with other brain regions, such as various cortical meaning-storage areas, as well as the “supramarginal and angular gyri of the inferior parietal lobes [which] are contiguous to Wernicke’s area,” and integrate highly (p. 217), along with visual, spatial, motor, memory, and even subcortical, suprapontine structures such as the basal ganglia and thalamus (within the cortico-striato-pallido-thalamo-cortical loop – language regulating and initiating) areas are all involved in auditory and language processing (pp. 216-7).

To further complicate matters, functional areas follow lateralization of the brain, that is, with the aforementioned auditory and language areas in the left hemisphere, the right hemisphere plays a vital role in helping people process information related to speech, emotion, and music (pp. 217-8; Carlson, 2010; Sparing, et al., 2007). For example, prosody is the intonation, dynamism, and rhythm of speech that, like music, can contribute to the communication of emotion. These functionalities are typically right hemisphere correlated, though some people (more women than men) have considerable bilaterality of speech (Zillmer, et al., 2008, pp 218-9). It goes, perhaps, without saying that language and perception of higher order thought processes, learning, and regulation also involve cognitive processing, further implicating highly integrated, polymodal cortical structures.

The authors of the study I reviewed, (Sparing, et al., 2007), cited research that explains both the traditional view of distinct/discrete hemispheric independence and the refutation of the classical view of “reciprocal cerebral hemispheric dominance” that modern neuroimaging shows a sharing of resources by speech/language and music processing centers (Perry; Riecker; Jeffries; Patel; Brown as cited in Sparing, et al., 2007, p. 319). While these very specialized brain areas are all interconnected and indeed ostensibly share resources, there is continued debate in the field as to the lateralization of cognitive abilities underlying music perception (Sparing, et al., 2007, p. 319). These authors investigated this by observing excitability of the brain during musical and linguistic tasks and the relation to left and right hand motor cortexes using Transcranial Magnetic Stimulation (TMS) while the participants sang, hummed, or talked (p. 319). Their findings that “production as well as reception of language predominantly increase the cortical excitability of the hand representation in the language-dominant (i.e. left) hemisphere [which] may suggest a closer relationship between the cortical networks mediating language processing, planning and execution of hand movements (Tokimura; Seya; Meister; Floel as cited in Sparing, et al., 2007, p. 319). These findings are of further interest because they demonstrate contrary evidence to the pre-study, extant literature that: “the relative increase of excitability of the left motor cortex during speaking aloud was less than the increase of excitability on the right hemisphere produced by both singing and humming” (p. 322), indicating that there is potentially greater lateralization with musicality and that we still have much to learn about brain polymodality/association.

“[T]he neural mechanisms required for musical perception must obviously be complex” (Carlson, 2010, p. 230). Certainly, many areas of the brain are involved: (beginning in the) subcortical auditory pathways, primary auditory cortexes, auditory association cortex (complexities, like pitch, etc.), superior temporal gyrus (pitch discrimination), inferior frontal cortex (harmony) right auditory cortex (beat, not unlike prosody), left auditory cortex (rhythmic patterns, in contradistinction to assumed, right-sided lateralization of prosodic content), cerebellum and basal ganglia (timing of rhythms and movements), even the brain stem shows more response to music than language (Carlson, 2010, pp. 230-1). While each adult individual has a specific hard-wiring and experience-driven, physiological correlation, musical ability appears to be primarily genetic and MRI studies show that those with amusia (severe and persistent deficit in musical ability, but without aphasia - speech deficits in either production/expressive or reception), have thicker auditory cortexes (right superior and inferior temporal gyri – STG and IFG), but thinner white matter of the IFG (p. 232). All this aside, it is clear that both the speech/language and musical processing abilities in the brain are highly specialized, interconnected/lateralized, and polymodal in nature, perhaps more so that we previously thought, and to ever-wider brain regions, previously held out to be quasi-uni-functional (remnants of one-to-one fallacy).

Paradoxically, the authors go on to discuss that their research shows that despite all the modern evidence, there is a preponderance of right hemisphere dominance in music processing (p. 321). They found that by using TMS, “the corticospinal projection of the left (i.e. dominant) hemisphere to the right hand during overt speech was facilitated. There was no effect on the right hemisphere during or after speaking. Moreover … excitability of the nondominant (i.e. right) motor cortex increases during both overt singing and humming, whereas no effect could be found on the left hemisphere” (p. 321). While this may seem obvious or cryptic, or both, the authors clarify with several calls for future studies and suggestion of use of TMS as “a complementary tool to investigate hemispheric lateralization of language-and music-related cortical networks…[and] to assess hemispheric lateralization by TMS ... to evaluate the effect of cognitive functions on motor cortex excitability as expressed in changes of the size of the TMS-induced motor evoked potentials (MEPs)” (p. 322).

In conclusion, by the end of this rather complex study, the authors concede what my other references also maintain, that the music and language functions of the brain are lateralized oppositely, in the right and left hemispheres, respectively. While there are theorists, including Darwin, who postulated that music was a proto-language that evolved, along with our brains, into the common speech of today, there has been no evidence to support this from modern imaging studies (p. 322). The conclusion is that further study is needed; I concur, and as in many of my posts, find it necessary to state that the brain and its functions do not follow a one-to-one correspondence and that polymodality and association, along with plastic and neurogenerative phenomena guarantee future opportunities for the contributions of bio-neuro-psychologists.

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Sparing, R., Meister, I. G., Wienemann, M., Buelte, D., Staedtgen, M.,
& Boroojerdi, B. (2007). Task-dependent modulation of functional connectivity between hand motor cortices and neuronal networks underlying language and music: A transcranial magnetic stimulation study in humans. European Journal of Neuroscience, 25(1), 319-323. doi:10.1111/j.1460-9568.2006.05252.x

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Change up: Painting, Dementia, and FTLD

2009-11-20T00:11:00.000-08:00

There are over 50 causes of dementia that affect either cortical or subcortical (or as in Alzheimer’s Disease - AD, traditionally considered a cortical dementia) and mixed types (see also Zillmer, Spiers, & Culbertson, 2008, pp. 406-7). The most common causes are vascular, infectious, and toxic. Generally, dementias are also divided into three types: progressive (cortical dementias like AD, Picks, Wilson’s; subcortical: Huntington’s Disease - HD, Parkinson’s Disease - PD, AIDS dementia, and Creutzfeldt-Jakob Disease - CJD), static (toxic: Alcoholic dementia, heavy metal poisoning; infectious: herpes encephalitis; and others like trauma, tumor, etc.), and reversible dementias (like systemic: anemia and uremia; B12 deficiency as in Korsakov’s Syndrome; endocrine as in Addison’s Disorder and thyroid disorders; and drug toxicity: from antipsychotics and anticholinergics) (p. 406).

Frontotemporal lobar degeneration (FTLD) is a cluster of diseases that have characteristics of primary dementia, warranting a DSM-IV TR diagnosis as a behavioral syndrome, that shows prominent and disproportionate atrophy of the anterior frontal and temporal lobes (Midorikawa, Fukutake, Kawamura, 2008, p. 224). By the DSM-IV TR, required for a dementia diagnosis are: memory impairment and in an additional area of cognition (language, praxis, executive function, etc.), impaired/decline in social/occupational functioning, clouded consciousness, and an organic contributor to etiology or absence of other conditions except an organic mental syndrome (see also American Psychiatric Association, 2000; Zillmer, et al., 2008, p. 407).

Primary dementia is significant for a loss of cognitive ability – memory, perception, verbal, and judgment – often seen in stroke patients and those suffering from AD (Carlson, 2010, p. 543). Additionally, aphasia is present in FTLD, with 2 subtypes, nonfluent aphasia and semantic aphasia. The 2 patients in the study I reviewed had semantic aphasia. Most interesting, however, was that these Japanese patients had no education in painting, did not paint prior to FTLD onset, and painted realistically. While the 2 patients studied did not show creativity in their paintings (that is, they were strictly painting what they saw) creativity does occurs with patients suffering from the nonfluent aphasia subtype (Midorikawa, et al., 2008, p. 228).

People with FTLD and primary dementia suffer from various problems in their day-to-day lives: difficulty recalling the names of certain objects (verbal deficit that worsens over time); difficulty recalling the meanings of words; abnormal behaviors such as intrusiveness and repetitive actions (that worsens); deficits in general verbal functioning (i.e., WAIS VIQ, etc.); frontal lobe function deterioration; preserved speech and comprehension ability, but with severe naming deficits; reading disturbances; other naming deteriorations (i.e. Western Aphasia Battery); sometimes apraxia (trouble following directions due to semantic deficit, with intact imitation and use) (p. 226); possible global deficits in visualizing and understanding objects (p. 228); visual semantic ability described as ‘a central semantic impairment’ (p. 229); marked atrophy in the left temporal lobe; and enlargement of the ventricle with possibilities for lacunar infarctions in the white matter. [important to note that these signs and symptoms are taken quasi-anecdotally, as the N=2] (p. 226). Additional symptoms not unlike those found in PD (including the typical muscular rigidity, slowness, resting tremor, and instability) are also possible in this kind of frontotemporal dementia (Carlson, 2010, pp. 537 & 546).

Interestingly, the patients in the study helped to show that “the assumption that the appearance of painting skills during FTLD does not reflect learning or cultural background, but rather is the expression of innate functions of the brain. In addition, our patients’ paintings were realistic in style, which might be an inherent phenomenon in humans, and not an advanced skill” (Midorikawa, 2008, p. 228).

The authors presented a couple of different theories for this finding: paradoxical functional facilitation (PFF) effects initiated by a disruption of inhibitory mechanisms and/or compensatory plasticity alongside a “decreased inhibition of ‘the right-sided and posteriorly located visual and musical systems’” (p. 228). The authors drew parallels to similar results by studies on children with autism in that “impoverished conceptual representation of the world may actually help rendering what we see’, and may arise from a common functional deficit. With these parallels, they concluded that it was perhaps more parsimoniously accounted for by a regression to childlike, quasi-autistic states. (2008).

Finally, while there are not any FDA approved treatments for FTLD, there are off-label treatments, garnered from experience treating AD, which can be used in addition to behavioral management (Caselli, & Yaari, 2008, p. 489). Currently, there are “six areas of pharmacotherapeutic consideration [which] are prevention (primary and secondary), intellectual decline, behavioral disorders (such as depression, anxiety, and psychosis), sleep disorders, frequently associated disorders (including motor neuron disease), and abrupt decline (pp. 489 & 497). While there are no curative treatments for this disorder, maintenance treatments and even treatments based on traditional Japanese medicine (Kampo - called Yokukansan), show promising results in symptom management (Kimura, Hayashida, Furukawa, Miyauchi, & Takamatsu, 2009, p. 38). Further important non-medical interventions concerning behavior are necessary: care for the care giver, maintenance of quality of life, containing weapons access, and limiting or eliminating driving privileges (Caselli & Yaari, 2008). Additionally, there are things that can be done behaviorally and for the caregivers to ensure that remaining/intact functions are used to a) slow degeneration (use it or lose it), b) increase agency and thereby quality of life (especially for caregivers who may be more reality oriented than patients), and c) treat co-morbid diseases and disorders and d) to take advantage of what intact functioning remains in order to provide reassurance, (acceptance stance) and emotional support to both the patients and those with whom they interact) (see also Midorikawa, et al., 2008, p. 229; Caselli & Yaari, 2008).

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Caselli, R. & Yaari, R. (2008). Medical management of frontotemporal dementia. American Journal of Alzheimer's Disease and Other Dementias, 22(6), 489-498. doi:10.1177/1533317507306654

Kimura, T., Hayashida, H., Furukawa, H., Miyauchi, D., & Takamatsu, J. (2009). Five cases of frontotemporal dementia with behavioral symptoms improved by yokukansan. Psychogeriatrics, 9(1), 38-43. doi:10.1111/j.1479-8301.2008.00261.x

Midorikawa, A., Fukutake, T., & Kawamura, M. (2008). Dementia and painting in patients from different cultural backgrounds. European Neurology, 60, 224-9. doi:10.1159/000151697

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Forget the excitotoxic tiger: Memory, traumatic stress, and the amygdalae

2009-11-16T23:52:00.000-08:00

Stress in both humans and animals has various effects, biopsychologically. One important effect (along with behavioral anxiety, hyperarousal, gastrointestinal motility, food intake changes, increased defecation, sleep disturbances, attentional deficits, and avoidance of novel stimuli, etc.) includes memory deficit (Vermetten, & Bremner, 2002, p. 127). Some of the physiological components of memory include the prefrontal cortex (PFC – especially in working memory), hippocampus (involved in declarative memory formation and sends efferent information to various areas for consolidation; even spatial memory in the right-posterior hippocampus; place/topographic, etc. – see also Carlson, 2010, pp. 471 & 483-4), the neocortex (damage to which causes semantic dementia – loss of facts), and the structure upon which I focus this post, the amygdala – involved in the emotional encoding of memory, and of course the hippocampi – which will not be discussed here in depth, the curious reader might consult any of the sources listed in the references section.

Stress has massive effects on memory processes involving “neurohormonal modulation of the laying down of memory traces” even thought to influence the strength of neuronal connections that influences consolidation (Vermetten, & Bremner, 2002, p. 138). In fact, “[i]ncreased level[s] of norepinephrine released during stress can modulate memory formation through action on the brain. … norepinephrine modulates [the following] aspects of memory: acquisition of new information… attentional component[s] of memory storage … and working memory” (pp. 138-9).

Norepinephrine isn’t the only neurochemical to influence the stressed brain, the glucocorticoids and glutamate also potentiate (especially in long term potentiation, LTP) severe damage to the structures and functions of the brain (Carlson, 2010, pp. 444-5). When stressed (damaged or diseased), synaptic vesicles are triggered to release glutamate that transporters do not remove, rather accumulate, in excess, extracellularly, allowing Ca+ ions to enter NMDA receptors leading to excitotoxicity and cell death (also happens in ischemic cascade in traumatic brain injury [TBI], stroke [cerebral vascular accident, CVA], autism, and Alzheimer’s Disease [AD]) (Carlson, 2010, pp. 446-8; Zillmer, Spiers, & Culbertson, 2008). Two other chemicals, dopamine (DA - especially in the PFC with working memory system, downregulated during stress) and epinephrine are endogenous memory modulators – and are especially active during arousal and stress (upregulated during stress) (see also Vermetten, & Bremner, 2002, p. 139).

The amygdala is involved in emotional memory and in the conditioned fear response (learning) mechanism (Carlson, 2010, pp. 369-71; Vermetten, & Bremner, 2002, p. 139). In fact, studies show that “the degree of activation of the amygdala during the encoding of emotionally arousing material (positive or negative) correlates significantly with subsequent recall of the material (declarative retention increase through enhanced hippocampal consolidation, though, with an upper limit – chronic over-arousal leads to impaired memory due to adrenalcortical upregulation – Zillmer, et al., 2008, p. 260). Lastly, the authors reviewed for this post (Vermetten & Bremner, 2002), provide an excellent (and very technical) synopsis of the major amygdalic connectivities (studied via lesion/damage) involved in stress, quoted here at length:

“Lesions of the central nucleus of the amygdala have been shown to completely block fear conditioning, while electrical stimulation of the central nucleus increases acoustic startle… The central nucleus of the amygdala projects to a variety of brain structures via the stria terminalis and the ventral amygdalofugal pathway. One pathway is from the central nucleus to the brainstem startle reflex circuit (nucleus reticularis pontis caudalis). … Pathways from the amygdala to the lateral hypothalamus effect peripheral sympathetic responses to stress. … Electrical stimulation of the amygdala in human subjects resulted in signs and symptoms of fear and anxiety including an increase in heart rate and blood pressure, increased muscle tension, subjective sensations of fear or anxiety … and increases in peripheral catecholamines. … There are also important connections between cortical association areas, thalamus and amygdala that are important in shaping the emotional valence of the cognitive response to stressful stimuli. In addition to thalamo-cortico-amygdala connections, there are direct pathways from thalamus to amygdala, which could account for fear responses below the level of conscious awareness” (pp. 139-40).

Maybe the most likely candidate for discussion of memory system damage is the boundary-ignoring, progressive dementia (traditionally thought of as a cortical dementia) known as Alzheimer’s Dementia [AD] (Zillmer, et al., 2008, p. 411). AD is a fatal illness, marked by both cortical and subcortical atrophy/degeneration; with postmortem autopsy (the only way the diagnosis is confirmed) revealing most damage to the cortical temporoparietal association areas (as well as the frontal – including subcorticofrontal nucleaus basalis of Meynert and olfactory areas – temporal, and parietal areas generally) and the subcortical limbic cortexes (where the amygdalae and hippocampi live) (p. 411).

In sum, the memory system is a very complex and interconnected one, impacted by experience and genetics, trauma and disease. I hope to incorporate this learning into my specialization with the work of those suffering the sequelae of trauma. Memory is a vast area, perhaps even a subspecialty in traumatology, and comprises many different areas of inquiry ranging from false memory, recovered memory, repression of memory, anterograde amnesia, retrograde amnesia, dissociative disorders, and, really, the entire foundation of traumatology. Were it not for memory, no one would have a problem with trauma, after the bodily reactions had passed – the sympathetic nervous reactions, the shaking, and the discharging. I recall the work of Peter Levine (Waking the Tiger) and his storying of the process an animal in the wild might go through after a brush with death, an attack. The animal might rest, shake and discharge, then get up and rejoin the heard. If only if it were that simple with humans.

Certainly, understanding the biopsychological underpinnings of memory and trauma are vital to my work. It is helpful to gain familiarity with the scientific thinking behind some of the interventions recommended by literature, and begin to see ripples and echoes of dovetailing work fitting nicely together, rounding out the toolkit to best help those who suffer their memories.

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Vermetten, E., & Bremner, J. (2002). Circuits and systems in stress. I. Preclinical studies. Depression and Anxiety, 15(3), 126-147. doi:10. 1002/da.10016

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Traumatic Predisposition or Neurotoxicity: Examining Hippocampal Volume and PTSD

2009-11-14T20:00:00.000-08:00

Traumatic Predisposition or Neurotoxicity: Examining Hippocampal Volume and PTSD

Peter A. Brown

California Institute of Integral Studies
School of Professional Psychology
Clinical Psychology

Table of Contents

Do Smaller Hippocampi predispose PTSD? 1

Hippocampal atrophy in PTSD: The Neurotoxicity Hypothesis 3

Conclusions: A Middle Way? 5

References 7

Traumatic Predisposition or Neurotoxicity: Examining Hippocampal Volume and PTSD

In much of the literature, there is an ongoing debate surrounding two hypotheses regarding subcortical (primarily limbic, hippocampal) relationships to Post Traumatic Stress Disorder (PTSD)/trauma: 1) the predisposition hypothesis, that is, those with smaller hippocampi (to begin with; genetically), are predisposed to the development of the familiar PTSD symptom cluster (intrusiveness/reexperiencing, avoidance, and hyperarousal – see also the DSM-IV-TR, American Psychiatric Association, 2004, pp. 463-8), and 2) the so-called neurotoxicity hypothesis, believed to be that the hippocampus actually atrophies in the post-traumatic brain.

The person suffering from PTSD is likely to have a dysfunctional hippocampus that does not distinguish a safe context from a dangerous one, thereby triggering amygdalic-emotional response (see also Carlson, 2010, p. 607). This subcortical process follows the ‘low road’ in amygdalic connectivity parlance, bypassing the (ventro-)medial prefrontal cortex ((v-)mPFC) which is unable to inhibit these triggers (or is itself impaired); the amygdala is highly connected, both ascending to cortical structures like the vmPFC and descending to other pontine structures including the spinal cord (Zillmer, Spiers, & Culbertson, 2008, p. 150).

Do Smaller Hippocampi predispose PTSD?

According to Sapolsky (2002), pivotal to the predisposition hypothesis is the need for correlation between more severe combat and smaller hippocampi, a finding that Gilbertson and colleagues (2002) did not support (p. 1113). The seminal Gilbertson study found that the hippocampal (and amygdalar) volume in monozygotic twin combat veterans was not only smaller in those who developed PTSD, but that it was likely smaller before combat and predisposed those veterans to traumatic reactions (2002).

Gilbertson and colleagues examined monozygotic twins (combat exposed Vietnam veterans and their stay-home twin brothers) in order to reveal whether or not smaller hippocampal volume post – combat experience was either a pre-existing condition or a direct result of traumatic experience (p. 1242). Demonstrating the superior design of this study and its predictive validity,

[b]ecause monozygotic twins are genetically identical, any differences in hippocampal volume between brothers were
interpreted as evidence for environmental effects, such as stress-induced neurotoxicity [as a result of combat exposure and
not as a result of exposure to combat with a smaller pre-existing hippocampal volume]. Alternatively, any differences in
hippocampal volume between the unexposed brothers of PTSD combat veterans…versus the unexposed brothers of non-
PTSD combat veterans…were taken as evidence for a pre-existing trait...Our results indicate that small hippocampal volume
constitutes a pre-existing vulnerability factor for pathological response to stress.” (pp. 1242-3)

Perhaps most important is the fact that the findings of the study show that combat exposed twins with larger hippocampi did not develop PTSD, thereby arguing “strongly against a stress-neurotoxic interpretation of the hippocampal diminution” (p. 1246).

Although unrelated to the combat veteran population, a recent study of limbic system volume (hippocampi and amygdalae) of adult survivors of childhood abuse with dissociative disorders (dissociative amnesia – DA; dissociative identity disorder – DID) reveals the tenor of etiological hypothesizing about PTSD and brain limbic volume: “Clinical symptoms and cognitive deficits have been frequently related to small hippocampal size of individuals who had been exposed to traumatic stress [i.e. that the traumatic even precipitated an atrophic mechanism], suggesting that hippocampal damage may be a powerful predictor for the severity and chronic character of PTSD [almost postulating that PTSD is so chronic because trauma damages the brain]” (Weniger, Lange, Sachsse, & Irle, 2008, p. 282). Alas, this study concludes with a position straddling the debate: “the small size of the amygdala and hippocampus and impaired cognition seems to be primarily related to PTSD [and not to dissociative disorders, per se, but in comorbid situations, the results are less clear], either by genetic factors or by factors related to suffering from chronic stress” (p. 289).

Hippocampal atrophy in PTSD: The Neurotoxicity Hypothesis

Many studies since the groundbreaking Bremner and colleagues paper in 1995 and the Gurvits and colleagues paper in 1996 (MRI studies showing establishing the initial correlates) established a evidence suggesting that the brain might be damaged due to psychological distress by action of “stress-induced disturbance of the hypothalamic-pituitary-adrenal axis” (Sapolsky as cited in Schmahl, et al., 2009, p. 294), glucocorticoids, and glutamate active in the limbic system (see also Carlson, 2010; Zillmer, et al., 2008). Dr. Alan Schore – in a chapter in Drs. Solomon and Siegel’s Healing Trauma: Attachment, Mind, Body, and Brain (2003) – on early relational trauma, echoes the flavor of the neurotoxic hypothesis, and possibly provides a link to the etiology of the hypothesis itself, if not as the trace of the 1990s “Decade of the Brain” Bremner and Gurvits’ papers, in his descriptions of developmentally toxic states. Schore expounds that developmental neurotoxicity occurs when the caregiver is unresponsive (or abusive) to the child induces hyperaroused states, which produce elevated catecholamines (neuromodulating in times of stress) and “hyperactivation of the excitotoxic N-methyl-D-aspartate (NMDA)-sensitive glutamate receptor, a critical site of neurotoxicity and synapse elimination in early development [due to pruning/synaptic apoptosis]” (Schore, 2003, p. 132). It is in passages such as this that make it easier to see how scientists hypothesized that psychological trauma may cause neurological damage due to neurotoxic activation of corticosteroids leading to hippocampal neuronal death – it was precisely this hypothesis that Gilbertson and colleagues tested, and refuted (2002).

Noting the polarity of hypotheses, in another recent study (Woodward, et al., 2006) examined hippocampal volume, PTSD, and alcoholism in combat veterans and found the opposite of Gilbertson and colleagues (2002): that PTSD uncomplicated by alcoholism did not show smaller hippocampal volumes, also drawing attention to the fact that in over 80% of the Gilbertson and colleague twins (one combat veteran, the other not) the brothers suffered from clinically significant alcoholism (Woodward, et al., 2006, p. 679). In another study (the Vietnam Era Twin Registry), upon which many of the combat veteran studies were based, also found genetic vulnerability to combat exposure/PTSD and alcoholism (p. 679). Interestingly, Sapolsky (2002), another researcher in this specialized area of research, and who was published in the same issue as the original Gilbertson study, noted that the alcoholism comorbidity confound was effectively ruled out because the twins (one combat, the other stayed home) had statistically (and genetically) identical hippocampi (p. 1112). The debate on comorbidity of alcoholism in both the Woodward and colleagues (2006) study and the Gilbertson and colleagues (2002) study seems to be a moot point, but there is still criticism despite the evidence. Interestingly, Schmahl and colleagues (2009) “did not find significant influence of [many common comorbidities, such as] eating disorders, agoraphobia, social phobia, substance abuse, or major depression” (p. 294). Finally, the Schmahl and colleagues findings suggest that the debate continues, that it is unclear how volumetric changes occur and that there may be a “supra-additive effect” on brain volume, when both (the studied) Borderline Personality Disorder and traumatic experience and/or PTSD are present (p. 294) (as PTSD is present in 60-70% of BPD patients, Zanarini, et al.; Zimmermann & Mattia as cited in Schmahl, et al., 2009, p. 289).

It seems clear that the debate is also one reminiscent of the nature-nurture question, in that there seems to be both genetic and environmental factors involved. Interestingly enough, Carlson (2010) reports that a few studies have identified genes thought to determine susceptibility to PTSD development, including those responsible for production of dopamine D2 receptors, dopamine transporters, and 5-HT transporters (Nugent, Amstadter, & Koenen as cited in Carlson, 2010, p. 607) (short allele promoter 5-HTT – increased stress sensitivity, proneness to depression/anxiety, see also Carlson, 2010, pp. 578-9 and 607). While perhaps promising and certainly interesting, Carlson’s line of thinking seems rather speculative and does not seem to control for many parsimonious and confounding variables, not to mention generalizability.

Conclusions: A Middle Way?

A final point that raises yet other possibilities in this ongoing debate regarding etiology of hippocampal volume correlates of PTSD, is that in a recent study, Hera and colleagues (2008) experimented with PTSD and cancer survivors in a very well designed study that found that there was no correlation (at 12 months post-diagnosis of cancer – considered a particularly insidious source of trauma) of smaller hippocampi and PTSD, but there was correlation with intrusive symptoms of PTSD (p. 307; see also DSM-IV-TR, APA, 2000). Further, the study seems to refute the predisposition hypothesis, while not exactly confirming the neurotoxic, in that “[t]he… negative findings [i.e., absence of smaller hippocampi in cancer survivors with PTSD]… may indicate that a smaller hippocampal volume is not likely to predispose cancer subjects [italics added] to developing PTSD” (Hera, et al., 2008, p. 305). The authors offered the hypothesis that intrusive symptomology (not full-blown PTSD) in cancer patients may have alternative neuropathophysiologic underpinnings, yet undetermined – suggestive of a possible separate cancer-related PTSD construct, featuring the intrusive symptom cluster (p. 307).

The relevance of the debate between neurotoxic responses to trauma versus preexisting small hippocampi is manifold. It is clear that the evidence goes both ways and that further research is needed. That said, the traumatology specialty might be able to use both hypotheses in the development of innovative applications in prevention and treatment of PTSD, possibly even modification of the PTSD construct, on biopsychological bases. For example, Sapolsky (2002) suggests that small volumetric hippocampi become the modern “flat foot” disqualification for military service, a sort of heart-murmur-like rule-out precluding a soldier from serving in combat (p. 1113). He further suggests that, should the neurotoxicity hypothesis stand, the field might develop a kind of post-traumatic golden hour of response along with antidote to the cascade of glucocorticoids and glutamate in the brain (p. 1113), perhaps reminiscent of propranolol preventative treatments (Pitman, et al., 2004, pp. 241-2).

Which ever way this baby and its bathwater go, it is clear that the best the field has at present is a controversy aiming at a simple solution to a very complex problem. There is some hope, evidenced by preliminary single case findings from researchers treating patients with PTSD with Eye Movement Desensitization and Reprocessing (EMDR) for 90 minutes per week for 8 weeks, that psychotherapy increased total baseline hippocampal volume by some 11% (albeit, this is a rather anecdotally) (Letizia, 2007, pp. 475-6). Perhaps future research, triangulation of data, pluralistic integration, comorbidity studies, longitudinal research, and even epidemiological research (as well as further treatment outcomes with larger sample sizes than the Letizia, 2007, example) will pave the way for refined theories applicable to the biopsychological treatment of PTSD.

References

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR. Washington, DC:
Author.

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., & Pitman, R. K. (2002). Smaller hippocampal
volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5(11), 1242-1247.
doi:10.1038/nn958

Hara, E., Matsuoka, Y., Hakamata, Y., Nagamine, M., Inagaki, M., Imoto, S., Murakami, K., Kim, Y., & Uchitomi, Y. (2008).
Hippocampal and amygdalar volumes in breast cancer survivors with posttraumatic stress disorder. The Journal of
Neuropsychiatry and Clinical Neurosciences, 20(3), 302-308. doi:10.1176/appi.neuropsych.20.3.302

Letizia, B., Andrea, F., & Paolo, C. (2007). Neuroanatomical changes after eye movement desensitization and reprocessing
(EMDR) treatment in posttraumatic stress disorder. The Journal of Neuropsychiatry and Clinical Neurosciences, 19(4), 475-
476. doi:10.1176/appi.neuropsych.19.4.475

Pitman, R., Sanders, K., Zusman, R., Healy, A., Cheema, F., Lasko, N., Cahill, L., Orr, S. (2004). Pilot study of secondary
prevention of posttraumatic stress disorder with propranolol. Curr Psychiatry Rep., 6(4), 241-2.

Sapolsky, R. M. (2002). Chicken, eggs and hippocampal atrophy. Nature Neuroscience, 5(11), 1111-1113.
doi:10.1038/nn1102-1111

Schmahl, C., Berne, K., Krause, A., Kleindienst, N., Valerius, G., Vermetten, E., & Bohus, M. (2009). Hippocampus and amygdala
volumes in patients with borderline personality disorder with or without posttraumatic stress disorder. Journal of Psychiatry
& Neuroscience, 34(4), 289-295.

Schore, A. (2003). Early relational trauma, disorganized attachment, and the development of a predisposition to violence. in
M. Solomon & D. Siegel (Eds.), Healing trauma: Attachment, mind, body, and brain (pp. 107-67). New York: W.W. Norton &
Company.

Weniger, G., Lange, C., Sachsse, U., & Irle, E. (2008). Amygdala and hippocampal volumes and cognition in adult survivors of
childhood abuse with dissociative disorders. Acta Psychiatrica Scandinavica, 118(4), 281-290. doi:10.1111/j.1600-
0447.2008.01246.x

Woodward, S. H., Kaloupek, D. G., Streeter, C. C., Kimble, M. O., Reiss, A. L., Eliez, S., Wald, L. L., Renshaw, P. F., Frederick, B.
B., Lane, B., Sheikh, J. I., Stegman, W. K., Kutter, C. J., Stewart, L. P., Prestel, R. S., & Arsenault, N. J. (2006). Hippocampal
volume, PTSD, and alcoholism in combat veterans. The American Journal of Psychiatry, 163(4), 674-681.
doi:10.1176/appi.ajp.163.4.674

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Process modified Stroop test reveals vmPFC not only emotionally bound

2009-11-10T20:06:00.001-08:00

efore discussing the role of the orbitofrontal cortex, I might refer the reader to my other posts throughout the semester, as to the absence of one-to-one structural-functional relationships of the brain, otherwise termed polymodality or association (see also Zillmer, Spiers, & Culbertson, 2008). Second, it is important to consider that the various constructs as used in the materials to which I refer in this article are consistently revised through iterative scientific methodology. Lastly, making light of the nature of both the aforementioned, it is vital to remember that emotional behavior is a very complex construct and there are even more complexities when science works to attribute complexities in causal relationships. With these in mind, I integrate various sources and examine a very interesting article I found that challenges and “invites the hypothesis that the ventromedial prefrontal cortex may not be as 'silent' with respect to mediating cognitive functions [and only involved in emotional regulation] as previously thought (Cato, Delis, Abildskov, & Bigler, 2004, p. 464).

The ventro-medial prefrontal cortex (vmPFC – located at the base of the anterior frontal lobes, adjacent to midline), which includes the medial orbitofrontal cortex (OFC) and the subgenual anterior cingulate cortex (ACC), is involved in regulating emotionally driven behavior (Carlson, 2010, p. 375). Important to note are the connections from the temporal cortex, the olfactory system, and the amygdala (memory, emotion, limbic system) (p. 375). According to Carlson (2010) and others, it is clear that the vmPFC is responsible for inhibiting emotional behavior, largely through the study of "natural experiments," case material, and neuroimaging (Larner & Leach, 2002, p. 26).

One such natural experiment is the legendary case of Phineas Gage. Injured by a railroad tamping iron through the cheek and out the top of his skull, Phineas Gage was never the same after his traumatic injury – his marked dispositional change, from irreverence, capriciousness, profanity and irresponsibleness (Larner & Leach, 2002, p. 26), to an inability to carry out plans, whimsicality, and thoughtlessness of others (Carlson, 2010, p. 376) are today recognized as hallmarks of OFC injury that are sometimes referred to as “pseudopsychopathy” (Larner & Leach, 2002, p. 26) or “acquired sociopathy,” differing from antisocial personality disorder (APD) by the ability to feel remorse and lack of vicious planning involved in APD (Zillmer, et al., 2008, p. 256).

Other issues commonly found in OFC injuries, prominent in large lesions, are environmental dependency syndrome. These are stimulus bound behaviors like utilization behavior (hand a patient pajamas, and regardless of context, they may undress and put them on), grasp reflex, and manual groping (p. 256). However, Carlson (2010), like many others, claim that vmPFC injury typically leave cognitive functions intact, following the usual syndrome of emotional dysregulation (and its correlates), going so far as to state: “[t]here was no relationship between cognitive abilities and real world competencies, which strongly suggests that emotional problems lie at the base of the real-world difficulties [a construct referring to judgment, planning, social inappropriateness, and financial and occupational status] exhibited by people with vmPFC damage” (p. 377). However, both Zillmer and colleagues (2008) – who bring in theoretical notions regarding impaired empathy and somatic marking (i.e., impaired automatic tagging of situations that help with response selection; typically assessed neuropsychologically with the gambling task (Bechera and colleagues as cited in Zillmer, et al., 2008, pp. 256-7) and one article I found, refuted this notion, showing that “[o]n the one hand, patients with VM-PFD may truly be spared from cognitive deficits and suffer from isolated emotional and behavioral impairments. Another possibility is that VM-PFD does lead to cognitive deficits in addition to emotional-behavioral dysfunction, and traditional neuropsychological tests have generally failed to identify such deficits in these patients" (Cato, et al., 2004, p. 454).

Cato’s study revealed that through the use of more sensitive neuropsychological testing that “the bifurcation of prefrontal cortex into two functional subregions [long recognized as a method to help parse a structure-function relationship and to reductively study the PFC], with higher-level cognitive functions mediated primarily by dorsolateral prefrontal regions [dlPFC] and emotional-behavioral regulation subserved primarily by ventromedial prefrontal cortex [vmPFC], may be inaccurate” (p. 464). The testing uses “process-oriented neuropsychological measures designed to quantify subtle cognitive deficits that may exist over and above the emotional or behavioral changes typically found in VM-PFD [ventro-medial prefrontal damage] patients (p. 454) and included two commonalities “(1) task demands that tapped multiple executive functions simultaneously, including cognitive shifting; and (2) scoring systems that went beyond the traditional measures of time-to-completion or level of accuracy, and also quantified and normed error types” (p. 463). This is important because their results followed a patient “whose VM-PFC damage was remarkably similar to that of Phineas Gage,” with all the typical symptom presentation and whose most salient problems related to emotional-behavioral regulation. The difference was that upon testing, Cato's patient was found to have marked cognitive deficits (p. 464).

Cato and colleagues argued that the cognitive functions may be organized in the frontal lobes along a continuum, where higher level processes are located most anterior (i.e., within the vmPFC), and simpler executive controls were more susceptible not to the vmPFC per se, but more concentrated in the dlPFC (p. 464). Their conclusion was that a process oriented approach to neuropsychological testing (adding a task switching task to the Stroop test) revealed deficits post vmPFC lesion (p. 464). In their words: “the highest levels of cognitive and emotional integration may occur in ventromedial prefrontal cortex, which, when compromised, may affect an individual’s ability to perform multilevel executive-function and memory tasks...[illustrating] how the use of multilevel executive-function tasks (e.g., inhibition plus switching) may capture higher-level deficits that may otherwise be missed by traditional procedures” (p. 464).

In conclusion, it is clear that biopsychology has much to learn by way of ongoing and iterative study of the human brain, whether in Gageian naturalistic experiment, animal modeling, computer simulation, or imaging. As the evidence builds, including those seminal 19th century studies, a clearer picture of the complexity of structure-function polymodal association becomes important to consider. Certainly, without the intriguing case of Phineas Gage and the Cato study’s patient, these associations might never be fully understood. I find it quite marvelous that with the triangulation of data from tests like the Stroop (plus switching task), MRIs, and historical records, the field advances to include ever more complexity and subtlety that gives future patients, their families, and caregivers, more information and possibilities for hope than ever before.

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Cato, M., Delis, D., Abildskov, T., & Bigler, E. (2004). Assessing the elusive cognitive deficits associated with ventromedial prefrontal damage: A case of a modern-day Phineas Gage. Journal of the International Neuropsychological Society, 10(3), 453-465. doi:10.1017/S1355617704103123

Larner, A. & Leach, J. (2002). Phineas Gage and the beginnings of neuropsychology. ACNR, 2(3), 26.

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Alternative blog reference

2009-11-04T11:29:00.000-08:00

So, I have chosen to stay with blogger because of the connectivity via google. That said, I would like to refer you to my previous blogspot for earlier posts.

http://peterallenbrown.wordpress.com/

best

pb

Drop what you're doing: Cataplexy and corticomotor structure and function

2009-11-04T11:25:00.000-08:00

The motor cortex is located on the precentral gyrus, caudal to the prefrontal cortex, and rostral to the somatosensory cortex and central sulcus, extending from the midline, laterally (Carlson, 2010, p. 273). Whereas the control of sensory systems is largely in the posterior cortex, movement is largely anterior and takes several forms: reflex actions, automatic repetitive actions (like walking), semivoluntary actions (yawning), and voluntary actions (picking up an object) (Zillmer, Spiers, & Culbertson, 2008, p. 189).

The motor cortex is organized (according to one theory) in a top-down, hierarchical fashion (another theory suggests a parallel process within the motor cortex, several circuits working simultaneously, see also Haines as cited in Zillmer, et al., 2008, p. 189). The motor cortex follows this pattern thus: first, highly integrated sensory information from the sensory association areas (parietal lobes, subcortical basal ganglia, and the cerebellum) and gets funneled through the primary motor cortex (responsible for fine details for movement, mapped as a motor homunculus) down through three other areas, the secondary motor cortex, the supplemental motor area (or the supplementary motor area or medial premotor area – functions in organization and sequential timing of movement) (pp. 189-91) (SMA - Carlson, 2010, p. 274); the premotor area (PMA or premotor cortex – plays a role in planning and movement readiness), and the cingulate motor area (CMA or cingulate motor area – likely involved in emotional and motivational impetus for movement, though less is known about this, but its proximity to the anterior cingulate suggests its emotional component) with the areas in the parietal lobes (posterior, Brodmann’s areas 5 & 7 – spatial mapping and motor programming coordination) and dorsolateral prefrontal cortex (dlPFC - involved in premotor planning and deployment Zillmer, et al., 2008, pp. 189-92).

In order to control movement, there are two groups of cortical efferent pathways, descending from the structures listed above (funneled down through the primary motor strip down through the midbrain, pons, medulla, and terminating in the spinal cord): the lateral (containing the corticospinal, corticobulbar, and rubrospinal tracts – controlling independent limbs for grasping objects and face & tongue movement) and the ventromedial group (the vestibulospinal – involved in posture, the tectospinal tract – eye, trunk, head coordination, the lateral and medial reticulospinal tract – involved in walking, and the ventral corticospinal tract – involved with both locomotion and posture) (Carlson, 2010, pp. 274-7).

These brain structures and descending pathways have myriad disorders that are beyond the scope of this post; however, one very interesting phenomenon is that of narcoleptic-cataplexy (NC). This is a condition by which the victim has a sudden and pathologic onset of REM sleep, where “the associated motor inhibition relates to a variety of nervous system dysfunctions, including massive nonreciprocal excitation of spinal inhibitory interneurons and active inhibition of motoneurons” (Zillmer, et al., 2008, pp. 462-3). This unusual and extreme form of narcolepsy is a complex sleep-wake disorder and is a sudden and brief loss of muscle tone (atonia) triggered by strong (mostly positive) emotions such hearing a funny joke (Schwartz, Ponz, Poryazova, Werth, Boesiger, Khatami, & Bassetti, 2008, p. 514). This cataplexic response is when suprapontine (that which lies supra, or above, the pons) structures fail to control the activation of the ponto-medullary mechanisms that normally underlie muscle atonia in REM-sleep (p. 514). Interestingly enough, Schwartz and colleagues found that when people see humorous pictures activation in the hypothalamus (reduced) and amygdala (increased) show up on MRI concluding that in cataplexy, people have a dysfunction in the hypothalamic-amygdala due to positive emotions and that hypocretin (a hypothalamic peptide that regulates sleep-wake, motor and feeding) modulates emotional inputs within the amygdala (pp. 514-5).

These results beg the question can this information be used in other areas where amygdalic overactivation is a problem (as in PTSD)? Time will tell.

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Schwartz, S., Ponz, A., Poryazova, R., Werth, E., Boesiger, P., Khatami, R., & Bassetti, C. L. (2008). Abnormal activity in hypothalamus and amygdala during humour processing in human narcolepsy with cataplexy. Brain: A Journal of Neurology, 131(2), 514-522. doi:10.1093/brain/awm292

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

A Rose by Any Other Name: PTSD and the Olfactory System

2009-10-30T19:59:00.000-07:00

In this post, I review and discuss an article on aggression and impulsivity in combat veterans with PTSD tied to Olfactory Identification Dysfunction (OID) (see also Dileo, Brewer, Hopwood, Anderson, & Creamer, 2007). While the human olfactory system has the second highest number of sensory receptor cells – after the visual system (Carlson, 2010, p. 256), is the oldest sensory system evolutionarily speaking (Zillmer, Spiers, & Culbertson, 2008, p. 186), and is the least understood (p. 186), it also has axons (in the olfactory tract of the olfactory bulbs, where the glomeruli synaptically connect to the mitral cells) that project directly to the amygdala and to two other limbic structures called the piriform cortex and the entorhinal cortex (Carlson, 2010, pp. 256-7). This is important for a couple of reasons. First, because the olfactory system does not pass through the thalamus before reaching the cortical (conscious) regions (i.e., Orbitofrontal cortex, OFC, PFC, etc.), rather it links directly to the subcortical limbic system (Zillmer, et al., 2008, p. 189). Second, the olfactorily enervated limbic system, a system largely preconscious, has a direct and practically immediate effect on emotion, mood, and even memory (see also Zillmer, et al., 2008, p. 189). When these systems are disordered, things like Anosmia (think: a-NOSE-mia, loss of smell), dysosmia (distorted smell sensation), phantosmia (experience of a phantom/hallucinatory smell), and hyposmia (diminished taste sensation) are prevalent (Zillmer, et al., 2008, p. 189).

Even Freud was interested in the role of smell and psychological disorders, yet the idea was mostly abandoned until much more recently when scientists began exploring the olfactory correlates of Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and even schizophrenia (i.e., hyposmia and dysosmia as early markers of AD and PD; phantosmia in schizophrenia) (p. 189). Fortunately, the neuropsychological community now has a method of testing for some of these early symptoms, by way of the Pennsylvania Smell Identification Test (UPSIT) – a scratch and sniff test – (Doty, Shaman, & Dann as cited in Zillmer, et al., 2008, p. 189), which Dileo and colleagues also used in their PTSD research (2007).

The deep connectivity to the “smell brain” (or “reptilian brain,” as it is sometimes called) enjoys a burgeoning evidence base and has been found to augment PTSD research and treatment. Dileo and colleagues (2007) add to this research by taking the thinking one step further with the combat veteran population (Vietnam era, outpatient, n=31, with community controls) (p. 523). The authors reasoned that since the complex functioning of the Obitoprefrontal Cortex (OFC) is often impaired in those suffering from PTSD, and since this area of the brain executively applies inhibitory responses, and the OFC is highly enervated to the basolateral amygdala, the OFC is very involved in emotional modulation (2007, pp. 523-4). Aggressiveness and impulsivity is thought to occur due to a failure of medial prefrontal structures to assert executive control over subcortical, limbic, amygdalic firing, the natural question, because of the direct link to the olfactory system, was to test these veterans who are often aggressive and impulsive due to their diagnosis, to determine the correlation of OID. As one might expect, and as other research demonstrates (see also Dileo, et al., 2007, p. 524), the OID is now thought to be a useful measure of OFC integrity and thereby a good predictor of PTSD-associated aggressivity and impulsivity (p. 524). In fact, the “OFC mediates odor identification [and refining of smells] as found via lesion and neuroimaging…[and because the OFC is connected with the limbic system and parallels the circuits for smell identification] OID’s have been strongly associated with impaired inhibition of affect, delusions, and maladaptive behavior (Martzke, Kopala, & Good, as cited in Dileo, et al., 2007, p. 524) and are found in combat veterans with PTSD (p. 528). Most importantly, the study concluded that the presence of OIDs are an important diagnostic indicator in predicting aggression and impulsivity, though as of yet, it remains difficult to say how effective OIDs can be in explaining the complexity of the OFC (p. 529).

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Dileo, J. F., Brewer, W. J., Hopwood, M., Anderson, V., & Creamer, M. (2008). Olfactory identification dysfunction, aggression and impulsivity in war veterans with post-traumatic stress disorder. Psychological Medicine, 38(4), 523-531. doi:10.1017/S0033291707001456

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Happy same-race face familiarity and the right ventral stream

2009-10-25T22:03:00.000-07:00

I have often extolled the ideas of polymodality or association, that the brain does not maintain a one-to-one structure-function correlation, and in visual processing this is also the case (see also Zillmer, Spiers, & Culbertson, 2008). While there is not a common visual processor, despite the name “occipital lobe,” there does exist a “seemingly instantaneous… culmination of separate but locally connected visual-perceptual processes” (p. 200). Not only are these seemingly instantaneous processes happening linearly, they also happen in parallel, giving us what is called bottom up percept formation and top-down building, though the latter is a matter of debate (p. 200).

I might like to include a word or two from a previous post in response to another learner about polymodal circuits in the brain.

The “what” pathway is occipital input along the occipital-temporal (associational) pathway to the inferior temporal region, helps us to recognize objects and perceive things (Zillmer, et al., 2008, p. 160; and for a great discussion on autism spectrum disorders and the Fusiform Face Area or FFA which is part of the social-emotional brain/circuit, which includes, amongst other regions, temporal, frontal, and limbic/other subcortical nuclei, see pp. 316-18). The “where” pathway, which, as you might guess, is similar occipital input orients more to the occipital-parietal pathway and to the posterior parietal lobe, processes this way to give us “where,” or spatial recognition. (Brown, post to a colleague on Capella course page, 2009).

In this post, I will cover one article on the neural correlates of same-race face recognition using positive/happy stimuli. The study in question demonstrated that same-race faces showing positive stimuli (in this case, three races where used, Japanese – the participants were all Japanese – other Asian, and Caucasian) positively correlate to greater amygdalic, posterior cingulate cortex (PCC), and superior temporal gyrus (STG) (the STG because these same-race faces where subjectively more familiar than the others) (Iidaka, Nogawa, Kansaku, & Sadato, 2008, p. 91). These results were also corroborated in many other studies that the authors thoughtfully cited and from which they drew a very clear, logical pattern and generated hypotheses.

Additional findings included that “the PCC is the neural correlate that is specifically involved when the Japanese subjects judge the happy expression on a same-race face;” that the amygdala responded to the presentation of both positive and negative emotional content; that the superior temporal sulcus (STS) is more active when greater personal familiarity is present in the stimulus; that “regions adjacent to the posterior STS may play a similar role as the PCC with regard to the same-race face processing;” and lastly, that because the PCC is implicated in memory retrieval, this region is thought to correlate to a sense of familiarity when the subjects viewed a happy face from their own race (pp. 97-8).

So, what goes wrong when lesions to these areas of the brain occur? Typically, these disorders are referred to as apperceptive and associative visual agnosias, such as prosopagnosia or the inability to recognize people by their faces (Zillmer, et al., 2008, p. 207). While prosopagnosia is thought to be a disorder of higher order processing relayed through the thalamus (p. 204), it is clear that the “what”/ventral stream, a stream that helps to connect visual perception with meaning (p. 206), receives impulses from the subregions of the visual association cortex, the V2 area, and the striate cortex (Carlson, 2010, p. 196). The left hemispheric ventral stream is associated with letters and numbers (symbols) whereas the right is more specific to recognition of faces and other objects (Zillmer, et al., 2008, p. 207). Damage to the right side can result in visual agnosia, such as prosopagnosia; whereas left sided damage results in neglect and problems distinguishing between left and right (p. 207). Cognitive neuropsychologists generally classify these agnosias into two groups: apperceptive visual agnosias (problems with object perception – like seeing in bits and pieces) and associative visual agnosias (problems assigning meaning to objects) (p. 207). If both hemispheres are involved, Balint’s syndrome may be involved, which includes visual agnosia with visuospatial difficulties such as mis-reaching and neglect (p. 207).

These ideas are fascinating in their polymodality and association in tandem, often overlapping, parallel streams. I might pose the following questions for thought: how can researchers acknowledge polymodality, while noting the relative unitariness of various constructs such as “problems differentiating left from right” or degree of happy, same-race face familiarity? Does this have some implication for the physico-behavioral mapping of continuous neurophysiology? What are the implications of extra-regional lesion – that is, when the boundaries of a lesion exceed the region’s known, discrete function?
These and other questions will perhaps keep you up tonight. Rest assured, however, there will be another day to explore this wild west of science.

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Iidaka, T., Nogawa, J., Kansaku, K., & Sadato, N. (2008). Neural correlates involved in processing happy affect on same race faces. Journal of Psychophysiology, 22(2), 91-99. doi:10.1027/0269-8803.22.2.91

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.

Is PTSD neurotoxic?

2009-10-23T09:49:00.000-07:00

In this brief article I will address biopsychological research of Post Traumatic Stress Disorder (PTSD). The study reviewed (Gilbertson, Shenton, Ciszewski, Kasai, Lasko, Orr & Pitman, 2002) utilized a “case-control” monozygotic twin design. This kind of study is used to explore the influence of heredity on a particular trait (in this case hippocampal volume in PTSD discordant twins, one of whom was exposed to combat in Vietnam, see also Gilbertson, et al., 2002) (Carlson, 2010, p. 166).

Briefly, and as temporal background to frame this particular research, structural magnetic resonance imaging (MRI) studies report that hippocampal volume in PTSD patients is noticeable smaller and it is hypothesized that psychological trauma may cause neurological damage due to neurotoxic activation of corticosteroids leading to hippocampal neuronal death (Gilbertson, et al., 2002, p. 1242). (in fact, this was the hypothesis under study). In this monozygotic twin study, the authors tested this neurotoxic hypothesis, by way of examining combat exposed Vietnam veterans and their stay-home twin brothers in order to revealing whether or not smaller hippocampal volume post – combat experience was either a pre-existing condition or a direct result of traumatic experience (p. 1242). Finally, “[b]ecause monozygotic twins are genetically identical, any differences in hippocampal volume between brothers were interpreted as evidence for environmental effects, such as stress-induced neurotoxicity [as a result of combat exposure and not as a result of a exposure to combat with a smaller pre-existing hippocampal volume]” (p. 1242).

While the study also examined several other variables concomitant to a severe PTSD diagnosis, for example, alcohol abuse and depression, the major finding is stated best by the authors themselves: “the key finding here concerns the identical twins of the higher severity PTSD combat veterans who were not themselves exposed to combat; they showed hippocampal volumes that were comparable to their combat-exposed brothers but significantly smaller than those of combat veterans without PTSD and their non-combat–exposed twins” (p. 1245). This clearly indicates that people with genetically (“given”) smaller hippocampal volumes are more likely to develop severe, unremitting PTSD than those with larger volumes (p. 1245), ceteris parabus. In other words – size matters. This effectively refutes the neurotoxicity hypothesis, therefore “reference to hippocampal ‘atrophy’ in PTSD may be a misnomer” (p. 1245).

This seminal study effectively settled a longstanding controversy of biopsychology, that the brain was injured by trauma due to neurotoxicity. While this is not absolutely ruled out by this study, it is clear that even when comorbid alcohol abuse and depression are circumvented via case-control design, that people who have smaller hippocampal volume are at greater risk for developing severe PTSD, especially when exposed to the terror of combat, and even then, independent of combat severity (p. 1245).

It is important to note that the hippocampus is involved in fear processing, memory (especially declarative memory – or, memory that is explicit, factual, and assessable to conscious awareness; this is highly correlated with the hippocampus and the medial temporal lobe, amongst other areas of the prefrontal cortex – the left dlPFC for encoding and the right PFC for retrieval, according to the Hemispheric-Encoding-Retrieval-Asymmetry (HERA) model, Zillmer, Spiers, & Culbertson, 2008, pp. 227-9), and in the important conditioning and extinction mechanism in animals and, likely, humans (having an effect on neuroendocrine regulation of the hypothalamic–pituitary–adrenal axis) (Gilbertson, et al., 2002, pp. 1245-6). Lastly, it is heredity that is likely the responsible etiology of smaller hippocampi observed in this study of twin Vietnam War-era brothers (though with a dizygotic twin study, this might have been further clarified) (p. 1246). Further sealing up the argument is the fact that in the study those veterans who had combat exposure and larger hippocampal volume and did not develop PTSD refutes the neurotoxic and/or shared environment hypotheses (though without a dizygotic study, this remains unclear) and adds strength to the aforementioned findings of this seminal study demonstrating PTSD susceptibility in those with smaller hippocampal volume (p. 1246).

References

Carlson, N. (2010). Physiology of behavior, (10th ed.). Boston: Allyn & Bacon.

Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., & Pitman, R. K. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5(11), 1242-1247. doi:10.1038/nn958

Zillmer, E., Spiers, M., & Culbertson, W. (2008). Principles of neuropsychology, (2nd ed.). Belmont, CA: Thomson Wadsworth.