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Neuropsychology: Self-Test on TBI - KEY

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

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

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

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

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

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.