Neuro(bio-)psychology and trauma studies: 2010

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.

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