Traumatic Brain Injury

Traumatic Brain Injury
Sue Meares

Outline Epidemiology Neuropathology Classification: Severity of TBI
Glasgow Coma Scale Post-traumatic Amnesia Outcome – Cognitive and Behavioural Case presentation

Traumatic Brain Injury (TBI)
Definition: Damage to the brain as a result of the application of mechanical energy from external physical forces, above the threshold of the tissue to withstand it without anatomical or physiological alteration. Generalli, T.A., (2005)

TBI: Epidemiology General incidence of hospitalised TBI:
200 per 100,000 of population 80% of cases are mild TBI US Census Bureau survey of mild to moderate TBI 600 per 100,000 people 25% seek no medical care 14% seen in doctor’s offices 35% seen in the Emergency Department 25% are hospitalised Bruns & Hauser (2003) Epilepsia. 44 (Suppl. 10), 2-10. Sosin, D.M., Sniezek, J.E. Thurman, D.J. (1996). Brain Injury. 10,

Incidence of TBI in Australia
TBI in Australia in 22,710 hospitalisations; 107 per 100,000 people Male/Female: 2-3:1 Males aged years; 300 per 100,000 people Australian Institute of Health & Welfare (2007). Bulletin No 55. Cat no. AUS96.

TBI: Epidemiology Mechanism of injury:
Children, and adults > 45 years – falls Adolescents and young adults – violence and motor vehicle accidents TBI occurs more often in: lower socioeconomic classes, unemployed, substance abuse, poor academic performance (Ponsford, J., with Sloan, S.& Snow, P., 1996). Hospitalised TBI Mechanism TBI Principal Diagnosis TBI Additional Diagnosis Falls 42% 30% Transportation 29% Assault 14% 16% Helps et al., (2008). Hospital separations due to traumatic brain injury, Australia AIHW. (CAT no. INJCAT 116)

Neuropathology Four mechanisms of traumatic brain injury: Focal Injury
Diffuse Injury Penetrating Injury Blast Injury

Focal or Contact injuries (Direct):
- require an object to strike the head, or physical contact between brain and skull - results in a focal/coup injury (coup injury = point of impact) Pathology: Vascular (haemorrhages), Traumatic axonal injury Diffuse Injuries (Indirect): - do not require contact - unrestricted movement where the brain moves within the cranial cavity - diffuse injuries occur due to acceleration/deceleration Pathology: Traumatic axonal injury ** Most TBIs involve contact (focal) and movement (diffuse) of the brain within the skull

Pathology: Local tissue necrosis (death)
Penetrating injuries: produce damage when an object passes through the protective covering of the skull resulting in direct brain damage Main cause gunshot wounds Mortality rate much higher than in closed TBI, 6.6-1 Damage due to laceration, crushing of brain tissue, intracranial haematomas (a mass of blood in tissues) and ischemia (an inadequate supply of blood to tissue) Tissue compressed remains injured High velocity objects create a shock wave that causes stretch injuries Low-velocity injuries may be restricted to the tract of injury Pathology: Local tissue necrosis (death) Blast injuries: seen in military or terrorist situations where the shock waves from an explosive device may result in brain injury Primary – CNS injury unclear (over-pressurization shock wave in other body systems - ear, lungs, GI tract) Secondary – Penetrating brain trauma Tertiary – Focal and acceleration/deceleration trauma, skull fractures Quaternary – Chemical exposure, burns Pathology: Brain swelling

Neuropathology: Classification of traumatic brain injury Smith C
Neuropathology: Classification of traumatic brain injury Smith C. (2011) Neuropathology. In Silver, J.M.,et al. Textbook of Traumatic Brain Injury. Focal/Contact Brain injury Diffuse Brain Injury Injury to scalp Traumatic axonal injury/Diffuse vascular injury Skull fractures Brain swelling Contusions/cerebral lacerations Global ischemic injury Intracranial haemorrhage Focal lesions secondary to raised intracranial pressure

Focal injury to the scalp:
Head injury vs brain injury vs TBI: Head injury = External injuries to the face, scalp and calvarium (skullcap): scalp laceration, bruising, abrasion skull fractures may or may not be associated with TBI

Focal Injury: Skull Fracture Four major types:
Linear: Depressed: Diastatic: Basilar: - # posterior skull base or # anterior skull base - bruising mastoid process - racoon eyes - CSF leaks nose, eyes - cranial nerve palsy (facial, ocular, auditory)

Surface contusions/lacerations
Surface contusion (a bruise) = pia-arachnoid is intact Laceration = pia-arachnoid is torn Hallmark of brain damage Moderate (78%), Severe (10%) and Mild (6%) contusions found in 94% of fatalities Characteristic distribution: Focal damage to frontal poles, inferior aspects of frontal lobe, cortex above and below operculum of Sylvian fissures; temporal poles and lateral and inferior aspects of temporal lobes Inferior involvement corresponds to bony structures base of skull Surface contusion may form into a mass lesion, causing swelling and raised intracranial pressure If pia-arachnoid torn may bleed into subdural space

Focal and Acceleration/Deceleration: Coup/ Contrecoup injury
Coup contusion occurs site of impact Coup and contrecoup contusion can occur individually and together Contrecoup usually associated with translational (linear) acceleration Contre cavitation – rapid increase in acceleration raises intracranial pressure at trauma point (coup) and decreased pressure at contrecoup Decreased pressure can cause cavitation bubbles which may burst causing local tissue damage Cavitation also implicated in outcome in penetrating trauma CSF is denser than brain tissue, may rush to coup area forcing brain to other side of skull causing contrecoup

Intracranial Haemorrhage:
Most common cause of death in patients who experience a “lucid” interval and then deteriorate Types Extradural (epidural) Intradural Subdural Subarachnoid Discrete intracerebral or intracerebellar haematoma not in continuity with surface of the brain

Intracranial Haemorrhage : 1. Extradural (epidural) haematoma
Formed when dura mater stripped away from the skull by bleeding from blood vessels or a fracture Present in 5-15% of fatal brain injury - in 5-10% coexists with an intradural haematoma Associated skull fracture in 85% of adults In two-thirds the extradural is due to a fracture of the squamous part of the temporal bone, remaining cases frontal or parietal fracture, occasionally posterior fossa The bleeding is generally arterial, is rapid, enlarges quickly stripping the dura from the scalp After approximately 2 weeks haematomas become smaller and are completely resolved in 4-6 weeks If detected early in most cases there is little underlying associated brain damage.

Brain CT Scans: Extradural
Acute right temporoparietal extradural Right frontal acute extradural

Intracranial Haemorrhage: 2. Intradural: (i) Subdural
Acute subdural haematoma forms in the space between the dura and brain (within first 48 hours) Produced by torn veins on brain’s surface and inner side of dura Can cover entire hemisphere and usually larger than EDH Poorer prognosis than EDH - more underlying brain damage 70% of cases due to fall or assault; 70% have a skull fracture In 50% the fracture is contralateral to side of haematoma Peak incidence 50 – 60 years Associated with swelling of ipsilateral cerebral hemisphere Subacute subdural haematoma – initial SDH increases (develops 2-14 days) Chronic subdural haematoma (develops weeks or months) May produce distortion and herniation of brain More common in older, alcoholic, those on anticoagulants

Brain CT scan: Subdural
Acute Subdural Chronic Subdural

Intracranial Haemorrhage: 2. Intradural: (ii) Subrachnoid
Occurs due to bleeding into the subarachnoid space Most subarachnoid haemorrhages occur in association with surface contusions Blood over inferior and lateral aspects of frontal and temporal lobes Larger bleed may constrict cerebral arteries (vasospasm) If posterior fossa subarachnoid May be associated with base of skull fracture May develop into hydrocephalus

Base of brain - haemorrrhagic defects and associated subarachnoid on underaspects of frontal lobes and in relation to temporal poles (18 hours post-injury, Gennarelli & Graham, 2005)

Intracranial Haemorrhage: 2
Intracranial Haemorrhage: 2. Intradural: (iii) Intracerebral and intracerebellar haematomas Present in 16-20% fatal brain injury cases May occur from multiple contusions or from direct rupture of blood vessels in brain Common in frontal and temporal lobes Delayed intracerebral haematoma may develop several days after the injury Burst” lobe – an intracerebral or intracerebellar haematoma in continuity with the subdural haematoma (25% of fatalities) When small haematomas found deep in midline structures (parasaggital white matter, corpus callosum, structures in the walls of 3 ventricles) more associated with diffuse traumatic axonal injury

Brain CT scan: Intracerebral haematoma

Surgical Treatment in Intracranial Haemorrhage (Baron & Jallo, 2007)
In patients where intracerebral collection causing mass effect (i.e. > 5mm of midline shift) Epidurals > 30cc in volume Acute subdural > 1cm in thickness; >5mm of midline shift, or subdural where patient has neurological changes (GCS) and raised intra-cranial pressure Procedure is through craniotomy or decompressive craniectomy Open depressed skull fractures with dural laceration to prevent infection

Brain Injury Secondary to Raised Intracranial Pressure
Intracranial pressure (ICP): determined by the volume of 3 elements in the skull: brain tissue volume, blood volume and CSF Normal pressure 0-10mm Hg Increase in one component compensated for by another (blood & CSF ) External ventricular drain inserted (monitors ICP and permits CSF drainage) >20mm Hg abnormal and raised ICP decreased cerebral blood flow and tissue perfusion leading to ischemia brain herniation – brain tissue herniated across dural areas (falx, tentorium) through foramen magnum, leading to respiratory depression respiratory depression or arrest due to brainstem compression Ischemia Hypoxia-Ischemia: related to reduction in cerebral blood flow reduction in cerebral perfusion may occur within hours (due to metabolic alteration) stretching and distortion of blood vessels (mass effect, ICP, herniation) hypotension due to multiple injuries vasospasm resulting in hypoperfusion

Acceleration/Deceleration Injury Ommaya and Gennarelli (1974)
Acceleration/Deceleration Injury Ommaya and Gennarelli (1974). Brain, 97, A/D forces cause mechanical strains in a “centripetal sequence” Sequence begins at the surface and progressively affects deeper structures 3 predictions: 1. When trauma produces LOC - cortex and subcortical white matter affected 2. Damage to brainstem will not occur without more severe damage to cortex and subcortical structures because midbrain last area to be affected by centripetal force 3. Cognitive symptoms such as confusion and disturbance of memory can occur without LOC, but the reverse cannot occur Therefore: Direction of force can determine injury severity A continuum of injury severity exists – from the surface inward (mild, moderate and severe TBI) A/D forces alone are sufficient to cause TBI

Diffuse Injury: Traumatic Axonal Injury
Acceleration/Deceleration brain injuries classically associated Diffuse Axonal Injury Characterised as diffuse degeneration of white matter (axons) (Strich, 1956), and shearing injury (Strich, 1961): torn axons, shearing of axon clusters, sheared axonal substance (axoplasm), swelling of damaged axons Diffuse Axonal Injury replaced by term Traumatic Axonal Injury (TAI; damaged axons are grouped, not strictly diffuse throughout brain) Shearing strains are exaggerated at substrates of different densities (i.e. grey and white matter, brain and blood vessels, and brain and CSF) and at positions of least brain movement Typical pattern: Axonal injury in the corpus callosum (CC), dorsolateral segments of the rostral brain stem and adjoining cerebeller peduncles, internal capsule May range from microscopic changes in white matter of cortex, CC, brain stem and cerebellum (mild TAI), grossly obvious focal lesions isolated to the CC (moderate TAI), and additional lesions in the brain stem in severe TAI TAI principal pathological substrate producing neurological impairment Classical view is that axons are torn at injury, but experimental studies now suggest axonal injury and death is a process not an immediate event Axons stretched when traumatic defect in cells occur at time of trauma 24-72 hours for swelling to occur Delayed cell death

Diffuse injury - Acceleration/Deceleration Bigler, E. D
Diffuse injury - Acceleration/Deceleration Bigler, E.D. (2000) The Lesion(s) in Traumatic Brain Injury: Implication for Clinical Neuropsychology. CCN Meeting, Sydney. A -dorsal view with frontal lobes pointing right, representing the physical forces involved in angular acceleration (combination of linear and rotational forces ) B -frontal view, depicting similar twisting action but due to linear forces as observed from a frontal pole perspective C -stretching (tensile) action across the lateral surface of the right hemisphere

Macroscopic haemorrhages midline structure (including brain stem)
Severe TBI Injuries Macroscopic haemorrhages midline structure (including brain stem) over time shrink to sunken cystic scars Microscopic axonal injuries Days – numerous axonal swellings and axonal bulbs in deep structures (parasaggital cortex, corpus callosum, internal capsule and long tracts in brainstem) Days to weeks – bulbs less prominent, cluster of microglia and macrophages and astrocytosis Months to years – small healed superficial contusions, extensive white matter degeneration, relatively intact grey matter, enlarged ventricles

Traumatic axonal injury – 17 month survival in a vegetative state (Gennarelli & Graham, 2005)
Marked symmetrical dilation of the ventricles Absence of surface contusions

Brain Swelling May be focal or diffuse
May be due to increase in cerebral blood volume or due to oedema (an increase in water content in brain tissue) Vasogenic Oedema: disruption of blood-brain barrier due to injury to cells that line blood vessels of brain 1. Swelling adjacent contusion/cerebral laceration/intracerebral haemorrhage Fluid in extracellular space in white matter Detected CT/MRI hrs, peaks 4-8 days 2. Swelling of one hemisphere Occurs after subdural evacuated; cause not clear - reperfusion of vascular bed, blood vessels dilate, blood-brain barrier leaky Mass effect from intracerebal haemorrhage, contusions – midline shift, compression of ventricles, hydrocpehalus

Complications: Infection (meningitis and brain abscess) Hydrocephalus
Following depressed skull fracture, base of skull fracture, surgery and insertion of ICP monitors (extra-ventricular drains) Hydrocephalus Following subarachnoid haematoma, oedema– obstruction to CSF flow, or difficulty in reabsorption of CSF may need placement of ventricular catheter into ventricles to drain CSF into body cavity (e.g. abdomen) Post-traumatic Epilepsy (Baron & Jallo, 2007) Incidence 5% Greater risk with penetrating brain injury, intracranial haemorrhage, compound depressed skull fracture (fibrosis of meninges or gliosis of underlying brain tissue) or early seizure (within first week), GCS ≤ 10

Classification: Severity of TBI
Severity of TBI is related to cognitive and behavioural outcomes Two aspects measured: Coma/impaired consciousness Post-traumatic amnesia

Severity of TBI: Coma/Impaired consciousness
Glasgow Coma Scale (GCS, Teasdale & Jennett, 1974) serial measurement of presence, duration and depth of impaired consciousness and coma used to describe altered consciousness from mild confusional state to deep coma 3 aspects measured: verbal responses, motor responses and eye opening highly reliable when used by trained persons

Severity of TBI: GCS GCS used to describe altered consciousness from mild confusional state to deep coma A coma score can be obtained (range 3-15; sum of highest score can be calculated) Coma has been defined when GCS ≤ 8 (e.g., no greater than 1 on eye opening, 2 on verbal response and 5 on motor response) A score of 3-deepest level of consciousness (no movements, sounds or eye opening) Injury Severity Classification GCS Mild Moderate 9 -12 Severe 3 - 8

Severity of TBI:GCS Which GCS represents severity of TBI?
GCS mild TBI – 30 minutes post-injury or on presentation to healthcare (Carroll et al., 2004) GCS 3-12 moderate-severe TBI: Initial GCS in Emergency Department Worst/Best Day 1 GCS, lowest pre-intubation GCS Profile of GCS over 24 – 48 hours (including scene) Vulnerability of GCS to drugs and alcohol Anaesthesia/surgery, opioids, sedation (intubation) Day of injury alcohol may/may not lower GCS (Lange et al; 2010) Effect of other injuries on GCS scores Intubation/tracheostomy/facial/eye injuries may prevent accurate GCS assessment

Severity of TBI: Post-traumatic Amnesia
The period following coma/impaired consciousness during which the patient is confused and disorientated (Levin & Goldstein, 1989) Post-traumatic amnesia (PTA) is characterised by intellectual and behavioural disturbances Hallmark of PTA is amnesia where the patient is unable to record events in a continuous (Russell & Nathan, 1946) or connected manner Duration of PTA defined as from the time of injury until return of continuous memory and includes the period of coma/impaired consciousness Duration of PTA related to severity of diffuse traumatic axonal injury PTA is one of the best predictors of outcome following TBI (more accurate than GCS)

Severity of TBI: Post-traumatic amnesia
Teasdale, G.M. (1995) Head injury. Journal of Neurology, Neurosurgery and Psychiatry, 58, PTA Duration Severity < 5 minutes Very mild 5-60 minutes Mild 1-24 hours Moderate 1-7 days Severe 1- 4 weeks Very severe More than 4 weeks Extremely severe

Severity of TBI : GCS and PTA duration
Carroll et al., (2004). Methodological issues and research recommendations for mild traumatic brain injury: The WHO Collaborating Centre Task force on mild traumatic brain injury. Journal of Rehabilitation Medicine (Suppl. 43), GCS PTA Duration Severity 13-15 Up to 24 hours Mild 9-12 1-24 hours Moderate 3-8 1-7 days Severe 1- 4 weeks Very severe More than 4 weeks Extremely severe Note that individuals may have PTA of more than one day where the initial GCS is 9 or more and in such cases, TBI severity is generally based on PTA duration rather than the initial GCS.

Outcome Moderate to Severe TBI may cause lasting cognitive and behavioural impairments Moderate TBI accounts for 8-10% of TBIs and Severe around 10% The extent of impairment reflects a number of factors: 1. The severity of diffuse traumatic axonal injury Indexed by: Coma Length of post-traumatic amnesia Extent of generalized atrophy 2. The location and depth of focal cerebral lesions

4. The course of recovery:
3. Other factors that may moderate recovery and influence cognitive status: Occurrence of significant non-brain physical injuries at time of injury (hypotension, hypoxia) Age Education, Intellectual capacity (cognitive reserve) Preexisting morbidities (e.g., alcohol use, hypertension, prior concussion/mild TBI; previous severe TBI) Psychological complications (e.g. mood, anxiety, pain) Sleep disturbance 4. The course of recovery: - PTA Rapid recovery Continued, slower recovery ? Plateau or greater cognitive impairment with increasing time post-injury

Neuropsychological domains affected:
Attention Residual deficits prevalent after severe TBI Distractible patients may be unable to focus on tasks Abnormalities of divided attention common (e.g. in dual task conditions i.e. performing simultaneous tasks) Limited capacity in effortful processing of non-routine vs well learned tasks (conscious vs automatic processing) Speed of information processing General slowness of mental activity As task becomes more effortful processing decreases become more apparent Patients may be slow to put together and express ideas and to grasp large amounts of information Slowed processing may undermine performance on timed tasks (e.g. Perceptual Reasoning Scale of WAIS-IV; Reaction time tasks) .

Memory Learning and recall of information (verbal and visual)
May be intrusions (semantic associations on word lists or from similar material presented during the assessment) Recognition memory may or may not be intact Executive contributions to learning – failure to organise strategies to learn Working memory deficits may affect learning (Logical Memory subtest WMS-IV)

Executive or Adaptive function (capacities that enable a person to engage successfully in independent, purposive, self-serving behaviour) Deficits are a critical determinant of functional outcome after TBI May lack self-awareness of extent of deficits Inability to adapt, regulate and control one’s responses in accord with novel and unusual task demands Able to perform routine, stereotyped activities that do not involve response control However, when the person is asked to generate alternative solutions by which to solve a task, to shift from one idea to another or to effect change in their behaviour on the basis of feedback as to the correctness of their response they exhibit deficits

Behavioural changes Personality changes most significant problems at 1, 5, and 15 years post TBI (O’Shanick et al., 2011) Impaired self-monitoring and regulation Impaired social perceptiveness Problems with initiation Profound concreteness Emotional change Inability to learn from social experience Over time, family burden increases, becoming more linked to personality changes and less to neurological severity Patient and family agree least about emotional-behavioural problems

Behavioural changes Frequency of depressive disorders after TBI range from 6% to 77% (Levin & Grossman 1978; Rutherford et al., 1997; Varney et al., 1987) Preinjury history of mood or anxiety disorder significantly more frequent in patients who develop post-TBI major depression Overall rate of psychotic disorder may range from 0.7%-9.8% (may be associated with injuries to the left hemisphere/temporal lobe) Bryant et al. (2000) reported Post-traumatic Stress Disorder in 26 (27.1%; N=96) of severe TBI patient 6 months post-injury Aggressive behaviour: orbito-frontal syndrome associated with behavioural excess – impulsivity, disinhibition, hyperactivity, distractibility and mood lability Inferior orbital surface of frontal lobe and anterior temporal lobes may be associated with aggression

Case Presentation: Carol Referral Information: A 50-year old married woman with a six-month history of distractibility, poor concentration and reduced recall of recent information Time of Assessment: 31 January, 2011 Current Complaints and History: Carol reported that since July, 2010 she was forgetful, easily distracted, and was clumsy and had dizzy spells and balance problems. Carol reported being diagnosed with breast cancer in December 2008 for which she underwent surgery and chemotherapy. She was worried her problems were due to the treatment. She reported she became depressed after the cancer diagnosis.

Interview with Carol’s husband: Since Carol sustained a traumatic brain injury in 1998, her memory had worsened over the years. She was easily distracted, and forget to pay bills, phone numbers and misplaced objects (keys). Her conversation tended to reflect information learnt in the past. Prior to the injury Carol was a quiet person. Personality change included being more talkative, not saying on track, being more forceful in opinions, and becoming agitated in conservations. He reported Carol had dizzy spells sometimes associated with headache, others came “from out of the blue”. He described her mood like a cycle, that was good when with family. When down she spent money to cheer herself up.

Relevant Neurological History:
Assaulted at 1700 on 7 September, 1998 GCS at scene = 9/15 Ambulance report: Witness observed 10 minutes loss of consciousness. Admitted to St Vincent’s Hospital at 1753. GCS on acute admission 12/15, 13/15, 12/15, 13/15; 12-13/15 for first 24 hours CT brain scan: bifrontal and right temporal contusions, right temporal subdural haemtoma, effacement of the right lateral ventricle and an undisplaced fracture of the right occipital bone PTA not measured Husband reported Carol was confused and disoriented for 3 days To questioning Carol reported her first memory was waking up in a ward at St Vincent’s and seeing her facial injuries in a mirror. She said it was already more than a week after the injury.

Relevant Psychological History:
Developed post-traumatic stress disorder with associated agoraphobia post-injury Episodes of major depression Two episodes of suicidality Demographic and social history: Born and educated in Hong Kong Indicated her first language was English and fluent in Mandarin 16 years of formal education (6 years primary, 4 years high school, 4 years university) Education took place in both English and Mandarin Accountant Employment terminated in 2000

Neuropsychological Measures Effort tests:
Test of Memory Malingering Raw Score Trial 1 48/50 Trial 2 50/50 WMS-IV Effort score Raw Score Base rate Reliable Digit Span 9 >25% Logical Memory II Recognition 24 Verbal Paired Associates II Recognititon 37 Visual Reproduction II Recognition 6

WAIS-IV Education Adjusted Composite Score Summary
Age Adjusted Scores Education Adjusted Index Composite Score (95% CI) Qualitative Description VC 93 (88-99) Average Low Average PR 90 (84-97) WM 100 (93-107) PS 89 (82-98) FSIQ )

WMS-IV Education Adjusted Composite Score Summary
Age Adjusted Scores Education Adjusted Index Composite Score (95% CI) Qualitative Description AMI 81 (76-88) Low Average Mild to Moderate Impairment VMI 92 (87-98) Average VWM 80 (74-89) Mild Impairment IMI 87 (81-94) Mild to Moderate Impairment DMI 81 (75-89)

Test of Premorbid Function: SS 114, High Average
Test of Premorbid Functioning (TOPF) WAIS-IV Actual-Predicted Comparison Composite Actual Predicted Estimation Interval Difference Critical Value Significant Difference Base rate FSIQ 91 111 83-139 -20 5.08 Y 13.4% VCI 93 85-137 -18 5.97 11.5% PRI 90 112 78-146 -22 6.24 23.5% WMI 100 81-143 -12 7.05 41.4% PSI 89 76-148 -23 10.71 24.7%

Test of Premorbid Functioning WMS-IV Actual – Predicted Comparison
Composite Actual Predicted Estimation Interval Difference Critical Value Significant Difference Base rate IMI 80 111 77-145 -31 7.45 Y 11.3% DMI 81 76-146 -30 7.4 12.1% VWMI 113 79-147 -33 8.02 7%

Failure to Maintain Set
Rey Auditory Verbal Learning Test Trials 1 2 3 4 5 Total B 6 Delay Recog 7 29 10 Trial 1 to 5: Mild to Moderate - Moderate to Severely Impaired Total learning: Moderately Impaired Trail 6: Moderately to Severely Impaired Delay: Mild to Moderately Impaired Controlled Oral Word Association Test Raw score FAS 53 High Average Animals 23 Wisconsin Card Sorting Test Percentile Categories 6 > 16% Perseverative Errors High Average Failure to Maintain Set

Psychological Measures
Depression Anxiety Stress Scales – 42 item Severity range Depression Severe Anxiety Moderate Stress Mild PTSD Checklist - Specific Cluster met Reexperiencing Yes Avoidance No Arousal PTSD Diagnosis Met

Conclusion: Available information (brain CT scan, retrospective report of duration of PTA, informant interview with husband) consistent with Carol having sustained a very severe TBI in In prrevious assessment demographic adjustment not available. Unusual decrement from premorbid levels in current Low Average Intellectual Ability and Low Average verbal concept formation, verbal reasoning and learnt knowledge. Cultural and education differences may have affected her performances on verbal and knowledge based tasks. Cultural factors may have affected performance on other tasks of verbal and non-verbal ability. Current performance on memory tasks consistent with mild to moderate memory problems and with information from husband: Hypothesised due to deficits post TBI and possible cognitive decline with increasing time since TBI. Psychological review suggested Severe depression, Moderate anxiety and Mild stress. Carol met criteria for PTSD at a subsyndromal level. Concerns of cognitive deterioration may be due to underlying psychological distress associated with depression following breast cancer. Subjective report of cognitive decline in breast cancer patients reported to be independent (unrelated) to any objective evidence of neuropsychological compromise Recommendations: Psychological and Psychiatric review; Anxiety Management strategies; Memory aids (diary, mobile phone); Strategies to assist with socialising

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