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Figure 4

Mechanisms of Traumatic Brain Injury

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Figure 2

The Glasgow Outcome Scale (GoS)

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Figure 3
Rancho Los Amigos Levels of Cognitive Functioning

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Figure 1

Symptoms of Traumatic Brain Injury Pathology

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Cognitive Assessment of Traumatic Brain Injury

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Cognitive Assessment of Traumatic Brain Injury

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Neuropsychological and functional outcome is related to the severity of the traumatic brain injury, with long-term cognitive deficits and function impairment common after moderate and severe traumatic brain injuries.

The Glasgow Outcome Scale (see Figure 2; Jennett & Bond, 1975) provides a broad categorisation of global functional disability following traumatic brain injury. A substantial percentage of clients who sustain severe traumatic brain injuries are at risk for moderate to severe disability.

Cognitive impairment following traumatic brain injury is highly individualized and difficult to predict. As severity of the injury increases, there is a greater likelihood of global cognitive deficits, that may include reduced speed of processing, attention, memory ability, and reasoning skills (Dikmen et al., 1995). Instruments examining these various cognitive domains, as well as measures of general intellectual function, should be included in the neuropsychological assessment of traumatic brain injury, and can inform a global measure of functioning using the Rancho Los Amigos Levels of Cognitive Functioning Scale (see Figure 3; Gouvier et al., 1987).

STUDENTS WOULD BE EXPECTED TO PROVIDE ADDITIONAL DETAILS ON SPECIFIC ASSESSMENT APPROACHES AND TASKS TO COMPLETE THIS SECTION.

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Bigler, E. D. (2004). Neuropsychological results and neuropathological findings at autopsy in a case of mild traumatic brain injury. Journal of the International Neuropsychological Society, 10, 794-806.

Dikmen, S., Machamer, J.E., Winn, R., & Temkin, N.R. (1995). Neuropsychological outcome 1-year post head injury. Neuropsychology, 9, 80-90.

Eisenberg, H. M., & Levin, H. S. (1989). Computed tomography and magnetic resonance imaging in mild to moderate head injury. In H. S. Levin, H. M. Eisenberg & A. Benton (Eds.), Mild Head Injury (pp. 133-141). New York: Oxford University Press.
Eslinger, P.J. (2002). Neuropsychological interventions: Clinical research and practice. New York, NY: Guildford Press.

Gouvier, W. D., Blanton, P. D., LaPorte, K. K., & Nepomuceno, C. (1987). Reliability and validity of the Disability Rating Scale and the Levels of Cognitive Functioning Scale in monitoring recovery from severe head injury. Archives of Physical Medicine and Rehabilitation, 68, 94-97.

Haslam, C., Batchelor, J.,Fearnside, M. R., Haslam, S. A., Hawkins, S., & Kenway, E. (1994). Post-coma disturbance and post traumatic amnesia as nonlinear predictors of cognitive outcome following severe closed head injury: Findings from the Westmead head injury project. Brain Injury, 8, 519-528.

Jennett, B. (1989). Some International Comparisons. In H. S. Levin, H. M. Eisenberg & A. R. Benton (Eds.), Mild Head Injury (pp. 23-36). New York: Oxford University Press. Jennett, B. & Bond, M. (1975). Assessment of outcome after severe brain damage. Lancet, 1, 480-484.
Lezak, M.D., Howieson, D.B., & Loring, D.W. (2004). Neuropsychological Assessment (4 ed.) New York, NY: Oxford University Press.

Mckee, A.C. & Daneshvar, D.H. (2015). The neuropathology of traumatic brain injury. Handbook of Clinical Neurology, 127, 45–66.

Podell, K., Gifford, K., Bougakov, D., & Goldberg, E. (2010). Neuropsychological assessment in traumatic brain injury. The Psychiatric Clinics of North America, 33, 855–876.

Povlishock, J. T. (1996). An overview of brain injury models. In R. K. Narayan, J. E. Wilberger & J. T.Povlishock (Eds.), Neurotrauma. New York: McGraw-Hill.

Prigatano, G.P. & Altman I.M. (1990). Impaired awareness of behavioural limitations after traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 71, 1058-1064.

Richardson, J. (2000). Clinical and neuropsychological aspects of closed head injury. East Sussex, England: Psychology Press Ltd.

Sohlberg, M.M. & Mateer, C.A. (1990). Evaluation and treatment of communicative skills. In J.S. Kreutzer & P. Wehman (Eds.), Community integration following traumatic brain injury. Baltimore, MD: Brooks.

Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: A practical scale. Lancet, 2, 81-84.
Virk, S., Williams, T., Brunsdon, R., Suh, F., & Morrow, A.  (2015).  Cognitive remediation of attention deficits following acquired brain injury: A systematic review and meta-analysis.  NeuroRehabilitation, 36, 367-377.

Wilson, B.A. (1991). Theory, assessment, and treatment in neuropsychological rehabilitation. Neuropsychology, 5, 281-291.
Zasler, N. (2000). Medical aspects. In S. A. Raskin & C. A. Mateer (Eds.), Neuropsychological management of mild traumatic brain injury (pp. 23-38). New York: Oxford University Press.

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Cognitive Rehabilitation after Traumatic Brain Injury

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Cognitive Rehabilitation after Traumatic Brain Injury

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Cognitive rehabilitation interventions usually require innovative and individualised approaches, due to the variable nature of deficits, personal background, and treatment goals from one client to the next (Wilson, 1991). The rehabilitation approach should be directed at functional deficits that remain after acute medical management, in order to facilitate optimal adjustment. Most often the approach will focus on (1) restoration of function, to improve specific skills, and/or (2) compensatory training in order to adapt to persisting cognitive or behavioural problems (Eslinger, 2002).

MEMORY DEFICITS:

Memory rehabilitation should take into account the kinds of memory that are spared and impaired, the particular memory processes that are compromised, and the regions of the brain that are affected. Repetitive practice drills and exercises can be applied in an attempt to restore damaged memory processes. Teaching specific strategies can be utilised to optimise residual function. Finally, external aides and environmental supports may be introduced and implemented to compensate for or bypass lost function. STUDENTS WOULD BE EXPECTED TO PROVIDE ADDITIONAL DETAILS ON SPECIFIC REHABILITATION APPROACHES AND METHODS TO COMPLETE THIS SECTION.

EXECUTIVE FUNCTION DEFICITS:

Executive deficits typically manifest as a disturbance in the ability to effectively self-regulate behaviour in order to achieve an intended effect, and include failures in anticipatory processes, feedback mechanisms, and error detection. Interventions for executive dysfunction can address these shortcomings, through the use of overt predictions, verbal mediation, adaptive problem solving, and formal self-monitoring strategies. STUDENTS WOULD BE EXPECTED TO PROVIDE ADDITIONAL DETAILS ON SPECIFIC REHABILITATION APPROACHES AND METHODS TO COMPLETE THIS SECTION.

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The Neuropsychological Profile of Traumatic Brain Injury

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The Neuropsychological Profile of Traumatic Brain Injury

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Some of the common symptoms of traumatic brain injury are presented in Figure 1, categorised by location of the neuropathology. For planning rehabilitation of traumatic brain injury, neuropsychological assessments are usually introduced once the client is out of PTA or at specific time points such as three or six months after injury (Podell, Gifford, Bougakov, & Goldberg, 2010). Following injury, the cognitive functioning of individuals usually gradually improves and eventually levels off, the time taken to do so being quite variable (Lezak, Howieson, & Loring, 2004).

Attention deficits are very common (Virk et al,, 2015). When severe, clients can experience significant distractibility, difficulty maintaining focused attention, and poor working memory function. Slowed thinking processes also commonly feature.

Unless direct damage to the left hemisphere has been sustained, a classic aphasia syndrome in clients with traumatic brain injury is relatively rare (Sohlberg & Mateer, 1990).

Some memory problems are usual present, but severity varies greatly (Lezak, Howieson, & Loring, 2004). Memory deficits usually consist of problems in the acquisition and retrieval of information.
Executive deficits after traumatic brain injury are often the most handicapping, as they interfere with the ability to flexibly and fluently apply knowledge and skills (Lezak, Howieson, & Loring, 2004). In addition, a common problem after traumatic brain injury occurring with frontal lobe injury is diminished awareness of one's deficits (Prigatano & Altman, 1990). Due to this lack of insight, clients may not be motivated for rehabilitation or for properly monitoring their performance in activities of daily living.

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Accurate and consistent classification of head injury severity is essential for studies of traumatic brain injury outcome.  The identification of several neurological factors that can be correlated with severity of head injury has subsequently enhanced injury classification and outcome prediction. In particular, three acute measures of injury severity are frequently utilised: (1) duration of loss of consciousness (LOC; Richardson, 2000), Glasgow Coma Scale (GCS) score (Teasdale & Jennett, 1974), and duration of posttraumatic amnesia (PTA, Haslam et al., 1994).

Alteration or loss of consciousness is considered indicative of diffuse brain damage (Jennett, 1989) with injury to progressively deeper structures associated with an increasing duration of unconsciousness (Eisenberg & Levin, 1989).  The GCS is a 15 point scale used to determine levels of consciousness and has gained wide acceptance as an indicator of the overall severity of head injury (Richardson, 2000).  The scale involves separate assessment of motor responses, verbal responses, and eye opening.  PTA refers to the period of confusion and inability to form new memories experienced after head injury.  PTA is thought to reflect cognitive disturbance secondary to brain damage and duration of PTA provides a retrospective means of assessing the severity of head injury (Zasler, 2000).  Table 1 demonstrates how based on these neurological factors, the severity of traumatic brain injury can be categorised.

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Table 1

Classification of Traumatic Brain Injury Severity

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The Neuropathology of Traumatic Brain Injury

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The Neuropathology of Traumatic Brain Injury

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In most instances, traumatic brain injury is the result of acceleration or deceleration (A/D) forces or direct impact.  Damage from a direct blow to the head begins with the inward molding of the skull at the point of contact. The point of contact is referred to as the coup, and a contusion is likely to appear under the site of impact (see Figure 4). Inertial forces can also cause countercoup lesions, in which the brain sustains a contusion in the area opposite the blow (Mckee & Daneshvar, 2015).

Cerebral contusions are often most severe on gyral crests. However, head injury particularly affects the frontal lobes of the brain (Bigler, 2004).  This area of the brain is uniquely vulnerable in head injuries because of the manner in which the frontal lobes rest against the rough, bony projections and irregularities of the sphenoidal ridge (Richardson, 2000).  Following impact, shearing forces give rise to contusions of the anterior and inferior surfaces of the frontal lobes (Richardson, 2000).

Furthermore, A/D injury without specific impact to the head may generate rotational forces cause microscopic tearing and other changes to the brain. These focal and diffuse lesions are relatively independent of the original site of impact (Povlishock, 1996) producing a spectrum of damage referred to as diffuse axonal injury (Bigler, 2004).

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