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Dr. Chakara

Brain Injury Medicine: Cognitive Impairments After TBI

Originally Published in BRAIN INJURY MEDICINE, Second Edition, July, 2011.

By: Dr. Freeman Chakara, Paul J. Eslinger, Giuseppe Zappalà and Anna M. Barrett
Tel: (717) 397-1400
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Website: www.providencebehavioral.com


Traumatic brain injury (TBI) causes several types of damage to the brain that affect the cerebral cortex, subcortical nuclear structures, and their widespread white matter connections (see chapters by Kochanek et al. and Hovda for more details). The resulting cascade of pathological changes disrupts neural functioning at multiple levels, from individual cellular and vascular structures to the larger brain networks they comprise (see Figure 1). This rapid deformation of brain anatomy and physiology leads to clinical neurological and neurobehavioral impairments that affect a person's cognition, vegetative and emotional functions, as well as social behaviour capacities (1). This chapter is organized to provide an overview and synthesis of the cognitive impairments that are commonly associated with TBI in adults. Cognitive and behavioral symptoms are often major concerns in all types of TBI, as indicated by the many other chapters relating to cognition and behavior, including Kreutzer (Neuropsychological Assessment and Treatment Plans), Cicerone (Cognitive Rehabilitation), Murdoch (Assessment and Treatment of Speech and Language Disorders), Coelho (Cognitive-Communication Deficits), McAllister (Emotional and Behavioral Sequelae), and Arciniegas (Pharmacotherapy of Cognitive Impairments) among others. The importance of these topics stems from the fact that rehabilitation outcomes and any long-term effects of TBI on personal, social and occupational functioning can often be related to cognitive abilities along with behavioral and emotional control. Indeed, cognitive measures are among the most important predictors of patients' return to work and independent living, even among those with good medical recoveries (2, 3).

TBI and post-concussion syndromes occur along a spectrum recognized as mild to severe, with clinical profiles increasingly recognized as a rational and expected "hierarchy" (or cluster) of clinical symptoms, mainly determined by the intensity, severity and location of the injury in the brain along a "gradient" of disturbances. In addition to these direct brain-behavior effects of TBI, clinicians and families must realize that there can be many complicating medical and psychological conditions that can contribute to post-TBI cognitive, behavioral and emotional impairments. These complicating factors are detailed in several chapters throughout the text and underscore the complex and nature of TBI. Despite their prevalence, cognitive impairments must be carefully evaluated on an individual basis, as they can be influenced by pre-existing conditions (e.g., learning disabilities, attention deficit hyperactivity disorder, substance abuse, prior head trauma), co-morbid conditions (e.g., seizures, major depression, pain, and medication side-effects) and differences in TBI damage and recovery. As an example, recent study identified a significant effect of major depression in lowering cognitive functions after TBI (4), with similar effects occurring with chronic headache and other pain, dizziness, diplopia, sleep disturbance, and stress vulnerability. Hence, a multidisciplinary and comprehensive approach to TBI and specifically to cognitive and behavioral impairments is necessary for best treatment outcomes. This is particularly important as TBI is considered a significant predisposing factor in the dementia literature.


Neurocognitive (or neuropsychological) assessment encompasses clinical and psychometric testing procedures that survey and objectively measure the effects of cerebral damage on cognitive, behavioral, social and emotional functioning (5,6). These procedures help identify and define the nature and extent of TBI effects utilizing standardized cognitive tests and survey instruments, together with comprehensive interview and clinical assessment. Neuropsychological test scores can change in different ways depending upon TBI pathophysiology. To this end, a variety of specific assessment techniques have been developed to evaluate a patient's relative strengths and weaknesses in multiple domains such as memory, speech and language, attentionconcentration, spatial cognition, executive functions, and social cognition (see chapter by Kreutzer for further details). Scores are then interpreted in reference to available normative data that provide the typical range and variation in test performance.

Interpretation of neuropsychological test scores is meant to identify the type and severity of cognitive impairments that in turn reflect general location and severity of brain injury. Most clinicians employ a flexible battery approach that focuses on specific problem areas identified through clinical exam and observation. The flexible battery approach emphasizes evaluating the patient's pattern of performance; that is, the possible causes for their impaired test score. For example, impaired memory test scores may reflect attentional and encoding deficiencies, working memory limitations, memory consolidation deficits, poor access to and retrieval of information or some combination of these underlying cognitive difficulties. Delineating specific processing impairments will also provide a more direct and efficient approach to remediation services that target impaired processes. Therefore, neuropsychological assessment, along with assessments provided through diverse medical and therapy services, is geared toward identifying how best to detect, characterize, and intervene in the remediation of cognitive, behavioral, social and emotional impairments that are caused by TBI. The following sections cover specific cognitive processing domains that are particularly important in TBI.


Information processing measures are designed to determine the speed and accuracy of basic sensory-perception and perceptual-motor responses. These processes are mediated by diverse cortical and subcortical regions along with white matter connections that are vulnerable to TBI related damage. Head trauma may alter reaction time capacities in several ways. Sarno et al. (7) demonstrated that severe TBI was associated with prolonged simple and choice reaction times to visual, auditory and tactile stimuli. Tactile stimuli presented particular difficulty in comparison to vision and audition (i.e., sensory-specific deficit) as well as in combination with those modalities (i.e., cross-modal deficits). This is an important study emphasizing acquired change in the typical sensory detection and integration processes that are critical for consistent functioning within stimulating and changing environments. Investigators have confirmed that reaction time can also be compromised after mild TBI (8,9), particularly as task difficulty increased and when inter-hemispheric transfer of information was required. Tinius (9) considered such results to be similar to adults with attention deficit disorder. Even when simple reaction time tasks are completed in normal fashion after TBI, deficits can emerge under conditions of increasing task difficulty, greater informational load, and even fatigue (10) that lead to inconsistent, slowed, and erroneous responses.


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Dr. Freeman Chakara, is a Board Certified Neuropsychologist and founder of Providence Behavioral Health Services. He provides Forensic Neuropsychological Evaluations for children and adults with known or suspected Brain Dysfunction. For the last twelve years, Dr. Chakara has evaluated children and adults for disorders of Attention, Memory, Language, Spatial Cognition, Executive Function, Sensory-Motor, and Socio-Behavioral Disorders.

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