Essay: Cognitive Effects of Brain Injury

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[. . .] The type of information processed by these declarative memory networks is relatively lateralized, with verbal information mediated by the dominant hemisphere and visuospatial information mediated by the non-dominant hemisphere (Cozzarelli, 2010). Remembering (retrieval of) declarative information requires the activation of the selected neural networks that originally encoded it. Volitional recall is initiated by prefrontal structures; for a relatively limited period of time after initial presentation, such recall also requires the participation of the hippocampal portion of these representational networks. After memories are encoded and consolidated, however, retrieval becomes less hippocampally-dependent (and, eventually, independent of the hippocampus) and instead is frontallydependent .

In addition to their amenability to volitional recall, declarative memories are highly associative and their recall can be triggered by activation (via external or internal stimuli) of any of the networks that participated in their encoding, including those involved in early sensory processing. Memory impairment is often labeled as 'amnesia' (Cozzarelli, 2010). In our experience, we find the use of this term in clinical practice to be potentially problematic: while it is technically correct to use the term 'amnesia' to denote a loss of memory of any kind (consistent with its etymology), its use in common parlance too often connotes loss of memory for autobiographical or other remotely learned information -- vis-a-vis the characters in movies or other fiction who awake from an injury with a complete (psychogenic) amnesia for their life stories (Cozzarelli, 2010). In lieu of describing a patient's memory problems as an amnesia (anterograde, retrograde, or both), it is more useful descriptively and more informative neuroanatomically to identify the type of memory impairment observed in the patient.

Conversely, inability to recall previously learned information spontaneously coupled with semantic or recognition cue-facilitated recall is more likely to reflect injury to or dysfunction of dorsolateral prefrontal-subcortical circuits (Silver, McAllister, Yudofsky, 2005). Typically, disturbances in the ability to learn new information (described in much of the brain injury literature as anterograde amnesia) predominates over the loss of previously, and especially remotely, learned material (or retrograde amnesia). Information learned proximate to the brain injury is more likely to be lost than is more remotely encoded information, a phenomenon referred to as Ribot's Law. Patients with brain injury commonly have disturbances of immediate recall and working memory that are associated and overlap with attentional deficits as discussed above. Delayed recall is frequently impaired after brain injury, occurring in 33%of cardiac arrest survivors at 12 months in one reported series and 29% of survivors at six months after cardiac arrest in another (Silver, McAllister, Yudofsky, 2005). These findings are consistent with other series, although some report even higher rates of impairments in both immediate and delayed recall. Impaired retrieval of remotely learned declarative information (retrograde amnesia) is less commonbut also reported. The development of impairments in new learning and also recall of previously learned information are consistent with the vulnerability of medial temporal structures and frontal cortices, respectively, to brain injury.

Regions at particular risk in brain injury include the CA1 field of the hippocampus, cortical layers III, V, and VI, and the putamen. In addition to vulnerable cell types, the white matter within the border zones between cerebral artery territories, through which the cortical areas involved in declarative memory are connected, is also vulnerable to hypoxic-ischemic injury. The variance in the rates of memory impairment appears to reflect between-study disparities in the mechanisms by which brain injury is acquired (i.e., cardiac arrest vs. other) and the severity of those injuries (Zasler, Katz, Zafonte, 2007).

Consistent with the anatomy of injury, and contrary to conventional wisdom about the cognitive sequel of brain injury, isolated memory impairments (i.e., 'pure' anterograde amnesia) are rarely observed after brain injury; instead, memory impairments usually involve impaired new learning and retrieval and they typically occur in combination with motor impairments and/or executive dysfunction (Silver, McAllister, Yudofsky, 2005). Given the multifaceted nature of post brain injury and brain disease memory impairments, the evaluation of memory among persons with brain injury requires a relatively comprehensive interview and examination of learning and recall. In our experience, it is common for patients, family members, and caregivers to lump attentional disturbances, problems with language and recognition, and executive dysfunction under the rubric of "memory problems."

Executive Dysfunction

Disturbances of executive function are common among survivors of brain injury and usually co-occur with memory disturbances. Executive function denotes a variety of cognitive processes including judgment, insight and self-awareness, anticipation, planning and organization, problem solving, and also extends to the executive control of attention, working memory, declarative and procedural memory, language (e.g., lexical fluency), praxis, and visuospatial function. While executive function is frequently ascribed to the "frontal lobes," it is important to be clear -- particularly in the context of executive dysfunction following brain injury -- that this domain of cognition is supported by the dorsolateral prefrontal-subcortical circuit (Zasler, Katz, Zafonte, 2007). This circuit is composed of: the dorsolateral prefrontal cortex; the dorsolateral head of the caudate nucleus; the globus pallidus interna and the rostrolateral substantia nigra (the "direct" circuit); the dorsal globus pallidus and the lateral portion of the subthalamic nucleus (the "indirect" circuit); and the ventral anterior and dorsolateral thalamus. The dorsolateral prefrontalsubcortical circuit functions in parallel to, and interacts with, the lateral orbitofrontal-subcortical circuit (mediating comportment) and the anterior cingulatesubcortical network (mediating motivation) (Zasler, Katz, Zafonte, 2007).

Additionally, other areas of the brain project into and receive information from this circuit, including the other frontal-subcortical circuits, the limbic system, and the cerebellum. The development of executive dysfunction after brain injury is predictable given the vulnerability of cortical layers III, V, and VI, the cerebellar Purkinje cell layer, and the white matter within the border zones between cerebral vascular territories (Kinnunen et al., 2011)

Injury at any of these locations may disrupt the function of the dorsolateral prefrontal-subcortical circuit and/or its interactions with other areas of the brain and thereby produce executive dysfunction. Problems in executive function may be incorrectly labeled as "memory problems;" their proper evaluation requires a careful history that is further informed by information obtained from the patient's family, coworkers, or caregivers. Patients with executive dysfunction may have limited insight into their problems making this collateral history all the more important. The MMSE, suggested above for the evaluation of attention and memory, does not adequately investigate this area of cognitive function. The Frontal Assessment Battery, the Behavioral Dyscontrol Scale, and the EXIT are useful tools for screening executive function at the bedside (Kinnunen et al., 2011).

When examining patients during the acute rehabilitation period or in the physician's office, one of these (or other) measures assessing executive function is needed to screen for the presence of impairments in this cognitive domain. When these measures do not identify impairments concordant with the patient's or informant's concerns about higher-level cognitive dysfunction, obtaining formal neuropsychological testing is appropriate. As with the evaluation of memory, formal neuropsychological assessment is the best method by which to identify subtle deficits in executive function, the presence and severity of other cognitive impairments, and the presence/influence of mood and other emotional disturbances on clinical presentation. In addition to disturbances of attention, processing speed, memory and executive function, language and calculation impairments, apraxia, agnosia, visuospatial dysfunction, Balint's syndrome, Anton's syndrome, alterations in personality and behavior, and affective dysregulation may also be produced by brain injury (Kinnunen et al., 2011). The reports describing the development of such problems generally involve patients with relatively severe brain injury, and those whose injuries are predominantly due to cardiac arrest.

These other post brain injury and brain disease cognitive and neurobehavioral impairments rarely occur in isolation, and instead co-occur with memory and/or executive dysfunction. While it is possible that injury to or dysfunction of the cortical areas or white matter subserving these cognitive functions may explain their development, their frequent co-occurrence with executive dysfunction raises the possibility that some of these problems may reflect disturbances in the executive control of other cognitive domains, emotion, and/or behavior rather than intrinsic impairments of language, praxis, gnosis, visuospatial function, and other aspects of perception and cognition (Zasler, Katz, Zafonte, 2007). In addition to employing measures specifically designed for the assessment of these other cognitive impairments, coupling neuropsychological studies with neuroimaging (or neuropathological) assessments will improve our understanding of the relative contributions of domain-specific and executive control disturbances to the clinical presentation of these problems.


Persistent cognitive impairments after brain injury and brain disease contribute to functional limitations and affect quality of life. Cognitive impairments is a huge problem for many survivors of brain injury and disease. At the severe end of the continuum of cognitive impairment are the disorders of consciousness, including coma, vegetative states, and the minimally conscious state. These are sometimes persistent, and occasionally permanent, disorders with complex medical, social, and legal considerations that must be addressed by clinicians and the families of these patients. In other cases, the disorders of consciousness are transient and give way to impairments of higher level cognition, including disturbances… [END OF PREVIEW]

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Cognitive Effects of Brain Injury.  (2012, August 8).  Retrieved May 20, 2019, from

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"Cognitive Effects of Brain Injury."  8 August 2012.  Web.  20 May 2019. <>.

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"Cognitive Effects of Brain Injury."  August 8, 2012.  Accessed May 20, 2019.