Introduction

Seizures can transiently disrupt neural networks, leading to brief cognitive and sensorimotor dysfunction. Epilepsy can have chronic effects upon functioning associated with permanent structural changes in the brain. For most with epilepsy, particularly those with well-controlled seizures on antiepileptic drugs (AEDs), the chronic cognitive effect of seizures will be mild. At the other end of the spectrum, however, there are individuals with profound impairment of cognitive functions, ranging from isolated deficits related to the region of the seizure focus to global disability from widespread changes in brain structure and function.

Measuring cognitive function

Neuropsychological assessment is useful for establishing baseline cognitive function against which change can be measured. This is helpful for evaluating cognitive complaints when they arise, for assessing disease progression, and for determining the effect of treatment. Neuropsychological assessment is mandatory for patients undergoing epilepsy surgery and is particularly important for those with poorly controlled seizures. Such assessment can be important for academic and vocational planning, for the provision of rehabilitative services, and to confirm localization of seizure onset zone for surgical planning.

Table 36.1 and 36.2 contain lists of cognitive and emotional domains that are typically assessed in the context of epilepsy and some of the more common measures employed. There are no standard test batteries used routinely to assess epilepsy, although some core tests are recommended by the NIH’s Common Data Elements project to facilitate comparisons between clinical centers. For evaluating change over time, some groups use reliable change indices (RCIs) or other statistical procedures (e.g., standard regression-based scores) to control for practice effects, although these methods can also obscure meaningful change if not used appropriately. The optimal neuropsychological report assesses whether or not there are factors causing a variable performance (e.g., interictal epileptiform discharges, motivational issues), considers the effects of AEDs, and highlights any localizing or lateralizing features of the results. Recommendations should include appraising the risk of decline in cognitive performance as it relates to treatments such as surgery and the possible benefit of rehabilitation strategies or social services for patients with deficits.

Table 36.1. Core neurocognitive functions to be assessed in epilepsy patients and suggested tests.

Note: WAIS, Wechsler Adult Intelligence Scale; WMS-III, Wechsler Memory Scale 3rd edition; MCG, Medical College of Georgia.
^a Embedded measures of task engagement refer to attempts to use improbable performances on standard clinical tests in order to recognize possible test invalidity.

Table 36.2. Sensory, motor, mood and personality, and quality of life variables to be assessed in epilepsy patients and suggested tests.

Note: WAIS, Wechsler Adult Intelligence Scale; AEDs, antiepileptic drugs.

Causes and mechanisms of cognitive dysfunction associated with epilepsy

Structural lesions can disrupt both local and global neural networks, generally resulting in predictable cognitive deficits. Structural lesions are common, often representing the etiology of the epilepsy (e.g., tumors, dysplasia). Sometimes lesions such as hippocampal atrophy in temporal lobe epilepsy (TLE) reflect the chronic effect of epileptiform activity upon the brain. Some patients also have structural lesions from prior surgical intervention.

Functional impairment of brain networks can also occur from transient chemical and electrical disruptions of brain circuitry from interictal and ictal abnormalities, synaptic and ion channel abnormalities, and medication side effects. When the functional disruption of brain circuitry is potentially reversible and not from a structural lesion, effective management of the underlying process can improve cognition (e.g., changing an AED causing adverse effects, decreasing epileptiform discharges, or altering synaptic neurotransmitter availability).

Mounting evidence indicates that cognitive functions are supported by large-scale distributed neural networks of varying complexity. The less complex systems mediate basic sensory and motor processing, while higher-order cognitive functions such as semantic memory and language are supported by interactions between widespread distributed neural systems. Cortical and subcortical gray matter structures function as processing nodes in these networks, which are then connected by white matter tracts. As already discussed, epilepsy and its treatments produce structural and functional disruption of these networks, as do the underlying neurological processes that cause the epilepsy and other associated comorbidities. Uncontrolled seizures themselves alter brain structure and function, as reflected by gray and white matter volumetric changes and altered functional connectivity demonstrated by resting state fMRI and diffusion tensor imaging (DTI). Disease-related variables such as seizure duration and frequency determine the severity of these brain changes.

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