Elsevier

Neurologic Clinics

Volume 27, Issue 4, November 2009, Pages 881-907
Neurologic Clinics

The Emerging Architecture of Neuropsychological Impairment in Epilepsy

https://doi.org/10.1016/j.ncl.2009.08.001Get rights and content

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The unique contribution of TLE

Psychomotor epilepsy or TLE has provided an especially important window into the neuropsychology of epilepsy. The term “psychomotor epilepsy” was used beginning in the 1930s to describe relatively poorly understood spells that some had called psychic equivalents.27, 28 The early electroencephalographic features were characterized in the context of clinical attacks wherein “….the patient, though he may perform apparently conscious acts, is not subject to command; he may exhibit involuntary tonic

The palm desert conferences on epilepsy surgery and the neuropsychology of epilepsy

Important events for the neuropsychology of TLE were the Palm Desert Conferences on Epilepsy Surgery.40 Before these international conferences there were varying opinions regarding the operational definition of surgical candidacy. Various reasonable criteria were proposed, including seizure frequency and severity, the number of failed medications, or the degree of social and occupational disability; but consensus remained to be achieved. At the second Palm Desert Conference a focus was placed

The distributed nature of cognitive impairment in mTLE

By definition the syndrome of mTLE is a disorder of childhood-adolescent onset.45 A core finding, clear from some of the earliest cognitive studies and routinely reported through the decades, is that an early age of onset of recurrent seizures is associated with a pernicious impact on a broad array of cognitive functions. This effect was reported as early as 192446 and subsequently confirmed in studies of adult patients with diverse seizure types,10, 47, 48, 49, 50 and even reported in

The distributed nature of anatomic abnormalities in chronic TLE

The cumulative neuroimaging literature, focusing here on structural neuroimaging, has shown that anatomic abnormalities in mTLE can be extensive. For reasons that remain to be understood, mTLE seems to be associated with abnormalities in surprisingly diverse neuronal systems, a pattern consistent with the generalized and distributed average neuropsychologic profile of TLE (see Fig. 1).

Initial quantitative MRI volumetric and voxel-based morphometry (VBM) studies identified atrophy of the

Distributed abnormalities in cortical surface features in TLE

Another example of the potential structural consequences of mTLE is provided by quantitative characterization of the cortical mantle, including indices of gyrification, cortical depth, and surface area. These indices provide important information concerning normal and abnormal brain development, the effects of normal aging, and disease impact.

Lee and colleagues70 were among the first to examine cortical surface features (sulcal curvature) in unilateral TLE, the bulk of evidence awaiting the

Distributed abnormalities in white matter and white matter tracts in TLE

In addition to gray matter abnormalities, a decrease in white matter volume is present in chronic TLE. Traditional volumetric studies have demonstrated distributed cerebral white matter abnormalities in patients with unilateral TLE, with abnormalities evident both contralateral and ipsilateral to the side of seizure onset, affecting temporal and extratemporal regions.86 Whole-brain VBM analyses have also demonstrated temporal and extratemporal abnormalities, although the findings are much less

TLE: a localization-related disorder?

The essential theme is that although the primary epileptic zone may be contained within the confines of the hippocampus and temporal lobe, considerable anatomic abnormality exists outside this region affecting a myriad of cortical, subcortical, and cerebellar regions and their direct and indirect connectivity. Importantly, the sum of these distributed structural abnormalities, not to mention associated abnormalities in other aspects of brain integrity, such as metabolism and blood flow, may

Linking distributed cognitive impairments with distributed neuroimaging abnormalities: the mosaic of structure-function relationships in chronic TLE

A developing literature has begun to characterize the links between cognition and the diverse regions of anatomic abnormality in TLE. This section touches on representative examples of these links. Although the focus is on associations between cognition and structural abnormalities, additional investigations albeit smaller in number have examined associations between cognition and behavior with other measures of brain integrity (eg, metabolism, functional MRI [fMRI] activation), and a few

The limitations of modal cognitive profiles

Modal or average cognitive profiles clearly help to convey a sense of the overall cognitive burden associated with TLE, an average burden that seems surprisingly onerous. Similarly, modal or average neuroimaging profiles convey a similar impression regarding the neuroanatomic burden. The symmetry between these modal cognitive and neuroimaging profiles helps to make the cognitive pathology understandable. Although helpful, these average profiles are just that, averages, and may not be

Is TLE unique?

The evidence presented indicates that patients with chronic TLE often exhibit cognitive and quantitative neuroimaging abnormalities that extend beyond the primary zone of seizure onset with significant associations between specific “extratemporal” structural abnormalities and cognitive impairments. These patterns may have their origin in considerable part from the effects of epilepsy and its causes on neurodevelopment as well as progressive abnormalities in a subset of patients. There is

Epilepsy and cognition: bridging the old and new literatures

This article describes a developing architecture of cognitive impairment in the epilepsies, moving from the long established traditional focus on the relationship between neuropsychological status and clinical epilepsy characteristics (eg, seizure frequency, seizure severity, duration of epilepsy, age of onset, etiology, medications), to one focusing on interrelationships between underlying anatomic, metabolic, and other neurobiologic correlates of the epilepsies with critical cognitive and

Conclusion

The landscape of cognitive impairment is clearly in transition from a long-standing focus on the relationship between cognitive function and clinical epilepsy features to one linking cognitive impairment to a multitude of neuroimaging parameters. Whether it will be possible to derive a broad understanding of cognition, clinical epilepsy features and neuroimaging markers remains to be determined. This represents an interesting research challenge for the future.

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      Mesial temporal lobe epilepsy (MTLE) is the most common form of epilepsy, often pharmacoresistant and surgically treated [6]. Hippocampal sclerosis (HS) is the most common pathological substrate of MTLE, although abnormalities can also extend to other limbic system structures, extramesial temporal lobe, subcortical, and extratemporal lobe regions [7,8]. Because of the implications of mesial temporal lobe (MTL) structures for memory consolidation, memory impairment has been considered the core deficit observed in patients [9,10].

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      Only the study by Diehl et al.13 reported that right UF damage was associated with visual reproduction impairment. Studies analyzing specific temporal and extratemporal structural abnormalities in correlation with cognitive impairment are scarce, and their results are controversial.32 The first report that suggested a relationship between diffusion parameters and memory in TLE was by Lui et al.33 in 2004, where the authors found increased apparent diffusion coefficient measurements in the hippocampal structures correlated with impaired memory in patients with TLE.

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