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DOI 10.1111/j.1528-1167.2008.02000.x

Медицинская библиотека · Epilepsia · 2009

Atypical language lateralization in epilepsy patients.

Möddel Gabriel, Lineweaver Tara, Schuele Stephan U, Reinholz Julia, Loddenkemper Tobias

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

PURPOSE: To investigate whether atypical language dominance in epilepsy patients is related to localization and type of lesions.

METHODS

Four hundred and forty-five epilepsy patients received bilateral Wada testing. Language was classified as left (L), right (R), bilateral-dependent (BD, speech arrest after left and right injections), or bilateral-independent (BI, no speech arrest after either injection). Groups were compared regarding handedness and magnetic resonance imaging (MRI) lesions. Lesions were classified as "early" (congenital), "late" neocortical (acquired after birth), and hippocampal sclerosis (HS).

RESULTS

Of all patients, 78% were L, 6% R, 7% BD, and 9% BI. Right-handers with left lesions did not differ from those without lesions. Left-handers with normal MRI did not differ from right-handers. Left-handers with early left lesions were most likely R (46%). Left-handers with late neocortical left lesions were most likely BD (37%); those with left HS were most likely BD (33%) or L (33%). In both latter groups, R language was rare (13% and 11%, respectively).

DISCUSSION: The data support the notion that R dominance may indicate development of functional language areas in the right hemisphere following an early insult. BD language may signal defective maintenance of right hemispheric language caused by a late left hemispheric insult at a time when left dominance has already started to develop. In contrast, BI language may represent a variant with functional language representation in both hemispheres.

Для цитирования: Möddel Gabriel, Lineweaver Tara, Schuele Stephan U, Reinholz Julia, Loddenkemper Tobias. Atypical language lateralization in epilepsy patients.. Epilepsia. 2009. DOI: 10.1111/j.1528-1167.2008.02000.x.

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