Functional anatomy of focal epilepsy

dysarthria, and ataxia developed over three days. Nystagmus, right tongue weakness, right hemiparesis, and bilateral Babinski signs were observed. CSF gamma globulin at that time was 27% of the total protein. By five weeks all signs and symptoms had improved. Later that year, she again developed a right hemiparesis with numbness and dysmetria. A year later, at age 22, she developed transient left leg weakness. For about ten years she was asymptomatic, then at age 32 she developed bulbar speech and facial and tongue weakness. Two days later she suddenly became nonfluent. She could say “yes” or “no” when addressed, but not always appropriately. She could say her name but had no other verbal output. Auditory comprehension for simple commands, trudfalse questions, and pointing to common objects was severely impared. Naming of objects, repetition of words or phrases, writing, reading, and reading comprehension were also severely affected. Poor comprehension precluded examination of praxis; however, she used her left limbs normally for daily activities. O n examination a left gaze preference, right homonymous hemianopia, right facial weakness, and hemiparesis were present. Complete blood count, sedimentation rate, sickle cell preparation, clotting profile, antinuclear antibody titer, lupus erythematosus preparation, latex fixation, Holter monitoring for 24 hours, and an echocardiogram were all normal. The electroencephalogram revealed continuous polymorphic delta activity in the left frontoparietal region. A nonenhancing radiodense white matter lesion was noted in the left periventricular region on computerized tomographic scan. Four-vessel cerebral angiography showed no abnormalities. Brainstem auditory evoked responses were normal, but visual evoked responses to pattern shift stimulation were abnormal bilaterally. An oligoclonal band pattern was observed in the CSF. Several months later the patient had substantially improved. At one year after her hospitalization she remains mildly anomic. Handwriting is poor and slightly agrammatical. Auditory comprehension is excellent. Questions concerning family, work, and social life are answered appropriately. Repetition for long sentences remains slightly impaired. Mild right-sided weakness is still evident, and reflexes are brisk. H e r gait is slightly wide based with circumduction of the right leg and decreased associated movements. MS rarely affects language but can result in aphasia [ 1 , 4 , 6 , 111. Rarely, MS stimulates major strokes [4, 131. Initially we considered a coincident stroke in this patient, but we failed to demonstrate a vascular lesion. The diagnosis of MS is usually based on clinical criteria which this patient met { 12). Poser [8] found aphasia in only 2 of 812 MS patients, and Muller [ S ] listed only 2 instances among 667 patients; most cases had resolved by the time of examination. Broca aphasia has been described in a patient with MS [GI; that report also included a description of 7 other patients with aphasia. Adams and Victor 111 stated that they had observed ‘‘several cases” of aphasia in MS, but none were described. In 2 patients with MS, Broca aphasia has been the presenting sign [ll}. Only one description of a global aphasia has been noted, and this was during a focal seizure 1141. Prominent language disturbances such as aphasia occur in other white matter diseases but rarely in MS [7, 9, lo]. Perhaps MS plaques in general are either not large enough or not dense enough to cause aphasia. Evidently, the plaque in this patient was large enough to encompass all language pathways, including connections from the Broca and Wernicke areas as well as the arcuate fasciculus.