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Severe Hemispatial Neglect as a Manifestation of Seizures and Nonconvulsive Status Epilepticus: Utility of Prolonged EEG Monitoring

Schomer, Andrew C.; Drislane, Frank W.

Journal of Clinical Neurophysiology: April 2015 - Volume 32 - Issue 2 - p e4–e7
doi: 10.1097/WNP.0000000000000107
Case Reports
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Purpose: Seizures and status epilepticus causing hemispatial neglect syndromes are seldom diagnosed, in part because, without motor signs, EEGs are not performed. Also, nonconvulsive seizures are often intermittent and missed on a single EEG. Two patients had severe neglect syndromes thought due to strokes. Correct diagnosis of epileptic seizures required longer-term EEG monitoring.

Methods: Review of clinical history, neurologic examination, imaging, and findings on prolonged EEG monitoring.

Results: A patient with a new onset of a profound left neglect had normal strength and language use, with no obvious clinical seizures. A right hemisphere embolic stroke was diagnosed, but MRI with diffusion-weighted imaging showed no evidence of ischemia. The initial EEG showed marked right parietal voltage suppression, with subsequent brief electrographic seizures and later, right parietal periodic discharges. The second patient had an earlier right subdural hematoma and focal motor seizures but was admitted with a new neglect syndrome and no clear clinical seizures. Head computed tomography showed no new lesion. EEG showed frequent right parieto–temporal epileptiform discharges and electrographic seizures. The neglect syndromes resolved with anticonvulsant treatment, but in both cases, electrographic seizures were intermittent, and there was no strict correlation between the clinical deficit and EEG manifestations of seizures.

Conclusions: Infrequently, the sudden onset of new hemispatial neglect can be caused by nonconvulsive seizures and nonconvulsive status epilepticus, even when there is no weakness and no clear clinical seizure activity. Nonconvulsive status epilepticus can cause primarily perceptual and cognitive syndromes. The correlation between the clinical deficits and seizure activity on the EEG, however, is imprecise. A single EEG may miss seizure activity, and repeated or prolonged EEG recording may be necessary to make the diagnosis.

Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, U.S.A.

Address correspondence and reprint requests to Frank W. Drislane, MD, Department of Neurology, Beth Israel Deaconess Medical Center, Kirstein 479, 330 Brookline Avenue, Boston, MA 02215, U.S.A.; e-mail: fdrislan@bidmc.harvard.edu.

© 2015 by the American Clinical Neurophysiology Society