Prolonged deficits after focal inhibitory seizures
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Updated: Aug 15, 2026

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System
Published on: January 1, 2018
Miguel Bussière1, David Pelz, Robert H Reid
1Department of Clinical Neurological Sciences, London Health Sciences Center, University of Western Ontario, London, Ontario, Canada.
Introduction:
Seizures are most commonly associated with positive phenomena such as tonic, clonic or myoclonic movements, automatisms, paresthesias and hallucinations. Negative phenomena, however, are not an uncommon manifestation of seizure activity. Examples of negative seizure phenomena include speech arrest, aphasia, amaurosis, amnesia, numbness, deafness, neglect and atonic seizures. Less commonly described in the literature are focal inhibitory motor seizures.
Methods And Results:
Two patients presenting with rapidly progressive, prolonged hemiparesis, sensory neglect and hemi-visual field obscuration are described. Computed tomography (CT) and magnetic resonance imaging (MRI) of the brain did not reveal progression of known structural lesions or new lesions. The superficial cortex of the hemisphere contralateral to the hemiparesis and sensory neglect enhanced diffusely with gadolinium on T1-weighted MRI images. Electroencephalography demonstrated periodic lateralized epileptiform discharges (PLEDs) in one patient and lateralized suppression and slowing in the other patient. Single photon emission computed tomography (SPECT) revealed hyperperfusion in the hemisphere contralateral to the hemiparesis and sensory neglect. The changes seen on MRI and SPECT resolved with resolution of the symptoms.
Conclusion:
Taken together with the clinical history, the results from these investigations suggest focal inhibitory seizure as the underlying etiology. A review of the literature and investigations helpful in making this difficult diagnosis are provided.
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