Neuroradiological and Electroencephalographic Features in a Case of Temporal Lobe Status Epilepticus

Abstract

A patient with medically intractable status epilepticus of temporal lobe origin is presented. A computed tomogram showed a low density area adjacent to the midbrain, possibly related to atrophy of the medial temporal lobe. Cerebral angiography revealed early filling veins and an anterior temporal blush. Magnetic resonance (MR) scanning (T2 weighted images) showed increased signal intensity in the region of the amygdala and anterolateral left temporal lobe. Ictal activity was recorded from scalp electrodes over the left temporal area, and many paroxysms were recorded from cortical surface electrodes. An anterior temporal lobectomy revealed only gliosis. The cerebral blood flow changes accompanying status epilepticus of focal origin are reviewed, and a possible relation of electroencephalographic, angiographic, and MR findings is discussed.

Focal Cerebral Magnetic Resonance Changes Associated with Partial Status Epilepticus

“…Two other patients reported to have focal cerebral MRI abnormality associated with partial SE did not undergo poststatus MRI to demonstrate resolution of the abnormality. In one of the 2 patients, anterotemporal lobectomy demonstrated only gliosis of resected tissue (Stone et al, 1986); in the other, MRI had been normal before SE (Bauer et a]., 1989). In these 5 cases and in our first case, the MRI abnormality involved a focal area either of white matter or of white and gray matter combined, demonstrating decreased signal intensity on T,-weighted and/or increased signal intensity on T,-weighted images, without mass effect.…”

Delayed, Transient Neurological Deterioration After Mild Head Injury. Case Report.

“…11,16,32) Neuroimaging signs of transient abnormalities in patients with status epilepticus characteristically involve a focal area either in the white matter or in the combined white and gray matter, appearing as low density areas by CT, and as decreased signal intensity on T 1 -weighted images and/or increased signal intensity on T 2 -weighted ones by MR imaging, without a mass effect. 9,13,31) Such changes are thought to be due to vasogenic edema induced by hyperemia. Increased oxygen consumption in the cortical epileptogenic zone and the resulting hypoxia are assumed to lead to an accumulation of CO 2 and lactic acid, which in turn causes vasodilation, loss of autoregulation, and increased cerebral blood flow.…”

Estatus parcial continuo, causa de hiperintensidad de la corteza cerebral en la resonancia nuclear magnética

“…, Patricio Quezada R. 3 y Luis Cartier R. Penfi eld en el año 1933 reportó, en exploraciones intraoperatorios vinculadas con actividad epiléptica persistente, cambios hemodinámicos locales, que posteriormente fueron defi nidos como patrones hipervasculares con los estudios angiográ-fi cos [4][5][6] . Sin embargo, la interpretación patogénica del fenómeno se comienza a confi gurar desde los primeros estudios hechos con la Resonancia Nuclear Magnética (RM) de cerebro en pacientes con crisis epilépticas focales [5][6][7] .…”

“…Sin embargo, la interpretación patogénica del fenómeno se comienza a confi gurar desde los primeros estudios hechos con la Resonancia Nuclear Magnética (RM) de cerebro en pacientes con crisis epilépticas focales [5][6][7] . La observación de las imágenes muestran hiperperfusión localizada y re-alce en las secuencias contrastadas, incremento de señales en T2W-FLAIR (fl uid-attenuaded inversión recovery) y Difusión (DWI: diffusion-weighted imaging), con variable grado de reducción en el coefi ciente de difusión aparente (ADC) [6][7][8] .…”