Subacute electrical stimulation of the hippocampus blocks intractable temporal lobe seizures and paroxysmal EEG activities.

PURPOSE: To investigate the clinical, electroencephalographic (EEG), and histopathologic effects of subacute electrical stimulation of the hippocampal formation or gyrus (SAHCS) on 10 patients with intractable temporal lobe seizures. METHODS: Bilateral, depth, hippocampal or unilateral, subdural, basotemporal electrodes were implanted in all 10 patients for a topographic diagnosis of the site and extent of the epileptic focus before a temporal lobectomy. In all patients, antiepileptic drugs (AEDs) were discontinued from 48 to 72 h before a program of continuous SAHCS, which was performed for 2-3 weeks. Stimulation parameters were biphasic Lilly wave pulses, 130/s in frequency, 450 micros in duration, and 200-400 microA in amplitude. The stimuli were delivered 23 of every 24 h for the 2-3-week SAHCS period. The effects of SAHCS on the number of clinical seizures per day and the percentage of interictal EEG spikes per 10-second samples of maximal paroxysmal activity at the epileptic focus were determined daily during the 16 days of SAHCS. At the completion of this program, patients underwent an en bloc temporal lobectomy, and the histopathologic effects of SAHCS on the stimulated tissue were analyzed by means of light-microscopy studies. RESULTS: In seven patients whose stimulation electrode contacts were placed within the hippocampal formation or gyrus and who experienced no interruption in the stimulation program, SAHCS abolished clinical seizures and significantly decreased the number of interictal EEG spikes at the focus after 5-6 days. The most evident and fast responses were found by stimulating either the anterior pes hippocampus close to the amygdala or the anterior parahippocampal gyrus close to the entorhinal cortex. Other surface, hippocampal, and basotemporal EEG signs predicted and accompanied this antiepileptic response. These included an electropositive DC shift and monomorphic delta activity at the medial hippocampal and parahippocampal regions, and a normalization of the background EEG activity and signs of slow-wave sleep in surface. depth, and subdural regions. In contrast, no evident antiepileptic responses or no responses at all were found in three patients when stimulation was either interrupted or when it was administered outside the hippocampus. Light microscopy analysis of the stimulated hippocampal tissue showed histopathological abnormalities attributable to the depth-electrode penetration damage or to the pial surface reaction to the subdural, Silastic electrode plate. However, no evident histopathological differences were found between the stimulated and nonstimulated hippocampal tissue. CONCLUSIONS: SAHCS appears to be a safe procedure that can suppress temporal lobe epileptogenesis with no additional damage to the stimulated tissue.

Quiste epidermoide hipotalámico e hiperprolactinemia secundaria / Hypotalamic epidermoid cyst and secundary hyprprolactinemia

La hiperprolactinemia secudaria a tumor hipotalámo es una patología poco frecuente de gran interés clínico. Se presenta el caso de una mujer de 32 añosde edad con padecimiento de siete meses de evolución manifestado por cefalea intermitente, disminución de la agudeza visual, amenorrea y galactorrea. Posteriormente inicia poliuria, polidipsia, hiperfagia, aumento ponderal y trastornos del sueño. a la exploración física se encontró defecto campimétrico visual, alteración de los pares craneales I, II, III y VII y lesión piramidal. Los estudios hormonales fueron compatibles con diabetes insípida y síndrome hiperprolactinémico. La tomografía computada evidenció la presencia de tumoración hipotalámica hiperémica con componenete quístico. La paciente fue intervenida quirúrgicamente, encontrándose tumor quístico de la línea media de la región hipotalámica, el cual no pudo ser extirpado en su totalidad, reportándose como diagnóstico anatomopatológico definitivo quiste epidermoide de la línea media. La evolución postquirúrgica de la paciente fue mala, fallecido 48 horas después de la cirugía.