[Hypothalamic hamartomas: control of seizures after partial removal in one case]. / Hamartomas hipotalámicos: control de las crisis después de la exéresis parcial en un caso.

OBJECTIVE: To describe a patient with intractable seizures and hypothalamic hamartoma that was only partially resected with complete control of seizures and improvement in behavior after surgery. CLINICAL CASE: He had gelastic seizures from the first months of life associated with hypothalamic hamartoma. We used magnetic resonance spectroscopy to localize and measure the lesion in the temporal lobes and in the hamartoma. The relative intensity of N-acetylaspartate to creatine (NAA/Cr) and NAA/choline (Ch) were not significantly different from normal control subjects for either temporal lobes, whereas the ratio NAA/Ch was decreased and the ratio NAA/Cr was highly increased in the hamartoma. Despite only partial resection of the hamartoma, seizures have been completely controlled and the patient has recovered normal social and work activity and is ending a normal life, that follow three years after surgery. CONCLUSIONS: These findings suggest that gelastic seizures associated with hypothalamic hamartoma are generated within the hamartoma itself, and that it is possible to control epilepsy and to improve intellectual and social problems with only partial resection of the mass.

Hippocampal cell loss in transient global cerebral ischemia in rats: a critical assessment.

The induction of transient global cerebral ischemia by permanent vertebral occlusion and temporary carotid ligation (four-vessel occlusion) is widely accepted as a valid tool for the study of pathogenesis and treatment of ischemia. The neural damage inflicted by this intervention is often assessed by measuring pyramidal cell loss in the CA1 hippocampal field. Nevertheless studies using this model in rats often fail to control variables that are relevant to the outcome, and/or apply biased methods to quantitate histological damage. We have applied unbiased stereological methods to estimate absolute numbers of surviving neurons in CA1 in Wistar rats subjected to either 10 or 20 min global ischemia using the Sugio et al. variant of the original four-vessel occlusion model. Animal mortality was high at both times, with neuron losses averaging 39% and 31%, respectively. Post-operative mortality was reduced substantially by using decompressive craniectomies and, even more effectively, by pre-treating the rats with low doses of phenytoin. Both maneuvers led to a severely increased CA1 neuron loss, which reached 50%, after an ischemia of 10 min. This finding strongly supports that mortality biases the sample. Other noteworthy findings that emerged from this study were a linear relationship between per-ischemic blood pressure increments and animal survival, and a negative correlation between cell survival and preferentially left-sided damage.

Animal survival related to acute blood pressure response in global cerebral ischemia in rats.

The increase in mean arterial blood pressure (MABP) during global cerebral ischemia constitutes a compensatory and protective mechanism, regulated by the Central Nervous System, in response to the accumulation of different toxic compounds in the brain stem. The relationship between MABP increases and improved tolerance by the animals to ischemia is discussed.

Characterization of the subtype of presynaptic alpha 2-adrenoceptors modulating noradrenaline release in cat and bovine cerebral arteries.

The possible existence of a heterogeneous population of alpha 2-adrenoceptors (alpha 2A and alpha 2B, demonstrated by binding studies) in adrenergic nerve endings of cat and bovine cerebral arteries modulating noradrenaline release was investigated. Electrical field stimulation elicited an increase of tritium secretion from these vessels preincubated with (+/-)-[3H]noradrenaline, which was reduced by the alpha 2-agonists, clonidine (1 microM) and B-HT 920 (0.01 and 0.1 microM), in cat cerebral arteries but only by B-HT 920 in bovine cerebral arteries. This reduction was inhibited by the antagonist of the alpha 2B-subtype, prazosin, and the antagonists of alpha 2A- and alpha 2B-subtypes yohimbine and particularly rauwolscine. The effect of B-HT 920 was partially inhibited by clonidine in bovine, but not in cat cerebral arteries. In both types of arteries, prazosin, yohimbine and the alpha 1-agonist methoxamine (all at 1 microM) failed to modify the stimulated radioactivity liberation, whereas it was increased by 1 microM rauwolscine, and by yohimbine plus prazosin in cat cerebral arteries. The basal tritium release was enhanced by rauwolscine and prazosin in cat cerebral arteries but only by the latter in bovine cerebral arteries. These results suggest: (1) the existence of presynaptic alpha 2-adrenoceptors, mainly of the alpha 2B-subtype, in these vessels negatively modulating noradrenaline release, their activity being greater in cat than in bovine cerebral arteries, and (2) clonidine has no agonistic but a weak antagonistic action in the latter vessels.