[Evaluation of cerebral glioma with advanced magnetic resonance techniques]. / Avaliação dos gliomas cerebrais. Por técnicas avançadas de Ressonância Magnética.

Magnetic Resonance Imaging (MRI) is the technique of choice for the radiological evaluation of cerebral gliomas. Determination of its malignant grade is important for therapeutic approach and prognosis. The authors focus on the utility of MRI advanced techniques, namely proton magnetic resonance spectroscopy, perfusion and diffusion. These techniques are complementary to conventional MRI and allow improved non-invasive early evaluation of malignant grade of gliomas. Moreover, these techniques are useful in the determination of the most malignant areas of the tumours, which are potential targets for stereotaxic biopsy and therapy. They also have particular utility on the distinction between residual tumor, recurrence and radiation necrosis.

Pathophysiology and long-term outcome of reversible tumor-like lesions induced by presenting status epilepticus.

BACKGROUND AND PURPOSE: Within the spectrum of reversible neuroimaging abnormalities induced by status epilepticus (SE) tumor-like lesions (TLL) have been rarely described. Their etiology, pathophysiology, and long-term outcome remain uncertain. These issues could be clarified by long-term magnetic resonance imaging (MRI) studies in TLL induced by presenting SE. METHODS: Prospective multi-sequence MRI and clinical and electroencephalographic long-term (18 to 60 months) follow-up studies were performed in 3 patients with reversible TLL induced by presenting SE. RESULTS: In the peri-ictal MRI, TLL are hypointense in T1-weighted, hyperintense in T2-weighted, and fluid-attenuated inversion recovery images with a marked subcortical component and sulci effacement. The diffusion and MR-spectroscopy studies disclosed intermixed areas of increased/decreased diffusivity associated with a lactate peak and a decreased N-acetylaspartate. At long-term follow-up, none of the patients had seizure recurrence or electroencephalographic epileptiform abnormalities; MRI showed residual focal atrophy and gliosis associated with neuronal loss/dysfunction. CONCLUSIONS: SE per se may induce TLL. MRI multi-sequence studies disclosed that they are mainly formed by focal vasogenic and cytotoxic edema resulting from the hypermetabolism associated with seizure activity. In spite of a clinical favorable long-term outcome, the demonstration of irreversible brain damage argues in favor of immediate treatment of SE.

Different electroclinical manifestations of the epilepsy associated with hamartomas connecting to the middle or posterior hypothalamus.

PURPOSE: The epilepsy associated with hypothalamic hamartomas (HHs) has typical clinical, electrophysiologic, and behavioral manifestations refractory to drug therapy and with unfavorable evolution. It is well known that only sessile lesions produce epilepsy, but no correlation has been established between the different types of sessile hamartomas and the diverse manifestations of the epilepsy. We correlate anatomic details of the hamartoma and the clinical and neurophysiologic manifestations of the associated epilepsy. METHODS: HHs of seven patients with epilepsy (ages 2- 25 years) were classified as to lateralization and connection to the anteroposterior axis of the hypothalamus by using high-resolution brain magnetic resonance imaging. We correlated the anatomic classification with the clinical and neurophysiologic manifestations of the epilepsy as evaluated in long-term (24 h) video-EEG recordings. RESULTS: HHs ranged in size from 0.4 to 2.6 cc, with complete lateralization in six of seven patients. Ictal manifestations showed good correlation with the lobar involvement of ictal/interictal EEGs. These manifestations suggest the existence of two types of cortical involvement, one associated with the temporal lobe, produced by hamartomas connected to the posterior hypothalamus (mamillary bodies), and the other associated with the frontal lobe, seen in lesions connecting to the middle hypothalamus. CONCLUSIONS: A consistent clinical and neurophysiologic pattern of either temporal or frontal lobe cortical secondary involvement was found in the patients of our series. It depends on whether the hamartoma connects to the mamillary bodies (temporal lobe cases) or whether it connects to the medial hypothalamus (frontal lobe cases).