Corpus callosum diffusion abnormalities in refractory epilepsy associated with hippocampal sclerosis.

Objectives: To detect by diffusion tensor imaging (DTI) the extent of microstructural integrity changes of the corpus callosum (CC) in patients with hippocampal sclerosis (HS) and to evaluate possible association with clinical characteristics.

Methods: Fourty-two patients with temporal lobe epilepsy (TLE) and HS and 30 control subjects were studied with DTI. We grouped patients according to lesion side (left or right) HS.

Extratemporal abnormalities in phosphorus magnetic resonance spectroscopy of patients with mesial temporal sclerosis.

Objective: We evaluated extratemporal metabolic changes with phosphorus magnetic resonance spectroscopy (31P-MRS) in patients with unilateral mesial temporal sclerosis (MTS).

Method: 31P-MRS of 33 patients with unilateral MTS was compared with 31 controls. The voxels were selected in the anterior, posterior insula-basal ganglia (AIBG, PIBG) and frontal lobes (FL).

Serial and prolonged EEG monitoring in anti-N-Methyl-d-Aspartate receptor encephalitis.

Objective: To describe serial electroencephalographic (EEG) findings of three patients with anti-NMDAR encephalitis.

Methods: Three women (age 15-34years) with confirmed anti-NMDAR encephalitis underwent serial EEG recordings. Continuous EEG for 72h was performed in one case and 3-day video-EEG monitoring was obtained in two cases.

Phosphorus magnetic resonance spectroscopy in malformations of cortical development.

Purpose: The aim of this study was to evaluate phospholipid metabolism in patients with malformations of cortical development (MCDs).

Methods: Thirty-seven patients with MCDs and 31 control subjects were studied using three-dimensional phosphorus magnetic resonance spectroscopy ((31)P-MRS) at 3.0 T.

[Pitfalls in the clinical and electroencephalographic diagnosis of ceroid lipofuscinosis].

Neuronal ceroid lipofuscinosis (NCL) were traditionally classified according to age of onset and clinical features in four main groups. Recently, a combination of clinical, ultra structural and genetics data led to the recognition of eight forms of NCL, providing a more precise framework to classify atypical cases. By the other hand, it was shown that mutations in the same gene could be responsible for a large variety of clinical phenotypes.