Eating seizures and emotional facial paresis: evidence suggesting the amygdala is a common anatomophysiological substratum.

The medial basotemporal lobes (hippocampus, amygdala, parahippocampal gyrus) are considered to be parts of the system responsible for nonvolitional facial movements. In patients with temporal lobe epilepsy, lower facial weakness during emotional expression has been found to occur almost exclusively contralateral to the temporal lobe with the epileptogenic focus. Repetitive and chronic stimulation of the amygdala during eating has also been postulated as a probable mechanism for eating seizures. The authors present the illustrative aspects of both facial asymmetry and eating seizures in a case of mesial temporal lobe epilepsy (MTLE). This report provides evidence that the amygdala may be the common anatomical basis for three different aspects of this patient: emotional facial paresis, eating seizures, and sleep paroxysmal microarousals.

Reduction in temporal N-acetylaspartate and creatine (or choline) ratio in temporal lobe epilepsy: does this 1H-magnetic resonance spectroscopy finding mean poor seizure control?

BACKGROUND: Proton magnetic resonance spectroscopy (1H-MRS) is a potentially useful tool in the in vivo investigation of brain metabolites in intractable temporal lobe epilepsy (TLE). Focal N-acetylaspartate (NAA) reductions have been correlated with mesial temporal sclerosis (MTS) in surgically resected epileptogenic foci. OBJECTIVE: To evaluate the abnormalities in the metabolites NAA, creatine+ phosphocreatine (Cr), and choline containing compounds (Cho) in the temporal lobe of medically refractory patients with temporal lobe epilepsy, seizure free patients with temporal lobe epilepsy, and normal controls. PATIENTS AND METHODS: Ten refractory patients, 12 seizure free patients with temporal lobe epilepsy, and 10 age matched normal controls were studied by 1H-magnetic resonance spectroscopy. All patients had consistently unilateral temporal EEG abnormalities and a normal brain MRI. Proton MR spectra were obtained from an 8 ml volume in the medial temporal lobes in patients with temporal lobe epilepsy (ipsilateral to EEG foci) and the normal controls. The signals measured were expressed in terms of NAA/Cr, NAA/Cho, and Cho/Cr. RESULTS: When compared with seizure free patients with temporal lobe epilepsy and normal controls, the 10 refractory patients with temporal lobe epilepsy had a lower mean (SEM) NAA/Cr ratio (1.65 (0.53) v 2.62 (0.60), and 2.66 (0.73); p<0.002 and p<0.006) and a lower mean NAA/Cho ratio (1.59 (0.79) v 2.83 (1.33) and 2.58 (0.67); p<0.02 and p<0.007). Furthermore, the two patients showing the lowest NAA/Cr ratios (1.47 and 1.73) in the seizure free group had had a past period of poor seizure control. CONCLUSIONS: There were reduced temporal NAA/Cr and NAA/Cho ratios, suggesting neuronal loss or damage, associated with past or present poor seizure control in the patients with temporal lobe epilepsy, but it does not exclude the possibility of a future complete seizure control (seizure free patients with temporal lobe epilepsy at the time of 1H-MRS). This study warrants further 1H-MRS investigation with a larger series of patients with temporal lobe epilepsy.

The spino-latero-reticular system of the rat: projections from the superficial dorsal horn and structural characterization of marginal neurons involved.

The projections of the superficial dorsal horn to the lateral reticular nucleus of the medulla oblongata of the rat, and the morphological types of spinal cord lamina I neurons involved were studied after injecting the retrograde tracer cholera toxin subunit B in the caudal portion of the lateral reticular nucleus. Only injection sites located in the lateral part of the lateral reticular nucleus caused retrograde cell labelling in the superficial dorsal horn (laminae I-III). However, injection sites covering the lateral half of the lateral reticular nucleus and the region intermediate between its lateral border and the ventrocaudal tip of the trigeminal spinal nucleus also labelled cells in the neck of the dorsal horn. In contrast, injection sites confined to the intermediate region gave rise to an almost exclusive cell labelling in laminae I-III. Because the lateral part of the lateral reticular nucleus and the adjoining lateral region are rich in noradrenergic cells, it is suggested that these may be the specific targets of laminae I-III neurons. On the basis of the solid dendritic filling achieved, labelled lamina I cells were classified structurally. Most were fusiform cells (80%) and a minority pyramidal or flattened cells (10% each). Since fusiform cells also project selectively to the parabrachial nuclei, which together with the lateral reticular nucleus have been implicated in respiratory and cardiovascular reflexes, it is suggested that this cell type may convey nociceptive input originating autonomic responses. The pyramidal cells project also in large numbers to the mesencephalic periaqueductal gray which, like the lateral reticular nucleus, exerts descending inhibition on the dorsal horn nociceptive neurons. This suggests that this cell type may activate the spinal-midbrain pain modulatory loops centred on both nuclei.