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.
"The attention–arousal coupling sustained by the meal is also claimed to play a role in triggering the attacks. Repetitive and chronic stimulation of amygdala during eating is proposed as the mechanism underlying eating epilepsy (Senanayake, 1994; Guimaraes et al., 2005). Established and new antiepileptic drugs are not effective in controlling the seizures (Loiseau et al., 1986). "
[Show abstract][Hide abstract] ABSTRACT: Food intake triggers convulsions in fasted mice and rats treated with antimuscarinic drugs, scopolamine or atropine. Bearing some similarities in triggering factor and manifestations of the seizures in patients with eating-evoked epilepsy, seizures in fasted animals may provide insight into the mechanism(s) of this rare and partially controlled form of reflex epilepsy.
"The most commonly reported somatomotor manifestations in TLE semiology occur in the face, neck, and upper extremities (Bossi et al., 1984). Orofacial movements involve both upper and lower facial musculature and include blinking, eye closure, bilateral facial contraction, contralateral hemifacial contraction, ipsilateral facial clonic jerks, perioral movements such as " lip smacking, " and a general change in overall facial expression (Bossi et al., 1984; Kotagal et al., 1995; Guimarães et al., 2005; Hogan and Rao, 2006). Suggestions have been made that these motor manifestations are a consequence of secondary generalization of a temporal epileptogenic focus, occurring through reciprocal cortico-cortical projections from mesial temporal structures to lateral temporal cortices, converging to the primary motor and premotor lateral cortices (Bossi et al., 1984). "
[Show abstract][Hide abstract] ABSTRACT: To assess the frequency and significance of facial paresis (FP) in a well-defined cohort of mesial temporal lobe epilepsy (MTLE) patients.
One hundred consecutive patients with MRI findings consistent with mesial temporal sclerosis (MTS) and concordant electroclinical data underwent facial motor examination at rest, with voluntary expression, and with spontaneous smiling. Hippocampal, amygdaloid, and temporopolar (TP) volumetric measures were acquired. Thirty healthy subjects, matched according to age and sex, were taken as controls.
Central-type FP was found in 46 patients. In 41 (89%) of 46, it was visualized at rest, with voluntary and emotional expression characterizing true facial motor paresis. In 33 (72%) of 46 patients, FP was contralateral to the side of MTS. By using a 2-SD cutoff from the mean of normal controls, we found reduction in TP volume ipsilateral to MTS in 61% of patients with FP and in 33% of those without (p = 0.01). Febrile seizures as initial precipitating injury (IPI) were observed in 34% of the patients and were classified as complex in 12 (26%) of 46 of those with FP and in five (9%) of 54 of those without (p = 0.02). The presence of FP was significantly associated with a shorter latent period and younger age at onset of habitual seizures, in particular, with secondarily generalized tonic-clonic seizures.
Facial paresis is a reliable lateralizing sign in MTLE and was associated with history of complex febrile seizures as IPI, younger age at onset of disease, and atrophy of temporal pole ipsilateral to MTS, indicating more widespread disease.
[Show abstract][Hide abstract] ABSTRACT: Animals treated with scopolamine after fasting develop convulsions after they are allowed to eat ad libitum. This study was aimed at investigating the effect on these convulsions of liquid food intake, feeding by gavage, and placebo. Fasted mice treated with saline or scopolamine were allowed to eat solid food, slurry food or liquid food ad libitum, given placebo, or given liquid food by gavage. After 30 min, all animals were allowed to eat food pellets and observed for 30 min for the incidence and onset of convulsions. Scopolamine treatment caused convulsions only in the animals given solid food in the first 30 min; no convulsions were observed in the animals given slurry food, liquid food ad libitum, gavage, or placebo. When the animals that did not develop convulsions during the experiment were allowed to eat solid food, convulsions occurred. These findings indicate that complex mechanisms trigger scopolamine-induced convulsions in fasted animals eating solid food.
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