Eating seizures and emotional facial paresis: evidence suggesting the amygdala is a common anatomophysiological substratum.
ABSTRACT 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.
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Article: The facial motor system.[Show abstract] [Hide abstract]
ABSTRACT: Facial movements support a variety of functions in human behavior. They participate in automatic somatic and visceral motor programs, they are essential in producing communicative displays of affective states and they are also subject to voluntary control. The multiplicity of functions of facial muscles, compared to limb muscles, is reflected in the heterogeneity of their anatomical and histological characteristics that goes well beyond the conventional classification in single facial muscles. Such parcellation in different functional muscular units is maintained throughout the central representation of facial movements from the brainstem up to the neocortex. Facial movements peculiarly lack a conventional proprioceptive feedback system, which is only in part vicariated by cutaneous or auditory afferents. Facial motor activity is the main marker of endogenous affective states and of the affective valence of external stimuli. At the cortical level, a complex network of specialized motor areas supports voluntary facial movements and, differently from upper limb movements, in such network there does not seem to be a prime actor in the primary motor cortex.Neuroscience & Biobehavioral Reviews 11/2013; · 10.28 Impact Factor
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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.Epilepsy & Behavior 05/2009; 15(2):142-5. · 2.06 Impact Factor
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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.Epilepsia 07/2010; 51 Suppl 3:80-4. · 4.58 Impact Factor