Повышенная судорожная готовность и эпилепсия могут сдерживаться голоданием.

Archive of Neurology and Psychiatry, 20: 711-779, 1928.
Lennox W, Cobb S.
Controlled fasting was found to reduce the length, severity and number of seizures.

Calorie-restricted ketogenic diet increases thresholds to all patterns of pentylenetetrazol-induced seizures: critical importance of electroclinical assessment.
Epilepsia. 2008 Feb;49(2):320-8. Epub 2007 Oct 15.
Raffo E, François J, Ferrandon A, Koning E, Nehlig A.
INSERM U 666, 67085 Strasbourg, France.
PURPOSE: Thresholds to pentylenetetrazol (PTZ) seizures were usually based only on clinical symptoms. Our purpose was to use electroclinical patterns to assess the efficacy of a ketogenic and/or calorie-restricted diet on PTZ-induced seizures.
METHODS: Forty 50-day-old rats were divided in four weight-matched groups and fed controlled diets: normocalorie carbohydrate (NC), hypocalorie carbohydrate (HC), normocalorie ketogenic (NK), and hypocalorie ketogenic (HK). After 21 days, blood glucose and beta-hydroxybutyrate levels were determined and seizures were induced by continuous infusion of PTZ. The clinical and EEG thresholds to each seizure pattern were compared between the different groups.
RESULTS: The electroclinical course of PTZ-induced seizures was similar in all groups. The HK group exhibited higher thresholds than the  other ones for most clinical features: absence (p = 0.003), first overt myoclonia (p = 0.028), clonic seizure (p = 0.006),  and for EEG features: first spike (p = 0.036), first spike-and-wave discharge (p = 0.014), subcontinuous spike-and-wave discharges (p = 0.005). NK, HC, and NC groups were not significantly different from each other. Blood glucose and beta-hydroxybutyrate levels were not correlated with electroclinical seizure thresholds. After the clonic seizure, despite stopping PTZ infusion, a tonic seizure occurred in some animals, without significant difference regarding the diet.
CONCLUSION: This approach permitted a precise study of the electroclinical course of PTZ-induced seizures. In addition to the usually studied first overt myoclonia, we clearly demonstrated the efficiency of a calorie restricted KD in elevating thresholds to most electroclinical seizure patterns. We confirmed the lack of efficiency of the KD to reduce seizure severity once the seizure has started.

Calorie restriction and glucose regulation.
Epilepsia. 2008 Nov;49 Suppl 8:94-6.
Yamada KA.
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Ketogenic diets (KDs) are effective treatments for epilepsy. The mechanisms of action are poorly understood. In some experime ntal seizure models, calorie restriction and hypoglycemia may augment the antiseizure effects of KDs. In addition, inhibiting  glycolysis or diverting glucose from the glycolytic pathway inhibits seizures and possibly epileptogenesis, suggesting an interaction between energy regulation and the anticonvulsant actions of these interventions. Children on KDs frequently exhibit poor weight gain and have lower blood glucose levels compared to children on standard, balanced diets. Young rodents  on a KD also exhibit slow weight gain, lower blood glucose and insulin levels, and elevated leptin levels. This review considers the possibility that calorie restriction, low serum glucose, and KDs share common cell signaling pathways to alter  brain excitability. AMP-activated protein kinase (AMPK) is an attractive candidate signaling protein that could link energy balance to gene expression in such a way so as to reduce brain excitability.

Caloric restriction inhibits seizure susceptibility in epileptic EL mice by reducing blood glucose.
Epilepsia. 2001 Nov;42(11):1371-8.
Greene AE, Todorova MT, McGowan R, Seyfried TN.
Biology Department, Boston College, Chestnut Hill, Massachusetts 02167, USA.
PURPOSE: Caloric restriction (CR) involves underfeeding and has long been recognized as a dietary therapy that improves health and increases longevity. In contrast to severe fasting or starvation, CR reduces total food intake without causing nutritional deficiencies. Although fasting has been recognized as an effective antiseizure therapy since the time of the ancient Greeks, the mechanism by which fasting inhibits seizures remains obscure. The influence of CR on seizure susceptibility was investigated at both juvenile (30 days) and adult (70 days) ages in the EL mouse, a genetic model of multifactorial idiopathic epilepsy. METHODS: The juvenile EL mice were separated into two groups and fed standard lab chow either ad libitum (control, n=18) or with a 15% CR diet (treated, n=17). The adult EL mice were separated into three groups; control (n=15), 15% CR (n=6), and 30% CR (n=3). Body weights, seizure susceptibility, and the levels of blood glucose and ketones (beta-hydroxybutyrate) were measured over a 10-week treatment period. Simple linear regression and multiple logistic regression were used to analyze the relations among seizures, glucose, and ketones.
RESULTS: CR delayed the onset and reduced the incidence of seizures at both juvenile and adult ages and was devoid of adverse side effects. Furthermore, mild CR (15%) had a greater antiepileptogenic effect than the well-established high-fat ketogenic diet in the juvenile mice. The CR-induced changes in blood glucose levels were predictive of both blood ketone levels and seizure susceptibility.
CONCLUSIONS: We propose that CR may reduce seizure susceptibility in EL mice by reducing brain glycolytic energy. Our preclinical findings suggest that CR may be an effective antiseizure dietary therapy for human seizure disorders.

Studies in Epilepsy