Catamenial epilepsy occurrence and patterns in a mixed population of women with epilepsy.

We evaluated the occurrence and distribution of patterns of catamenial epilepsy in a heterogenous cohort of women with epilepsy on no hormonal therapies, enrolled in a prospective, observational study. The primary aim of the study was pregnancy rate in women with epilepsy with no prior reproductive problems. In this analysis, we included women who recorded one or more menstrual cycles with one or more seizures. We measured progesterone concentrations for one to three cycles. We defined catamenial patterns as twofold or greater average daily seizure frequency around menstruation (C1), ovulation (C2), and for anovulatory cycles, from midcycle through menstruation (C3). Twenty-three of the 89 enrolled women with epilepsy were eligible for this analysis; 12 of 23 met criteria for catamenial epilepsy; five of 23 demonstrated only a C1 pattern, two of 23 only a C2 pattern, five of 23 a combined C1/C2 pattern, and the one woman with anovulatory cycles did not demonstrate a C3 pattern. There were no differences in likelihood of demonstrating a catamenial pattern between those who reported a prior catamenial pattern and those who did not (p = .855). This analysis demonstrates the utility of app-based tracking to determine a catamenial pattern. Larger prospective studies could confirm these findings and inform potential therapeutic trial designs for catamenial epilepsy.

Progesterone and its derivatives for the treatment of catamenial epilepsy: A systematic review.

OBJECTIVE: Catamenial epilepsy (CE) is defined as an increase in seizure frequency during specific phases of the menstrual cycle in women with epilepsy. The treatment usually includes a combination of non-hormonal and hormonal therapies. This systematic review summarizes the available data on the efficacy of progesterone and its derivates to treat CE. METHODS: We performed a systematic search of the literature to identify studies reporting data on the use of progesterone and its derivatives (any type and dose) for the treatment of CE. The main outcome included the efficacy of progesterone and its derivatives on seizure frequency. RESULTS: Nineteen articles (457 patients) were included; four were randomized controlled trials (two comparing progesterone vs placebo and two comparing norethisterone vs placebo). Progesterone was generally administered during the luteal phase (from day 15 to 25) or during perimenstrual exacerbations (from day 23 to 25), with an average dose of 10-30 mg/day to a maximum of 300 mg/day. The therapy, usually well tolerated, was ineffective in the randomized controlled trials; conversely, it was associated with an overall reduction in seizure frequency in case reports and uncontrolled studies. CONCLUSIONS: Although data from uncontrolled studies suggest that hormone therapy with progesterone may be useful in the treatment of CE, its efficacy has not been demonstrated in controlled trials. The possible antiseizure effect of progesterone could be mediated by its active metabolite allopregnanolone, making the plasmatic measurement of these hormones mandatory to evaluate efficacy. Further randomized controlled trials should investigate the efficacy of progesterone and its derivatives, addressing these pharmacological issues.

Anticonvulsant Effect of Asparagus racemosus Willd. in a Mouse Model of Catamenial Epilepsy.

Asparagus racemosus Willd. (Family Liliaceae), also known as female reproductive tonic, is traditionally used across the Sub-Himalayan region in Uttarakhand, India for treatment of epilepsy and disorders of female reproductive system. Therefore, in this study, we investigated the anticonvulsant effect of A. racemosus in a mouse model of catamenial epilepsy. We artificially increased progesterone and neurosteroid levels (a state of pseudo-pregnancy) in adult Swiss albino female mice by injecting pregnant mares' serum gonadotropin (PMSG) (5 IU s.c.), followed by human chorionic gonadotropin (HCG) (5 IU s.c.) after 46 h. In the following 10 days, A. racemosus treatment was given along with measurement of progesterone, estradiol, and corticosterone levels in the blood. Neurosteroid withdrawal was induced by finasteride (50 mg/kg, i.p.) on treatment day 9. Twenty-four hours after finasteride administration (day 10 of treatment), seizure susceptibility was evaluated with the sub-convulsant pentylenetetrazole (PTZ) dose (40 mg/kg i.p.). Four hours after PTZ, animals were assessed for depression like phenotypes followed by euthanasia and separation of brain parts (cortex and hippocampus). The results showed that PMSG and HCG treatment elevated progesterone and estradiol levels. Treatment with finasteride increased seizure susceptibility and depression due to decreased progesterone and elevated estrogen levels coupled with decreased monoamine and elevated corticosterone levels. A. racemosus treatment, on the other hand, significantly decreased seizure susceptibility and depression like behaviors, possibly because of increased progesterone, restored estradiol, corticosterone, and monoamine levels. We concluded that herbal formulations using A. racemosus root extracts may be used as monotherapy or adjuvant therapy along with available AEDs for the better and safe management of catamenial epilepsy as well as comorbid depression.

Precision treatment with nicotine in autosomal dominant sleep-related hypermotor epilepsy (ADSHE): An observational study of clinical outcome and serum cotinine levels in 17 patients.

PURPOSE: To report the clinical outcome of nicotine exposure in patients with autosomal dominant sleep-related hypermotor epilepsy (ADSHE), along with serum concentrations of the major nicotine metabolite cotinine. METHODS: We recruited 17 ADSHE patients with CHRNA4 mutations (12 with p.S280F and 5 with p.L291 dup). Clinical characteristics were collected from hospital records. A telephone interview was performed on the use and seizure-reducing effect of nicotine applying a six-point rating scale from "none" to very good". Serum concentrations of cotinine were measured in 14 nicotine users. RESULTS: All patients but one had ever used nicotine. Nine had used snuff; seven were current users. Eleven had used transdermal nicotine; nine were current users. Seven reported long-lasting seizure control, all used nicotine, four transdermal nicotine and three snuff. In 78% of patients using continuous transdermal nicotine, the effect was rated as good or very good. Cotinine concentrations were 453 ± 196 (mean ± SD) nmol/l in seven patients using transdermal nicotine only vs. 1241 ± 494 nmol/l in seven using other forms of nicotine. No correlation with seizure control was found. Three patients experienced improvement with transdermal delivery compared to snuff. CONCLUSION: This is the hitherto largest observational study supporting a favorable effect of nicotine in this specific seizure disorder. Better seizure control from transdermal nicotine compared to only day-time consumption suggests benefit from exposure throughout the night. According to current clinical experience, patients with uncontrolled ADSHE harboring relevant mutations should be offered precision treatment with transdermal nicotine.

Symptomatic eating epilepsy: two novel pediatric patients and review of literature.

Eating epilepsy (EE) is a form of reflex epilepsy in which seizures are triggered by eating. It is a rare condition but a high prevalence has been reported in Sri Lanka. In EE, the ictal semiology includes focal seizures with or without secondary generalization or generalized seizures. Some cases are idiopathic while focal structural changes on imaging, if present, are often confined to the temporal lobe or perisylvian region. On the other hand, some cases support the hypothesis of a genetic aetiology. The prognosis of EE is extremely variable due to the different nature of the underlying disorder. We describe two patients with symptomatic eating epilepsy, a 13-year-old boy with a bilateral perisylvian polymicrogyria and a 2-year-old boy with a genetic cause. The presence of structural lesions or the dysfunction of specific cortical regions in the context of a germline genetic alteration might lead to a hyperexcitation fostering the epileptogenesis. We review the available literature to clarify the aetiopathogenesis and the mechanisms underlying EE to improve the diagnosis and the management of these rare conditions.

Epileptic seizures triggered by eating in dogs.

BACKGROUND: Seizures triggered by eating (STE) behavior are very rare in humans and have not been documented previously in dogs. OBJECTIVES: To document the occurrence of STE in dogs and describe their clinical features. ANIMALS: Ten client-owned dogs with STE diagnosed at 5 European referral centers. METHODS: A call for suspected cases of STE was made online. This call was followed by a retrospective review of medical records, combined with a questionnaire to be completed by both the owner and the board-certified neurologist who made the diagnosis. Cases were included if >50% of the seizures that occurred were related to eating and if a minimum diagnostic evaluation for seizures had been performed. RESULTS: Four cases only had STE and 6 cases had both STE and spontaneous seizures. Four of the dogs were retrievers. The most common seizure type was focal epileptic seizures evolving to become generalized. Nine dogs were diagnosed with idiopathic epilepsy. One dog had a presumptive diagnosis of glioma involving the margins of the parietal, temporal, and frontal cortex (the perisylvian region), an area known to have a key role in eating-associated epilepsy in people. Treatment strategies included a combination of pharmacological management and eating habit changes. CONCLUSIONS AND CLINICAL IMPORTANCE: We have identified a form of reflex epilepsy in dogs, with STE behavior. Further studies are warranted to improve the characterization and management of STE.

Epilepsia refleja por agua caliente: a propósito de un caso en un lactante / Hot-water epilepsy: case report in an infant

La epilepsia refleja por agua caliente es un tipo de convulsión poco frecuente cuya fisiopatología se desconoce. Estas crisis reflejas suelen iniciarse pocos segundos tras el contacto con el agua y, comúnmente, a temperaturas de 37-48 ºC. Los automatismos y las crisis parciales complejas, con o sin generalización secundaria, son el modo de manifestación principal.La exploración neurológica y el electroencefalograma intercrítico no suelen presentar alteraciones, lo que puede condicionar un retraso en el diagnóstico, por lo que es fundamental la sospecha clínica.El tratamiento antiepiléptico se inicia cuando se asocia a otro tipo de epilepsia o cuando ciertas medidas sencillas, como el descenso de la temperatura del agua en el baño, no controlan las crisis. Es posible la desaparición espontánea. Cuando es necesaria la terapéutica farmacológica, existe, normalmente, buena respuesta.Se presenta el caso de un lactante con diagnóstico de epilepsia refleja por agua caliente.

Hot-water epilepsy is a rare type of seizure whose pathophysiology is unknown. These reflex seizures usually begin a few seconds after contact with water, commonly at temperatures between 37-48 ºC. Automations and complex partial crises, with or without secondary generalization, are the main manifestation mode of this type of reflex epilepsies.Neurological examination and intercritical electroencephalography are usually normal, which may condition a delay in diagnosis, and the clinical suspicion is fundamental.Antiepileptic treatment is initiated when associated with another type of epilepsy or when certain simple measures, such as lowering the water temperature in the bath, do not control crises. Spontaneous disappearance is possible; when pharmacological therapy is necessary, there is usually a good response.We present the case of an infant diagnosed with hot-water epilepsy.

Remarkable effect of transdermal nicotine in children with CHRNA4-related autosomal dominant sleep-related hypermotor epilepsy.

OBJECTIVE: Autosomal dominant sleep-related hypermotor epilepsy (ADSHE) is characterized by hypermotor seizures and may be caused by gain-of-function mutations affecting the nicotinic acetylcholine receptor (nAChR). Benefit from nicotine consumption has been reported in adult patients with this disorder. For the first time, the effect of transdermal nicotine is evaluated in children. METHODS: Transdermal nicotine was applied to three boys, two aged 10 years (7 mg/24 h) and one six years (3.5 mg/24 h). Autosomal dominant sleep-related hypermotor epilepsy was caused by the p.S280F-CHRNA4 (cholinergic receptor, nicotinic, alpha polypeptide 4) mutation. The children suffered from frequent, persistent nocturnal seizures and had developed educational and psychosocial problems. Seizure frequency and cognitive and behavioral parameters were assessed before and after treatment. RESULTS: A striking seizure reduction was reported soon after treatment onset. Hypermotor seizures disappeared; only sporadic arousals, sometimes with minor motor elements, were observed. Psychometric testing documented improvement in cognitive domains such as visuospatial ability, processing speed, memory, and some areas of executive functions. SIGNIFICANCE: Nicotine appears to be a mechanistic treatment for this specific disorder, probably because of desensitization of the mutated receptors. It may control seizures resistant to conventional drugs for epilepsy and impact socioeducational function in children. This mode of precision therapy should receive more attention and should be available to more patients with uncontrolled CHRNA4-related ADSHE across the age span.

Reflex epileptic features in patients with focal epilepsy of unknown cause.

OBJECTIVES: There is a gap of knowledge regarding reflex seizures in patients with focal epilepsy of unknown cause (FEUC). We aimed to evaluate the prevalence, demographic and clinical characteristics of reflex seizures in patients with FEUC to provide an insight to the underlying ictogenic mechanisms and to draw attention to this important but under-investigated topic. PATIENTS AND METHODS: After carefully questioning for reflex triggers, 186 patients diagnosed according to ILAE criteria and followed-up for a minimum of 5 years were included. The demographic and clinical properties as well as electrophysiological and neuroimaging data of these patients were reevaluated and compared to the patients without reflex seizures. RESULTS: The reflex seizure rate was 6.5 % in patients with FEUC. Patients with reflex features had lower monotherapy rates (p = 0.005) and higher major depression rates (p = 0.001) than patients without reflex features. The distribution of the patients according to their reflex triggers were as follows: hot-water induced (n = 3, 25 %), photosensitive (n = 2, 16.7 %), eating- induced (n = 2, 16.7 %), musicogenic (n = 2, 16.7 %), startle induced (n = 2, 16.7 %) and both musicogenic and startle type (n = 1, 8.3 %) respectively. The drug resistance rate of patients with reflex seizures was 25 % (n = 3). One patient with drug resistant reflex seizures showed benefit from epilepsy surgery and became seizure-free during last 3 years of follow-up. CONCLUSION: A careful and thoroughly history taking specifically questioning and focusing on seizure inducing factors in patients with FEUC is needed to confirm the presence of reflex seizures in patients with FEUC, who had higher rates of polytherapy and major depression. Elaborative evaluation of reflex features in FEUC might contribute to effective seizure control, ensure new therapeutic approaches, enlighten the obscurity and the resulting anxiety of having a diagnosis of FEUC in epilepsy patients.

Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis in Leucine-Rich Glioma-Inactivated 1 (Lgi1) Mutant Rats.

The dysfunction of astrocytic inwardly rectifying potassium (Kir) 4.1 channels, which mediate the spatial potassium-buffering function of astrocytes, is known to be involved in the development of epilepsy. Here, we analyzed the Kir4.1 expressional changes in Leucine-Rich Glioma-Inactivated 1 (Lgi1) mutant rats, which is a model of autosomal dominant lateral temporal lobe epilepsy in humans, to clarify the role of astrocytic Kir4.1 channels in Lgi1-related epileptogenesis. Priming acoustic stimulation (at postnatal day 16) conferred seizure susceptibility on Lgi1 mutant rats, which evoked audiogenic seizures with test stimulation at eight weeks. In the seizure-susceptible Lgi1 mutant rats (before test stimulation), astrocytic Kir4.1 expression was down-regulated region-specifically in the cerebral cortex, hippocampus, and amygdala. In addition, prophylactic treatments of Lgi1 mutant rats with valproic acid (VPA, 30 mg/kg and 200 mg/kg) for two weeks prevented both the development of seizure susceptibility and the down-regulation of Kir4.1 expression in astrocytes. The present study demonstrated for the first time that the astrocytic Kir4.1 expression was reduced in the Lgi1-related seizure model, suggesting that the down-regulation of Kir4.1 channels in astrocytes is involved in audiogenic epileptogenesis caused by Lgi1 mutation. In addition, VPA seemed to have a prophylactic effect on Lgi1-related seizures.

Overexpression of the immediate-early genes Egr1, Egr2, and Egr3 in two strains of rodents susceptible to audiogenic seizures.

Genetic animal models of epilepsy are an important tool for further understanding the basic cellular mechanisms underlying epileptogenesis and for developing novel antiepileptic drugs. We conducted a comparative study of gene expression in the inferior colliculus, a nucleus that triggers audiogenic seizures, using two animal models, the Wistar audiogenic rat (WAR) and the genetic audiogenic seizure hamster (GASH:Sal). For this purpose, both models were exposed to high intensity auditory stimulation, and 60min later, the inferior colliculi were collected. As controls, intact Wistar rats and Syrian hamsters were subjected to stimulation and tissue preparation protocols identical to those performed on the experimental animals. Ribonucleic acid was isolated, and microarray analysis comparing the stimulated Wistar and WAR rats showed that the genomic profile of these animals displayed significant (fold change, |FC|≥2.0 and p<0.05) upregulation of 38 genes and downregulation of 47 genes. Comparison of gene expression profiles between stimulated control hamsters and stimulated GASH:Sal revealed the upregulation of 10 genes and the downregulation of 5 genes. Among the common genes that were altered in both models, we identified the zinc finger immediate-early growth response gene Egr3. The Egr3 protein is a transcription factor that is induced by distinct stress-elicited factors. Based on immunohistochemistry, this protein was expressed in the cochlear nucleus complex, the inferior colliculus, and the hippocampus of both animal models as well as in lymphoma tumors of the GASH:Sal. Our results support that the overexpression of the Egr3 gene in both models might contribute to neuronal viability and development of lymphoma in response to stress associated with audiogenic seizures. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

Effects of marketed antiepileptic drugs and placebo in the human photosensitivity screening protocol.

A study of epilepsy patients with a reproducible range of photoparoxysmal responses (PPR) (epileptiform discharges evoked by flashing lights) has been used as a "proof-of-concept" trial to determine if novel potential antiepileptic drugs (AEDs) should proceed in development. The standard design for this trial requires a 3-day inpatient stay and is single-blind. We evaluated two marketed and effective AEDs-one narrow-spectrum [carbamazepine (CBZ)], and one broad-spectrum [levetiracetam (LEV)]-using a novel double-blinded, cross-over outpatient version of the trial to detect acute drug effects of the two marketed AEDs on photosensitivity. We tested 6 patients with a known stable photosensitivity response, using single oral doses of CBZ 400 mg and LEV 1000 mg, compared to 2 test days with single placebo doses. Patients who received LEV had the lowest mean PPR (compared with placebo and CBZ). The mixed effect model showed a significant effect of LEV in all eye closure conditions (p < 0.001). There was no evidence of a significant change in PPR after CBZ or placebo treatment. In conclusion, LEV 1000 mg, but not CBZ 400 mg, was effective in suppressing photosensitivity within a 6-h period compared with placebo showing the ability of our novel photosensitivity trial design to demonstrate effects of broad-spectrum AEDs. We cannot confirm the ability of the photosensitivity trial to detect the narrow-spectrum AED CBZ in our design. The novel outpatient study design is feasible and is expected to reduce costs compared with previous methodology.

Reflex myoclonic epilepsy in infancy: a critical review.

Benign myoclonic epilepsy in infancy, classified among the generalised idiopathic epilepsies, is characterised by the occurrence of myoclonic seizures in the first three years of life in otherwise normal infants. Some authors have described cases of myoclonic seizures as a reflex response to sudden unexpected tactile or acoustic stimuli and this clinical entity has been proposed as a separate nosographic syndrome, referred to as "reflex myoclonic epilepsy in infancy" (RMEI). We reviewed all published articles and case reports on RMEI in order to clarify clinical and electroencephalographic findings, with particular attention to outcome and treatment. RMEI appears to be a benign variant of idiopathic myoclonic epilepsy in infancy with specific features that occur in neurologically and developmentally normal children. This rare clinical entity is often under-described and under-diagnosed, and for this reason should be brought to the attention of paediatricians in order to avoid extensive investigations and reassure parents of the lack of long-term complications.

Corpus callosotomy in a patient with startle epilepsy.

Startle epilepsy is a syndrome of reflex epilepsy in which the seizures are precipitated by a sudden and surprising, usually auditory, stimulus. We describe herein a girl who had been suffering with startle-induced seizures since 2 years of age. She had focal, tonic and tonic-clonic seizures, refractory to antiepileptic treatment. Daily tonic seizures led to very frequent falls and morbidity. Neurologically, she had no deficit. Interictal EEG showed slow waves and epileptiform discharges in central and fronto-central regions. Video-polygraphic recordings of seizures, triggered by stimuli, showed generalised symmetric tonic posturing with ictal EEG, characterised by an abrupt and diffuse electrodecremental pattern of fast activity, followed by alpha-theta rhythm superimposed by epileptic discharges predominantly over the vertex and anterior regions. Magnetic resonance imaging showed no abnormalities. Corpus callosotomy was performed when the patient was 17. Since surgery, the patient (one year follow-up) has remained seizure-free. Corpus callosotomy may be considered in patients with startle epilepsy and tonic seizures, in the absence of focal lesions amenable to surgery. [Published with video sequences].

A rat model for LGI1-related epilepsies.

Mutations of the leucine-rich glioma-inactivated 1 (LGI1) gene cause an autosomal dominant partial epilepsy with auditory features also known as autosomal-dominant lateral temporal lobe epilepsy. LGI1 is also the main antigen present in sera and cerebrospinal fluids of patients with limbic encephalitis and seizures, highlighting its importance in a spectrum of epileptic disorders. LGI1 encodes a neuronal secreted protein, whose brain function is still poorly understood. Here, we generated, by ENU (N-ethyl-N-nitrosourea) mutagenesis, Lgi1-mutant rats carrying a missense mutation (L385R). We found that the L385R mutation prevents the secretion of Lgi1 protein by COS7 transfected cells. However, the L385R-Lgi1 protein was found at low levels in the brains and cultured neurons of Lgi1-mutant rats, suggesting that mutant protein may be destabilized in vivo. Studies on the behavioral phenotype and intracranial electroencephalographic signals from Lgi1-mutant rats recalled several features of the human genetic disorder. We show that homozygous Lgi1-mutant rats (Lgi1(L385R/L385R)) generated early-onset spontaneous epileptic seizures from P10 and died prematurely. Heterozygous Lgi1-mutant rats (Lgi1(+/L385R)) were more susceptible to sound-induced, generalized tonic-clonic seizures than control rats. Audiogenic seizures were suppressed by antiepileptic drugs such as carbamazepine, phenytoin and levetiracetam, which are commonly used to treat partial seizures, but not by the prototypic absence seizure drug, ethosuximide. Our findings provide the first rat model with a missense mutation in Lgi1 gene, an original model complementary to knockout mice. This study revealed that LGI1 disease-causing missense mutations might cause a depletion of the protein in neurons, and not only a failure of Lgi1 secretion.

Music and epilepsy: a critical review.

The effect of music on patients with epileptic seizures is complex and at present poorly understood. Clinical studies suggest that the processing of music within the human brain involves numerous cortical areas, extending beyond Heschl's gyrus and working within connected networks. These networks could be recruited during a seizure manifesting as musical phenomena. Similarly, if certain areas within the network are hyperexcitable, then there is a potential that particular sounds or certain music could act as epileptogenic triggers. This occurs in the case of musicogenic epilepsy, whereby seizures are triggered by music. Although it appears that this condition is rare, the exact prevalence is unknown, as often patients do not implicate music as an epileptogenic trigger and routine electroencephalography does not use sound in seizure provocation. Music therapy for refractory epilepsy remains controversial, and further research is needed to explore the potential anticonvulsant role of music. Dopaminergic system modulation and the ambivalent action of cognitive and sensory input in ictogenesis may provide possible theories for the dichotomous proconvulsant and anticonvulsant role of music in epilepsy. The effect of antiepileptic drugs and surgery on musicality should not be underestimated. Altered pitch perception in relation to carbamazepine is rare, but health care professionals should discuss this risk or consider alternative medication particularly if the patient is a professional musician or native-born Japanese. Studies observing the effect of epilepsy surgery on musicality suggest a risk with right temporal lobectomy, although the extent of this risk and correlation to size and area of resection need further delineation. This potential risk may bring into question whether tests on musical perception and memory should form part of the preoperative neuropsychological workup for patients embarking on surgery, particularly that of the right temporal lobe.

cAMP-dependent phosphorylation of microtubule-associated protein-2 during treatment of sodium valproate and audiogenic kindling.

Administration of anticonvulsant sodium valproate alleviated audiogenic seizures in Krushinskii-Molodkina rats, which was accompanied by a decrease in cAMP-dependent phosphorylation of microtubule-associated protein MAP2 in the hippocampus ex vivo. In contrast, audiogenic kindling resulted in a marked increase in MAP2 phosphorylation at cAMP-dependent protein kinase-specific sites. These changes in the state of MAP2 phosphorylation providing restructuring of dendrites in response to specific influences modulate neuronal activity and are the important mechanisms of neuronal plasticity.

Unilateral opercular lesion and eating-induced seizures.

Eating-induced seizures are an uncommon presentation of reflex epilepsy, a condition characterized by seizures provoked by specific stimuli. Most reports have identified aetiology associated with malformations of cortical developmental, hypoxic brain injury, previous meningoencephalitis or static encephalopathy. We present a patient with eating-induced reflex seizures, which began several years after treatment for an opercular primitive neuroectodermal tumour (PNET), and who subsequently underwent in-depth clinical and video-EEG analysis for her seizures. This patient noted rapid improvement with decreased frequency of seizure activity after treatment with valproic acid. We discuss the aetiology of reflex epilepsy, the anatomical basis of eating-induced epilepsy, and review the current literature.

Gene expression profiling reveals the mechanism of action of anticonvulsant drug QYS.

We have examined the gene expression profiling of inferior colliculus from DBA/2J mice with high-intensity noise induced audiogenic seizure (AGS). We have also tested the effects of Qingyangshenylycosides (QYS), a traditional Chinese medicine, on the audiogenic seizure, and examined how the drug affected the gene expressions in inferior colliculus. Our results demonstrated that the latency was increased and the Tonus% of AGS was decreased in the animals treated with QYS, indicating that the drug effectively prevented audiogenic seizure. Gene expression analysis using Agilent oligo microarray showed that total of 134 genes were either up- or down-regulated during AGS. QYS prevented many of the AGS induced gene expression changes. Nevertheless, some of the AGS induced genes were further enhanced or reversed by QYS treatment. Our gene expression profiling data provided important information regarding the molecular mechanisms of AGS and the mechanism of action of QYS. Further analysis of the function of these genes may help to identify therapeutic targets for epilepsy.