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Sleep-related hypermotor epilepsy is a subgroup of sleep-related epilepsies and is very rare among focal epilepsies. It is a type of epilepsy that can be confused with the primary diseases of sleep and is diagnosed late. Here, we present a case diagnosed with elect roenc ephal ograp hy (video-EEG) monitoring 13 years later.

Objective: Neurological manifestations associated with coronavirus disease-2019 (COVID-19) are broad and heterogeneous. Although the predominant clinical presentation is respiratory dysfunction, concerns have been raised about the neurological hallmarks. Many reports suggest some findings on electroencephalography (EEG) can be relevant to COVID-19. Materials and Methods: Patients with COVID-19 admitted to hospital and referred for EEG from March 1, 2020 to February 15, 2021, were retrospectively enrolled. When research databases were queried with the terms “COVID-19 (ICD code: 10: U07.3) and “EEG”, total number of patients obtained was 32. Number of patients excluded due to unconfirmed diagnose with COVID-19 was 12. Twenty adult patients with certain diagnose of COVID-19 who underwent 21-electrode routine EEG during the outbreak with neurological deterioration were identified. Results: Background abnormalities was evident in one of fourth patients (n=5, 25%). Mild diffuse slowing (n=3, 15%) and focal slowing (n=3, 15%) with left frontotemporal tendency (n=2, 10%) were observed. Epileptiform abnormalities and seizures were detected showing focal (n=4, 20%) or generalized onset (n=1, 5%). Conclusion: Here we performed a retrospective single-centre study to evaluate the electroencephalographic findings in patients diagnosed with COVID-19 since it remains unknown. it needs to be more clarified with increasing number of recordings

BackgroundMigraine without aura (MwoA) is a very frequent and remarkable comorbidity in patients with idiopathic/genetic epilepsy (I/GE). Frequently in clinical practice, diagnosis of MwoA may be challenging despite the guidance of current diagnostic criteria of the International Classification of Headache Disorders 3 (ICHD-3). In this study, we aimed to disclose the diagnostic gaps in the diagnosis of comorbid MwoA, using a zone concept, in patients with I/GEs with headaches who were diagnosed by an experienced headache expert.MethodsIn this multicenter study including 809 consecutive patients with a diagnosis of I/GE with or without headache, 163 patients who were diagnosed by an experienced headache expert as having a comorbid MwoA were reevaluated. Eligible patients were divided into three subgroups, namely, full diagnosis, zone I, and zone II according to their status of fulfilling the ICHD-3 criteria. A Classification and Regression Tree (CART) analysis was performed to bring out the meaningful predictors when evaluating patients with I/GEs for MwoA comorbidity, using the variables that were significant in the univariate analysis.ResultsLonger headache duration (

Summary Gelastic seizures are typically associated with hypothalamic hamartoma. Given the rarity of gelastic seizures, pathways for the motor and emotional aspects of laughter have been hypothesized but remain unclear. Only few case reports of patients with tuberous sclerosis complex who developed gelastic epilepsy have been reported. In this case study, we report a case of TS that presented itself mainly with dermatologic manifestations and without any neurological findings other than gelastic seizures. Ictal EEG revealed an active epileptic activity on the right fronto-temporal region. Clinical and laboratory findings were consistent with gelastic epilepsy that originated from temporal and extra-temporal lobes. Seizures were controlled using carbamazepine and levetiracetam polytherapy. In our case, there is no evidence of cortical and subcortical tubers, subependymal glial nodules, giant cell astrocytomas or aneurysm.

Objectives:Lacosamide is a third-generation antiepileptic agent that selectively enhances slow inactivation of sodium channels that take part in generation and propagation of action potentials and results in the diminution of neuronal excitability. Because of this new mechanism of action, it is expected to be efficacious in patients with drug-resistant epilepsy. In this study, we aimed to assess the efficacy and tolerability of lacosamide add-on treatment in refractory epilepsy patients by presenting our experience in a tertiary referral center.Methods:Medical records of refractory focal epilepsy patients who were followed in epilepsy outpatient clinic between October 2014 and May 2017 were retrospectively reviewed in this study. Patients who were treated with add-on lacosamide and completed minimum of six months follow-up period were included. ≥50% reduction in seizure frequency was defined as treatment response.Results:In this study, 88 patients were included. The percentage of seizure-free patients after six months follow-up was 4.6% and the treatment response rate was 55.6%. We also evaluated the effect of concomitant use of sodium channel blockers, the presence of abnormal findings on magnetic resonance imaging and the introduction stage of lacosamide. No significant difference was observed in the response rate regarding the mentioned parameters. 19% of the patients reported side effects, the majority of which were dizziness, vertigo and somnolence. None of them discontinued treatment because of side effects.Conclusion:Our findings suggest that lacosamide add-on therapy is effective in refractory focal epilepsy and has an appropriate tolerability and safety profile since none of the patients stopped treatment due to side effects.

There is a mutual interaction between sex steroid hormones and epilepsy. Although female and male sex hormones and their metabolites access the brain via the blood brain barrier, they can also be synthesized de novo from cholesterol within the glia and neurones (neurosteroids). While estrogens enhance neuronal excitability, progesterone and its metabolites exert anticonvulsant effects. Testosterone, on the other hand, has a less consistent effect on seizure susceptibility, depending on the ratio of its conversion to estrogens. This paper focuses on the effects of neurosteroidal sex hormones on seizure susceptibility. Further study is required to identify the future role of their use in the treatment of epilepsy.

Lafora disease (LD) is a progressive myoclonus epilepsy with autosomal recessive inheritance. Clinical course is progressive and includes myoclonic, cerebellar, and extrapyramidal signs, generalized tonic-clonic seizures, and cognitive decline. Valproic acid, zonisamide, levetiracetam, clonazepam, and piracetam are among the treatment options. Carbamazepine (CBZ), oxcarbazepine, phenytoin, and lamotrigine (LM) should be avoided to prevent worsening of symptoms. Though evidence is limited, perampanel is the only drug to achieve sustained improvement in frequency of seizures, and effective control of neurological and cognitive decline in patients with LD. Described in the present report is a case of typical LD with clinical worsening on CBZ and LM treatment. Electroencephalographic and pathologic findings are reported.

Scientific BACKGROUND: Bilateral thalamic infarct is quite rare and encountered at the rate of 0.6%. Emboly from an artery to another, cardioembolism, migrain and the existence of an only perforing artery are among the causes of bilateral thalamic infarct. During the course of many hematologic diseases, tendency to thrombosis increases, and therefore, stroke can also be witnessed. OBJECTIVE: Upon scanning the literature, concurrence of myelodysplastic syndrome and bilateral thalamic infarct have not been encountered. Thus, a subject with myelodysplastic syndrome was aimed to be discussed due to the development of bilateral thalamic infarct in the light of the literature. CASE: A 52 years old women was consulted with the complaint of headache and weakness on her right side as an inpatient in hematology unit. On the neurological examination of the patient followed by hematology unit for a decade with the diagnosis of myelodysplastic syndrome, right hemiparesis including her face was determined. On the sensorial examination, there was a decrease in all her sensorial modalities on the right, but there was only loss of sensorial vibration on the left. On cranial MRI, bilateral thalamic infarct was detected. No other pathologies except for myelodysplastic syndrome were found in the etiology. CONCLUSION: It should also be remembered that a blood disease such as myelodysplastic syndrome could be among the causes of bilateral thalamic infarct