Epileptic Disorders
SCIE-ISI SCOPUS (SonsInc.)
1950-6945
1950-6945
Cơ quản chủ quản: WILEY , John Wiley & Sons Inc.
Các bài báo tiêu biểu
The challenges to individuals with epilepsy extend far beyond the seizures. Co‐morbidities in epilepsy are very common and are often more problematic to individuals than the seizures themselves. In this review, the pathophysiological mechanisms of cognitive impairment are discussed. While aetiology of the epilepsy has a significant influence on cognition, there is increasing evidence that prolonged or recurrent seizures can cause or exacerbate cognitive impairment. Alterations in signalling pathways and neuronal network function play a major role in both the pathophysiology of epilepsy and the epilepsy comorbidities. However, the biological underpinnings of cognitive impairment can be distinct from the pathophysiological processes that cause seizures.
Epilepsy is a brain condition characterized by the recurrence of unprovoked seizures. Generally, prognosis refers to the probability of attaining seizure freedom on treatment and little is known about the natural history of the untreated condition. Here, we summarize aspects of the prognosis and prognostic predictors of treated and untreated epilepsy and of its different syndromes. Usually, epilepsy is a fairly benign condition. Most epilepsies have a good prognosis for full seizure control and eventual discontinuation of AEDs, but epilepsy syndromes have differing outcomes and responses to treatment. Prognostic factors include aetiology, EEG abnormalities, type of seizures and the number of seizures experienced before treatment onset, and poor early effects of drugs. Early response to treatment is an important positive predictor of long‐term prognosis, while the history of a high number of seizures at the time of diagnosis, intellectual disability, and symptomatic aetiology are negative predictors. Different prognostic patterns can be identified, suggesting that the epileptogenic process is not static. Epilepsy carries a greater than expected risk of premature death. Aetiology is the single most important risk factor for premature death.
The aim of our study was to define the frequency of seizures in a population of outpatients attending a cognitive function clinic in Italy and to identify risk factors for seizures in patients with Alzheimer's disease.
In this retrospective study, we analyzed our clinical records to gather information on patients' demographic, metabolic, cardiovascular and cognitive features. We sought to determine the significance of abnormal neuroimaging findings and the use of potentially epileptogenic drugs on the onset of seizures. From the records of 583 patients referred to the clinic for cognitive disturbances, we identified 145 patients with Alzheimer's disease.
Of these 145 patients, 14 (9.7%) had a history of complex partial or generalised seizures, or both. Of the risk factors identified, onset of seizures was associated with male gender and none of the patients with seizures had diabetes. The risk of seizure onset was higher in Alzheimer's disease patients with hyperlipaemia and severe dementia. No other risk factors were identified, although hypertensive patients seemed to be protected.
Seizures in Alzheimer's disease are frequent and often under‐recognized. In elderly patients, especially those with Alzheimer's disease, correct diagnosis and treatment are important to prevent disease from worsening and disability from increasing. Patients with dementia should routinely undergo history‐taking designed to elicit a history of seizures and define patients at high risk.
Several animal models are discussed in order to outline features of difficult‐to‐treat or drug‐resistant epilepsy. These models can be categorised as those which show a poor response to different antiepileptic drugs and those in which subgroups of drug‐resistant animals are selected, based on interindividual differences. Non‐responders to antiepileptic drugs have been described in the amygdala kindling model, as well as the chronic phase of post‐status epilepticus models. Epileptic dogs which do not respond to standard antiepileptic drugs may serve as a translational model to provide a more clinical environment for drug testing. Drug resistance or a poor response to several antiepileptic drugs has been reported for the 6‐Hz model, lamotrigine‐pretreated kindled rats, pentylentetrazole‐induced seizures in rats pre‐exposed to pilocarpine, as well as following intrauterine exposure of rats to methylazoxymethanol. Using models to select non‐responders is highly time‐consuming and elaborate, limiting their use in routine drug‐screening procedures. Current efforts to identify biomarkers of drug resistance may simplify the selection process,
Anorgasmia is the inability to reach orgasm during sexual intercourse, and, although it is believed that around 90% of anorgasmia problems are related to psychological issues, the use of serotoninergic drugs, including antidepressants and atypical antipsychotics, is a common cause of situational anorgasmia. Pregabalin is a new antiepileptic drug, structurally related to gabapentin, and commonly used as adjunctive therapy for partial epilepsy and treatment of neuropathic pain in adults. Herein, we describe three men with epilepsy, who experienced severe anorgasmia after pregabalin add‐on treatment.
Một phụ nữ 23 tuổi không có tiền sử về các rối loạn giọng nói, hô hấp hoặc giấc ngủ trước đó đã nhận liệu pháp kích thích dây thần kinh phế vị (VNS) để điều trị động kinh cục bộ kháng trị và phát triển cơn thở khò khè liên quan đến giấc ngủ trong quá trình điều chỉnh thông số. Việc giảm cường độ VNS trong quá trình nghiên cứu giấc ngủ polysomnography đã loại bỏ hoàn toàn cơn thở khò khè. Chúng tôi kết luận rằng trong những trường hợp hiếm hoi, VNS có thể gây ra cơn thở khò khè liên quan đến giấc ngủ, mở rộng phổ các rối loạn thông khí liên quan đến giấc ngủ đã biết liên quan đến liệu pháp VNS. Việc điều chỉnh thông số trong quá trình polysomnography có thể giải quyết cơn thở khò khè ban đêm do VNS gây ra.
Duplication of
mutations account for a large proportion of Dravet syndrome patients, and are reported in other cases of epilepsy, such as some families with genetic epilepsy with febrile seizures plus (GEFS+). While most Dravet syndrome cases are caused by
To describe the clinical course and pathological diagnosis of a 12‐year‐old female who presented with an acute syndrome of right hemispheric epilepsy and cortical dysfunction and brain MRI demonstrating atrophy of the left cerebral and right cerebellar hemispheres.
The patient presented with occasional partial seizures consisting of a left calf sensation followed by left leg clonic jerking. Initial brain MRI showed left cerebral and right cerebellar atrophy with T2 hyperintensity in the left parietal region. After six months, the seizure frequency increased and semiology evolved to include frequent clonic movements of the left side of the face, arm and leg and epilepsia partialis continua (EPC) of the left arm and leg. There was progressive weakness of the left leg and, to a lesser extent, her left arm. MRI at this time demonstrated an additional T2 hyperintensity in the right frontal lobe. An extensive evaluation for paraneoplastic, mitochondrial, and genetic epilepsy syndromes was unrevealing. On biopsy evaluation, chronic T‐cell mediated encephalitis was demonstrated within bilateral frontal lobes. Treatment with immunomodulatory therapy resulted in some improvement in her seizure frequency and motor function.
Rasmussen's encephalitis can be a challenging diagnosis. The patient's clinical history, including EPC, with bilateral frontal lobe biopsies confirming a T‐cell mediated encephalitis supports a diagnosis of bilateral Rasmussen encephalitis. This case highlights the diagnostic challenges and treatment dilemmas that arise in an adolescent presenting with bilateral inflammatory lesions of Rasmussen's encephalitis. [