作者
Gülnihal Kutlu,Abidin Erdal,Yasemin Bıçer Gömceli,Levent Ertuğrul İnan
摘要
D resistant epilepsy is defined as failure of adequate trials of 2 tolerated, appropriately chosen, and used antiepileptic drug (AED) schedules (whether as monotherapies or in combination) to achieve sustained freedom from seizure.1 Early recognition of drug resistant epilepsy is significant for trying alternative therapeutic approaches in the patient including surgery, ketogenic diet, and vagal nerve stimulation. Therefore, the diagnosis of drug resistant epilepsy is very important, but pseudo-resistant epilepsy is not uncommon. Pseudo-refractory epilepsy is usually due to incorrect diagnosis, use of incorrect and/or low dose AED, and poor compliance of patients. Nonepileptic paroxysmal events, including psychogenic non-epileptic seizure (PNES) especially syncope, certain sleep and movement disorders, can be mistaken for epilepsy. An incorrect seizure classification may cause the wrong drug choice. On the other hand, inadequate dosing of an AED may be another reason for pseudorefraction. Poor compliance with AEDs is also seen frequently.2,3 The aim of this study was to investigate causes of seizures and subsequent effective management approaches in patients with pseudo-refractory epilepsy. In the present study, patients who were followed up in our epilepsy department were investigated retrospectively. The files of 2920 patients seen between June 2002 and December 2011 were retrospectively reviewed by the same neurologist in the Department of Epilepsy in Ankara Research and Educational Hospital, Ankara, Turkey. Patients with pseudo-refractory epilepsy were determined according to the following criteria: 1. Patients who did not have enough control of seizures despite at least 2 different AED regimens before being admitted to our department. 2. Patients had no seizure at least one year after the revision of the diagnosis and/ or treatment of epilepsy in our epilepsy department. Information on demographic data, medical and epilepsy history, seizure types and frequency, routine EEG, and neuroimaging findings were collected for all patients. An EEG with or without seizure induction, home video recording, and cardiology consultation were also investigated in patients whose diagnosis of epilepsy was doubtful. One hundred and twenty-two patients were examined, but 17 patients were excluded as they had seizures after the adjustment of treatment (12 of them had PNES, but their seizures continued despite the adjustment of treatment). They may have only PNES that was resistant to treatment and/or they had drug resistant epileptic seizures. Five patients had poor compliance; their seizures again did not stop after good compliance. Therefore, 105 were included in this study. All patients who did not respond to treatment in spite of at least 2 different AED regimens were accepted as refractory. The mean age was 29±11.53 years (age range 16-70). Seventy-four patients (70.5%) were female and the remaining 31 patients male. No risk factors were determined in 65 (61.9%) patients. There was head trauma in 12 (11.4%) patients, positive family history for epilepsy in 10 (9.5%) patients, febrile convulsion in 9 (8.6%) patients, anoxic birth in 5 patients, and history of CNS infection in 4 patients. Six patients had hypertension, and 2 patients had diabetes mellitus as a comorbid condition. Sixty-three patients were administered polytherapy, with 10 using 3 or more AEDs. Monotherapy was given to 42 patients. However, patients treated with monotherapy used at least one other AED regimen in their previous history. When routine electroencephalograms were examined, there was no EEG abnormality in 55 (52.4%) patients. Forty-eight patients had generalized/focal epileptiform abnormality (20 of them had generalized epileptiform abnormality and 28 focal epileptiform abnormality). Generalized mild slowing in the EEG was observed in 2 patients. Among 105 patients, 101 underwent cranial MRI. The cranial MRI was normal in 97 patients while, hippocampal sclerosis was present in 3 patients, and diffuse atrophy was seen in one patient. The reasons for pseudo-refractory epilepsy are summarized in Table 1. Incorrect diagnosis of epilepsy was observed in 57 patients, and PNES was considered as a diagnosis in 47. Thirty-two (68%) of them were female. After a review of the files, 37 patients with PNES had a seizure with induction during the EEG recording, and the diagnosis of PNES was made according to the induction of those typical seizures with normal EEG except artifacts. Permission of patients was taken before the induction. First of all, we tried to stimulate seizure with self-induction, normal saline was given to the patient intravenously and seizure semiology and EEG findings before, during, and after seizure were examined. All patients knew that it was not a real drug. The diagnosis of the remaining 7 patients with PNES