비케톤성 고혈당증 유발발작의 임상양상과 예후
The Clinical Presentations and Prognosis of Non-Ketotic Hyperglycemia Induced Seizure
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Background: Seizure can be triggered by the non-ketotic hyperglycemia (NKH). Recently we analysed 18 cases of NKH induced seizure to identify the causes for NKH, seizure types, prognosis, and the differences of clinical presentation between the patient with chronic brain structural lesion (CBSL) and the patient without. Methods: Eighteen patients with NKH induced seizure were selected from the database. Data regarding brain images, clinical symptoms, co-morbid illnesses, blood laboratories, and prognosis were collected. Patients were divided into two groups according to the presence of CBSL. Results: The patients with CBSL showed more generalized tonic-clonic seizure (GTCS) than without. Focal seizures in this group appeared to be originated from the pre-existing lesion in many situations. The poor compliance to anti-diabetic treatment and physical stresses were most common causes for NKH. One year seizure remission without anti-epileptic drug treatment was achieved in 17 of 18 patients. Conclusions: The patients with CBSL might have more GTCS than without. The impairment of inhibitory mechanism surrounding the focal irritative zone might be one of plausible explanation for this phenomenon. The prognosis was favorable. Further large studies are required.
Abstract
Background: Seizure can be triggered by the non-ketotic hyperglycemia (NKH). Recently we analysed 18 cases of NKH induced seizure to identify the causes for NKH, seizure types, prognosis, and the differences of clinical presentation between the patient with chronic brain structural lesion (CBSL) and the patient without. Methods: Eighteen patients with NKH induced seizure were selected from the database. Data regarding brain images, clinical symptoms, co-morbid illnesses, blood laboratories, and prognosis were collected. Patients were divided into two groups according to the presence of CBSL. Results: The patients with CBSL showed more generalized tonic-clonic seizure (GTCS) than without. Focal seizures in this group appeared to be originated from the pre-existing lesion in many situations. The poor compliance to anti-diabetic treatment and physical stresses were most common causes for NKH. One year seizure remission without anti-epileptic drug treatment was achieved in 17 of 18 patients. Conclusions: The patients with CBSL might have more GTCS than without. The impairment of inhibitory mechanism surrounding the focal irritative zone might be one of plausible explanation for this phenomenon. The prognosis was favorable. Further large studies are required.
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