Effects of carbamazepine on serum levels of folic acid and homocysteine

Epilepsy is resistant to drug treatment in about one third of cases, but the mechanisms underlying this drug resistance are not understood. The aim of this study is to assess carbamazepine [CBZ] effect on homocysteine and folic acid occurrence in patients with epilepsy. A total of 45 epileptic outpatients treated by CBZ and 28 sex and age matched healthy controls. The mean of homocysteine and folic acid in epileptic patients were significantly higher 16.46 +/- 1.79 micro mol/L; 8.46 +/- 0.35 ng/ml compared with healthy controls 8.54 +/- 0.64; 10.61 +/- 0.63 [p = 0.0001; p = 0.006, respectively]. Epileptic patients were divided into two groups, therapy-response, and therapy-resistant. Homocysteine serum concentration was significantly higher in the first group of patients [therapy-resistant] compared with healthy controlled group 19.77 +/- 2.96 versus 8.54 +/- 0.64 [p = 0.0001], respectively. However, folic acid concentration was significantly lower in the first group of patients [therapy-resistant] compared with healthy controlled group 7.58 +/- 0.3 versus 10.61 +/- 0.63 [p = 0.001] respectively. In therapy-response group, homocysteine serum concentration was significantly different compared with healthy controlled group [12.3 +/- 1.11 versus 8.54 +/- 0.64], but it remained within the normal value. There was no significant difference in levels of folic acid between the therapy-response group and healthy controlled group 9.55 +/- 0.61 versus 10.61 +/- 0.63 [p = 0.21]. This study demonstrates that epileptic patients taking antiepileptic drug [CBZ] have increased serum levels of homocysteine. Serum homocysteine levels in patients treated with CBZ were higher - up to 50%. The elevated levels of homocysteine may occur due to deficiency of folic acid that is necessary for homocysteine metabolism

Neurosarcoidosis manifesting as glioma-like lesion

This case deals with a very rare manifestation of sarcoidosis, neurosarcoidosis mimicking a glioma in the left temporal lobe. Clinical presentation, neruoradiological and surgical findings are briefly discussed

Histopathological findings in chronic pharmacoresistant temporal epilepsy: a pathognomonic combination of lesions maintaining neuron injury?

Progression and pharmacoresistance of epileptic seizures is clinically not yet well predicted and comprehensible. This was a pathological study of surgical specimens of resected temporal lobe and hippocampus in chronic pharmacoresistant temporal epilepsy, in order to determine any lesions that might play a role in the onset or in the maintenance of this type of epilepsy, and any lesions that might result in as wide a variety of lesions as have been reported in the different studies in the literature. This was a prospective histopathological study of successive mesial temporal and extrahippocampal structures removed from patients suffering from refractory epilepsy. Serial cut sections of 1.5 - 2 mm were studied between October 1997 and December 2004 in the Epilepsy Centre of Damascus University. A retrospective review was done later. Sixty-six consecutive surgical specimens from 66 patients with refractory epilepsy lasting for 1 - 32 years [mean = 16.2 years] were received and studied. Our series included 33 males and 33 females [2 - 45 years; average 22 years]. Pathological study revealed some constant lesions observed in all cases: signs of neuronal injury with cell lysis, apoptosis followed by neuronal loss, cortical dysplasia/ dysgenesis, hippocampal and temporal gliosis and focal degenerative cystic changes. Other observations were as follows: neuroglial tumours and malformations [20 cases, 30%], subependymal cortical heterotopia [13 cases, 20%], gyral fusion [16 cases, 24%] with abnormal elongation of the sulcus in [6 cases 9%], inflammation [10 cases, 15%], vascular tumours/ malformations [5 cases, 7.5%], gliomas [5 cases, 7.5%], severe atrophy [2 cases, 3%], small meningeal nodule [1 case, 1.5%], and old haemorrhage [1 case, 1.5%].In this series, a large variety of lesions were found with constant signs of neuronal injury and loss. A presumable epileptogenic focus was found in many cases [58%], and the multiplicity and multifocality of lesions were well documented. A good understanding of the sequencing of the processes leading to cell injury might contribute in the prevention of progression of epileptic seizure in previously susceptible patients