Effects of the antiepileptic drugs on peripheral nerve function.

OBJECTIVE: We aimed to compare the effects of antiepileptic drugs and provide findings of peripheral nerve impairment using standard electrophysiological techniques. MATERIALS AND METHODS: Young adult outpatients with epilepsy on monotherapy for no less than 6 months with carbamazepine (CBZ), valproic acid (VPA), oxcarbazepine (OXC) and topiramate (TPM) were examined. Patients who had any other disease that could effect nerve conduction studies and who had neuropathic symptoms were excluded. RESULTS: Each group contained 15 patients and 20 healthy subjects were examined as the control group. Prolonged latency of median sensory nerve (P = 0.004), ulnar sensory nerve (P = 0.01) and sural nerve (P = 0.003) with a diminished nerve conduction velocity was observed in the CBZ group (P = 0.014, P = 0.002, P = 0.025, respectively). No correlation was found between VPA, OXC and TPM and the nerve conduction studies (P > 0.05). CONCLUSIONS: Valproic acid, oxcarbazepine and topiramate don't have effects on nerve conduction studies. Mild electrophysiological changes contribute to carbamazepine therapy.

N-hexane induced polyneuropathy: a clinical and electrophysiological follow up.

BACKGROUND: Chronic exposure to relatively high levels of n-hexane either by inhalation or skin contact can result in peripheral nerve lesions. We present the clinical and electrophysiological features of 5 patients who have been exposed to n-hexane at similar industrial occupations in the progressive phase. METHODS: All patients underwent routine laboratory tests, cerebrospinal fluid examination, and sural nerve biopsy. Conventional sensory and motor nerve conduction studies were applied at admission and at the end of the 12 month. RESULTS: The average incubation period of the 5 cases was 10.2 months and the average period of the initial symptoms was 3.8 months. Numbness and weakness of the lower extremities were the initial symptoms that had ascended to the upper extremities in three of the patients. Deep tendon reflexes were either diminished or abolic. There was distal atrophy only in patient 5. All were treated with vitamin B complex and physical therapy and training. They were removed from further exposure to n-hexane after aetiological confirmation, but motor disturbance continued to worsen in the patient 5. The patients were visited every 3 months. Sensory functions were regained earlier than motor functions. All the patients, including one who was severe quadriparetic in the early stages, regained their full motor capabilities within 6 months to 21 months. CONCLUSION: Occupational n-hexane causes subacute neuropathy and the duration of exposure is important for the neurological outcome. We suggest that the prognosis of n-hexane induced neuropathy is well if correct diagnosis is made and further exposure is ceased.

The sensitivity of clinical diagnostic methods in the diagnosis of diabetic neuropathy.

This study assessed the sensitivity of various methods for the clinical diagnosis of diabetic peripheral neuropathy. A total of 147 randomly selected patients with diabetes mellitus and 65 age- and sex-matched healthy controls were evaluated by various clinical (the neuropathy symptom score [NSS], the neuropathy disability score [NDS], vibration perception thresholds [VPTs], Tinel's sign and Phalen's sign), laboratory (fasting plasma glucose and glycosylated haemoglobin levels) and electro-physiological (nerve conduction studies, H-reflex and F-wave measurements) methods. In the patient group, 8.2% had an abnormal NSS, 28.5% had a positive Phalen's sign, 32.6% had a positive Tinel's sign, 42.8% had an abnormal VPT and 57.1% had an abnormal NDS. Significant correlations were found between electro-physiologically confirmed neuropathy and the two provocation tests and abnormal VPTs. In conclusion, assessment with a complete neurological examination and standard electrophysiological tests is very important for the diagnosis of diabetic peripheral neuropathy and the prevention of morbidity in patients with or without symptoms.

Seizure development after stroke.

Although there have been many studies on seizures following stroke, there is still much we do not know about them. In this study, we evaluated the characteristics of seizures in stroke patients. There were 2267 patients with a first-ever stroke, and after excluding 387 patients, 1880 were available for analysis. Of these 1880 patients, we evaluated 200 patients with seizures and 400 patients without seizures. We investigated the seizures according to age, gender, stroke type, the aetiology of ischaemic stroke and the localisation of the lesion. The seizures were classified as early onset and late onset and the seizure type as partial, generalised or secondarily generalised. Seizures occurred in 200 (10.6%) of 1880 strokes. The number of patients with seizures were 138 (10.6%) in ischaemic stroke group and 62 (10.7%) in haemorrhagic stroke group. Patients with ischaemic strokes had 41 embolic (29.7%) and 97 thrombotic (70.3%) origin, and these were not statistically significant in comparison with controls. Cortical involvement for the development of seizures was the most important risk factor (odds ratios = 4.25, p < 0.01). It was concluded that embolic strokes, being younger than 65 years old, and cortical localisation of stroke were important risks for developing seizures.