The effect of oxcarbazepine on bone metabolism.

OBJECTIVE: Long term use of several antiepileptic drugs is known to cause alteration in bone metabolism. Therefore, we investigated the effect of new antiepileptic drug, oxcarbazepine, on bone metabolism. METHODS: Twenty eight patients who were on oxcarbazepin therapy (18 female, 10 males; mean age: 27.82 +/- 10.98 years (range: 15-45)) with no additional antiepileptic drug use history in one year period prior to the study and 28 control subjects were involved in the study. Measurement of calcium, phosphate, alkaline phosphatase and Vitamin D3 levels and bone density measurements with DEXA method were performed in patient and age-matched control groups. The baseline parameters were compared with the control group and with those measured at the end of one year. RESULTS: The biochemical (calcium, phosphate, alkaline phosphatase and Vitamin D3) parameters and densitometry values after one year of therapy were not different than the baseline values indicating that those were not affected by the therapy (P > 0.05). CONCLUSIONS: In previous studies, anticonvulsant drugs that induce enzymes increase bone degradation by causing vitamin D deficiency. According to the results of this study, oxcarbazepin with little effect on enzyme induction was shown not to affect bone mineral metabolism.

Managing atypical and typical herpetic central nervous system infections: results of a multinational study.

There have been many studies pertaining to the management of herpetic meningoencephalitis (HME), but the majority of them have focussed on virologically unconfirmed cases or included only small sample sizes. We have conducted a multicentre study aimed at providing management strategies for HME. Overall, 501 adult patients with PCR-proven HME were included retrospectively from 35 referral centres in 10 countries; 496 patients were found to be eligible for the analysis. Cerebrospinal fluid (CSF) analysis using a PCR assay yielded herpes simplex virus (HSV)-1 DNA in 351 patients (70.8%), HSV-2 DNA in 83 patients (16.7%) and undefined HSV DNA type in 62 patients (12.5%). A total of 379 patients (76.4%) had at least one of the specified characteristics of encephalitis, and we placed these patients into the encephalitis presentation group. The remaining 117 patients (23.6%) had none of these findings, and these patients were placed in the nonencephalitis presentation group. Abnormalities suggestive of encephalitis were detected in magnetic resonance imaging (MRI) in 83.9% of the patients and in electroencephalography (EEG) in 91.0% of patients in the encephalitis presentation group. In the nonencephalitis presentation group, MRI and EEG data were suggestive of encephalitis in 33.3 and 61.9% of patients, respectively. However, the concomitant use of MRI and EEG indicated encephalitis in 96.3 and 87.5% of the cases with and without encephalitic clinical presentation, respectively. Considering the subtle nature of HME, CSF HSV PCR, EEG and MRI data should be collected for all patients with a central nervous system infection.

Myasthenia gravis: how to treat?

Myasthenia Gravis is an acquired autoimmune disorder caused by a neuromuscular transmission defect which is clinically characterized by fluctuating weakness of voluntary muscles and fatigability. It can be diagnosed by clinical features, clinical, pharmacological and electrophysiological tests and serological evaluation. Treatment modalities include symptomatic treatment in the form of cholinesterase inhibitors and plasmapheresis and immunotherapy in the form of immunosuppressant medications, immunomodulating therapy and thymectomy. No single regimen is appropriate for all patients and up to now no mode of therapy has been proven to be clearly superior. The response to any form of treatment is difficult to assess because the severity of symptoms fluctuate. We retrospectively analyzed the clinical records of 33 myasthenia gravis patients which were managed at our clinic between 1995-2003. All patients were treated with anticholinesterase medications sometime during their treatment. Most patients recieved immunosupressant and/or immunomodulator therapy. Patients were referred for thymectomy when indicated. We evaluated the outcome with different treatment modalities, focusing on the role of thymectomy. We also investigated the possible correlations between clinicopathological features and clinical outcome. We conclude that as for the medical treatment of myasthenia gravis azathioprine plus steroid improves the outcome; and for the surgical treatment, early thymectomy should be performed in all generalize myasthenia patients.

The subclinical incidence of CTS in pregnancy: Assessment of median nerve impairment in asymptomatic pregnant women.

PURPOSE: The true incidence of pregnancy related carpal tunnel syndrome (PRCTS) is unknown. Most of the diagnoses of PRCTS are made based only on clinical symptoms. Here, we report a prospective controlled clinical trial assessing the electrophysiological changes in pregnant women to provide objective measure of the median nerve function. METHODS: Pregnant women in the third trimester (n=69) and age-matched non-pregnant women (n=40) asymptomatic for CTS were included in the study. Nerve conduction studies of the median and ulnar nerves across the carpal tunnel were bilaterally performed with the standard techniques. RESULTS: All the median sensory nerve conduction studies (amplitude, latency and velocity) performed from the ring finger and palmar region to wrist showed significant prolongation of median nerve conduction in the pregnant women compared with the control group (*p

Combined effects of ACE and MMP-3 polymorphisms on migraine development.

Migraine is a primary headache disorder which involves both genetic and environmental components. Since angiotensin-converting enzyme (ACE) and matrix metalloproteinase (MMP) share the same homology, we investigated whether the MMP-3 and ACE I/D gene variants are involved in migraine risk and whether the ACE variant might act in combination with the MMP-3 genetic variant in patients with migraine. This is the first study to evaluate the association between MMP-3 and ACE polymorphisms, and migraine. Genotypes were determined by polymerase chain reaction. The frequencies of 5A5A genotypes of the MMP-3 and D allele of ACE were significantly elevated, but II genotypes of the ACE and 6A allele of MMP-3 significantly decreased in all patients. The combined DD/5A5A and ID/5A5A genotypes increased the risk of migraine. Individuals who were homozygous for the deletion (D) allele showed increased ACE activity. Subjects with the 5A5A genotype and/or D allele or with the combined DD/5A5A or ID/5A5A might be more susceptible to migraine development. In contrast, subjects with the II and/or 6A6A genotypes may be protected from migraine development. The greater activity of the 5A5A and DD genotypes might result in vascular reactivity that is more pronounced in migraine. Taken together, our data suggest that numerous genes may influence ACE activity. Discovery of new genes might better clarify the pathogenesis of migraine and open an avenue to therapeutic strategies against migraine.

Evaluation of neuromuscular transmission by using monopolar needle electrode.

OBJECTIVE: To evaluate the value of single-fibre electromyography (SFEMG) with monopolar electrode (MNPE) in revealing neuromuscular transmission dysfunction. MATERIAL AND METHODS: We examined the extensor digitorum communis muscle by using single-fibre electrode (SFE) and MNPE sequentially, in randomly assigned 20 healthy volunteers and in 17 patients with known myasthenia gravis (MG). The high-pass filter setting was 3 kHz for MNPE. Ten individual jitter values were calculated for each electrode in every muscle. Repetitive nerve stimulation (RNS) test on trapezius muscle was performed on 15 patients. RESULTS: In controls, the mean jitter values were 27 +/- 9 (10-59) micro s with SFE, and 21 +/- 7.2 (9-56) micro s with MNPE (P = 0.001). In the MG group, the mean jitter values were 52.4 +/- 38 (12-221) micro s with SFE, and 51.8 +/- 34.7 (12-179) micro s with MNPE. Both electrodes identified junction dysfunction in 14 patients. RNS revealed decrement in four patients but 11. CONCLUSION: SFEMG with SFE is still the gold standard; however, SFEMG with MNPE is superior to RNS like SFEMG with SFE.