Objectives: Obesity is defined as a risk factor for carpal tunnel syndrome (CTS). In this study, the presence or absence of recovery in median nerve conduction velocities after weight loss in obese patients was assessed in order to determine whether excess weight or other factors influence the higher prevalence of CTS in obese patients. Methods: Patients with body mass indexes (BMIs) ≧30 were included in the study. CTS symptoms, age, gender, height, body weight, and concomitant diseases were evaluated. Nerve conduction studies (NCS) were obtained on one upper extremity. All patients were included in dietetic programs. Three months later, NCS were repeated and compared with the first NCS. Results: BMIs were statistically significantly lower on the second visits 3 months later (p = 0.0001). No statistically significant difference was observed in the second NCS of electromyographically diagnosed cases with CTS (p > 0.05). Conclusion: We expected a recovery in median nerve conduction velocities in patients with CTS after weight loss. In the literature, even in untreated cases with CTS, spontaneous improvements in second NCS have been reported. This finding suggests that factors other than excess body weight may be influential in the higher prevalence of CTS in obese patients. A more detailed, genetic-factor-targeted investigation may prove more beneficial to clarify this issue.

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This study reflect that TNF-α-308G/A polymorphism may be one of the many genetic factors for migraine susceptibility in the Turkish population.

and Brazil [1][2][3][4] . A small number have also been identified in Turkey [5][6][7][8][9] . The largest case studies of HWE patients have been performed in India by Mani et al, Gururaj et al, and Satishchandra et al, respectively 1 . Satishchandra et al reported that HWE accounts for 3.6−3.9% of all epilepsy cases. They speculated that genetic factors and the high temperature of bath water may underlie this finding. Although studies report that 7−32.4% of HWE cases are found in families in which more than one individuals are affected 1,10 , the pathogenic and genetic mechanisms underlying the expression of HWE in humans remain to be demonstrated. ABSTRACT:Objective: To assess the clinical features of several members of the same family diagnosed with both hot water epilepsy (HWE) and cerebral lesions. Methods: Age at onset and types of seizure, precipitating factors, EEG findings, and neuroimages were evaluated. Results: The family consisted of six generations, including one consanguineous parent. Of eight family members diagnosed with epilepsy, seven suffered from HWE. Age at onset of seizures ranged within childhood. Seven patients with HWE experienced complex partial seizures, with or without secondary generalization; one experienced simple partial seizures as well as complex partial seizures. Three patients experienced spontaneous seizures as well as HWE. Interictal EEG revealed abnormalities in two patients. Magnetic resonance imaging revealed cerebral lesions in one patient, probably attributable to ischemic changes. Magnetic resonance images were consistent with findings of ischemic gliosis in two patients, and either demyelinating or ischemic gliosis in one patient. Conclusions: Descriptions of HWE families with different ethnic backgrounds may permit more definite conclusions regarding the mechanisms epileptogenesis, and the genetic defects that underlie this disease.

We report the clinical and electrophysiological features of a large Turkish family with genetically confirmed X-linked spinal and bulbar muscular atrophy (SBMA). Family members were identified by field work. A detailed history was obtained from each subject, and each subject received a detailed neurological examination. To confirm the CAG repeat expansion in the AR gene, genomic DNA was extracted from the peripheral blood of patients. The family consisted of 128 individuals over five generations, with two consanguineous parents, one slightly affected female, and 12 affected males with SBMA. We studied the five surviving male patients and one surviving female carrier. The age at disease onset, phenotypic features, and disease severity varied among the family members. DNA analysis was performed on five individuals, belonging to five generations of the family. Four affected males and a slightly affected female carrier were shown to carry an expanded CAG repeat in the androgen receptor gene. This family report is consistent with previous studies suggesting that SBMA may be present with a wide clinical spectrum in affected family members. Further descriptions of SBMA affected families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease.