Role of anti-GQ1B antibody in differential diagnosis of acute ophthalmoparesis.

Miller Fisher syndrome (MFS) is a triad of total external ophthalmoplegia, ataxia, and areflexia, while botulism has the usual clinical presentation of involvement of cranial muscles and palsies with blurred vision, diplopia, ptosis, dilated pupils, and facial paralysis, caused by a bacterial neurotoxin which attacks proteins involved in presynaptic vesicle release. In this report, we needed to make the differential diagnosis between MFS and botulism in a patient who presented with acute ophthalmoparesis and a history of diarrhea three days before, which started two days after consuming tinned food. Routine laboratory, neurophysiologic, and imaging investigations were normal. A clinical diagnosis of Miller Fisher syndrome was reached by anti-ganglioside GQ1B and GM1 Ig G and M antibody investigations which proved positive. The patient was treated with intravenous immunoglobulin two weeks after (in the late period) the symptoms started and he has recovered completely. Systemic autoimmune diseases should be considered in patients with bilateral ophthalmoparesis. As in the present patient, the evaluation of specific antibodies helps in the diagnosis and thus early effective treatment is possible.

Potential effects of zinc on information processing in boys with attention deficit hyperactivity disorder.

PURPOSE: The aims of the present study were to investigate the relationship between plasma zinc levels and amplitudes and latencies of P1, N2, and P3 in parietal and frontal areas in children with ADHD, and to compare these zinc levels and event-related potentials (ERPs) indices with controls. METHODS: 28 boys with ADHD were divided into two groups according to plasma zinc levels: low zinc group (N=13, zinc level <80 microg/dL) and zinc non-deficient group (N=15, zinc level >or=80 microg/dL). ERP indices from parietal and frontal brain regions were recorded in children with ADHD and in 24 normal boys by using an auditory oddball paradigm. Plasma zinc levels were measured by an atomic absorption spectrophotometer. RESULTS: The plasma zinc levels were significantly lower in both ADHD groups (means are 65.8 microg/dL in low zinc group and 89.5 microg/dL in zinc non-deficient group) than controls (mean: 107.8 microg/dL; both p values <0.017). In ADHD compared to controls, the amplitudes of P3 in frontal and parietal regions were significantly lower, and the latency of P3 in parietal region was significantly longer (all p values <0.017). In low zinc ADHD group compared to zinc non-deficient ADHD group, the latencies of N2 in frontal and parietal region were significantly shorter (all p values <0.017). In addition, there was a medium but significant positive correlation between plasma zinc levels and amplitude and latency of frontal N2 wave in ADHD. CONCLUSIONS: These results can suggest that plasma zinc levels might have an effect on information processing in ADHD children, and lower zinc levels seem to affect N2 wave. Since N2 wave changes may reflect a different inhibition process, further studies are warranted to investigate the effect of zinc on inhibitory process in children with ADHD, and in low zinc and non-deficient ADHD groups.

Evaluation of event-related potentials in Klinefelter syndrome and idiopathic hypogonadotrophic hypogonadism.

BACKGROUND: Many studies have evaluated patients with idiopathic hypogonadothropic hypogonadotropism (IHH), but few of these studies utilize event-related potentials (P300). AIMS: To assess the cognitive functions of hypergonadotropic vs. hypogonadotropic patients. SETTINGS AND DESIGN: The study group consisted of 41 untreated IHH patients, 32 untreated Klinefelter syndrome (KS) patients, and 30 healthy control subjects. METHODS AND MATERIAL: In this study, the latency and amplitude of P300 was evaluated in 41 untreated IHH and 32 untreated KS patients and compared to healthy control subjects (average age: 30 years). Also evaluated were the patients' hormone levels. RESULTS AND CONCLUSIONS: In this study, the amplitude of P300 was found to be reduced, and the latency prolonged in IHH patients in comparison to KS patients and control subjects. In KS patients, there was no difference in latency of P300, but the amplitude was reduced when compared with the control group. Cognitive dysfunction in patients with hypogonadotropism is related to androgen hormone levels. This deficiency can affect development of the central nervous system (CNS), causing defects of CNS to varying degrees during the perinatal period. Androgen deficiency is considered to exert its effects during the period of cognitive ability development, manifest in IHH patients but not KS patients.

The antioxidant effect of beta-Glucan on oxidative stress status in experimental spinal cord injury in rats.

This study was performed to investigate the antioxidant effect of beta-Glucan in experimental spinal cord injury (SCI). Injury was produced using weight-drop technique in rats. beta-Glucan was given by intraperitoneal injection following trauma. The rats were sacrificed at the sixth day of injury. Oxidative stress status was assessed by measuring the spinal cord tissue content of Malonyldialdehyde (MDA), Superoxide Dismutase (SOD) and Gluthatione Peroxidase (GSH-Px) activities. No effect of beta-Glucan on SOD and MDA activities was found but, GSH-Px levels were found to decrease to the baseline (preinjury) levels when it was compared to untreated group (U=0.000; p=0.002). According to our results, beta-Glucan works like a scavenger and has an antioxidant effect on lipid peroxidation in spinal cord injury.