Red cell distribution width levels in Parkinson's disease patients.

Parkinson's disease (PD) is a neurodegenerative disorder with motor and non-motor impairment. It has been known for a while that oxidative stress, protein changes and mitochondrial dysfunction have the role of contribution to the pathogenesis. Disturbance of red blood cell function may play a role in the pathophysiology of neurodegenerative diseases such as Huntington's, Parkinson's and Alzheimer's disease. RDW was found to be strongly associated with inflammatory markers in diseases such as acute pancreatitis, myocardial injury and hepatocellular carcinoma. The data about RDW levels and PD are scarce. In this study, we aimed to investigate the RDW values and their relationship with the severity of the disease in patients with Parkinson's disease. 94 patients with Parkinson's disease were included into the study, 97 healthy individuals without history of PD were considered as control group. The United Parkinson's Disease Rating Scale (UPDRS) and the modified Hoehn and Yahr staging scale were used to assess the severity of PD. Although RDW levels were significantly higher than the healthy subjects, there was not any relation between the severity of PD, duration of the disease, RDW levels, other blood parameters, mean UPDRS score or mean mH&Y score. In conclusion, RDW levels are higher than the healthy subjects in PD patients but there is no relation between RDW levels and disease duration. Larger studies are needed to explain the role of RDW as an inflammatory marker.

Visual evoked potential abnormalities in migraine patients.

BACKGROUND: Visual processing in migraine has been targeted indicating that the visual pathways are involved in the migraine pathophysiology. We aimed to assess the nature of visual evoked potential (VEP) changes in migraine patients and to evaluate the role of VEP in the diagnosis of migraine. MATERIALS AND METHODS: We examined 31 female and 10 male patients with a migraine headache diagnosis according to the criteria of the International Headache Society. Control subjects had neither migraine and other types of primary headache nor familial history. VEP were elicited using a checkerboard by monocular and binocular pattern reversal stimulation. The latencies of N75, P100 and N145 and peak-to-peak amplitude of N75-P100 were measured. We compared VEP latencies and amplitudes of the monocular and binocular stimulation within each population. RESULTS: The N75 and P100 latencies were found to be significantly longer in the study group than the control group (p = 0.014 and p = 0.034, respectively) while the amplitudes in the study group were lower (p = 0.014). N145 latency was found to be longer in patients with longer duration of disease (p < 0.05). P100 latency was found to be significantly longer in patients with aura than the patients without aura (p = 0.029). N75 latency, recorded by left monocular stimulation, was elongated and the amplitude was diminished with left hemicranial headache. CONCLUSION: Measurement of VEP latency and amplitude is a valuable and reliable test for the diagnosis of migraine. Our results reflect a persisting dysfunction of precortical visual processing which might be relevant in the pathogenesis of migraine.

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.

Common peroneal and tibial nerve paralysis secondary to herpes zoster infection: a case report.

BACKGROUND: The usual presentation of herpes zoster (HZ) is a self-limiting vesicular rash, often accompanied by post-herpetic neuralgia. However, HZ can give rise to other complications, that have unusual presentations and serious sequelae like segmental motor paralysis of the limbs that is a relatively rare complication. CASE: A 68-year-old man presented with foot drop on the right side had a history of HZ infection on and around the knee and the popliteal fossa. He was treated with acyclovir by a dermatologist and 10 days after the inital symptoms he developed weakness on the right ankle and on the muscles distal to the knee. In a few days foot drop has developed and he was unable to walk without help. Three months later he was admitted to the neurology out patient clinic. On his electrophysiological examination common peroneal nerve could not be stimulated on the right side. The distal latency of the tibial nerve has prolonged, CMAP amplitude has diminished and the nerve conduction velocity has slowed down. Latency of the sural nerve has prolonged with a small SNAP amplitude and a slow nerve conduction velocity on the right side. Electromyography revealed denervation on the muscles inervated by tibialis anterior and common peroneal nerves distal to the knee. CONCLUSION: The double mononeuropathy of the tibial and common peroneal nerves secondary to HZ was not found in the published data. HZ should be considered as a possible cause of the paralysis of peripheral nerves and more attention should be paid to it.

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.

A comparison of sural nerve conduction studies in patients with impaired oral glucose tolerance test.

OBJECTIVE: Monitoring of the sural nerve is a sensitive method for detection of neuropathies. We examined different methods of studying sural nerve conduction in a group of patients with impaired glucose tolerance (IGT) in the same study. MATERIALS AND METHODS: Several parameters of sural nerve were investigated in 20 patients. First, sensory nerve conduction studies of the sural nerve were performed on the distal-leg and the proximal-leg segments. Second, dorsal sural nerve studies were conducted. Third, the sural/radial sensory nerve action potential (SNAP) amplitude ratios were calculated. The results were compared with those obtained from 21 healthy controls. RESULTS: Abnormal results revealing peripheral neuropathy were found in only one patient and dorsal sural SNAP was absent in another patient (5%). Although the results of nerve conduction studies were within normal ranges except the patient with peripheral neuropathy, the lower extremity nerves and especially sural nerves have been found to be more affected and the parameters revealed large differences between groups (P < 0.05). Only dorsal sural nerve latency related to fasting blood glucose level in patients (<0.05). DISCUSSION AND CONCLUSIONS: Sural nerve studies should be of value to determine neuropathy in IGT patients. This study supported the idea that IGT is a transitional state before diabetes and also the importance of the dorsal sural nerve latencies for early detection of neuropathy.