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.

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.

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.

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.