Sera were collected from a total of 122 children, comprising 117 cases with undifferentiated fever and 5 cases with dengue hemorrhagic fever (DHF), during June to September 1994 in Karachi, Pakistan. Sera were tested by the IgM-capture ELISA using dengue type 1 (D1), dengue type 2 (D2), West Nile (WN), and Japanese encephalitis (JE) viral antigens. Among 92 single sera from undifferentiated fever cases, IgM antibodies were detected in 5 cases by D1, 8 cases by D2, and 5 cases by WN antigens, respectively. Corresponding number of positives among 25 paired sera from undifferentiated fever cases were 3 by D1, 6 by D2, and 1 by WN antigen. Four out of 5 DHF cases possessed anti-D1 as well as anti-D2 IgM antibodies. Only a single DHF case was positive for anti-WN IgM antibodies. Anti-JE IgM antibodies were not detected in any of the tested serum specimens. Clinical manifestations of undifferentiated fever patients were generally non specific, but the percentage of children with anemia, hepatomegaly and splenomegaly was higher in patients possessing anti-dengue IgM antibodies than those without. Among the groups with anti-dengue IgM antibodies, those possessing only anti-D2 but not anti-D1 IgM antibodies showed higher percentages with cough, edema, and splenomegaly. The results indicated that up to 26% of the undifferentiated fever cases were caused by dengue virus infection in Karachi, Pakistan.

Antibodies, Viral↗

PubMedDate not supplied

Characteristics of cranial nerve palsies in diabetic patients.

The incidence of palsy in the third, sixth and seventh cranial nerves was studied with regard to central nervous system involvement in diabetic patients. Among 1961 diabetic patients, 19 (0.97%) demonstrated cranial nerve palsies. Nine out of these 19 patients showed facial palsy; 6 palsy of the oculomotor nerve; 2 palsy of the abducent nerve; and 3 both oculomotor and abducent nerve palsies. In contrast, only 5 out of 3841 non-diabetic patients (0.13%) had any cranial nerve palsies; all 5 were cases of facial palsy. The incidence of cranial palsies in diabetic patients was significantly higher than that in non-diabetic patients (P less than 0.01). Concerning age, sex, the state of glycemic control, diabetic complications and method of treatment, there were no differences disclosed in the diabetic patients with cranial nerve palsy. The incidences of diabetic complications were compared between the patients with facial palsy and those with ophthalmoplegia. Only one out of 9 patients with facial palsy (11%) had diabetic complications, whereas 7 out of 10 patients with ophthalmoplegia (70%) demonstrated diabetic complications and the difference was significant. Thus ophthalmoplegia appears to be more closely related to diabetic metabolism while facial palsy is less strongly correlated with diabetes.

Abducens Nerve↗

PubMedDate not supplied

Central and peripheral motor conduction time in chronic alcoholics with polyneuropathy and/or spasticity.

We measured central and peripheral motor conduction time to demonstrate lesions in the upper and lower motor neurons of 11 chronic alcoholics with polyneuropathy without spasticity, 7 chronic alcoholics with spasticity with and without alcoholic polyneuropathy, and 16 healthy volunteers as controls. Peripheral motor conduction time was significantly prolonged in all extremities in all of the chronic alcoholics, and was accompanied by a considerable reduction in motor conduction velocity. Central motor conduction time was considerably prolonged in the lower extremities of the alcoholics with spasticity compared with both the controls and the alcoholics without spasticity. Central motor conduction time in the patients with alcoholic polyneuropathy without spasticity was slightly prolonged in comparison with the controls, but not significantly. Based on the electrophysiological findings, we conclude that peripheral neuropathy is a lesion common to chronic alcoholics whether or not they have clinically evident polyneuropathy. Chronic alcoholics with spasticity have significantly longer central motor conduction time in the lower extremities. Spasticity in chronic alcoholics develops not independently but concomitantly with peripheral neuropathy, suggesting that peripheral neuropathy develops earlier than spasticity.

Action Potentials↗

PubMedDate not supplied

Magnetic stimulation of peripheral nerve; site of stimulation estimated from H reflex.

In order to find out the difference in the site of stimulation between electrical and magnetic stimulation of a peripheral nerve, H reflexes were recorded in 20 healthy persons. Electrical stimulation was performed with the stimulator placed along the tibial nerve (A) and at right angles to the tibial nerve (B). Magnetic stimulation (Magstim Model 200) was performed with a large (14 cm in diameter) magnetic coil (C) and a small (7 cm in diameter) magnetic coil (D). The magnetic coil was held parallel to the skin and its center was placed on the point where the cathode had been placed in the electrical stimulation. The mean value of the sum of M wave latency and H reflex latency in C was 1.4 msec, 1.7 msec and 0.8 msec shorter than those in A, B and D, respectively. The mean value of the sum of M wave latency and H reflex latency in D was 0.6 msec shorter than that in A and 0.9 msec shorter than that in B. When the center of the magnetic coil is placed over the peripheral nerve, two loci of the nerve, 7-8 cm apart from each other with the large magnetic coil and 3-4 cm apart from each other with the small magnetic coil, are considered to be stimulated simultaneously.

Adult↗

PubMedDate not supplied

Magnetic stimulation of peripheral nerves. Comparison of magnetic stimulation with electrical stimulation.

We measured total peripheral motor conduction time by two different methods, magnetic stimulation and electrical stimulation, to reveal which is better in determining actual peripheral motor conduction time. In the upper extremities, the difference between magnetic stimulation and electrical stimulation was within a mean time of 1.39 +/- 0.8 msec, while that in the lower extremities was 2.3 +/- 1.1 msec. In any 4 extremities, total peripheral motor conduction time obtained by magnetic stimulation was significantly shorter than that measured by electrical stimulation employing conventional F-wave response. We conclude that stimulus sites 8.8 +/- 5.1 cm distal to spinal motoneurons in the upper extremities, and 10.5 +/- 5.3 cm distal in the lower extremities were stimulated by magnetic stimulation of the peripheral nerves. Electrical stimulation employing conventional F-wave measurement is superior to magnetic stimulation for actual total peripheral nerve conduction study.

Adult↗

PubMedDate not supplied

Sympathetic dysfunction mediating cardiovascular regulation in alcoholic neuropathy.

We evaluated autonomic function in alcoholic neuropathy by non-invasive hemodynamic studies using servo-plethysmo-manometry and laser Doppler flowmetry. In 16 alcoholics compared with 17 age-matched healthy controls, the extent of AP responses to phase IV of the Valsalva maneuver, cold pressor test and isometric exercise decreased significantly, indicating sympathetic hypofunction. Five patients had paradoxical depressor response to cold pressor test, which was reproducible by submersion of the hand in warm water. The data suggest involvement of the higher autonomic center. Reflex bradycardia in phase IV of the Valsalva maneuver and the variation coefficient of R-R intervals in the electrocardiogram were lower, indicating parasympathetic hypofunction. Cutaneous blood flow response in the foot upon local warming and submersion of the hand in cold water was significantly impaired, but that in the contralateral hand was not. Abnormalities in the autonomic function tests may result from a toxic effect of ethanol on the peripheral and central autonomic nervous system and the cardiovascular system. The results indicate not only parasympathetic (vagal) but sympathetic dysfunction mediating cardiovascular regulation in patients with alcoholic neuropathy.

Adult↗