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      Visual Evoked Potentials in Konzo, a Spastic Paraparesis of Acute Onset in Africa

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          Abstract

          Aim: To assess whether or not visual evoked potentials (VEPs) are abnormal in konzo, a para/tetraparesis of sudden onset, and to correlate the findings to the clinical picture of the disorder. Methods: VEPs were recorded in 23 patients (9 men and 14 women, mean age: 23 ± 10 years) suffering from konzo, and 38 healthy subjects (20 men and 18 women, mean age: 27 ± 15 years). The mean P100 latencies and peak-to-peak N75-P100 amplitudes of each eye were measured and compared in the two groups. The mean interocular P100 latency and amplitude differences were calculated and also compared. Results: VEPs were abnormal in 11/23 patients (48%) consisting of P100 prolongation (7 subjects), absence of P100 wave (2 subjects) or an atypical waveform (2 subjects). The mean P100 latency value of the konzo group was significantly increased as compared with the mean (+ 2.5 SD) of the reference values from healthy subjects (p < 0.05). There was a statistically significant decrease of amplitude in konzo patients compared to normal subjects (p < 0.05) with, however, only 2 patients outside the 95% confidence limits. Six patients (27%) had abnormal VEPs despite normal visual acuity. These abnormalities were symmetric and a relation could be found between neither the duration nor the severity of the disease and the VEP perturbation. Conclusion: The main features of these abnormalities are delayed P100 latency and decreased amplitude. These findings indicate involvement of visual pathways and seem to suggest the presence of axonal loss in the prechiasmal visual pathways in konzo. This study provides evidence that the neurodamage in konzo extends to the visual pathways.

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          Most cited references6

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          Geographical and seasonal association between linamarin and cyanide exposure from cassava and the upper motor neurone disease konzo in former Zaire.

          High cyanide intake from consumption of insufficiently processed cassava has been advanced as a possible aetiology of the upper motor neurone disease konzo. However, similar neurodamage has not been associated with cyanide exposure from any other source. With an ecological study design, we compared 22 cases of konzo, 57 unaffected household members and 116 members from unaffected households, a total of 195 subjects, in konzo-affected savanna villages with 103 subjects in adjacent non-affected forest villages in the Paykongila area in the Bandundu Region, Zaire. In the dry season, the mean value (+/- SEM) of urinary thiocyanate, the main cyanide metabolite, was higher in the three groups in konzo-affected villages (563 +/- 105, 587 +/- 44 and 629 +/- 47 micromol/l) than in unaffected villages (241 +/- 17 micromol/l). In affected villages in the dry season when konzo incidence was high, mean urinary thiocyanate was also higher than the levels found in the wet season when incidence was low. The wet season values (mean +/- SEM) were 344 +/- 60, 381 +/- 35 and 351 +/- 27 micromol/l. Urinary levels of inorganic sulphate were low in all groups, indicating low intake of the sulphur amino-acids which provide a substrate for cyanide detoxification. These findings support an aetiological role for cyanide in konzo. However, urinary linamarin, the cyanogenic glucoside and source of cyanide in cassava, was more closely associated with the occurrence of konzo. The mean value (+/- SEM) of urinary linamarin in the konzo cases was 632 +/- 105 micromol/l and in their household members 657 +/- 52 micromol/l, which was significantly higher than in members of control households in the same village (351 +/- 28 micromol/l) and in unaffected villages (147 +/- 18 micromol/l). This suggests that a specific neurotoxic effect of linamarin, rather than the associated general cyanide exposure resulting from glucoside breakdown in the gut, may be the cause of konzo.
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            Cassava cyanogens and konzo, an upper motoneuron disease found in Africa

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              Visual evoked cortical magnetic responses to checkerboard pattern reversal stimulation: a study on the neural generators of N75, P100 and N145.

              In an attempt to elucidate the neural generators of pattern reversal visual evoked potentials (PR-VEPs), we measured the visual evoked magnetic fields (PR-VEFs) using a 37-channel magnetoencephalography in six healthy young adults. A half-field checkerboard pattern was phase-reversed at a rate of 1 Hz to stimulate the right or left visual half-field, thus yielding 12 PR-VEFs in total from the six subjects. The simultaneously recorded scalp PR-VEPs showed three distinct components of N75, P100 and N145. Three corresponding components were also identified in the PR-VEFs with similar peak latencies (N75m, P100m and N145m). P100m and N145m were clearly identified in all 12 PR-VEFs, whereas N75m was observed in only nine of 12 PR-VEFs. The equivalent current dipoles (ECDs) of N75m, P100m and N145m were located closely to each other in the occipital cortex around the calcarine fissure contralateral to the stimulated visual field, when they were overlaid on the MRI. The reliability of dipole estimation was highest in P100m, followed by N145m while N75m showed the least reliability. The direction of the current flow of ECDs of N75m and N145m was from the medial to the lateral in the occipital cortex when viewed in a coronal section, whereas that for P100m was toward the medial. The ECD location of P100m changed according to the retinotopic organization when the upper or lower quadrant of the visual field was stimulated, with the ECDs being located in the lower or upper part, respectively, of the visual cortex. Our results therefore indicate that the neural origins of N75m, P100m and N145m of PR-VEFs are in the primary visual cortex on the contralateral side of the stimulated visual half-field, while the three components are physiologically distinct.
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                Author and article information

                Journal
                OPH
                Ophthalmologica
                10.1159/issn.0030-3755
                Ophthalmologica
                S. Karger AG
                0030-3755
                1423-0267
                2003
                December 2003
                30 October 2003
                : 217
                : 6
                : 381-386
                Affiliations
                Departments of aOphthalmology and bNeurology, Kinshasa University Hospital, Kinshasa, Democratic Republic of Congo; cDepartment of Ophthalmology, Haukeland University Hospital, and dCentre for International Health, University of Bergen, Bergen, Norway; eCenter for Research on Occupational and Environmental Toxicology, Oregon Health Science University, Portland, Ore., USA; fDepartment of Neuro-Ophthalmology, Moorfields Eye Hospital and the National Hospital for Neurology and Neurosurgery, London, UK
                Article
                73066 Ophthalmologica 2003;217:381–386
                10.1159/000073066
                14573969
                df5ed085-1552-41b5-9322-7ef92912d566
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 07 March 2003
                : 23 May 2003
                Page count
                Figures: 1, Tables: 2, References: 24, Pages: 6
                Categories
                Original Paper

                Vision sciences,Ophthalmology & Optometry,Pathology
                Visual evoked potential,Konzo,Upper motor neuron

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