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      Upbeat Nystagmus due to a Small Pontine Lesion: Evidence for the Existence of a Crossing Ventral Tegmental Tract

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          Abstract

          We report a patient with an isolated large upbeat nystagmus (UBN) in the primary position of gaze. Eye movements were filmed and recorded using electro-oculography. The upward vestibulo-ocular reflex gain, evaluated by pitching the head forward, was markedly reduced compared to when pitching the head back. The lesion was a probable lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level. This UBN case, with one of the smallest brainstem lesions reported so far, supports the existence in humans of the crossing ventral tegmental tract, described in the cat and transmitting excitatory upward vestibular signals to the third nerve nucleus. It is also suggested that the decussation of this tract lies at the same upper pons level as in the cat but in a slightly more ventral location, i.e. in the posterior basis pontis.

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          Vertical nystagmus: clinical facts and hypotheses.

          D Miléa, C Pierrot-Deseilligny (2005)
          The pathophysiology of spontaneous upbeat (UBN) and downbeat (DBN) nystagmus is reviewed in the light of several instructive clinical findings and experimental data. UBN due to pontine lesions could result from damage to the ventral tegmental tract (VTT), originating in the superior vestibular nucleus (SVN), coursing through the ventral pons and transmitting excitatory upward vestibular signals to the third nerve nucleus. A VTT lesion probably leads to relative hypoactivity of the drive to the motoneurons of the elevator muscles with, consequently, an imbalance between the downward and upward systems, resulting in a downward slow phase. The results observed in internuclear ophthalmoplegia suggest that the medial longitudinal fasciculus (MLF) is involved in the transmission of both upward and downward vestibular signals. Since no clinical cases of DBN due to focal brainstem damage have been reported, it may be assumed that the transmission of downward vestibular signals depends only upon the MLF, whereas that of upward vestibular signals involves both the MLF and the VTT. The main focal lesions resulting in DBN affect the cerebellar flocculus and/or paraflocculus. Apparently, this structure tonically inhibits the SVN and its excitatory efferent tract (i.e. the VTT) but not the downward vestibular system. Therefore, a floccular lesion could result in a disinhibition of the SVN-VTT pathway with, consequently, relative hyperactivity of the drive to the motoneurons of the elevator muscles, resulting in an upward slow phase. UBN also results from lesions affecting the caudal medulla. An area in this region could form part of a feedback loop involved in upward gaze-holding, originating in a collateral branch of the VTT and comprising the caudal medulla, the flocculus and the SVN, successively. Therefore, it is suggested that the main types of spontaneous vertical nystagmus due to focal central lesions result from a primary dysfunction of the SVN-VTT pathway, which becomes hypoactive after pontine or caudal medullary lesions, thereby eliciting UBN, and hyperactive after floccular lesions, thereby eliciting DBN. Lastly, since gravity influences UBN and DBN and may facilitate the downward vestibular system and restrain the upward vestibular system, it is hypothesized that the excitatory SVN-VTT pathway, along with its specific floccular inhibition, has developed to counteract the gravity pull. This anatomical hyperdevelopment is apparently associated with a physiological upward velocity bias, since the gain of all upward slow eye movements is greater than that of downward slow eye movements in normal human subjects and in monkeys.
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            Connections and oculomotor projections of the superior vestibular nucleus and cell group 'y'.

            Malcolm Carpenter, Robert J. Cowie (1985)
            Attempts were made to determine brainstem and cerebellar afferent and efferent projections of the superior vestibular nucleus (SVN) and cell group 'y' ('y') in the cat using axoplasmic tracers. Injections of HRP, WGA-HRP and [3H]amino acids were made into SVN and 'y' using two different infratentorial stereotaxic approaches. Controls were provided by unilateral HRP injections involving the oculomotor nuclear complex (OMC), the interstitial nucleus of Cajal (INC) and the deep cerebellar nuclei (DCN). Large injections of SVN almost invariably involved 'y' and dorsal parts of the lateral vestibular nucleus (LVN). Smaller injections involved central and ventral peripheral parts of SVN. Discrete injections of 'y' involved small dorsal parts of LVN. Afferents to SVN are derived mainly from the vestibular nuclei (VN) and parts of the vestibulocerebellum. SVN receives afferents: bilaterally from caudal portions of the medial (MVN) and inferior (IVN) vestibular nuclei and 'y'; contralaterally from ventral and lateral parts of SVN and rostral MVN; and ipsilaterally from the nodulus, uvula and medial parts of the flocculus. Purkinje cells (PC) in medial parts of the flocculus project to central regions of SVN, while PC in the nodulus and uvula appear to project mainly to dorsal peripheral regions of SVN. SVN receives sparse projections from the ipsilateral INC, the contralateral central cervical nucleus (CCN) and virtually no projections from the reticular formation. SVN projects via the medial longitudinal fasciculus (MLF) to the ipsilateral trochlear nucleus (TN), the inferior rectus subdivision of the OMC, the INC, the nucleus of Darkschewitsch (ND) and the rostral interstitial nucleus of the MLF (RiMLF). Contralateral projections of SVN cross in the ventral tegmentum caudal to most of the decussating fibers of the superior cerebellar peduncle and terminate in the dorsal rim of the TN and the superior rectus and inferior oblique subdivisions of the OMC; sparse crossed projections enter the INC and the ND. Cerebellar projections of SVN end as mossy fibers in the ipsilateral nodulus, uvula and in medial parts of the flocculus bilaterally. Retrograde transport from unilateral injections of the OMC indicate that afferents from SVN arise ipsilaterally from central and dorsal regions and contralaterally from dorsal peripheral regions. Ventral cell group 'y' receives small numbers of afferent fibers from caudal central parts of the ipsilateral flocculus. No fibers from ventral 'y' could be traced to other vestibular nuclei, the OMC or the cerebellum.(ABSTRACT TRUNCATED AT 400 WORDS)
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              Vertical vestibulo-ocular reflex, smooth pursuit and eye-head tracking dysfunction in internuclear ophthalmoplegia.

              P Ranalli, J Sharpe (1988)
              Vertical smooth eye movements were quantified by magnetic search coil oculography in 7 patients with internuclear ophthalmoplegia (INO), 4 bilateral and 3 unilateral, and compared with age-matched normal subjects. The upward and downward vestibulo-ocular reflex (VOR) had reduced gain and abnormal phase lag in both unilateral and bilateral INO during active head motion at frequencies from 0.25 to 2 Hz. The phase lag was attributed to disruption of vestibular eye velocity signals and relative preservation of eye position signals. Fixation of a stationary target enhanced smooth eye movement gain during vertical head motion but it remained subnormal. Vertical smooth pursuit gain was mildly reduced. All patients had normal gaze (eye plus head) gain when tracking with both the head and eyes despite defective cancellation of the vertical VOR; they employed high amplitude head tracking to compensate for the uncancelled VOR. Cancellation was more impaired than smooth pursuit. Dissociation between cancellation and ocular pursuit was also demonstrated by a model of VOR cancellation that uses measured pursuit gain with the head immobile to predict gaze gain of eye-head tracking. The model predicted eye-head tracking gain in normal subjects but not in patients with INO. The results indicate that the medial longitudinal fasciculi or neighbouring tegmental tracts convey bidirectional signals for vertical pursuit, cancellation, and vestibular smooth eye movements in man, and that smooth pursuit and cancellation of the VOR can be dissociated in INO.
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                Author and article information

                Journal
                Journal ID (publisher-id): ENE
                Journal ID (nlm-ta): Eur Neurol
                Journal ID (doi): 10.1159/issn.0014-3022
                Title: European Neurology
                Publisher: S. Karger AG
                ISSN (Print): 0014-3022
                ISSN (Electronic): 1421-9913
                Publication date Subscription-year: 2005
                Publication date (Print): January 2006
                Publication date (Electronic): 01 February 2006
                Volume: 54
                Issue: 4
                Pages: 186-190
                Affiliations
                aINSERM 679 et Service de Neurologie 1 et bService d’Ophtalmologie, Hôpital de la Salpêtrière, AP-HP, Paris, et cService de Médecine Interne, Hôpital de Lagny, Lagny, France
                Article
                Publisher ID: 90295 Other ID: Eur Neurol 2005;54:186–190
                DOI: 10.1159/000090295
                PubMed ID: 16352905
                SO-VID: 9242ec72-e8aa-4b3b-bdd4-57f6d9333a47
                Copyright © © 2005 S. Karger AG, Basel
                License:

                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
                Date received : 14 July 2005
                Date accepted : 19 October 2005
                Page count
                Figures: 3, References: 14, Pages: 5
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Ventral tegmental tract,Vertical nystagmus,Upbeat nystagmus,Vestibulo-ocular reflex
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Ventral tegmental tract, Vertical nystagmus, Upbeat nystagmus, Vestibulo-ocular reflex

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