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Albert F Fuchs - One of the best experts on this subject based on the ideXlab platform.
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anatomical connections of the primate pretectal Nucleus of the optic tract
The Journal of Comparative Neurology, 1994Co-Authors: Michael J Mustari, Chris R. S. Kaneko, Albert F Fuchs, Farrel R RobinsonAbstract:The pretectal Nucleus of the optic tract (NOT) plays an essential role in optokinetic nystagmus, the reflexive movements of the eyes to motion of the entire visual scene. To determine how the NOT can influence structures that move the eyes, we injected it with lectin-conjugated horseradish peroxidase and characterized its afferent and efferent connections. The NOT sent its heaviest projection to the caudal half of the ipsilateral dorsal cap of Kooy in the inferior olive. The rostral dorsal cap was free of labeling. The NOT sent lighter, but consistent, projections to other visual and oculomotor-related areas including, from rostral to caudal, the ipsilateral pregeniculate Nucleus, the contralateeral NOT, the lateral and medial terminal nuclei of the accessory optic system bilaterally, the ipsilateral dorsolateral pontine Nucleus, the ipsilateral Nucleus Prepositus Hypoglossi, and the ipsilateral medial vestibular Nucleus. The NOT received input from the contralateral NOT, the lateral terminal nuclei bilaterally, and the ipsilateral pregeniculate Nucleus. Although our injections involved the pretectal olivary Nucleus (PON), there was neither orthograde nor retrograde labeling in the contralateral PON. Our results indicate that the NOT can influence brainstem preoculomotor pathways both directly through the medial vestibular Nucleus and Nucleus Prepositus Hypoglossi and indirectly through both climbing and mossy fiber pathways to the cerebellar flocculus. In addition, the NOT communicates strongly with other retino-recipient zones, whose neurons are driven by either horizontal (contralateral NOT) or vertical (medial and lateral terminal nuclei) fullfield image motion. © 1994 Wiley-Liss, Inc.
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discharge patterns in Nucleus Prepositus Hypoglossi and adjacent medial vestibular Nucleus during horizontal eye movement in behaving macaques
Journal of Neurophysiology, 1992Co-Authors: Jenny Mcfarland, Albert F FuchsAbstract:1. Monkeys were trained to perform a variety of horizontal eye tracking tasks designed to reveal possible eye movement and vestibular sensitivities of neurons in the medulla. To test eye movement s...
The Johns Hopkins School Of Medicine - One of the best experts on this subject based on the ideXlab platform.
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Reversal of vertical nystagmus with convergence in anti-DPPX encephalitis
Spencer S. Eccles Health Sciences Library University of Utah, 2019Co-Authors: Daniel R. Gold, Departments Of Neurology, Otolaryngology Head Neck - & Surgery, Emergency Medicine, And Medicine, The Johns Hopkins School Of MedicineAbstract:This is a man who initially presented with spontaneous upbeat and torsional nystagmus, which led to the diagnosis of anti-DPPX encephalitis (for further details on this patient's course and for a video of his nystagmus, see reference 1). Over 6-12 months, his spontaneous (mainly) upbeat nystagmus (UBN) transitioned to spontaneous downbeat nystagmus (DBN). In this video, he has gaze-evoked nystagmus (e.g., right-beating in right gaze and left-beating nystagmus in left gaze) with a downbeat component. While spontaneous downbeat nystagmus was present in primary gaze, with convergence, this transitioned to upbeat nystagmus. Vertical nystagmus reversing with convergence is a finding often seen in patients with Wernicke's encephalopathy. While the semicircular canals (posterior, horizontal, and anterior) are the angular acceleration detectors in the labyrinth, the otoliths (utricle and saccule) are the linear acceleration detectors and are responsible for the translational vestibulo-ocular reflex (t-VOR). In order for the t-VOR to generate appropriate eye movements, orbital position and vergence angle must be taken into account(2). Brainstem structures responsible for processing otolithic inputs include the medial and inferior vestibular nuclei (MVN and LVN), which have projections to the cerebellar nodulus (which also has a role in modulating the t-VOR)2. In patients with acute Wernicke's encephalopathy(2), gaze-evoked nystagmus can be attributed to damage involving the MVN-Nucleus Prepositus Hypoglossi (NPH) complex, while the horizontal (angular) VOR is commonly impaired since the horizontal semicircular canal afferents synapse in the MVN. With Wernicke's the transition from spontaneous upbeat nystagmus (attributed to damage involving the Nucleus of Roller and Nucleus intercalatus, which both inhibit the flocculus) to downbeat nystagmus with convergence can also be explained by damage to the MVN and LVN given their role in the t-VOR. In this patient with anti-DPPX encephalitis, impairment of MVN-LVN and/or nodulus are all possible explanation or the transition of DBN to UBN with convergence. It is possible that the initial spontaneous upbeat-torsional nystagmus resulted from asymmetric pontomedullary damage involving the vertical semicircular canal (SCC) pathways (multiple MRIs showed no clear T2/FLAIR or T1-enhancing posterior fossa lesions). Several theories exist for the transition of spontaneous UBN to spontaneous DBN: 1) Given the proximity of the paramedian tract nuclei (PTN), the chronic downbeat nystagmus could relate to vertical SCC pathway recovery with persistent PTN damage - i.e., a similar mechanism to the prevailing theory for transition of acute UBN to chronic DBN in Wernicke's encephalopathy. Since the PTN normally excites the flocculus, damage to the PTN can cause relative hypoactivity of the flocculus and an upward bias (slow phase drift since anterior canal [upward or anti-gravity] pathways are overactive) with resultant downbeat nystagmus. 2) The patient also developed gaze-evoked nystagmus in lateral and up and down gaze after 6-12 months, likely related to dysfunction of the flocculus/paraflocculus rather than the MVN-NPH given its presence in horizontal and vertical gaze. The spontaneous DBN and saccadic pursuit and VOR suppression that also developed are also suggestive of a flocculus/paraflocculus syndrome. It is therefore possible that the acute asymmetric vertical SCC pathway injury recovered, but flocculus/paraflocculus impairment developed chronically.1. Doherty L, Gold D, Solnes L, Probasco J, Venkatesan A. Anti-DPPX encephalitis: prominent nystagmus reflected by extraocular muscle FDG-PET avidity. Neurol Neuroimmunol Neuroinflamm 2017;4:e361. 2. Kattah JC, McClelland C, Zee DS. Vertical nystagmus in Wernicke's encephalopathy: pathogenesis and role of central processing of information from the otoliths. J Neurol 2019
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Mesodiencephalic stroke causing unilateral riMLF and INC ocular motor syndromes
Spencer S. Eccles Health Sciences Library University of Utah, 2018Co-Authors: Daniel R. Gold, Departments Of Neurology, Otolaryngology Head Neck - & Surgery, Emergency Medicine, And Medicine, The Johns Hopkins School Of MedicineAbstract:This is a 65-year-old man who experienced the sudden onset of diplopia (with horizontal and vertical components), dysarthria and imbalance. An MRI performed the following day showed a left mesodiencephalic stroke. The patient was seen in clinic 10 days later (when the video was taken), and by that time the diplopia was purely vertical. The patient had ocular motor findings due to involvement of two distinct rostral midbrain structures: 1) Left interstitial Nucleus of Cajal (INC) a. Incomplete ocular tilt reaction including a left hypertropia from skew deviation (25 prism diopters) and ocular counterroll (top poles rotated toward the right ear on dilated fundus exam), but without a head tilt i. The utriculo-ocular motor pathway (or graviceptive pathway, which mediate afferents from utricle and vertical semicircular canal fibers) begins in the right labyrinth, decussates at the pontomedullary junction, and ascends via the left medial longitudinal fasciculus (MLF) to the left INC. The higher eye will be ipsilesional when the utriculo-ocular motor pathway is affected rostral to (or higher than) the decussation of this pathway - this can be remembered as HIGH-HIGH. If the lesion is lower than the decussation, the lower eye will be ipsilesional - this can be remembered as LOW-LOW. b. Vertical gaze-evoked nystagmus (but none horizontally) i. The INC is responsible for vertical and torsional gaze holding, while the medullary Nucleus Prepositus Hypoglossi-medial vestibular Nucleus complex is responsible for horizontal gaze holding 2) Left rostral interstitial MLF (riMLF) a. Torsional nystagmus, top poles beating toward the RIGHT ear (with torsional nystagmus associated with a LEFT INC, the top poles should beat ipsilaterally, or top poles toward the LEFT ear). With a unilateral riMLF lesion, if torsional nystagmus is seen, it will beat contralaterally as in this case. b. Slow vertical saccades, slower downward compared to upward. This is because the innervation for upward saccades is bilateral (i.e., unilateral riMLF innervates bilateral superior rectus and inferior oblique) while the innervation for downward saccades is unilateral (i.e., unilateral riMLF innervates ipsilateral inferior rectus and superior oblique). The riMLF contains the vertical and torsional excitatory burst neurons. Vertical smooth pursuit and vertical vestibulo-ocular reflexes were normal. c. Absent ipsitorsional quick phases in the roll plane when the patient's head was slowly tilted to the left side. When his head is tilted slowly to the right, the eyes will counterroll with top poles toward the left ear due to the physiologic ocular tilt reaction, but as the head continues to tilt, a quick torsional phase will need to be generated toward the right ear. Since the riMLF contains the vertical and torsional burst neurons, quick torsional phases toward the left (ipsilesional) ear cannot be generated with a left head tilt in this patient, although they were normal with head tilt to the right side due to the intact right riMLF. The initial diplopia with vertical AND horizontal components may have been related to skew deviation AND a pseudo-abducens palsy on the RIGHT (since the descending inhibitory convergence pathways decussate from the left mesodiencephalic region to innervate the right medial rectus subNucleus), respectively. Or, there may have been 3rd fascicle or nuclear involvement initially causing medial rectus weakness. However, this is purely conjecture because no detailed ocular motor examination was available in the hospital records. The patient was seen 1 month later and at that time there had been significant improvement in his skew deviation, and spontaneous torsional nystagmus had resolved completely. Three months after the stroke, there was no vertical misalignment in straight ahead gaze, although there was still a small left hypertropia in downgaze. However, his slow vertical saccades remained. The patient also happened to have asteroid hyalosis in the vitreous OD much more than OS (apparent in the video)
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Gaze-evoked and centripetal nystagmus in Creutzfeldt-Jakob disease
Spencer S. Eccles Health Sciences Library, 2018Co-Authors: Daniel R. Gold, Departments Of Neurology, Otolaryngology Head Neck - & Surgery, Emergency Medicine, And Medicine, The Johns Hopkins School Of MedicineAbstract:This is a 65-year-old woman who experienced a progressive cerebellopathy over several months. Initially, she presented with mild gait imbalance and positional vertigo, and there was only apogeotropic positional nystagmus (more pronounced in supine roll test compared to Dix-Hallpike) with a very slight downbeat component (peak slow phase velocity [SPV] 2-3 degrees/second). In right roll, there was a 16 d/s peak SPV left-beating nystagmus and she was maximally symptomatic in this position. In left roll, there was a -7 d/s peak SPV right-beating nystagmus and she was less symptomatic. Ocular motor and vestibular exams (including head impulse and video head impulse testing) were normal. A presumptive diagnosis of left apogeotropic horizontal canal benign paroxysmal positional vertigo was made, although there was no response to repeated positional maneuvers over one week. Contrast-enhanced MRI was normal with respect to the posterior fossa. Clear gait and limb ataxia were apparent in the following weeks, and a variety of central ocular motor abnormalities developed including dysmetric saccades, impaired smooth pursuit (with relatively spared vestibulo-ocular [VOR] suppression horizontally given loss of the horizontal VOR), fixation-removed downbeat nystagmus, gaze-evoked and rebound nystagmus. Extensive testing looking for infectious, inflammatory and neoplastic disorders was unrevealing. By the second MRI, the thalamic hemispheres were slightly hyperintense on T2-weighted/FLAIR and diffusion weighted imaging (DWI). CSF RT-QuIC and 14-3-3 protein were positive, and CSF T-tau protein was abnormal at >4000, confirming the diagnosis of Creutzfeldt-Jakob disease (CJD). Regarding her gaze-holding function, after sustained lateral gaze for greater than 10 seconds, nystagmus reversed direction from gaze-evoked nystagmus (e.g., in right gaze, slow phase drift toward primary gaze and fast phase back to the right - centrifugal nystagmus) to centripetal nystagmus (e.g., in right gaze, slow phase drift to the right and fast phase back toward primary gaze). Gaze-evoked nystagmus (GEN) is common with cerebellar disease, as is rebound nystagmus. GEN results from impaired function of the neural integrators (Nucleus Prepositus Hypoglossi and medial vestibular Nucleus for horizontal gaze-holding and interstitial Nucleus of Cajal for vertical and torsional gaze-holding), while the flocculus/paraflocculus helps to improve neural integrator function1. Therefore, horizontal and vertical GEN is commonly seen with cerebellar disease. With GEN, compensatory mechanisms attempt to minimize the slow phase drift back toward primary position, and this compensatory bias will shift the resting position of the eyes peripherally(2). Ideally, this shift in the null region should be balanced with the slow phase drift back to center. Imbalance between compensatory and pathological biases can create its own slow phase drift. In the case of rebound nystagmus, if the patient looks to the right, in an effort to minimize the leftward slow phase drift back toward center, compensatory mechanisms will pull the null region farther out to the right. When the patient looks from right to straight ahead gaze, the now left-beating (rebound) nystagmus is akin to a GEN and continues until the compensatory and pathological biases are in equipoise(1, 2). Likewise, centripetal nystagmus probably also represents a compensatory shift in the null region farther to the right as compared to the actual eye position in right gaze, the result being a rightward slow phase drift followed by a centripetal fast phase. Thus, the appearance of centripetal nystagmus may represent an over-compensation, usually brought on by sustained eccentric gaze(1). In patients with CJD who have cerebellar manifestations, gaze-evoked and rebound nystagmus have been commonly reported, in addition to less common ocular motor signs like periodic alternating nystagmus (not seen in this patient) and centripetal nystagmus(3), although these findings are not specific for the diagnosis of CJD. 1. Buttner U, Grundei T. Gaze-evoked nystagmus and smooth pursuit deficits: their relationship studied in 52 patients. J Neurol 1995;242:384-389. 2. Leech J, Gresty M, Hess K, Rudge P. Gaze failure, drifting eye movements, and centripetal nystagmus in cerebellar disease. Br J Ophthalmol 1977;61:774-781. 3. Helmchen Ch, Buttner U. Centripetal nystagmus in a case of Creutzfeldt-Jacob disease. Neuro-Ophthalmology 1995;15:187-192
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Test your knowledge: The acute vestibular syndrome with gaze-evoked nystagmus and bilaterally abnormal head impulse testing due to middle cerebellar peduncle and flocculus hemorrhage
Spencer S. Eccles Health Sciences Library University of Utah, 2018Co-Authors: Tony Brune, Department Of Neurology, The Johns Hopkins School Of MedicineAbstract:This is a 70-year-old woman with a history of atrial fibrillation on warfarin presenting with acute prolonged vertigo and imbalance. In addition to the findings demonstrated in the first part of the video, what else should be seen to reassure the examiner that the etiology of her vertigo is benign? A. Right beating nystagmus in left gaze, a right hypertropia with alternate cover testing, abnormal head impulse test (HIT) to the left, and normal hearing. B. Left beating nystagmus in left gaze, a right hypertropia increasing in left and downgaze and in right head tilt with alternate cover testing, normal HIT to the left, and normal hearing. C. Left-beating nystagmus in left gaze, no vertical heterophoria/heterotropia, abnormal HIT to the left, and decreased hearing on the left. D. Right-beating nystagmus in left gaze, no vertical heterophoria/heterotropia, abnormal HIT to the left and normal hearing. A. Incorrect. The Head Impulse, Nystagmus, Test of Skew (HINTS) ‘Plus' (added test of auditory function) examination consists of four pieces of the bedside examination which accurately differentiates central and vestibular causes of acute vestibular syndrome (acute prolonged vertigo, spontaneous nystagmus, imbalance, nausea/vomiting, head motion intolerance). A benign exam (usually indicative of acute vestibular neuritis) consists of: 1) unidirectional, contralesional, mixed horizontal-torsional nystagmus; 2) an abnormal ipsilesional HIT; 3) no evidence of skew deviation on alternate cover testing; 4) normal hearing. When hearing is involved, labyrinthine ischemia should be strongly considered, especially in someone with vascular risk factors without clear evidence of infectious labyrinthitis or Ramsay Hunt syndrome. The presence of a hypertropia in the setting of acute vertigo is generally assumed to represent a skew deviation until proven otherwise, and this is suggestive of central utricle pathway injury (rarely, a patient can have a "peripheral" skew due to involvement of the utricle within the labyrinth or utricle fibers in the 8th cranial nerve). Left hypotropia could accompany an abnormal HIT to the left with a left vestibular nuclear lesion (caudal to the decussation of the utricle-ocular motor pathways) and rarely due to left-sided 8th nerve/labyrinthine injury. B. Incorrect. In this case, the left-beating nystagmus in left gaze would be consistent with bidirectional, direction-changing or gaze evoked nystagmus (GEN) since there was right-beating nystagmus in right gaze. In peripheral disorders, the spontaneous right-beating nystagmus would increase in the direction of the fast phase (in accordance with Alexander's law) or to the right, but should not transition to left-beating in left gaze. Commonly, horizontal GEN is seen with pathology involving the medial vestibular Nucleus, Nucleus Prepositus Hypoglossi, or cerebellar flocculus (or their connections). A normal HIT is also highly suggestive of a central etiology, commonly a posterior inferior cerebellar artery distribution infarct. A right hypertropia increasing in left and downgaze and in right head tilt would be most consistent with a right 4th nerve palsy (especially if there is excycloduction in the right eye). Occasionally an unrelated congenital or longstanding acquired 4th nerve palsy can lead to a falsely "central" HINTS exam, as any hyperdeviation seen with alternate cover testing should be assumed to be a skew deviation until proven otherwise in the acutely vertiginous patient. Rarely, a nuclear or fascicular 4th nerve palsy can be accompanied by dizziness/vertigo or imbalance and nystagmus (especially with involvement of the adjacent brachium conjunctivum, also known as the superior cerebellar peduncle). C. Incorrect. Concerning findings in this case include gaze-evoked nystagmus and acute hearing loss. The internal auditory artery, a branch of the anterior inferior cerebellar artery, supplies the cochlea and vestibular inner ear structures. Therefore, examination findings as above must be treated as a stroke equivalent. D. Correct. These features are all compatible with left unilateral vestibular loss, which in the acute setting, is usually due to vestibular neuritis. Summary of case and diagnosis (watch the remainder of the video): Additional findings include left-beating nystagmus in left gaze and up-beating nystagmus in upgaze (GEN); and abnormal HIT to both sides, more prominent on the left than the right; she also presented with a hypertropia and vertical diplopia, which quickly resolved within 24 hours. As discussed above, the combination of these findings is most consistent with a central etiology. In her case, she suffered a spontaneous hemorrhage mainly involving the right middle cerebellar peduncle due to anti-coagulation. There was also involvement of the right flocculus, and it has been shown that with acute unilateral flocculus strokes, the vestibulo-ocular reflex (VOR) is often impaired contralesionally more than ipsilesionally. Not only were the corrective (overt) saccades more prominent to the left than to the right with bedside testing, but with video HIT testing, the gain (calculated as area under the eye velocity curve [green traces] to the area under the head velocity curve) to the left was 0.44 while it was 0.57 to the right. Generally, gains of
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Test Your Knowledge - Central and peripheral vestibular and ocular motor signs due to a large vestibular schwannoma
Spencer S. Eccles Health Sciences Library University of Utah, 2018Co-Authors: Daniel R. Gold, Departments Of Neurology, Otolaryngology Head Neck - & Surgery, Emergency Medicine, And Medicine, The Johns Hopkins School Of MedicineAbstract:Which of the following is least likely to be the correct localization or etiology given the findings seen in the video? 1) Acute right 8th cranial neuropathy 2) Right-sided vestibular schwannoma 3) Right vestibular Nucleus infarction 4) Right anterior inferior cerebellar artery distribution stroke Answers: 1) Incorrect. With a right-sided peripheral 8th cranial neuropathy (as in vestibular neuritis), there should be 1) an abnormal head impulse test (HIT) to the right, 2) absence of a skew deviation, and 3) left-beating unidirectional nystagmus, increasing in left gaze (in accordance with Alexander's law. In this case, there was bidirectional (direction-changing) or gaze-evoked nystagmus in lateral gaze, suggestive of a central disorder. 2) Correct. This patient has a right sided vestibular schwannoma causing a right unilateral vestibular loss (right 8th cranial nerve compression), and given its cerebello-pontine angle location and its size, there was also right-sided compression of the brainstem/cerebellum causing right-beating gaze-evoked nystagmus (GEN) in right and up gaze (upbeating in upgaze). There is left-beating nystagmus in left gaze that is most likely due to a combination of gaze-evoked nystagmus (unilateral posterior fossa lesions can cause bilateral gaze-evoked nystagmus, usually greater ipsilesional than contralesional) AND right unilateral vestibular loss. The combination of gaze-evoked (larger amplitude, lower frequency) nystagmus in one direction and vestibular (smaller amplitude, higher frequency) nystagmus in the other is also referred to as Bruns nystagmus and is commonly related to cerebello-pontine angle tumors. In this case, there is not a clear distinction between the two types of nystagmus, presumably related to the large size of the tumor and the fact that gaze-evoked nystagmus is present in all directions of gaze. However, when looking to the left, a slight torsional nystagmus (top poles beating toward left ear) can be appreciated in the video - mixed horizontal-torsional nystagmus is seen in unilateral vestibular loss (seen to the left), as opposed to the pure horizontal gaze-evoked nystagmus (seen to the right). For a more typical example of Bruns nystagmus, see https://collections.lib.utah.edu/details?id=1248764; 3) Correct. Since the horizontal canal afferents synapse in the medial vestibular Nucleus (MVN), it is possible to have an abnormal HIT that is "central". Since the MVN-Nucleus Prepositus Hypoglossi (NPH) complex is responsible for horizontal gaze-holding, unilateral or bilateral injury can also cause gaze-evoked nystagmus. Since the MVN-NPH complex may be preferentially affected by Wernicke's encephalopathy, this provides the explanation for gaze-evoked nystagmus and loss of the horizontal vestibulo-ocular reflex (with relative sparing of vertical VOR) in this condition. 4) Correct. A stroke in the distribution of the right anterior inferior cerebellar artery (AICA) can cause right labyrinthine ischemia (causing right unilateral vestibular loss, although generally accompanied by ipsilesional hearing loss due to cochlear ischemia), and simultaneous brainstem/cerebellar ischemia which can result in gaze-evoked nystagmus (e.g., right flocculus)
Guy Cheron - One of the best experts on this subject based on the ideXlab platform.
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the hypothesis of the uniqueness of the oculomotor neural integrator direct experimental evidence in the cat
The Journal of Physiology, 1996Co-Authors: Emile Godaux, Guy CheronAbstract:1. As far as horizontal eye movements are concerned, the well-known hypothesis, not yet experimentally proved, of the common neural integrator states that the eye-position signal is generated by a common network, regardless of the type of versional movement. The aim of this study was to evaluate the validity of this hypothesis by checking whether the sensitivity to eye position of the neurones of the Nucleus Prepositus Hypoglossi (NPH) (the main component of the system integrating the different incoming velocity signals) would be the same regardless of the type of versional movement. 2. The discharge of sixty-five NPH neurones was recorded in the alert cat during spontaneous eye movements made in the light and in response to sinusoidal rotations of the head in complete darkness. 3. For each NPH neurone, the sensitivity to eye position was determined from measurements carried out during intersaccadic fixation. The discharge rate of the studied neurone was plotted against eye position. The slope of the resulting regression line gave the sensitivity (measured during intersaccadic fixation in the light) of the neurone to eye position, which was termed K(f). 4. A new method was developed to measure the sensitivity to eye position (K(v)) of neurones during vestibular slow phases. The difficulty came from the fact that, during slow phases, eye velocity and eye position changed simultaneously and that each of those two variables could influence neuronal activity. For each neurone, the instantaneous firing rate was measured each time the eye passed through a given position during any slow phase generated during any vestibulo-ocular reflex. At a given position, the discharge rate of the neurone under study was plotted against the eye velocity. From the resulting linear regression line, two interesting values were obtained: its slope, corresponding to the sensitivity of the neurone to eye velocity, R(v), (at that given eye position) and its 'y'-intercept, F(0), the interpolated firing rate when the eye velocity was zero. This procedure was repeated for different eye positions. The values of F(0) were then plotted against the eye positions. The slope of the resulting regression line gave the sensitivity (measured during vestibular stimulation) of the neurone to eye position, which was termed K(v). 5. The errors on the individual values of K(f) and K(v) were assessed in order to allow a statistical comparison at the single unit level. 6. We found that, for each of our sixty-five neurones, the sensitivity to eye position measured during intersaccadic fixation in the light was equal to the sensitivity to eye position measured during the vestibulo-ocular reflex (VOR) elicited in complete darkness. We conclude that our results favour the hypothesis of a unique horizontal oculomotor integrator for all versional movements.
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effect of muscimol microinjections into the Prepositus Hypoglossi and the medial vestibular nuclei on cat eye movements
Journal of Neurophysiology, 1994Co-Authors: Philippe Mettens, Emile Godaux, Guy Cheron, H L GalianaAbstract:1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the Nucleus Prepositus Hypoglossi (NPH) and the medial vestibular Nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)
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differential effect of injections of kainic acid into the Prepositus and the vestibular nuclei of the cat
The Journal of Physiology, 1993Co-Authors: Emile Godaux, Philippe Mettens, Guy CheronAbstract:1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate. 2. Previously, microinjections of kainic acid (KA) into the region of the Nucleus Prepositus Hypoglossi (NPH) and of the medial vestibular Nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey. However, the relatively large volumes (1-3 microliters) and concentrations (2-4 micrograms microliters-1) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 microgram microliter-1) either into the rostral part of the MVN or into different sites along the NPH of the cat. 3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s. 4. In each injection experiment, the location of the abducens Nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens Nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens Nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes.(ABSTRACT TRUNCATED AT 400 WORDS)
Emile Godaux - One of the best experts on this subject based on the ideXlab platform.
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the hypothesis of the uniqueness of the oculomotor neural integrator direct experimental evidence in the cat
The Journal of Physiology, 1996Co-Authors: Emile Godaux, Guy CheronAbstract:1. As far as horizontal eye movements are concerned, the well-known hypothesis, not yet experimentally proved, of the common neural integrator states that the eye-position signal is generated by a common network, regardless of the type of versional movement. The aim of this study was to evaluate the validity of this hypothesis by checking whether the sensitivity to eye position of the neurones of the Nucleus Prepositus Hypoglossi (NPH) (the main component of the system integrating the different incoming velocity signals) would be the same regardless of the type of versional movement. 2. The discharge of sixty-five NPH neurones was recorded in the alert cat during spontaneous eye movements made in the light and in response to sinusoidal rotations of the head in complete darkness. 3. For each NPH neurone, the sensitivity to eye position was determined from measurements carried out during intersaccadic fixation. The discharge rate of the studied neurone was plotted against eye position. The slope of the resulting regression line gave the sensitivity (measured during intersaccadic fixation in the light) of the neurone to eye position, which was termed K(f). 4. A new method was developed to measure the sensitivity to eye position (K(v)) of neurones during vestibular slow phases. The difficulty came from the fact that, during slow phases, eye velocity and eye position changed simultaneously and that each of those two variables could influence neuronal activity. For each neurone, the instantaneous firing rate was measured each time the eye passed through a given position during any slow phase generated during any vestibulo-ocular reflex. At a given position, the discharge rate of the neurone under study was plotted against the eye velocity. From the resulting linear regression line, two interesting values were obtained: its slope, corresponding to the sensitivity of the neurone to eye velocity, R(v), (at that given eye position) and its 'y'-intercept, F(0), the interpolated firing rate when the eye velocity was zero. This procedure was repeated for different eye positions. The values of F(0) were then plotted against the eye positions. The slope of the resulting regression line gave the sensitivity (measured during vestibular stimulation) of the neurone to eye position, which was termed K(v). 5. The errors on the individual values of K(f) and K(v) were assessed in order to allow a statistical comparison at the single unit level. 6. We found that, for each of our sixty-five neurones, the sensitivity to eye position measured during intersaccadic fixation in the light was equal to the sensitivity to eye position measured during the vestibulo-ocular reflex (VOR) elicited in complete darkness. We conclude that our results favour the hypothesis of a unique horizontal oculomotor integrator for all versional movements.
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effect of muscimol microinjections into the Prepositus Hypoglossi and the medial vestibular nuclei on cat eye movements
Journal of Neurophysiology, 1994Co-Authors: Philippe Mettens, Emile Godaux, Guy Cheron, H L GalianaAbstract:1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the Nucleus Prepositus Hypoglossi (NPH) and the medial vestibular Nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)
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differential effect of injections of kainic acid into the Prepositus and the vestibular nuclei of the cat
The Journal of Physiology, 1993Co-Authors: Emile Godaux, Philippe Mettens, Guy CheronAbstract:1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate. 2. Previously, microinjections of kainic acid (KA) into the region of the Nucleus Prepositus Hypoglossi (NPH) and of the medial vestibular Nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey. However, the relatively large volumes (1-3 microliters) and concentrations (2-4 micrograms microliters-1) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 microgram microliter-1) either into the rostral part of the MVN or into different sites along the NPH of the cat. 3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s. 4. In each injection experiment, the location of the abducens Nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens Nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens Nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes.(ABSTRACT TRUNCATED AT 400 WORDS)
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neural connections of the pontine reticular formation which connects reciprocally with the Nucleus Prepositus Hypoglossi in the rat
Neuroscience, 1999Co-Authors: H Iwasaki, Kazutaka Kani, Toshihiro MaedaAbstract:Abstract The pontine reticular formation connected with the Nucleus Prepositus Hypoglossi was studied in the rat using anterograde and retrograde tracer techniques. The area reciprocally connected with the Nucleus Prepositus Hypoglossi was evident in the pontine reticular formation of the rat. The region had intensive reciprocal connections with the ipsilateral subthalamic region, the contralateral pontine reticular formation and the Nucleus Prepositus Hypoglossi. Furthermore, it was confirmed that the region received cholinergic projections mainly from the pedunculopontine tegmental Nucleus and the laterodorsal tegmental Nucleus, and aminergic projections from the dopaminergic cell groups A13 and A11, noradrenergic cell groups A7, A6 and A5, and the serotoninergic B9 cell group. This region in the rat was considered to be the preoculomotor structure in the function of horizontal gaze corresponding to the paramedian pontine reticular formation in other animals.
