Ocular Motor Disorders Research Articles

Comparison of the effects of pretreatment with competitive or noncompetitive NMDA antagonists on vestibular compensation

Unilateral labyrinthectomy (UL) results in a syndrome of ocular motor and postural disorders which abates over time in a process of behavioural recovery known as vestibular compensation. We have previously reported that a single systemic pre-UL injection of the organic Ca 2+ channel antagonist verapamil or the noncompetitive N-methyl- d-aspartate (NMDA) receptor antagonist MK-801 reduces the behavioural effects of UL in guinea pigs. The present study was conducted to determine if similar effects would be obtained with single injections of the competitive NMDA receptor antagonists 3-[(±)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP) or cis-4-(phosphonomethyl)-piperidine-2-carboxylic acid (CGS 19755). Guinea pigs received an IP injection of 5 mg/kg CPP 2.5 h pre-UL, 5 or 10 mg/kg CPP 1 h pre-UL, 10 or 20 mg/kg CGS 19755 1 h pre-UL, or 1 ml/kg vehicle (saline) 1 h pre-UL, and the effects on the compensation of spontaneous nystagmus were measured over the following 52 h post-UL. Pretreatment with CPP had no significant effect on spontaneous nystagmus frequency or its compensation over 52 h post-UL. However, pretreatment with CGS 19755 resulted in a significant decrease in spontaneous nystagmus frequency without any acceleration of the rate of compensation.

Ocular Motor Disorders of the Brain Stem (Baillière's Clinical Neurology

Ocular Motor Disorders of the Brain Stem (Baillière's Clinical Neurology

Reflex horizontal saccades in multiple sclerosis

The authors used infrared oculography to measure reflex horizontal saccades in 50 normal subjects and 65 patients with multiple sclerosis. MS patients were divided into three groups on the basis of a current or past history of ocularmotor disorder or neither. Saccadic duration and peak velocity characteristics were modelled using simple mathematical functions. Data were segregated by eye and direction and anatomical interpretations made on the basis of abnormalities found. The authors were able to show that duration more so than velocity data, using small angles, was sensitive to clinical and presumed ‘subclinical’ abnormalities. Saccadic latency did not correlate with visual pathway problems, and dysmetria frequently occurred in patients with a previous history of ocular palsy. In contrast to previous studies the authors have demonstrated that careful measurement of small saccades provides clinically robust and useful information, and suggest that this approach could be extended to aid in the evaluation ...

Das okulomotorische System — Simulation von physiologischen und pathologischen horizontalen sakkadischen Augenbewegungen - The Oculomotor System - Simulation of Physiological and Pathological Horizontal Saccadic Eye Movements

Horizontal saccadic eye movements were analyzed by way of the input- and output-functions of the oculomotor system. On the basis of the parameters of the model, it was possible to simulate both physiological and pathological saccades. In this paper we present the results of simulation experiments that were performed to study the influence of various ocular motor disorders. The parameters of the model proved a useful diagnostic aid.

Abnormalities of horizontal gaze. Clinical, oculographic and magnetic resonance imaging findings. II. Gaze palsy and internuclear ophthalmoplegia.

The site of lesions responsible for horizontal gaze palsy and various types of internuclear ophthalmoplegia (INO) was established by identifying the common areas where the abnormal MRI signals from patients with a given ocular-motor disorder overlapped. Patients with unilateral gaze palsy had lesions in the paramedian area of the pons, including the abducens nucleus, the lateral part of the nucleus reticularis pontis caudalis and the nucleus reticularis pontis oralis. Patients with abducens nucleus lesions showed additional clinical signs of lateral rectus weakness. Lesions responsible for bilateral gaze palsy involved the pontine tegmental raphe. Since this region contains the saccadic omnipause neurons, this finding suggests that damage to omnipause cells produces slowing of saccades rather than opsoclonus, as previously proposed. All INOs, regardless of the presence of impaired abduction or convergence, had similar MRI appearances. Frequently the lesions in patients with INO, were not confined to the medial longitudinal fasciculus (MLF) but also involved neighbouring structures at the pontine and mid-brain levels. There was a statistically significant association between the clinical severity of the INO and the presence of abnormal abduction or convergence. The findings suggest that the lesions outside the MLF, which may affect abducens, gaze or convergence pathways, are responsible for the presence of features additional to INO, depending on the magnitude of functional disruption they produce.

Neuronal activity in the guinea pig medial vestibular nucleus in vitro following chronic unilateral labyrinthectomy

Unilateral labyrinthectomy (UL) causes ocular motor and postural disorders which disappear over time in a process of recovery known as vestibular compensation. Vestibular compensation is due to CNS plasticity which generates a partial recovery of resting activity in the vestibular nucleus ipsilateral to the UL, however the mechanism of this neural recovery is unknown. It has been suggested that other areas of the CNS may substitute non-vestibular sensory inputs for the missing labyrinthine input, thereby causing vestibular compensation. The present results show that resting activity can be recorded from medial vestibular nucleus (MVN) neurons in vitro, in brainstem slices from guinea pigs which have compensated for an ipsilateral UL. This result suggests that MVN neurons are capable of generating resting activity without inputs from many other CNS areas. Perfusion with high Mg 2+ solution did not abolish resting activity in most cases, suggesting that part of the resting activity may be generated spontaneously by the neurons, possibly through changes in the electrical excitability of the cell membrane.

Dissociated nystagmus as a common sign of ocular motor disorders in HIV-infected patients.

In order to determine if ocular motor disturbances due to brainstem and cerebellar dysfunction provide a frequent and early marker for HIV infection of the brain, neurological examination was performed in 133 HIV-infected persons who were consecutively admitted to our hospital. In 22 patients (17%) we found no other reason for cerebellar or pontomesencephalic signs than HIV encephalopathy. Ocular motor disorders accounted for the most frequent signs of cerebellar and pontomesencephalic dysfunction. Ocular motor disorders mainly consisted of dissociated nystagmus (n = 12), gaze-evoked nystagmus (n = 10) and impaired smooth pursuit (n = 6). Cerebellar ataxic gait and dysmetria were present in 3 patients. Since dissociated nystagmus was the primary ocular motor disorder, we assume that the medial longitudinal fasciculus may be a predilected circumscribed area for HIV infection of the brain. We suppose that cerebellar and pontomesencephalic disorders may be an early marker for HIV encephalopathy because they were the only neurological signs found in 12 patients.

Effects of ablation of flocculus and paraflocculus of eye movements in primate.

1. Eye movements were recorded in four rhesus monkeys, before and after bilateral ablations of the flocculi and portions of the paraflocculi (“flocculectomy”). Animals were trained to fixate and follow targets so that pursuit, saccades, and vestibular and optokinetic nystagmus could be quantitated. 2. The vestibuloocular reflex (VOR) was mildly affected by flocculectomy. In darkness the VOR gain (eye velocity/head velocity) for steps of head velocity (normal range, 0.84-0.96) increased postoperatively in one monkey to 1.17, decreased in another to 0.62, and did not change significantly in the other two (0.96, 0.94). VOR phase lead at 0.05-Hz oscillation in darkness (normal range, O,O--LOO) increased in two monkeys by 12 and 9.5 O but did not change significantly in the others. 3. Visual suppression of inappropriate vestibular nystagmus was impaired. During oscillation at 0.25 Hz with a head-fixed visual scene, the average amount of attenuation of the VOR decreased from 5 1% preoperatively to 20% postoperatively. Visual suppression of caloric nystagmus was comparably affected. 4. Smooth tracking of small targets moving in space was impaired either with the head still (smooth pursuit) or moving (cancellation of the VOR by fixating a target rotating with the head). The average gain (gaze velocity/target velocity) in either case was about 0.65 (normal, 0.95-0.98). The pursuit deficit was less than that reported after total cerebellectomy, suggesting other cerebellar structures also participate in smooth tracking. 5. Optokinetic nystagmus (OKN) was present postoperatively but, in response to a constant-velocity stimulus, the initial slowphase velocity decreased by 50% and the rise time to a steady state nearly doubled. For stimuli belowr 6O”/s the average steady-state gain was only mildly diminished to 0.86 (normal, 0.98) and the time course of optokinetic afternystagmus (OKAN) in darkness was normal. The response to higher velocity optokinetic stimuli was impaired. These abnormalities can largely be attributed to the coexisting pursuit deficit although the protracted rise to a steady state suggests a change in the ability of the brain stem optokinetic system to handle large amounts of retinal slip. 6. Flocculectomized monkeys showed horizontally, gaze-paretic nystagmus with exponentially decaying centripetal drift (time constant, 1.56 s) and vertically, downbeat nystagmus with exponentially decaying (in three monkeys) or exponentially increasing (in one monkey) slow phases. All animals showed rebound nystagmus. These results implicate the flocculus and possibly the paraflocculus in the control of the time constant and stability of the brain stem oculomotor integrators. 7. Saccadic velocities and accuracy were normal but flocculectomized monkeys showed brief (40150 ms duration), approximately exponential, postsaccadic drift with amplitudes up to 15% of the size of the saccade. The eyes usually drifted in the same direction as the saccade but each monkey showed an idiosyncratic pattern depending on saccade direction and eye position. Postsaccadic drift may reflect a mismatch between the phasic (pulse) and tonic (step) innervational changes that create saccades.

Bilateral adrenal medullary hyperplasia: a clinicopathological entity.

A 36-year-old white patient is described. He received treatment for hypertension and showed slightly increased excretion of 17-OHCS- and 17-ketosteroids but no increase in values for 3-methoxy-4-hydroxymandelic acid in the urine. He was admitted to hospital for a myocardial infarction, which was found to be situated in the anterior wall. During his stay in hospital a sudden increase in blood pressure occurred, together with a typical attach of perspiration, loss of consciousness, and ventricular fibrillation. The assay by 3-methoxy-4-hydroxymandelic acid now showed markedly increased amounts. A phaeochromocytoma was thought to be the most probably diagnosis, but now withstanding therapy the patient died from cerebral lesions. At necropsy a recent anteroseptal myocardial infarction and some minor lesions were found but no tumour and notably no phaechromocytoma, neither in the adrenals nor elsewhere. Using Dobbie's morphometric technique, as described by Munro Neville (1969), changes in the adrenals were demonstrated, which were considered to represent primary adrenal medullary hyperplasia. Criteria for the diagnosis of this syndrome are discussed. Until now it had been presumed to be present in a number of cases but never convincingly demonstrated.

Anomalies of Ocular Motor Nerves : Neuroanatomic Correlates of Paradoxical Innervation in Duane's Syndrome and Related Congenital Ocular Motor Disorders

Anomalies of Ocular Motor Nerves : Neuroanatomic Correlates of Paradoxical Innervation in Duane's Syndrome and Related Congenital Ocular Motor Disorders

OCULAR ELECTROMYOGRAPHY IN BRAIN STEM DYSFUNCTION; CLINICAL AND ELECTROPHYSIOLOGICAL ANALYSIS OF A CASE WITH MULTIPLE EYE MOVEMENT DISORDERS.

The purpose of this paper is to show how electromyography (EMG) of the eye muscles serves to elucidate physiologic phenomena occurring in the presence of brain stem dysfunction. One of the basic tenets of ocular muscle physiology is that excitation of one set of muscles (agonists) is associated with the inhibition of the opposing set (antagonists), exemplified both ipsilaterally and contralaterally. Electromyography affords an opportunity to demonstrate these basic phenomena not only in the course of normal eye movements but also in conjugate and disconjugate gaze disorders and even, as in this case, in apparent (clinical) paralysis of eye movement. While many descriptions of ocular motor disorders are available, most reports discuss the defects in eye movement without specifically alluding to excitation or, in particular, to inhibition. This report will emphasize these phenomena and the correlation of clinical and electromyographic findings. From the electrophysiologic point of view, one of the

Protection of the Interproximal Space

The study of the ocular-motor nerves must be exhaustive from their source (nuclei in the brainstem) down to the effector muscles (orbit). Visual disturbances have to be analysed by differentiating between a decrease in visual acuity and ocular-motor disorders. Imaging tests are dominated by MRI, including fine slices and gadolinium injection. A study of the Circle of Willis vessels is often useful, and essential in the case of type III impairment. A further CT scan is essential for analysis of the foramina, base of the skull and orbital walls. Impairment of CN VI requires a CT scan of the apex of petrous. The study of the cavernous sinuses must be in-depth (T2 and T1 after gadolinium and elimination of fats) and always comparative. Impairment of CN III is often complex, difficult to identify precisely (complete or partial, with or without a pupil impairment, associated with other neurological signs) and requires a reasoned study based on anatomical, semiological and pathological knowledge. Other than tumour diseases, it is necessary to consider less well known malformative, ischemic and inflammatory aetiology.