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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nystagmus seen only with convergence is unusual. We describe four cases of acquired convergence-evoked pendular nystagmus in patients with multiple sclerosis. The nystagmus was horizontal and asymmetric in all patients. Eye movement recordings in one subject showed a conjugate rather than a convergent-divergent relationship of the phase of movement between the two eyes. All patients had evidence of optic neuropathy and cerebellar dysfunction. Occlusion of either eye during fixation of near targets led to divergent drift of the covered eye and a decrease in nystagmus. Intravenous scopolamine reduced nystagmus in one patient. Base-in prisms alleviated symptoms of oscillopsia at near and improving reading visual acuity. Convergence-evoked pendular nystagmus may be more common than currently appreciated, particularly among patients with multiple sclerosis.
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PMID:Acquired convergence-evoked pendular nystagmus in multiple sclerosis. 1009 46

One of the most frequent disorders of the brainstem in multiple sclerosis (MS) is internuclear opthalmoplegia (INO). The aim of this study is to show how it is possible to monitor the course of MS grading INO on the basis of electro-oculographic findings. We selected 130 patients with a diagnosis of clinically defined multiple sclerosis (78 males and 52 females, mean age 43.5 years) from a population of 354 MS patients. Both saccadic eye movements and spontaneous, vestibular (VOR), visuo-vestibular (VVOR) and optokinetich nystagmus (OKN) were assessed. Slowing of the adducting eye was considered as a sign of lesion of the interocular pathways. Statistical analyses showed that the most sensitive test was VVOR, the least sensitive being randomised saccades. An impairment of random saccades was always associated with abnormal results on all other tests. It seems thus possible to grade the involvement of the medial longitudinal fasciculi (MLF) in MS from an abnormality limited to the VVOR test up to an impairment of randomised saccadic movements. Grading brainstem involvement in MS is particularly important in therapeutic trials and during rehabilitation.
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PMID:Grading brainstem involvement in multiple sclerosis - by means of electro-oculography. 1087 5

Spontaneous sinusoidal oscillations of the eyes are a feature of disorders affecting central myelin, including multiple sclerosis. The mechanism responsible for these oscillations (pendular nystagmus) is unknown. We tested the hypothesis that pendular nystagmus is due to instability of the neural integrator, a network of neurons that normally guarantees steady gaze by mathematically integrating premotor signals. It was possible to make a model of the neural integrator unstable, and abnormal feedback then produced sustained oscillations so that it simulated pendular nystagmus. One prediction of the model is that a large premotor signal, such as is required to generate a rapid (saccadic) eye movement, will transiently suppress the activity of some neurons in the network, and that this will "reset" the oscillations, i.e., produce a phase shift; larger saccades will produce greater phase shifts. Alternatively, if the source of pendular nystagmus is outside the neural integrator (i.e., is present on velocity inputs to the stable integrator), then it may not be possible to reset the oscillations with a saccadic eye movement. We compared the phase relationships of pendular nystagmus prior to and following saccades in six patients with multiple sclerosis (MS). All patients showed phase shifts (median 64 degrees) of their ocular oscillations following large (more than 10 degrees) saccades; smaller saccades (less than 5 degrees) caused smaller phase shifts (median 17 degrees). Our findings suggest that, in MS, pendular nystagmus arises from an instability in the feedback control of the neural integrator for eye movements, which depends on a distributed network of neurons in the brainstem and cerebellum.
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PMID:Experimental tests of a neural-network model for ocular oscillations caused by disease of central myelin. 1096 19

Patients with acquired forms of nystagmus may suffer from oscillopsia and blurred vision; abolishing or reducing nystagmus ameliorates these symptoms. Ideally, treatment of nystagmus should be directed against the pathophysiologic mechanism responsible. Identification of nystagmus pattern is important in directing therapy and occasionally requires electronic eye movement recording for precise characterization. Patients with acquired pendular nystagmus, particularly those with multiple sclerosis, often benefit from gabapentin, a drug with few side effects. Scopolamine, clonazepam, and valproate are also useful in some patients. A new drug, memantine, was effective in treating pendular nystagmus in one study, but it has not yet been approved for use in the United States. Periodic alternating nystagmus usually responds to baclofen. Central vestibular nystagmus, including downbeating and upbeating forms, can be treated with baclofen or clonazepam. In some patients, treatment of an underlying condition, such as periodic ataxia, Whipple's disease, and Chiari malformation, abolishes nystagmus and improves vision. If pharmacologic therapy fails, optical devices can be considered in selected patients. Injections of botulinum toxin and surgery to weaken extraocular muscles are prone to induce diplopia and may precipitate plastic-adaptive ocular motor changes that eventually negate the beneficial effect.
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PMID:Acquired Nystagmus. 1109 97

Vertical vestibuloocular reflexes (VVOR) were examined in 45 patients with multiple sclerosis. It is proposed to study VVOR basing on stimulation of the vertical semicircular labirynthine canals with active sagittal nodding of the head. Central lesion of the vestibular system is characterized by VVOR hyperreactivity, total failure of VVOR suppression by glance, two types of VVOR domination (typical--up and atypical--down), interocular asymmetry (dissociated nystagmus).
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PMID:[Vertical vestibuloocular reflexes in affection of central parts of vestibular system (communication III)]. 1118 80

A 42-year old woman was admitted to our hospital because of sudden onset of dizziness and oscillopsia. Neurologic examination revealed horizontal, binocular pendular nystagmus, which increase their amplitude on left lateral gaze. She also showed that mild right blephaloptosis, right facial spasms, increased tendon reflexes and positive pathological reflexes of four limbs and mild chorea-like movement of both feet. MRI showed an abnormal high intensity area on a T2weighted and proton density images located at the right tegmentum mesencephali. She was diagnosed as clinically probable multiple sclerosis according to the Poser's criteria. The nystagmus was suppressed by clonazepam and diazepam. To our knowledge, it is a first report of acquired pendular nystagmus associated with the lesion of tegmentum mesencephali. We speculate that the involvement of the tract of paramedian pontine reticular formation causes the nystagmus and the dysfunction of GABAnergic neurons might play an important role of the nystagmus.
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PMID:[Acquired pendular nystagmus associated with the lesion of tegmentum mesencephali in a patient with probable multiple sclerosis]. 1129 65

The aim of this study was to further investigate optokinetic reflex function in multiple sclerosis. Gaze-holding in darkness, optokinetic nystagmus, optokinetic afternystagmus and latency to circularvection were measured using electro-oculography and a rotating optokinetic drum. Gaze-holding was not significantly different between the multiple sclerosis and control groups; however, four of 23 multiple sclerosis patients exhibited eccentric gaze-evoked nystagmus. There were no significant differences in either optokinetic nystagmus frequency or latency to circularvection. However, optokinetic nystagmus slow phase velocity during rise time and amplitude during beat time were significantly reduced in the multiple sclerosis group (p < 0.05 and p < 0.0001, respectively). The time constant of optokinetic afternystagmus was also significantly reduced in the multiple sclerosis group (p < 0.005). These results indicate that optokinetic nystagmus and optokinetic afternystagmus are significantly impaired multiple sclerosis.
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PMID:Optokinetic reflex dysfunction in multiple sclerosis. 1138 18

Acquired nystagmus occurs frequently in patients with multiple sclerosis and is often the cause of illusory motion of the environment (oscillopsia), and blurring of vision. Based primarily on the beneficial effect of gabapentin on acquired pendular nystagmus (APN), a GABAergic mechanism in controlling nystagmus has been hypothesised. If increasing GABA concentrations in the CNS are critical for the treatment of nystagmus, then a selective GABAergic drug should be highly successful. However, as gabapentin is not a selective GABAergic agent, vigabatrin, a "pure" GABAergic medication, and gabapentin, were compared in a single blind cross over trial in eight patients with definite multiple sclerosis. Patients were randomly assigned to begin with gabapentin (1200 mg daily) or vigabatrin (2000 mg daily). Neuro-ophthalmological and electro-oculographic (EOG) evaluations were performed four and three times, respectively. Treatment efficacy was based on improving visual acuity and EOG indices (amplitude or frequency of nystagmus, or both) by at least 50% of pretreatment values. Three out of eight patients dropped out due to adverse effects. In the remaining five patients gabapentin improved symptomatic pendular or gaze evoked jerk nystagmus in four. Three patients decided to continue gabapentin therapy. Importantly, vigabatrin proved useful in only one out of five patients, suggesting that gabapentin effectiveness may be related to additional non-GABAergic mechanisms of action. Interaction with cerebral glutamate transmission by inhibition of NMDA receptor might be an alternative hypothesis for the therapeutic action of gabapentin.
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PMID:Gabapentin but not vigabatrin is effective in the treatment of acquired nystagmus in multiple sclerosis: How valid is the GABAergic hypothesis? 1141 74

The effects of the anticonvulsant gabapentin were measured on vision and eve movements in three patients with acquired pendular nystagmus. In two patients, the nystagmus was associated with multiple sclerosis and, in the other, it followed brainstem stroke. A single oral 600 mg dose of gabapentin produced improvement of vision due to changes in ocular oscillations in all three patients. The effect was sustained after five weeks of treatment in two patients who elected to continue taking gabapentin 900-1500 mg/day. The results of this pilot study suggest that a controlled trial of gabapentin should be conducted to evaluate its role in the treatment of acquired forms of nystagmus.
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PMID:A pilot study of gabapentin as treatment for acquired nystagmus. 1153 72

Advances in understanding the organization of the ocular motor system, including its anatomy and pharmacology, have provided new insights into the pathogenesis of various forms of nystagmus. The discoveries of fibromuscular pulleys that govern the pulling directions of the extraocular muscles has provided a new conceptual framework to account for the different axes of rotation of vestibular and other types of movements that may contribute to nystagmus. Theoretical and experimental evidence has suggested that acquired pendular nystagmus, which is commonly due to multiple sclerosis, arises from the neural network that normally guarantees steady gaze by integrating premotor signals. Pharmacologic inactivation studies have implicated both gamma-aminobutyric acid (GABA) and glutamate as important transmitters in the neural integrator and suggested new drug therapies. New electro-optic devices may eventually prove to be effective treatment for the visual symptoms cause by acquired nystagmus. The demonstration of proprioceptive mechanisms in the distal extraocular muscles has provided a rationale for new operative treatments for congenital nystagmus.
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PMID:Nystagmus. 1189 58


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