Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an unselected series of 644 cases of multiple sclerosis, 25 cases with acquired pendular nystagmus were found. Ten additional cases of pendular nystagmus in multiple sclerosis were investigated, and four cases from the literature are analysed. Acquired pendular nystagmus is purely sinusoidal in form, ceases with eye closure, is accompanied by oscillopsia, often monocular and vertical in direction, and never accompanied by optokinetic inversion. This is different from congenital nystagmus. Acquired pendular nystagmus in multiple sclerosis shows a high correlation with holding tremor of head and arm and with trunk ataxia, and must therefore be viewed as a result of lesions of cerebellar nuclei or their fibre connections with the brain-stem. Supporting evidence is discussed. The results fit into a theory of cerebellar function according to which the cerebellar nuclei are involved in the maintenance of positions.
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PMID:Acquired pendular nystagmus with oscillopsia in multiple sclerosis: a sign of cerebellar nuclei disease. 483 52

Acquired pendular nystagmus (APN) is regularly accompanied by oscillopsia and impairment of static visual acuity. Therapeutic approaches to APN remain controversial, and there is no generally accepted therapeutic approach. We tested 14 patients who had suffered from APN caused by multiple sclerosis for several years; 12 patients presented with fixational pendular nystagmus (increasing during fixation) and 2 with spontaneous pendular nystagmus. All 11 patients with fixational pendular nystagmus who were given memantine, a glutamate antagonist, experienced complete cessation of the nystagmus. In contrast, scopolamine caused no (6 of 8) or only a minor (10-50%) reduction of the nystagmus (2 of 8). It was concluded that memantine is a safe treatment option for APN.
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PMID:Drug therapy for acquired pendular nystagmus in multiple sclerosis. 900 39

Acquired pendular nystagmus (APN) complicates multiple sclerosis and other neurological disorders, causes visual impairment, and frequently resists treatment. Vision could be improved by a visual aid that gates or shifts the seen world in lockstep with the APN. Since the pathological oscillations are embedded in normal eye movements, such a device must track the nystagmus selectively. We evaluated the ability of an adaptive filter to perform this tracking and improve acuity when coupled to either of two devices--a shutter that permitted brief glimpses of the world synchronized with the nystagmus, or simulated image-shifting optics. In 10 normal subjects whose decimal acuity averaged 1.46 +/- 0.20, acuity fell to 0.36 +/- 0.08 under viewing conditions simulating APN. The synchronized shutter restored acuity to 0.60 +/- 0.12, while image-stabilization raised it to 1.17 +/- 0.13. Adaptive filters provide a practical means by which to track nystagmus. The most effective visual aid would couple such filters to image-stabilizing optics.
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PMID:Application of adaptive filters to visual testing and treatment in acquired pendular nystagmus. 1554 48

Acquired pendular nystagmus (APN) complicates multiple sclerosis and other neurological disorders, causes visual impairment, and is often refractory to available treatments. Vision could be improved by an optical aid that shifts the seen world in lockstep with the APN. An essential component of such a device is the image-shifting mechanism, which must be light, accurate, suitable for battery operation, and capable of image shifting at the frequencies and amplitudes seen in APN. We determined that a three-lens image-shifting mechanism used in commercial image-stabilizing lenses has the potential to satisfy all these requirements. In combination with software designed to track nystagmus, the optical mechanism proved capable of improving visual acuity in 12 normal subjects experiencing simulated two-dimensional nystagmus. Acuity was restored to within an average of 0.12 logMAR (range 0.0-0.22) of the subjects' values without the simulated nystagmus. These results support the feasibility of an assistive device for patients with APN.
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PMID:Image-shifting optics for a nystagmus treatment device. 1554 49

For several forms of acquired nystagmus, animal models exist, mathematical hypotheses have been proposed, and treatments are available. What insights could acquired nystagmus provide for congenital forms of nystagmus? Acquired periodic alternating nystagmus (PAN) is caused by instability of the velocity storage mechanism for vestibular eye movements; an adaptive mechanism produces the oscillations that have a period of about 4 minutes. Surprisingly, the ability of individuals with congenital forms of nystagmus to adapt their eye movements to new visual demands has received little study. Acquired pendular nystagmus (APN) may arise from instability in the neural integrator for eye movements; identification of the neurotransmitters contributing to normal gaze holding made it possible to identify candidate drugs for treatment of APN. Similar knowledge of the biology underlying of congenital forms of nystagmus might similarly suggest effective drugs. Downbeat nystagmus (DBN) is caused by cerebellar disease, which includes structural lesions affecting the flocculus and paraflocculus, and calcium channelopathies, such as episodic ataxia type 2 (EA2), for which a mouse model and effective treatment is available. Since some congenital forms of nystagmus are genetic in origin, then the possibility arises that they may be caused by a channelopathy, a hypothesis that suggests novel drugs for evaluation in randomized controlled trials.
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PMID:What can acquired nystagmus tell us about congenital forms of nystagmus? 1670 74

Advances made in understanding the pathophysiology of eye movement disorders have only recently with the publication of the first well-planned studies been translated into better treatment strategies. The following chapter summarizes the pharmacological treatment options for a variety of oculomotor syndromes. Cortisone is useful, for example, for acute vestibular neuritis to improve the restitution of the labyrinthine function. For the widespread benign paroxysmal positioning nystagmus, a series of liberating movements that free the semicircular canal from the causative otoconia is now a well-established therapy. Treatment for the central vestibular syndrome of up- and downbeat nystagmus consists of drugs like the potassium canal blocker 4-aminopyridine, which influence the cerebellar circuits involved in the disorder's pathophysiology. Acquired pendular nystagmus, one of the oculomotor syndromes often caused by multiple sclerosis, results in the severe impairment of reduced visual acuity. Memantine, a weak NMDA antagonist, has now been proven effective here. Finally, anticonvulsants like carbamazepine are the drugs of choice for disorders involving a nerve-blood vessel contact that induces symptoms of vestibular paroxysmia or superior oblique myokymia.
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PMID:Therapeutic considerations for eye movement disorders. 1731 84

Acquired pendular nystagmus (APN) occurs with multiple sclerosis (MS) and oculopalatal tremor (OPT); distinct features of the nystagmus have led to the development of separate models for their pathogenesis. APN in MS has been attributed to instability in the neural integrator, which normally ensures steady gaze. APN in OPT may result from electrotonic coupling between neurons in the hypertrophied inferior olivary nucleus, which induces maladaptive learning in cerebellar cortex. We tested these two hypotheses by analyzing the effects of gabapentin, memantine, and baclofen on both forms of nystagmus. No drug changed the dominant frequency of either form of APN, but the variability of frequency was affected with gabapentin and memantine in patients with OPT. The amplitude of APN in both MS and OPT was reduced with gabapentin and memantine, but not baclofen. Analyzing the effects of drug therapies on ocular oscillations provides a novel approach to test models of nystagmus.
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PMID:Pharmacological tests of hypotheses for acquired pendular nystagmus. 2195 Oct 11

We review the latest literature on the neuropharmacological treatments for acquired nystagmus.Nystagmus may have a significant [corrected] impact on health, yet there is little scientific evidence on which to make firm recommendations for treatment. Acquired pendular nystagmus may respond to gabapentin or memantine; downbeat and upbeat nystagmus to aminopyridines; and periodic alternating nystagmus to baclofen. To improve treatment we need multi-centre, randomised controlled trials using standardised techniques in reporting objective outcomes, with good follow-up duration and careful reporting of side effects.
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PMID:The pharmacological treatment of acquired nystagmus. 2266 44

Acquired pendular nystagmus (PN) occurs commonly in multiple sclerosis (MS) and results in a highly disabling oscillopsia that impairs vision. It usually consists of pseudo-sinusoidal oscillations at a single frequency (3-5 Hz) that often briefly stop for a few hundred milliseconds after saccades and blinks. The oscillations are thought to arise from instability in the gaze-holding networks ("neural integrator") in the brainstem and cerebellum.(1,2) Here we describe a patient with monocular PN in whom vibration on the skull from a handheld muscle massager strikingly diminished or stopped her nystagmus.
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PMID:Damping of monocular pendular nystagmus with vibration in a patient with multiple sclerosis. 2554 81

Acquired pendular nystagmus is comprised of quasi-sinusoidal oscillations of the eyes significantly affecting gaze holding and clarity of vision. The most common causes of acquired pendular nystagmus include demyelinating disorders such as multiple sclerosis and the syndrome of ocular palatal tremor. However, several other deficits, such as pharmacological intoxication, metabolic and genetic disorders, and granulomatous disorders can lead to syndromes mimicking acquired pendular nystagmus. Study of the kinematic features of acquired pendular nystagmus has suggested a putative pathophysiology of an otherwise mysterious neurological disorder. Here we review clinical features of neurological deficits that co-occur with acquired pendular nystagmus. Subsequent discussion of the pathophysiology of individual forms of pendular nystagmus speculates on mechanisms of the underlying disease while providing insights into pharmacotherapy of nystagmus.
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PMID:Acquired pendular nystagmus. 2832 Jan 94


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