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)

Seventy five patients affected by senile dementia of the Alzheimer type (mean age 82) have been submitted to a standardized neurological examination of 88 items. Gait abnormalities were present in 57% of the cases. Extrapyramidal symptoms (akinesia or rigidity or tremor) were noticed in 64% of the cases but they were rarely associated with a typical parkinsonian syndrome. Myoclonus was observed in only 4 patients. The gait abnormalities were significantly associated with the presence of rigidity and grasp reflex but not with other primitive reflexes. The only symptoms to be correlated with dementia severity as assessed by the Mini Mental State were rigidity and optokinetic nystagmus abolition. Tremor and amyotrophy of the hands appeared to be negatively correlated to dementia severity.
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PMID:[Standardized neurologic study in senile dementia of Alzheimer's type]. 268 Apr 61

Chronic states of methylmercurialism were induced in squirrel monkey subjects. Principal neurological signs included ataxia, abnormal gait, incoordination and amaurosis. Although slight to moderate vacuolization occurred in supporting cell layers of the cristae and maculae, receptor cell function was essentially normal. Except for a lowered cold threshold, bithermal caloric-induced nystagmus was not significantly different from control values. Pre and postrotatory (Barany chair) tests revealed a reduction only in frequency related variables. The development of spontaneous and positional nystagmus (sometimes with eyes open) coupled with the behavioral signs and the evidence of normal receptor response suggested cerebellar dysfunction. Severe pathologic changes were present in the cerebral cortex, but no lesions were found in the cerebellar cortex. Substantial neuronal degeneration and gliosis, however, were observed in several subcortical nuclei, including cerebellar and vestibular nuclei.
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PMID:Horizontal nystagmus in methylmercury poisoned squirrel monkeys. 613 46

A 28-year old male was admitted to Musashino Red Cross Hospital on June 21, 1975, because of symptoms of increased intracranial pressure and cerebellar dysfunction. Thirteen months prior to admission he had a mild fever, tremor of right arm, headache, nausea and unsteady gait, but made a gradual recovery in about 40 days. A month prior to admission he had unsteady gate again wit dizziness, photophobia and lacrimation. Gait disturbance aggravated and he was admitted to another hospital, where he developed recent memory disturbance and cloudiness of consciousness. Spinal tap revealed initial pressure of 280 mm CSF. So a mass lesion possibly in the posterior fossa was suspected and the patient was referred to the neurosurgical department of musashino Red Cross Hospital. On admission he was moderately disorientated and disturbed in recent memory. Wide based gait, horizontal and vertical nystagmus were also noted. Angiography revealed rounding of the curve of the pericallosal artery but no space occupying lesions. External ventricular drainage was performed on July 25, 1975. After the operation, his orientation improved without change in dizziness, nystagmus and recent memory disturbance. Ventriculography showed hydrocephalus with cisternography revealed a block at the basal cisterns. PPDs was negative and typical sarcoid tubercles were found in the biopsy specimen of the cervical lymphnode. Kveim test was positive. But repeated chest roentgenogram failed to show bilateral hilar lymphadenopathy, or other changes consistent with pulmonary sarcoidosis. Steroid therapy resulted in marked symptomatic improvement.
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PMID:[A case of CNS sarcoidosis -case report of hydrocephalus due to mechanical obstruction secondary to sarcoid granulomata at the outlet of the fourth ventricle (author's transl)]. 723 30

Neurological, auditory, vestibular and ocular motor examinations were performed on 3 definite and 3 possible heterozygous carriers of a previously described X-linked multi-system disorder with early childhood onset, rapid progression and a fatal outcome (Arts et al., 1993). The symptoms, i.e., delayed motor development, ataxia, hearing loss and subnormal intelligence, were so evident in 2 of the possible carriers that they could be redesignated as probable carriers. Other symptoms in the definite and probable carriers were clubfeet, dysarthria, intention tremor and abnormal gait, while their signs included dysdiadochokinesia, ataxic paraplegia, abnormal muscle tendon reflexes and extensor plantar responses. All the symptomatic carriers developed moderate-to-severe sensorineural hearing loss with normal stapedial reflexes and brain stem auditory evoked potentials (BAEPs) in those in whom this could be evaluated. Speech discrimination was disproportionally poor unilaterally in one case from whom no BAEPs could be obtained because of her degree of hearing loss. Various combinations were found of high gain of the vestibulo-ocular reflex, spontaneous nystagmus and directional preponderance of vestibularly evoked nystagmus, slowing, hypometria or multi-stepping of saccades, saccadic intrusions of eye movements (macro square wave jerks, double saccadic pulses), impairment of smooth pursuit eye movements and optokinetic nystagmus, and failure of visual fixation suppression of vestibularly evoked nystagmus. Such findings indicate major involvement of the (vestibulo)cerebellum and the vermis. MRI in one carrier showed mild cerebellar atrophy.
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PMID:Multi-system signs and symptoms in X-linked ataxia carriers. 886 31

Phenytoin is an anti-convulsant drug commonly used to prevent seizures in patients with cerebral metastases. Phenytoin has complicated non-linear kinetics, is highly protein bound and has a small window between its therapeutic and toxic dose. This combination of factors means that small increases in dosage can all too quickly result in high plasma levels and toxic symptoms. Symptoms of phenytoin toxicity include: confusion, nystagmus, agitation, abnormal gait and hallucinations. This case report describes phenytoin toxicity in a patient receiving phenytoin 300 mg three times a day for a number of weeks. The patient was admitted to the unit for terminal care, where his phenytoin levels were found to be very high. Phenytoin was withheld until levels returned to within the normal range. During this time the patient became orientated and many of his symptoms resolved.
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PMID:A case of phenytoin toxicity in a patient with advanced lung cancer. 1716 67

This open-label multicenter study evaluated the long-term safety and efficacy of intrathecal ziconotide and included 78 patients with chronic pain who had completed one of two previous ziconotide clinical trials. Each patient's initial ziconotide dose was based on his or her dose from the study of origin and was adjusted as necessary on the basis of adverse events and analgesic effect. The median ziconotide dose was 6.48 mcg/day (range, 0.00-120.00 mcg/day) at the Initial Visit and ranged from 5.52 to 7.20 mcg/day across all study visits. The most commonly reported new adverse events that were considered ziconotide related were memory impairment (11.3%); dizziness, nystagmus, and speech disorder (8.5% each); nervousness and somnolence (7.0% each); and abnormal gait (5.6%). There was no evidence of increased adverse event incidence at higher cumulative ziconotide doses. Elevations in creatine kinase were noted, but the proportion of patients with creatine kinase elevations did not change from the Initial Visit to the Termination Visit (4.1% each). Stable mean Visual Analog Scale of Pain Intensity scores during the three years of the study suggested no evidence of increased pain intensity with increased duration of ziconotide exposure. Long-term treatment with ziconotide appeared to be well tolerated and effective in patients whose response to ziconotide and ability to tolerate the drug had been previously demonstrated.
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PMID:Long-term intrathecal ziconotide for chronic pain: an open-label study. 1871 48

A 10-year-old male koala started to fall from the tree while sleeping. Subsequently, the koala often fell down while walking and showed a gait abnormality, abnormal nystagmus and hypersalivation. At 12 years of age, the koala became ataxic and seemed blind. At 13 years of age, the koala exhibited signs of dysstasia and was euthanased. Necropsy revealed marked symmetrical atrophy of the cerebellum. Histopathologically, a severe loss of Purkinje and granule cells was evident in the cerebellum, while the molecular layer was more cellular than normal with cells resembling small neurons, which were positively stained with parvalbumin immunohistochemistry. Reactive Bergmann glial cells (astrocytes) were present adjacent to the depleted Purkinje cell zone. The very late onset and slow progression of the cerebellar cortical degeneration in this case is particularly interesting and appears to be the first report in the koala.
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PMID:Late onset cerebellar cortical degeneration in a koala. 1967 52

Ziconotide is a conopeptide intrathecal (IT) analgesic which is approved by the US Food and Drug Administration (FDA) for the management of severe chronic pain. It is a synthetic equivalent of a naturally occurring conopeptide found in the venom of the fish-eating marine cone snail and provides analgesia via binding to N-type voltage-sensitive calcium channels in the spinal cord. As ziconotide is a peptide, it is expected to be completely degraded by endopeptidases and exopeptidases (Phase I hydrolytic enzymes) widely located throughout the body, and not by other Phase I biotransformation processes (including the cytochrome P450 system) or by Phase II conjugation reactions. Thus, IT administration, low plasma ziconotide concentrations, and metabolism by ubiquitous peptidases make metabolic interactions of other drugs with ziconotide unlikely. Side effects of ziconotide which tend to occur more commonly at higher doses may include: nausea, vomiting, confusion, postural hypotension, abnormal gait, urinary retention, nystagmus/amblyopia, drowsiness/somnolence (reduced level of consciousness), dizziness or lightheadedness, weakness, visual problems (eg, double vision), elevation of serum creatine kinase, or vestibular side effects. Initially, when ziconotide was first administered to human subjects, titration schedules were overly aggressive and led to an abundance of adverse effects. Subsequently, clinicians have gained appreciation for ziconotide's relatively narrow therapeutic window. With appropriate usage multiple studies have shown ziconotide to be a safe and effective intrathecal analgesic alone or in combination with other intrathecal analgesics.
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PMID:Safety and efficacy of intrathecal ziconotide in the management of severe chronic pain. 1970 62

The precise anatomy and physiology of human walking remains poorly understood. The frontal lobes appear crucial, and, on the basis of clinical observation, contribute to the control of truncal motion, postural responses, and the maintenance of equilibrium and locomotion. The rich repertoire of frontal gait disorders gives some indication of this complexity. Variable combinations of disequilibrium with a wide stance base, increased body sway and falls, loss of control of truncal motion, locomotor disability with gait ignition failure, start hesitation, shuffling, and freezing are encountered in diseases of the frontal lobes. Furthermore, the pattern of gait may change as the frontal disease progresses. The slowness of walking, lack of heel-shin or upper limb ataxia, dysarthria or nystagmus distinguishes the wide stance base from cerebellar gait ataxia. A lively facial expression, normal voluntary movements of the upper limbs, upper motor neuron signs, and the absence of a rest tremor distinguish the hypokinetic elements from Parkinson's disease. Poor truncal mobility, impaired postural responses, and falls after the slightest perturbation eventually make walking impossible even though simple leg movements may still be possible while seated or lying. One or more of these features usually predominates in the initial presentation of a frontal gait syndrome. Accordingly, there is considerable variation in the manner of presentation and evolution of frontal gait disorders. The gait syndrome is accompanied by frontal motor and cognitive changes, which may be subtle or overshadowed by the gait disorder. This complexity of clinical presentation accounts for the plethora of descriptions from "frontal ataxia" to "gait apraxia". As suggested in the original descriptions of frontal ataxia, the spectrum of gait disturbance is likely to be due to damage to frontal cortex and its connections with subcortical structures including the basal ganglia, cerebellum, and the brainstem.
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PMID:Frontal lobe ataxia. 2182 22

Paraneoplastic cerebellar degeneration associated with anti-Ri antibodies mainly presents with opsoclonus-myoclonus-ataxia. We report here the case of a patient with anti-Ri-antibody paraneoplastic syndrome, who presented four years after treatment for small-cell lung cancer (SCLC) with oscillopsia and gait disorder. On neurological examination vertical nystagmus, ataxic gait and postural tremor of all four limbs was detected. He died one year after the onset of the symptoms because of a acute exacerbation of his severe chronic obstructive pulmonary disease. No SCLC relapse or new cancer has been detected during the one-year follow-up period.To our knowledge, our patient is the first case of anti-Ri associated disorder with oscillopsia and vertical nystagmus as the initially prominent clinical features. The findings of this case study support the variability of anti-Ri-antibody-associated paraneoplastic syndrome. Further studies must be directed to better characterize the mechanisms underlying this syndrome. Finally, paraneoplastic neurological syndromes should be kept in mind also when a neoplastic disease is not demonstrated.
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PMID:Anti-Ri-associated paraneoplastic cerebellar degeneration. Report of a case and revision of the literature. 2202 93


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