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)

The differential diagnosis of an acute peripheral vestibulopathy ("vestibular neuritis") and of an ischemic lesion in the cerebellar territory of the posterior-inferior cerebellar artery (PICA) is important. Both present with acute vertigo, vomiting, spontaneous nystagmus and difficulties in walking. We analyze the clinical, oculographic and NMR findings as well as the outcome in 10 patients with an ischemic stroke in the cerebellar territory of the PICA. On clinical grounds alone, it is not always possible to attribute the acute vestibular syndrome to a peripheral vestibular lesion or to a PICA insult. In our experience an important feature of a PICA insult is a discrepancy between the amount of vertigo, the severity of the walking difficulties, and the often weak and rapidly resolving spontaneous nystagmus. In contrast to a peripheral vestibulopathy, the vestibuloocular reflex is only minimally or not decreased in PICA insults, and gain asymmetries are accounted for by the presence of spontaneous nystagmus. However, only neuroimaging can finally differentiate between the two entities.
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PMID:[Acute vestibular syndrome in cerebellar infarct of the posterior inferior cerebellar artery (PICA infarct)]. 872 Jul 25

Clinical and MRI investigations were carried out on 27 patients with acquired pendular nystagmus in an attempt to delineate possible sites of lesions responsible for pendular nystagmus and mechanisms underlying the frequent ocular disconjugacy of this nystagmus. The aetiologies were multiple sclerosis (n = 21), brainstem stroke (n = 3) and other neurological conditions. In at least 59% of the patients, pendular nystagmus appeared > 1 year after the first symptom of the disease. Patients MRIs were characterized by multiple areas of abnormal signal and were analysed statistically to identify areas where lesions overlapped significantly between patients. Statistically significant overlap occurred in areas containing the red nucleus, the central tegmental tract, the medial vestibular nucleus and the inferior olive. Patients with horizontal pendular nystagmus showed predominantly pontine lesions whereas patients with torsional pendular nystagmus showed predominantly medullary involvement. The nystagmus was conjugate in 15 patients and disconjugate in amplitude or direction in 12. Internuclear ophthalmoplegia or asymmetrical visual acuity occurred in similar proportions in both groups. Patients with conjugate pendular nystagmus had a higher incidence of symmetrical, "mirror image' lesions on MRI than patients with disconjugate nystagmus. The abundance of abnormal MRI signals in our sample suggests that large or multiple structural lesions may be required to elicit pendular nystagmus, predominantly in the pons but also in the midbrain and medulla. The involvement of structures projecting to the inferior olive supports the hypothesis that oscillatory properties of olivary neurons causes the rhythm of pendular nystagmus. The delay observed between the onset of the underlying disease and the pendular nystagmus supports a mechanism operating via neural deafferentation. Disconjugancies in pendular nystagmus cannot be explained on the basis of the associated internuclear ophthalmoplegias nor on the basis of asymmetrical visual acuity. The association between symmetrical MRI lesions and conjugate nystagmus suggests that asymmetrical damage to brainstem structures concerned with binocular alignment may underlie disconjugate pendular nystagmus.
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PMID:Clinical and MRI correlates in 27 patients with acquired pendular nystagmus. 880 Sep 42

To get a better insight into the clinical differentiation between vertigo of cerebrovascular origin and of aural origin, we investigated radiologically proven stroke patients who presented with vertigo as an initial clinical manifestation. Of 154 stroke patients, 30 patients with vertigo (20%) had the relevant lesion, demonstrated with the initial computerized tomographic scan (13 patients) or the follow-up magnetic resonance imaging (MRI) study (17 patients) of the brain. Every lesion was in the vertebrobasilar arterial territory; 19 in the cerebellum, 8 in the pons, and 3 in the medulla oblongata. Although 12 of the 30 patients (40%) presented with vertigo in isolation at the onset of stroke, eight patients (27%) developed additional neurologic abnormalities from four hours to seven days later. Patients with isolated vertigo (13%) had the small lesion exclusively in the cerebellum of the PICA medial branch territory. The most frequent accompanying neurological sign was swaying in the cerebellar and medullary lesion, and dysarthria in the pontine lesion. The direction of nystagmus or swaying did not match the lesion side in some patients. Our findings suggest that cerebellar stroke may commonly manifest isolated vertigo or vertigo with swaying mimicking labyrinthine disorder, particularly at the onset of the disease. MRI study and tests for truncal ataxia and lateropulsion may be crucial for the detection of vertigo of cerebrovascular origin.
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PMID:Vertigo of cerebrovascular origin proven by CT scan or MRI: pitfalls in clinical differentiation from vertigo of aural origin. 896 9

We present a case of persistent hiccups (singultus) after a lateral medullary cerebrovascular accident. The patient presented with a two-day history of nausea and vomiting. Clinically, the patient had a loss of pain and temperature on the left side of the face, a loss of pain and temperature on the right side of the trunk, a mild left hemiparesis, and a left-sided ataxia. Nystagmus, diplopia, and hiccups were also evident. A left lateral medullary syndrome in the vascular distribution of the posterior inferior cerebellar artery was diagnosed. Work-up included a magnetic resonance imaging angiogram, which revealed an occlusion v high-grade stenosis of the basilar artery. The patient reported that the most distressing symptom was the chronic hiccups (25/min), which interfered with nutrition, sleep, and activity. While in the acute care hospital, the patient was treated with prochlorperazine, promethazine, and chlorpromazine. Each of these medications was unsuccessful in stopping the hiccups. After a search of the European literature revealed that baclofen was recommended as the drug of choice for stopping persistent hiccups, the patient was given 5 mg of baclofen by mouth three times per day, and the hiccups abated within 48 hours. The baclofen was discontinued after one week of therapy, and the hiccups did not return. We recommend consideration of baclofen for the treatment of persistent hiccups after lateral medullary syndrome because of its desirable side effects and reported success rate compared with other drugs used to treat chronic hiccups.
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PMID:Hiccups associated with lateral medullary syndrome. A case report. 912 21

The therapeutic efficacy of a regimen consisting of intravenous injection of Cardiocrome, containing cytochrome c, flavin mononucleotide and thiamine diphosphate for mitochondrial encephalomyopathy (MEM) was examined. This combined therapy was applied to nine patients with MEM, including four with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes. For the standard regimen, Cardiocrome was first injected daily, usually for 4 weeks, and later by means of intermittent injections for maintenance treatment. Clinical improvement was obtained in eight of the patients. Improvement was observed in the muscle symptoms of easy fatigability, motor disability and severity of stroke-like episodes, as well as in various other symptoms such as phosphate, tinnitus, headache, corneal edema, chilblains, thalamic pain, respiratory failure, and nystagmus. This clinical improvement was maintained for more than 1 year by additional intermittent injections. In conclusion, this therapy was fairly effective for the management of patients with MEM.
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PMID:Treatment of mitochondrial encephalomyopathy with a combination of cytochrome C and vitamins B1 and B2. 918 76

Stroke caused by occlusion of an intracranial artery following blunt head trauma is a rare event. Traumatic dissections of the middle cerebral artery have been reported while thrombosis is very rare. We describe a case of fatal thrombosis of the left middle cerebral artery that occurred in the time interval between 2 and 6 hours after an apparently minor head trauma in a motor vehicle accident. The 25-year-old woman was in normal health on admission to the hospital. Two hours later the patient manifested nystagmus and vomiting. Six hours later she was aphasic with right hemiparesis. Twenty-four hours later the patient was comatose. A third CT scan performed at that time showed a wide infarct of the left cerebral hemisphere and a hyperdense left middle cerebral artery. The patient died 5 days after the collision. The autopsy confirmed the presence of the cerebral infarct and revealed thrombosis of the left middle cerebral artery. Microscopically, the transverse rupture of the intima and of the elastic lamina along the whole circumference of the vessel was found at the beginning of the thrombosed tract. We conclude that the blunt head trauma caused a partial rupture of the wall of the left middle cerebral artery with consequent thrombosis of the vessel and cerebral infarct. Based on the anatomy of the middle cerebral artery and on the review of the morphological literature we propose that the 2 types of lesion, the dissection and the thrombosis, that may follow closed head trauma, might depend on a common denominator that is the primitive rupture of the intima and elastic lamina.
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PMID:Middle cerebral artery thrombosis following blunt head trauma. 949 32

We prospectively studied motor symptoms in 32 patients with CT- or MRI-proven acute pure parietal stroke. A transient, mild, 'pseudoparesis' of the hand (90%), was noted, improved by visual attention and prompting, associated with non-awareness of muscle power (53%), transient soft pyramidal signs (50%), unilateral akinesia (100%) and motor hemineglect (37%) in non-dominant lesions. Lower motoneurone-type atrophy was not observed in this acute phase. We called 'poikilotonia' the striking unpredictable variations in muscle tone, ranging from extreme hypertonia to hypotonia, found in all patients. When maintaining postures, patients showed large oscillations (100%), laterodeviation or levitation of the arm (60%), especially in the case of large or posterior lesions, or, occasionally (3%), motor persistence or even hemicatalepsy (3%). Limb kinetic and manipulatory apraxia, with inadequate organization and anticipation of motor sequences and synergies, motor arrests, perplexity, unrecognizable gestures and loss of bimanual coordination, was a constant finding (100%). Other apraxias (62%) and difficulty in copying intransitive gestures of the hand (84%) were associated with posterior lesions involving the supramarginal gyrus. When reaching towards objects, all patients showed abnormal anticipatory hand shaping, but visuomotor ataxia (3%) was only seen with bilateral posterior stroke. Sensory (70%) or pseudocerebellar (4%) ataxia, was seen in both anterior and posterior lesions. Avoidance behaviors (34%) were not uncommon, but had no localizing value. Of the dyskinesias, hand dystonia (84%) was frequent, but athetosis (16%), asterixis (15%), postural tremor (15%), myoclonus (9%) and stereotypia (9%), were uncommon. The abnormal eye movements were unilateral hypo-akinesia of exploratory saccades (43%), abnormal ipsilateral pursuit and contralateral optokinetic nystagmus in the case of posterior lesions, and oculomotor apraxia with bilateral posterior lesions. In conclusion, parietal motor syndrome can be recognized during bedside examination, and probably reflects the loss of multiple sensory feedback to motor programs, especially those directed to the extrapersonal space.
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PMID:Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively. 987 53

Caloric stimulation induced a transient reversal of multimodal hemispatial cognitive deficits in an 81-year-old woman with an acute left cerebral hemisphere stroke. The patient had unawareness of her right hand (asomatognosia), right-sided visual unawareness (hemineglect), aphasia and right-sided weakness (hemiplegia) prior to the stimulation. Transient improvements in impaired sensory, motor, linguistic and cognitive function developed within 30 s following application of the caloric stimulus and onset of horizontal nystagmus. The effect persisted for 3 min and ceased completely after 5 min. While several recent reports have described the capacity of caloric stimulation to transiently improve or reverse a wide range of attentional, cognitive and motor impairments, most examples are in right-hemisphere-damaged patients with long-standing brain injury. Typically, patients have been tested several months or years after the onset of the deficit. A possible mechanism for the temporary reintegration of multiple cognitive functions in this patient is discussed.
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PMID:Does vestibular stimulation activate thalamocortical mechanisms that reintegrate impaired cortical regions? 1009 98

The purpose of the present investigation was to determine the effect of galvanic vestibular stimulation on visuo-spatial neglect without inducing nystagmus and associated discomfort. Fourteen patients with right-hemisphere stroke with neglect were assessed with two visuo-motor tasks ("Line crossing" and "Star cancellation") on three occasions. Seven of the subjects received galvanic vestibular stimulation during the second condition (Experiment 1), whereas the other seven received stimulation during the third assessment (Experiment 2). Between-group comparisons of stimulation effects were performed by analyzing change on visuo-spatial neglect from the first to the second condition in the two experimental groups. A significantly larger effect was demonstrated on the "Line crossing" task in Experiment 1. This finding suggests a stimulation effect beyond practice/spontaneous recovery, and may provide new possibilities in rehabilitation research because the stimulation can be given without discomfort.
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PMID:Reduction of visuo-spatial neglect with vestibular galvanic stimulation. 1038 Jul 28

A 60-year-old hypertensive woman had a pontine hemorrhage that caused slight right hemiplegia, deep sensory disturbance on her right side and dysarthria. Three months after the stroke, she was transferred to our hospital for rehabilitation. Approximately 6 months later, she gradually began to complain of the visual oscillation. Continual, unceasing conjugate vertical/rotatory eye movements were observed. Fixation was momentary at best because of an inability to dampen the spontaneous eye movements. Electrooculography (EOG) showed bilateral vertical/rotatory sinusoidal eye movements of 2.5 Hz frequency and 10- to 35-degree amplitude. Both vertical and horizontal optokinetic nystagmus were absent. Caloric stimulation did not evoke any responses bilaterally. There were no rhythmical movements at similar frequencies in other parts of the body such as palatal myoclonus. MRI revealed not only hematoma mainly at the dorsal pontine tegmentum but also hypertrophy of the inferior olive nucleus, suggesting disruption of the central tegmental tract. Lesions of this tract may be one cause of pendular nystagmus. Several drug therapies were investigated for the nystagmus. There was no response to baclofen 15 mg. Trihexyphenidyl 4 mg was discontinued because of drug-induced hallucinations. Tiapride 600 mg and phenobarbital 90 mg were each slightly effective in reducing both frequency and amplitude of nystagmus. Treatment with clonazepam 1 mg resulted in the striking disappearance of nystagmus. She was aware of this and no longer experienced oscillopsia. Despite the visual benefit, however, the patient did not wish to continue this drug because of drowsiness and muscle relaxation. The potential long-term therapeutic application of clonazepam should be further investigated. To our knowledge, there have been no reports of successful treatment in acquired pendular nystagmus with clonazepam. Therefore, based on this favorable experience, it is suggested that clonazepam should be added to the list of potential therapies for pendular nystagmus.
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PMID:[Acquired pendular nystagmus after pontine hemorrhage]. 1065 2


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