Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0234376 (intention tremor)
 350 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a case of 89-year-old woman showing rhythmic skeletal myoclonus mainly on the right upper limb. This myoclonus appeared five days after the cerebral infarction. It was seen constantly both at rest and in posture, and decreased during voluntary movement. When the patient was under emotional stress, it spread to the submandibular, neck and trunks of upper limb. During sleep, this movement completely disappeared. There was no myoclonus in palato-pharyngo-laryngo-oculo-diaphragmatic muscle group. In the examination of the surface electromyography, the movement was not reciprocal between extensor and flexor muscles, and its cycle was about 3.5 Hz. It was different from the intention tremor because it did not increase during the movement phase on the finger nose test. The examination of MRI revealed a small infarction including right dentate nucleus and right superior cerebellar peduncle, and from which an infarction of the superior cerebellar artery territory was considered. Only a few cases of rhythmic skeletal myoclonus without palatal myoclonus have been reported in the literature. All of these cases had small infarction of the same region as the above case. Their myoclonus began 5 to 15 days after the onset of cerebral infarction. These periods were markedly shorter than that of intention tremor and palatal myoclonus. This fact suggest that the rhythmic skeletal myoclonus has a different mechanism from that of the palatal myoclonus.
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PMID:[Rhythmic skeletal myoclonus without palatal myoclonus]. 129 64

A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait ataxia and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
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PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49

We reported three cases with involuntary movements following pontine hemorrhage. All cases had various symptoms indicating brain-stem lesions, but the consciousness and motor functions were not severely disturbed. CT scans showed a small hematoma localized in unilateral pontine tegmentum in all cases. Intention tremor developed six to ten months after the hemorrhage when the initial neurological symptoms were almost relieved. Electromyogram (EMG) showed a rhythmic 3-4 Hz alternating or synchronized tremor pattern which was induced by finger-nose test and arm stretching. In one case which had showed bilateral horizontal gaze palsy indicating bilateral PPRF involvement in the acute stage, spontaneous vertical nystagmus was observed when the tremor developed. Electronystagmogram (ENG) and its differential calculus showed a pendular nature of the eye movement. This abnormal eye movement did not disappear while the patient was asleep. This case also developed a palatal myoclonus in the chronic stage. Magnetic resonance images (MRI's) obtained one to three years after the hemorrhage revealed a lesion localized in hemipontine tegmentum. The responsible lesion of these involuntary movements was thought to be located in pontine tegmentum from the MRI findings. The functional Prognosis of small hemorrhage in unilateral pontine tegmentum is generally good, but care should be taken for the possibility of late development of various types of involuntary movement.
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PMID:[Three cases of involuntary movements following pontine hemorrhage]. 319 Sep 36

In 58 patients with progressive supranuclear palsy (PSP), 19 (32.8%) had CT, MRI, or autopsy evidence of a multi-infarct (MI) state. The clinical findings in the infarct syndrome were similar to idiopathic PSP. Five MI-PSP patients had had a stroke, four had focal dystonia, two had hemiparesis, and one had an intention tremor of recent onset. In contrast, only 5.9% (12.9% of those with CT or MRI) of 426 Parkinson's disease patients had evidence of strokes. One case of PSP studied pathologically was attributed to cerebral amyloid angiopathy.
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PMID:Progressive supranuclear palsy and a multi-infarct state. 356 71

A 49-year-old woman was admitted to Utsunomiya Saiseikai hospital complaining of right breast swelling. There was half a year history of difficulty in walking. A diagnosis of breast cancer was made by biopsy. Neurological examination revealed scanning speech, nystagmus, intention tremor and ataxic gait, but brain CT scan and MRI showed neither metastatic, invasive lesions nor atrophy in the brain. Lumpectomy for breast cancer was performed. For immunocytochemical studies, the cytoplasm of neurons in sections of normal human cerebral cortex, cerebellum, spinal cord and dorsal root ganglia were stained by the patient's serum, but glial cells were not. Upon Western blot, the patient's serum reacted with a 40-kDa protein in extracts of both cerebrum and cerebellum obtained from normal rats. A diagnosis of paraneoplastic cerebellar degeneration (PCD) was made on the basis of clinical manifestations and detection of the antineuronal antibody. The antibody accompanying the breast cancer which stained neuronal cytoplasm and bound to a 40-kDa protein may be a subtype of antibody causing PCD.
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PMID:[Antineuronal autoantibody to a 40-kDa protein in a patient with cerebellar ataxia and breast cancer]. 761 51

We described two types of involuntary movement accompanied with a well-located thalmaic lesion shown by MR imaging in five patients. All patients had the involuntary movements of an upper limb contralateral to the thalamic lesion. Two patients (1 and 2) had choreoathetosis that became most prominent when their index finger approached their nose, where irregular and dysynchronous oscillation occasionally superimposed. This choreoathetosis was differentiated from pseudoathetosis caused by disturbance of proprioceptive sensations. The MRI lesion was located at the middle level of thalamus including nucleus centromedianus. The other three patients (3, 4 and 5) had a regular and rhythmic oscillation in their forearm. The oscillation began to appear after their index finger reached their nose on finger-to-nose test. We considered the oscillation as a postural tremor based on its rhythmicity and regularity. Patient 4 had additional tremor in movement. Their postural tremor continued while the arm kept the position. Surface electromyogram showed the reciprocal discharges between the forearm extensor and flexor muscles with a frequency of 3 to 4 Hz. This tremor was not accentuated during limb movement toward the nose nor was coarse, and was distinguished from intention tremor described by Charcot and Dejerine. This tremor was also different from hyperkinesis volitionnelle and movement oppositionist. The "rubral tremor" differed from the tremor shown in our cases for a lack of resting tremor. The responsible lesion shown by MRI located at caudal posterior thalamus including pulvinar in patient 3, or located at the upper level of thalamus in patient 4 and case 5 that was more rostral than the lesion of the choreoathetosis cases. In cases of cerebrovascular accidents, both types of involuntary movement appeared after several months from the stroke. This delayed appearance suggests that these involuntary movements were the result not only of functional disturbance of thalamus, but of secondary repairing mechanism occurring at the lesion.
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PMID:[Involuntary movements caused by thalamic lesion]. 799 88

Two female cases, 23- and 21-year-old, of supravalvular aortic stenosis associated with cerebellar hypoplasia, retinitis pigmentosa and myopathy were reported. No family history of mental retardation and cardiovascular anomalies was found. There was no consanguinity between the parents. Pregnancy, labor and delivery were reported to be uncomplicated. When they visited to our hospital at the age of 13 and 11 years, they had short stature, characteristic facial appearance (eg, wide mouth, elongated philtrum, low nasal bridge and broad forehead) and supravalvular aortic stenosis. Neurological examination disclosed mental retardation, retinitis pigmentosa, muscle wasting and contracture of bilateral knee and ankle joints. Gait was unsteady and bradykinetic. Their smooth pursuiting ocular movements were saccadic. No nystagmus was recorded. Mild intention tremor was present. The muscles were slightly hypotonic, but deep tendon reflexes were hyperactive in the lower extremities. The sensory system was normal. Results of chromosome analysis and urine amino acid analysis were normal. The serum creatine kinase was elevated to 1,000-3,000 U. Muscle biopsy revealed nonspecific myopathic changes such as variability of fiber diameter in both fiber types. Neither cell infiltration nor deposits of fat or glycogen was found. Cranial MRIs performed at the age of 22 and 20 years disclosed cerebellar hypoplasia and moderate enlargement of the fourth ventricle. The two cases resembled clinically those of Williams syndrome, but the MRI findings were not consistent with those of the syndrome. The disorder is considered to be either Williams syndrome complicated by some other relatively rare clinical features, or another heredofamilial disease partly resembling Williams syndrome.
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PMID:[Myopathy, cerebellar ataxia and Williams syndrome like features in siblings]. 819 69

This population-based study refers to 78 Swedish children with non-progressive ataxia from a total population of 3.1 million inhabitants. Inclusion criteria were ataxic gait without any signs of spasticity, dyssynergia, dysmetria and intention tremor. CT and/or MRI studies were available from 70 patients (90%). Infratentorial pathology was revealed in 27%, and findings were considered normal in 61%. If CT was normal, of recent date and of good quality, MRI did not add any new information. In half of the cases with pathological CT, however, MRI provided new information. The origin was considered prenatal in 45% (familial in 17%), perinatal in 4% and unclassifiable in 51%. 60% were mentally retarded; in the rest, cognitive development was near normal (18%) or normal (22%). Speech development was delayed in 88%, and 58% had visual dysfunction.
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PMID:Non-progressive ataxia: origins, brain pathology and impairments in 78 swedish children. 864 34

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

We describe five patients presenting with high fever and isolated cerebellar gait ataxia. In all these patients, neurological examination revealed dysmetria, intention tremor and postural tremor during sustained posture, all restricted to the legs. Brain MRI was normal. In four of these patients, the recording of leg tremor during sustained postures showed a 3-Hz frequency. Cerebellar gait ataxia resolved within 3-10 days. We suggest that the ataxic gait was due to a reversible dysfunction of the spinocerebellar part of the anterior lobe.
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PMID:Reversible cerebellar gait ataxia with postural tremor during episodes of high pyrexia. 888 94


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