Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doctors, nurses, and medical and nursing students administered a questionnaire on memory disturbances, tremor and clumsiness in their first-degree relatives who live or lived near them. We obtained data on 1,479 relatives, of whom 805 were alive and 674 had died. Of those alive and older than 65, 8.69% had severe memory disturbances, 1.11% a parkinsonian syndrome and 5.59% essential tremor. Of those who had died, 10.68% had suffered from severe memory disturbances before they died. The results of both groups are similar and in accordance with the data in the literature. In our opinion this new type of epidemiological study can be very useful in diseases which are easily detected by nonspecialists and in areas with hospitals and medical schools.
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PMID:A new type of epidemiological study: questionnaire administered by medical personnel. 129 94

A case with cortico-basal degeneration was reported with special reference to the immunohistochemical study. A 59-year-old housewife noted tremor and clumsiness of her left hand. On the initial examination she showed the hyperreflexia of the upper extremities and jaw jerk, parkinsonian symptoms such as Myerson sign, parkinsonian gait and rigidity in the left arm. She showed pronounced forced grasping in the left hand. At the age of 60 she showed a WAIS scale with verbal IQ of 99 and performance below the scale. She could not copy hand postures. Tremor was aggravated by action or anxiety, more prominent on the left hand. There was some incoordination on the finger-nose testing of left arm and on the knee-heel testing of both legs. She also showed homolateral dyskinesia. She had a left Babinski sign and sensory testing was normal. A CT scan showed slightly enlarged ventricles (Fig. 1). At the age of 61 she could not understand simple requests and speak few words spontaneously, showing severe dysarthria. There were palilalia and motor impersistence. CT scan showed more widening of the lateral ventricles. At the age of 62, she had lingual dyskinesia and tapping on her upper lip provoked myoclonic jerk on her arms. She died of pneumonia at the age of 65 years, 6 years from the onset. The brain weighed 1190 g. There were bilateral old subdural hematomas on the right parietal and occipital lobe and the left parietal lobe. There was atrophy of frontal and superior parietal region.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Widespread tau abnormality in a case of cortico-basal degeneration]. 129 53

Rubral tremor is a distinct clinical entity as described by Gorden Holmes. We have reported here a 44 years old woman with rubral tremor appearing about 2 months after an embolic attack of vertebral-basilar artery. On neurological examination there were left homonymous hemianopsia, dysarthria very mild weakness of left upper and lower limbs with clumsiness of her left lower limb and the tremor of the left upper limb. Muscle tone was increased in her left upper limb with dystonic posturing. The tremor of her left upper limb was present at rest with regular rhythm of 2.8 Hz. This tremor included the reciprocal movements such as radial and ulnar flexion of the left wrist and independent movements of different fingers. It was accentuated by postural adjustment and by guided voluntary movements and disappeared during sleep. Surface EMG demonstrated that the grouping discharge was seen not only alternatingly but also synchronously between agonists and antagonists. A brain MRI image revealed multiple lesions including right thalamus and left cerebellum. No lesions were detected in brain stem. On the basis of MRI, it was questionable whether the lesion involved the dentate nucleus in the left cerebellum although the lesion was located at the medulla near the dentate nucleus extending from the cortex. So-called rubral tremor could be generated in lesions of cerebello-rubro-thalamic system without rubral lesion itself.
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PMID:[Symptomatological rubral tremor caused by vertebral-basilar artery embolism]. 180 67

A 42 year old man presented with a slowly progressive gait disturbance, generalised weakness, dysarthria, clumsiness and tremor of his hands, and involuntary jerks. Hexosaminidase A activity in plasma, leucocytes and fibroblasts was considerably reduced, establishing the diagnosis of GM2 gangliosidosis. Clinical examination showed two previously unreported features, a clinically evident sensory neuropathy and internuclear ophthalmoplegia.
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PMID:An adult onset hexosaminidase A deficiency syndrome with sensory neuropathy and internuclear ophthalmoplegia. 183 93

A genetic study of idiopathic focal dystonias was undertaken by examining 153 first-degree relatives of 40 index patients with torticollis (14 patients), other focal cranial dystonias (16 patients), and writer's cramp (10 patients). Nine relatives with dystonia were identified in 6 families; 8 of these had symptoms such as clumsiness or tremor, but none were aware of any dystonia. A further 4 relatives, now decreased, were affected by history. Overall, 25% of index patients had relatives with dystonia. The results of segregation analysis suggested the presence of an autosomal dominant gene or genes with reduced penetrance as a common cause for focal dystonia. Segregation ratios were not significantly different from those ratios observed in generalized or segmental dystonia in the United Kingdom, and it is possible that a single autosomal dominant gene mutation is responsible for inherited dystonia in the majority of patients irrespective of distribution or severity.
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PMID:A genetic study of idiopathic focal dystonias. 204 48

Micrographia due to focal cerebral disorder is very rare. We described a patient with micrographia due to a left putaminal infarction. Following an infarction involving the left putamen and corona radiata, a 58-year-old right-handed man developed micrographia with the right hand, right facial palsy, right hand clumsiness and slight aphasia. Micrographia finally disappeared by the seventh month. No parkinsonian features were noted. Our case suggests that micrographia is a disorder of the motor control system of handwriting which exists in the contralateral putamen, and has no relation with extrapyramidal signs like rigidity, tremor or akinesia.
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PMID:[A case of micrographia with the right hand due to left putaminal infarction]. 259 41

Three placebo-controlled double-blind and crossover trials were carried out to analyze the effects of oral yohimbine (YOH) 0.8 mg/kg on mood and performance in 16 healthy students. Subjective assessments (visual analogue scales, side-effects on questionnaire) and objective measurements (digit symbols, flicker fusion, tapping, heterophoria) were done at baseline, and post treatment. YOH shifted the healthy subjects' mood towards feeling panicked, elevated systolic blood pressure and plasma prolactin concentrations, reduced digit symbol substitution, and induced drowsiness and passiveness. Caffeine (CAF) 10 mg/kg raised plasma cortisol and rendered the subjects slightly panicked. Muzziness, clumsiness, tremor, chills and nausea were common after both YOH and CAF. Diazepam (DZ) 0.3 mg/kg given at 60 min antagonized some effects of CAF but failed to antagonize YOH. Clonidine (CLO) 100 micrograms counteracted YOH effects on blood pressure but less the subjective and hormonal effects. CLO 200 micrograms partly antagonized the pressor, sedative but not the hormonal responses of YOH. DZ counteracted YOH effects on plasma cortisol on panic but not on other subjective measures or plasma prolactin. Since CLO did not abolish YOH-induced prolactin increase, it is suggested that these effects of YOH are mediated not only via adrenergic alpha 2-receptors; other mechanisms made important contributions.
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PMID:Anxiogenic effect of yohimbine in healthy subjects: comparison with caffeine and antagonism by clonidine and diazepam. 315 10

The presenting symptoms of Wilson disease and its natural history as related to age are described based on 283 cases collected in Japan. The disease presented with a variety of signs and symptoms; the most frequent were in order of frequency jaundice, dysarthria, clumsiness, tremor, drooling, gait disturbance, malaise and arthralgia. The mean age at onset of the disease was 12.0 years. Hepatic and osteoarthral symptoms developed early and neurological symptoms late. Fifty-eight cases developed neurological symptoms only, 28 cases had hepatic symptoms only, and in 26 cases hepatic symptoms were followed by neurological symptoms. A higher mortality rate was observed in hepatic, hepato-haematological and hepato-renal cases mainly due to acute hepatic failure resulting in death only a few weeks after onset. Cases having only neurological symptoms showed a more favourable prognosis with a longer survival.
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PMID:Presenting symptoms and natural history of Wilson disease. 359 45

We have studied a large family of which seven members suffer from a progressive disease with onset in the first decade. The first symptoms were gait ataxia and clumsiness in all cases, followed by progressive development of severe distal amyotrophy reminiscent of Charcot-Marie-Tooth disease. In four patients a postural tremor which was relieved by pharmacological agents was also evident in the limbs or head. Cerebellar atrophy was confirmed on CT scan. Motor nerve conduction velocities were in the low normal range, while sensory nerve conduction was markedly decreased. All patients had impaired proprioception and vibration sense. The laboratory investigation revealed a normal CSF protein level and elevated serum bilirubin. The patients reported in this study apparently suffer from an original recessive form of spinal and olivocerebellar degeneration associated with a neuronal form of Charcot-Marie-Tooth disease.
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PMID:Study of a family with progressive ataxia, tremor and severe distal amyotrophy. 721 50

1. Very little is known about the behaviour of children in their second year and even less in their Peer-group. Aggressive behaviour among peers seems to be established at this age and it is interesting to observe it within the Peer-groups. 2. A useful definition of aggression seems to be the following one: Aggression is any physical contact, direct or indirect, by which another person is hurt. 3. We observe five different forms of aggression: 3.1 Aggression by chance, without any aim, happening out of awkwardness and motoric clumsiness. This kind of aggression becomes rarer during the second year. 3.2 Manipulating one another, as shaking arm or leg of another child, pulling his hair, tapping his body and so on, giving the impression of the aggressor exploring his partner. This kind of aggression also becomes rarer during the second year. 3.3 Robbery of objects, i.e. toys being in the hands of another; the reaction of the victim is increasing during the second year. 3.4 Aggression in order to control the group and to establish leadership in connection with the development of a group hierarchy. 3.5 Pathologic Aggression, observed on a child of the group with brain dysfunction. The child overthrows others from behind, climbs on them and bites them in the ear, the neck or the cheek. 4. We still need more observation on Peer-groups of this age to know more about the beginning and development of the here described phenomena.
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PMID:[Aggression in peer groups during the second year of life]. 731 89


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