Cases reported "Tremor"

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1/504. mercury toxicity due to the smelting of placer gold recovered by mercury amalgam.

    A 19-year-old man developed tremor in both hands and fatigue after starting work at a placer gold mine where he was exposed to mercury-gold amalgam. Examination revealed an intention tremor, dysdiadochokinesis and mild rigidity. The 24-h urinary mercury concentration reached a peak of 715 nmol/l (143 ug/l) shortly before the clinical examination, after which he was removed from working in the gold room [mercury No. Adverse Effect Level: 250 nmol/l (50 ug/l)]. On review 7 weeks later his tremor had almost resolved and the dysdiadochokinesis and rigidity had gone. The 24-h urinary mercury concentration had fallen to 160 nmol/l (32 ug/l). The principal exposure to mercury was considered to be the smelting of retorted gold with previously unrecognized residual mercury in it. The peak air concentration of mercury vapour during gold smelting was 0.533 mg/m3 (mercury Vapour ACGIH TLV: 0.05 mg/m3 TWA). Several engineering and procedural controls were instituted. This episode occurred at another mine site, unrelated to Mount Isa Mines Limited. ( info)

2/504. Osmotic demyelination syndrome with two-phase movement disorders: case report.

    Osmotic demyelination syndrome (ODS) is characterized by regions of demyelination throughout the brain, which are most prominent in the pons. This demyelinating disease is associated with electrolyte disturbances and typically occurs in patients who are alcoholic or malnourished. movement disorders are not frequently recognized in patients with ODS. This report describes a 22-year-old woman with ODS after correction of profound hyponatremia. The main neurologic symptom was two-phase movement disorder. First, she had acute onset dystonia, then the movement disorder transformed to generalized rigidity and tremors in the delayed second phase. magnetic resonance imaging in the first phase revealed demyelinating lesions in the central pons, bilateral thalami and basal ganglia. In the second phase, the previous myelinolysis had been partially resolved. The clinical course of the two-phase movement disorder did not correlate with the resolving feature of neuroradiologic findings. During the second-phase movement disorder, the patient had a good response to propranolol and trihexyphenidyl. ( info)

3/504. neurophysiology of orthostatic tremor. Influence of transcranial magnetic stimulation.

    A 74-year-old patient suffers from painful muscle cramps when he stands since 30 years. He has no visible tremor but 16 Hz burst activity on EMG, indicating orthostatic tremor. Previous diagnosis was hysteria, stiff person syndrome or dystonia. This shows that EMG during standing should be part of the examination of patients with stiff muscles or muscle cramps. Tremor was not strictly orthostatic. It appeared in back muscles while sitting, when the patient supported a weight with outstretched arms. Phase between muscles differed between normal standing and standing on heels. Subthreshold transcranial magnetic stimulation modulated timing of the tremor bursts and inhibited them at higher intensity stimulation. ( info)

4/504. Anticonvulsant-induced dyskinesias: a comparison with dyskinesias induced by neuroleptics.

    anticonvulsants cause dyskinesias more commonly than has been appreciated. Diphenylhydantoin (DPH), carbamazepine, primidone, and phenobarbitone may cause asterixis. DPH, but not other anticonvulsants, may cause orofacial dyskinesias, limb chorea, and dystonia in intoxicated patients. These dyskinesias are similar to those caused by neuroleptic drugs and may be related to dopamine antagonistic properties possessed by DPH. ( info)

5/504. Tremor and seizures associated with chronic manganese intoxication.

    Tremor and seizures developed in a 2-year-old girl receiving total parenteral nutrition. T1-weighted images on MRI revealed areas of hyperintensity in the basal ganglia, brainstem and cerebellum. blood manganese was elevated. The symptoms and MRI abnormalities disappeared after withdrawal of manganese administration. The recommendation of daily parenteral manganese intake was discussed. ( info)

6/504. levodopa may improve orthostatic tremor: case report and trial of treatment.

    Primary orthostatic tremor is a regular fast lower limb tremor causing unsteadiness on standing. Treatment is generally unsatisfactory. A patient with primary orthostatic tremor who 9 years later developed levodopa responsive idiopathic Parkinson's disease is described. The patient exhibited the classic features of primary orthostatic tremor with relief of the tremor by walking or sitting while treated with levodopa. However, in the "off" state, when the benefits of levodopa disappeared, this orthostatic tremor was continuous and severely compromised the patient's gait. On the basis of this finding eight patients with primary orthostatic tremor were treated with levodopa. Five patients experienced benefit and elected to remain on long term treatment. This study is the first trial of therapy in primary orthostatic tremor and suggests that levodopa can lead to good symptomatic relief in this potentially disabling condition. ( info)

7/504. essential tremor in Papua, New Guinea.

    The clinical features of 175 cases of essential tremor are related. This disorder is prevalent among a population of the Eastern Highlands of papua new guinea. It affects predominantly women in middle and old age; only 27 per cent of the cases were males. The disorder is slowly progressive and significant disability appears in elderly women when the trunk muscles are involved. Epidemiological studies have shown that the presence of tremor can be correlated with linguistic distinctions between high and low prevalence populations. Although only 30 patients reported a first degree relative with tremor, the syndrome would seem to stem from a genetic predisposition. In a number of patients essential tremor appeared to be associated with Parkinson's disease. ( info)

8/504. Tremor induced by toluene misuse successfully treated by a Vim thalamotomy.

    A 22 year old man developed a vigorous tremor of 5 Hz in his right hand, after a 7 year history of toluene misuse. T2 Weighted MRI depicted marked decreases in the signal intensity of the basal ganglia, red nucleus, and thalamus on both sides. The stereotactic coagulation of the left nucleus ventrointermedius (Vim) of the thalamus abolished the tremors in his right hand. This patient clearly exhibited the pathological involvement of rubral lesions in generation of a toluene induced tremor on MRI. toluene induced tremor is an irreversible symptom which persists even after stopping toluene misuse, therefore in medically intractable cases, it should be positively treated by a Vim thalamotomy. ( info)

9/504. Unusual presentation of spinal cord compression related to misplaced pedicle screws in thoracic scoliosis.

    Utilization of thoracic pedicle screws is controversial, especially in the treatment of scoliosis. We present a case of a 15-year-old girl seen 6 months after her initial surgery for scoliosis done elsewhere. She complained of persistent epigastric pain, tremor of the right foot at rest, and abnormal feelings in her legs. Clinical examination revealed mild weakness in the right lower extremity, a loss of thermoalgic discrimination, and a forward imbalance. A CT scan revealed at T8 and T10 that the right pedicle screws were misplaced by 4 mm in the spinal canal. At the time of the revision surgery the somatosensory evoked potentials (SSEP) returned to normal after screw removal. The clinical symptoms resolved 1 month after the revision. The authors conclude that after pedicle instrumentation at the thoracic level a spinal cord compression should be looked for in case of subtle neurologic findings such as persistent abdominal pain, mild lower extremity weakness, tremor at rest, thermoalgic discrimination loss, or unexplained imbalance. ( info)

10/504. Clinical genetics of familial progressive supranuclear palsy.

    Recent studies have shown that progressive supranuclear palsy (PSP) could be inherited, but the pattern of inheritance and the spectrum of the clinical findings in relatives are unknown. We here report 12 pedigrees, confirmed by pathology in four probands, with familial PSP. Pathological diagnosis was confirmed according to recently reported internationally agreed criteria. The spectrum of the clinical phenotypes in these families was variable including 34 typical cases of PSP (12 probands plus 22 secondary cases), three patients with postural tremor, three with dementia, one with parkinsonism, two with tremor, dystonia, gaze palsy and tics, and one with gait disturbance. The presence of affected members in at least two generations in eight of the families and the absence of consanguinity suggests autosomal dominant transmission with incomplete penetrance. We conclude that hereditary PSP is more frequent than previously thought and that the scarcity of familial cases may be related to a lack of recognition of the variable phenotypic expression of the disease. ( info)
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