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)

Two patients with movement disorders are described and neurochemically studied. The first subject concerns a central anticholinergic syndrome in a 83 years old man treated with l-dopa and amantadine for red nucleus tremor. The second one is an association of parkinsonism and chorea in a 76 years old woman presenting with FAHR's syndrome. In both cases, CSF HVA levels were measured before and after oral probenecid load. The observations confirm the usefulness of this neurochemical strategy in order to classify aging patients with parkinsonism into dopasensitive and doparesistant groups.
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PMID:Further observations showing the impact of the probenecid test in movement disorders. 401 57

Mean homovanillic acid and 5-hydroxyindoleacetic acid concentrations were significantly low in the lumbar CSF of a group of patients with disseminated sclerosis (DS) who were severely disabled but not in the CSF of a less severely restricted group with DS. CSF concentrations were also low in a group of patients with superior cerebellar peduncular tremor due to DS and in a single patient with a similar tremor associated with a post-traumatic brain-stem lesion. The interpretation of abnormal CSF amine metabolite concentrations is discussed in the light of these findings.
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PMID:Amine metabolites in the cerebrospinal fluid of patients with disseminated sclerosis. 484 38

Twelve cases of chronic sensorimotor neuropathy associated with benign IgM paraproteinaemia are described. The onset was in the sixth or seventh decades and 9 cases were male. Tremor and ataxia were common features. The ESR was raised in 6 cases and the CSF protein content elevated in 10. There was severe reduction of motor nerve conduction velocity. Sera from all cases contained monoclonal IgM antibodies strongly reactive with human peripheral myelin, made up by the paraprotein. Histological studies on nerve biopsies taken from 8 cases all demonstrated a demyelinating neuropathy. Eight biopsies were examined by immunofluorescence. Monoclonal IgM was present on the myelin sheaths of surviving myelinated nerve fibres. The findings suggested that the neuropathy was of autoimmune origin and caused directly by the antimyelin antibody.
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PMID:Chronic demyelinating neuropathy associated with benign IgM paraproteinaemia. 633 2

Clinical and neuropsychological findings, EEG, and several blood and CSF parameters were investigated in 36 patients with Alzheimer's disease (AD) and 35 patients with senile dementia of Alzheimer type (SDAT). There were more women among senile patients and more familial cases among presenile patients. The average duration of the symptoms was longer in presenile patients (6.1 years) than in senile patients (3.9 years). This could be due to the lower resistance to the disease process in the senile group. Extrapyramidal signs, especially rigidity, were found in over 60% of all patients and in practically all patients with advanced dementia. Tremor was found in three patients only. Four presenile (11%) and two senile (6%) patients had epileptic seizures. All patients had abnormal EEG recordings, mainly in form of diffuse slowing. A positive correlation was found between the EEG abnormality and the severity of dementia in AD but not in SDAT. However, the difference between the correlation coefficients in AD and SDAT was insignificant. Between EEG and the duration of the disease there was no correlation. EEG was not more abnormal in very severe dementia than in severe dementia. Other findings were similar in AD and SDAT. It is concluded that it is artificial to separate AD and SDAT at the age of 65 and that they clinically compose a single entity. This entity could well be called Alzheimer's disease.
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PMID:Alzheimer's disease and senile dementia of Alzheimer type. A comparative study. 711 68

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

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

After coronary angiography a 66-year-old man developed manifest hyperthyroidism (fT3 8.7 pg/ml, fT4 3.7 ng/dl) marked by tremor, restlessness and sweating. The hyperthyroidism was controlled by high dosages of thiamazole (240 mg daily) and lithium (24-36 mmol daily). But the white cell count dropped from 8,000/microliters to 4,900/microliters on the eighth day. Although the thiamazole dose was reduced to 40 mg daily, the granulocytopenia became more severe and, on the 24th day of treatment, agranulocytosis occurred (neutrophilic granulocyte count 200/microliters), although the thiamazole had been discontinued. The patient was then isolated and treated prophylactically with ofloxacin. Simultaneously he received 5 micrograms/kg granulocyte-colony stimulating factor (G-CSF) subcutaneously daily for 7 days. On the sixth day of this treatment the granulocyte count was 520/microliters, next day 3,800/microliters, and after a further 2 days it overshot to 31,000/microliters, then gradually returning to normal values. -It is recommended that the use of G-CSF should be considered also for thyrostatic-induced agranulocytosis, because it may shorten this dangerous phase.
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PMID:[Granulocyte colony-stimulating factor (G-CSF) in the early stage of thyrostatic-induced agranulocytosis]. 751 60

Potassium channel blockade by 4-aminopyridine (4-AP) has been shown to initiate modest levels of functional recovery in spinal-injured dogs and people following intravenous administration; however, the relevant central nervous system (CNS) concentration mediating these effects is not known. We have determined the concentrations of 4-aminopyridine in plasma and cerebrospinal fluid following intravenous administration (0.5 mg/kg) in large (> 22 kg) dogs, using liquid column chromatography. Plasma levels are initially high (> 1 microgram/mL) and fall rapidly to levels less than 100 ng/mL by about 2 h postinjection. A characteristic secondary peak in plasma 4-AP is observed at about 1 h postinjection. Corresponding concentrations of 4-AP in CSF were relatively stable for nearly 2 h, never exceeding (as a mean) 50 ng/mL within the first 2 h postinjection. We suggest behavioral recovery in clinical cases of spinal cord injury in both dogs and humans is mediated by such low (< 50 ng/mL) concentrations of 4-AP bathing the lesion. Since the adverse side effects that accompany IV administration of the drug limit its potential clinical usefulness, we have evaluated the feasibility of an alternate route of administration, continuous metered delivery of 4-AP into the spinal cord's subarachnoid space. This is accomplished by using a surgically implantable pump and delivery catheter. The pump itself can be interrogated, and is fully programmable, by noninvasive telemetry. Intrathecal delivery rates of between 1 and 60 micrograms of 4-AP per hour never produced detectable levels of the drug in plasma or cervically sampled CSF in dogs independent of the amount or duration of infusion (hours to days). The levels of 4-AP in lumbar samples of CSF near the lumbar delivery site suggest a very steep gradient of the drug, with local concentrations easily reaching 1 microgram/mL or higher (10- to 20-fold higher than can be safely produced by IV administration). The most frequent adverse reaction to intrathecal 4-AP delivery was a mild hindlimb tremor, fully reversible following reduction in the rate of drug delivery or termination of delivery. This route of drug administration relative to clinical spinal cord injury is discussed.
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PMID:Plasma and cerebrospinal fluid concentrations of 4-aminopyridine following intravenous injection and metered intrathecal delivery in canines. 778 31

A 70-year-old man was admitted to our hospital because of a 15-year history of walking difficulty, disturbance of sensation in the palm for 2 years and hand tremor for 6 months. On admission, the scapulohumeral muscles showed fasciculation and atrophy. There was action tremor in the upper limb, and the proximal lower limb showed atrophy and weakness. Standing and walking were impossible. Deep tendon reflexes were decreased in lower limbs. Pathologic reflexes were not found. There was distal dominant sensory disturbance, and urination was difficult. Needle EMG showed a neurogenic pattern in 4 all limbs. MCV and F-latency were delayed. SCV in the median nerve and the amplitude in the sural nerve were decreased. Biopsy of the sural nerve revealed both axonal change and demyelination. Biopsy of the quadriceps femoris muscle showed neurogenic change with helper T-cell infiltration. Anti-HTLV-I antibody and ATL-like cells in both blood and CSF were positive. There were HTLV-I provirus DNA with a polyclonal pattern and the type of HLA as HAM. The HTLV-I infection was of the HAM type. As the present patient showed mainly neuropathy without pyramidal signs, was not considered to have HAM.
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PMID:[HTLV-I-associated neuropathy]. 778 27

Ten patients with haematological malignancy receiving allogeneic transplants from donors other than HLA-identical siblings were prepared for marrow transplantation with antithymocyte globulin, cyclophosphamide 120 mg/kg and fractionated total body irradiation 12 Gy, and were given cyclosporin, methotrexate and prednisolone as prophylaxis against graft-versus-host disease post-transplant. The harvested T replete donor marrow was incubated with recombinant human (rh) GM-CSF 10 micrograms/ml (supersaturating concentration) for 1 h at 37 degrees C on a gently shaking rocker platform. After incubation the marrow was washed twice in 5% human serum albumin/normal saline and infused into the recipient. Before and after incubation, there was no significant difference in cell viability, the nucleated cell count, the CFU-GM content nor the proportion of cells in S phase of the cell cycle. Compared with a preceding cohort of 16 patients treated on the same protocol but in whom the marrow was not incubated with GM-CSF, there was no difference in the incidence of graft failure or rate of neutrophil recovery.
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PMID:Lack of efficacy of a short ex vivo incubation of human allogeneic donor marrow with recombinant human GM-CSF prior to its infusion into the recipient. 785 31


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