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)

A 63-year-old man was admitted to our hospital with tremor and somnolence, followed soon by coma. Anemia and retinal bleeding were observed. The blood smear exhibited rouleaux formation and leukoerythroblastosis. A bone marrow aspiration resulted in dry tap. The biopsy specimens revealed remarkable infiltration of myeloma cells with fibrosis. The M-component of IgG-lambda type and hyper-ammonemia were detected in the serum. Liver and renal functions, however, were within normal range. His consciousness recovered after plasmapheresis. Two courses of VMCP (vincristine, melphalan, carboquone and prednisolone) did not affect the paraproteinemia. Five courses of VAD (vincristine, adriamycin and dexamethasone) could lower the level of IgG. He died of pneumonia. The plasma of some patients with multiple myeloma may contain unidentified factors which increase the plasma ammonia.
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PMID:[Coma, hyperviscosity syndrome, hyperammonemia and myelofibrosis in a patient with IgG, lambda type multiple myeloma]. 250 73

Infection of cattle with various stocks of Trypanosoma brucei rhodesiense indicated that 49% developed a fatal CNS disease comparable to that found in man. Duration of disease ranged from 85 to 1613 days post infection. All eight stocks of T. b. rhodesiense tested, including those from Ethiopia and Tanzania, induced CNS disease. Blood became positive three to five days after inoculation, and after an initial peak of parasitaemia remained positive for three to five months. Subinoculation of blood into rodents subsequently became negative, although trypanosomes persisted in the lymph nodes for at least 56 to 1613 days. Only animals with CNS disease had detectable parasites in the CSF, usually after the animals had undergone severe deterioration. At post mortem examination trypanosomes could usually be found in the lymph nodes and CSF, and occasionally in the blood. Clinical signs included fever, hyperkinesia, weight loss, cerebellar ataxia, tremor, salivation and hyperaesthesia. A mild to moderate anaemia accompanied a transient thrombocytopenia and leucopenia. Animals subsequently developed leucocytosis. A pleocytosis and elevated total protein in the CSF was found, which persisted in some animals for long periods. Histopathological examination of the brain showed prominent generalized perivascular infiltrates consisting mainly of lymphocytes and plasma cells. Mott's cells were regularly observed. Vascular changes were characterized by swollen endothelium, infiltration of the vascular wall by inflammatory cells, and in some instances perivascular oedema. In the most severe cases evidence of ischaemia consisted of large numbers of astrocytes, rarefaction of the parenchyma, and areas of necrosis with loss of normal architecture. Demyelination was limited to perivascular areas. Occasionally a moderate to severe pancarditis was found.
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PMID:Experimental infection of cattle with Trypanosoma brucei rhodesiense. 261 88

Slc/ddY mice (10 male, 10 female per group) were given a single p.o. intubation of tris (1,3-dichloro-2-propyl) phosphate (TDCPP) in olive oil and were observed for 14 days. LD50 values of male and female mice were 2.67 (2.52 approximately 2.83) and 2.25 2.25 (2.12 approximately 2.39) g/kg, respectively. The animals revealed ataxic gait, hyperactivity, and convulsion. Slc/ddY mice (12 male, 12 female er group) were administered diet containing 1.33, 0.42, 0.13, 0.04, and 0.01% of TDCPP for 3 months. Male and female mice of the 1.33% group showed emaciation, rough hair, and tremor; and all animals died within one month. Hematological studies showed slight anemia in males of the 0.42% group and females of the 0.42% and 0.13% groups. They also exhibited a tendency to increase ALP and GPT levels. The animals of the 0.42%, 0.13% and 0.04% groups exhibited tendency to increase liver weights and kidney weights in both sexes. Histopathologically, very slight focal necrosis was recognized in the liver in only 2 females of the 0.42% group. The NOEL under this condition is 0.01% in the diet of tris (1,3-dichloro-2-propyl) phosphate (male: 13.2 mg/kg/day, female: 15.3 mg/kg/day).
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PMID:[Acute and subacute toxicity studies of tris (1,3-dichloro-2-propyl) phosphate on mice]. 263 31

A 6 week old girl from a socially isolated family presented with seizures and was found to have a full fontanelle, retinal and subhyaloid haemorrhages, and anaemia. These findings were not the result of a shaking injury but of a ruptured intracerebral arterial aneurysm.
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PMID:Spontaneous subhyaloid and retinal haemorrhages in an infant. 378 95

A 43-year-old male was referred by a veterinarian who evaluated his dog for a seizure and suspected a toxic lead exposure for both. He refurbished houses, removing old paint, and complained of decreased cognition, fatigue, and muscle cramps. He had a depressed affect, postural tremor, right arm weakness with partial denervation on EMG, and borderline-low sensory nerve action potential (SNAP) amplitudes. A mild anemia and elevated serum and urine lead levels supported a diagnosis of lead neuropathy. Chelation therapy increased urine lead excretion without symptomatic improvement. His brother worked part-time with him and developed similar findings, but also had difficulty chewing, dysphagia, perioral twitching, gynecomastia, and multifocal denervation of extremity and facial muscles. His lead levels were not elevated, but an androgen receptor mutation identified on the X chromosome for both brothers confirmed the diagnosis of X-linked bulbospinomuscular atrophy (Kennedy's disease).
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PMID:X-linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy. 817 Apr 88

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial juvenile parkinsonism with dementia and autonomic failure--a case report]. 833 79

Seven related Bernese Mountain Dogs developed a syndrome Characterized by progressive cerebellar and hepatic disease. Clinically, stiffness in the hind limbs, mild incoordination, and a slight head tremor were first noticeable when pups were 4 to 6 weeks old. The condition progressed, causing pups to assume a wide-based stance. Other signs included head bobbing, spontaneous nystagmus, and, finally, paresis. Hematologic findings included leukocytosis with a left shift; normocytic, normochromic anemia; hypoproteinemia, low serum creatinine, and urea nitrogen concentrations; excessive fasting plasma ammonia concentration; and an increase in concentration of serum bile acids. Portal venography performed on 1 dog revealed a small liver and extensive extrahepatic varicosities. Necropsy revealed cerebellar hypoplasia, nodular liver, extensive abdominal varicosities, and ascites. Histologically, degeneration and depletion of Purkinje's cells and vacuolation, degeneration, and nodular regeneration of hepatic tissues were evident. Preliminary analysis of the pedigree was suggestive of an autosomal recessive pattern of inheritance.
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PMID:Clinical, hematologic, and biochemical features of a syndrome in Bernese mountain dogs characterized by hepatocerebellar degeneration. 863 71

Our previous studies showed that the passage of the Friend virus complex through rats generated variant MuLVs, designated PVC111, PVC211, PVC321 and PVC441, that induced neurological disorders associated with tremor and paralysis. In this study, we tested the pathogenicity of four different PVC viruses in mice. Although histopathological studies revealed spongiform degeneration in the spinal cords of NFS mice infected with each PVC virus, only PVC441 frequently induced tremor and paralysis. After a long latency, all of these viruses induced leukemia associated with severe anemia. Further studies with PVC441 revealed dose- and age-dependence for tremor induction. In contrast to NFS mice, BALB/c, DBA/2 and C57BL/6 mice infected with PVC441 virus showed no neurological symptoms, although the virus could be isolated from the tissues of central nervous system. Despite the absence of neurological symptoms, a high degree of neuronal degeneration in the lumbar spinal cord was found in PVC441-infected BALB/c mice. A low degree of neuronal degeneration was found in PVC441-infected DBA/2 or C57BL/6 mice. Genetic crosses of these resistant mice with susceptible NFS mice indicated that resistance to tremor induction by PVC441 was dominant in all mouse strains and suggested that various host genes may control the susceptibility of mice to tremor induction by PVC441 virus.
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PMID:Factors affecting induction of neurological disorders in mice by paralysis-inducing Friend-related PVC viruses. 874 Dec 58

Following several years absence from clinical follow up, an 18-year-old female on diet therapy for phenylketonuria presented with spastic paraparesis, tremor, disorientation, slurred speech, distractibility, deteriorating mental function and megaloblastic anaemia (Hb 64g/l mean corpuscular volume 121). Plasma phenylalanine levels were 100-600 mumol/l for the first 18 months of life but thereafter, because of serious psycho-social factors, > 1200 mumol/l. Her diet had strictly excluded all meats, eggs and dairy products but she had been ingesting her medical food (Lofenalac) only irregularly. Further investigation revealed a vitamin B12 level of 65.8 pmol/l (normal 150-670). Treatment with oral B12 quickly corrected her anaemia and there was a gradual improvement in speech, gait, tremor, disorientation and mood but mild spastic diplegia remained. This case prompted us to survey 37 adolescent and young adult phenylketonuria patients in our clinic -28 were on diet therapy, 9 were off (age 11-35 years, mean 21.6 years, 17 males, 20 females). Those on diet were not under ideal metabolic control. Six (16%) had subnormal serum B12 levels (< 150 pmol/l) and another six had borderline low values (150-200 pmol/l). None had specific neurological signs of subacute combined degeneration. Serum methylmalonic acid and homocysteine were not measured. On the basis of this survey we recommend that complete blood count, serum B12, RBC folate, methylmalonic acid and homocysteine be routinely measured in adolescents and young adults with phenylketonuria.
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PMID:Vitamin B12 deficiency in adolescents and young adults with phenylketonuria. 882 32

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99


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