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)

80 strictly selected patients with chronic renal insufficiency with plasma creatinine values of 1.4--14.5 mg% were examined according to a fixed scheme to determine the presence of symptoms and signs of renal encephalopathy. The general cerebral symptoms complained of were headache in 33.4% of the patient material, dizziness in 30.3%, easy fatigability in 62.5%, giddiness in 18.8% and insomnia in 37.5%. The most prominent neurological findings were hyperactive deep reflexes in 30% and action tremor in 23.8%. The symptoms of organic brain syndrome were impairment of memory in 32.5%, weakness of concentration in 28.8% and lability of affect in 63.7%. Diffuse EEG abnormalities were found in 26.2%. While the clinical neuropsychiatric symptoms did not show any statistically significant correlation with the various internal medical data, a trend was observed in the greater number of pathological EEGs with an increase in the impairment of renal function. Furthermore, there was a statistically significant correlation, (alpha less than or equal to0.015) between the occurrence of pathological EEGs and the plasma creatinine and BUN values. It is remarkable that the patients with abnormal EEGs had a relatively low mean creatinine level of 5.89 mg%. The strict dietetic management of the patients is regarded as one of the deciding factors for the relatively low frequency of neuropsychiatric symptoms in the material studied.
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PMID:Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention. I. CNS disturbances. 5 91

A family from Western Norway is described in which 5 out of 9 members in one generation developed a progressive encephalopathy in middle life. Massive, symmetrical calcifications located in basal ganglia, dentate nuclei and cerebral sulci of the brain were seen on roentgenograms of the skull. All affected members exhibited a clinical syndrome which included mental deterioration, extrapyramidal motor deficit, cerebellar ataxia and tremor. The biochemical investigation showed normal serum calcium and phosphorous and concentration of immunoreactive parathyroid hormone was normal. The Ellsworth-Howard test with exogenously administered parathyroid extract revealed a subnormal phosphorous diuresis while urinary excretion of cyclic AMP was normal. Thus, the defect appears to be an insufficient intracellular response to cyclic AMP. The late onset of symptoms is compatible with the slight disturbance in calcium-phosphorous metabolism we have demonstrated. The family probably represents an unusual type of pseudo-pseudohypoparathyroidism of which only one other family has been reported earlier. The investigations and pedigree analysis of the present kindred is suggestive of an autosomal recessive inheritance of the disorder.
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PMID:Cerebral calcinosis with late onset encephalopathy. Unusual type of pseudo-pseudohypoparathyreoidism. 20 54

Acute encephalopathy caused by gasoline sniffing is well recognized, but has been thought to be completely reversible. We report a patient who developed a progressive encephalopathy characterized by ataxia, tremor and dementia following repeated, deliberate gasoline inhalation. Blood and urine lead levels were consistently elevated and at autopsy, the formalin-fixed brain lead content was between 5200 and 6500 micrograms/100 gm of tissue. This case shows that repeated gasoline sniffing can result in irreversible encephalopathy and that both the acute and chronic encephalopathy probably result from organic lead intoxication and not from the gasoline itself.
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PMID:Acute and chronic progressive encephalopathy due to gasoline sniffing. 56 91

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

In rats with lymphostatic encephalopathy the duration of harmine tremor was lengthened, and the brain concentrations of harmine decreased more slowly than in sham-operated controls. The tremor began simultaneously in both rat groups at coinciding brain concentrations of harmine. In rats with lymphostatic encephalopathy harmine concentrations in brain at the termination of tremor lay in the same range as in sham-operated controls. The plasma concentrations of harmine were not changed by the disease. It is concluded that during lymphostatic encephalopathy the lymphatic drug elimination from brain is impaired whereas--at least for harmine--the blood-brain barrier functions as normal.
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PMID:Harmine action in rats with lymphostatic encephalopathy. 84 10

Acute myoclonic encephalopathy related to the ingestion of bismuth salts has been known for 3 years and would appear to be reversible. Of a total of 41 cases, 32 were observed for an average of more than a year. Alongside the commoner benign forms, there coexist severe forms, sometimes fatal, prolonged forms and complicated forms. Permanent deterioration, affecting memory above all, tremor, marked insomnia, headache and disturbed gait are amongst the most durable complications, sometimes definitive, whilst in four cases osteo-arthropathy of the shoulders was associated with permanent invalidism.
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PMID:[Bismuth myoclonic encephalopathies. Their course and lasting or definitive late complications]. 92 35

In normal and lymphostatic encephalopathic rats, aprotinin pretreatment alters the duration of the harmine tremor and the cerebral concentration of the alkaloid; low doses shorten the tremor and decrease the concentration, a high dose causes the opposite. Aprotinin may decrease or increase the blood-brain barrier permeability of harmine. Because the findings are similar in both groups of rats the blood-brain barrier for harmine is assumed to be intact in lymphostatic encephalopathy. However, sick rats possibly suffer from an impaired cerebral elimination of harmine.
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PMID:The effect of aprotinin on the harmine-induced tremor in lymphostatic encephalopathic and normal rats. 108 Jan 14

Two patients with acute encephalopathy with bilateral striatal necrosis are presented and the literature on the subject is reviewed. The disease is characterized by abrupt onset following a systemic infectious illness, with disturbance of consciousness, absence of speech, dystonic movements of the limbs, general stiffness, opisthotonus, tremor, facial grimacing, and stereotyped reaction to painful stimuli. After a variable period of time, there is gradual improvement of the neurological status with clearing of consciousness and recovery of motor functions. Mild CSF pleocytosis is the only abnormal laboratory test encountered. Cranial imaging shows from the beginning of the illness, bilateral involvement of the striatum that may persist indefinitely. The pathogenesis of this disorder remains unknown although an infectious or para-infectious mechanism seems to be the most likely possibility.
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PMID:Acute encephalopathy with bilateral striatal necrosis. A distinctive clinicopathological condition. 149 50

Clinical and laboratory findings are reported in nine patients who developed acute encephalopathy during the course of Lassa fever. The encephalopathy manifested 3-17 days after disease onset with confusion, followed rapidly by tremor (seven patients), grand mal convulsions (seven), abnormal posturing (three) and coma (eight); focal neurological signs and evidence of raised intracranial pressure were not seen. Eight patients died, most commonly from respiratory arrest following a protracted fit. Development of encephalopathy did not correlate with the presence of virus in cerebrospinal fluid (CSF), nor with virus antibodies in CSF and/or serum; thus, neither direct cytopathic nor immune-mediated mechanisms seem to be involved in its pathogenesis.
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PMID:Lassa fever encephalopathy: clinical and laboratory findings. 159 76

In recent years there are a considerable increase in alcohol consumption in Taiwan, which may have been accompanied by increased incidence of alcohol-related physical disease. This study was designed for an understanding of neurological problems in chronic alcoholic patients. One hundred and five cases of chronic alcoholics with neurological problems were collected. All had taken more than 100 g alcohol daily for more than 8 years. They were all males, with a mean age of 47.0 +/- 1.3 years, mean daily alcohol consumption of 185.1 +/- 9.0 g (mean +/- S.E.). These chronic alcoholic patients showed various neurological problems. Patients showing typical clinical features of alcoholic neurological disease are now rather rare. Most of the patients had manifestations of more than one problems: polyneuropathy (74.3%), alcoholic tremor (37.1%), hallucinosis (30.5%), myopathy (26.7%), head injury (24.8%), withdrawal seizures (18.1%), Wernicke encephalopathy (15.2%), paranoia (13.3%), and stroke (15.2%). Furthermore, we divided all the patients into 5 categories, they were: encephalopathy, 59 cases (56.2%); stroke, 16 cases (15.2%); cerebellar degeneration, 12 cases (11.4%); neuropathy, 78 case (74.3%); and myopathy, 28 cases (16.7%). The daily alcohol consumption and duration of daily drinking were different significantly (p less than 0.05) among five different syndrome categories.
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PMID:Neurological problems in chronic alcoholics. 165 33


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