Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

The mutual enhancement of the side effects of muscular tremor and rigidity caused by lithium and neuroleptic drugs should be recognised. However, at present the 'case' for a neuroleptic-lithium interaction producing severe organic brain syndrome is arguably weak; in the absence of standardised sampling for monitoring lithium serum concentrations such reports may simply reflect 'pure' lithium intoxication rather than a drug interaction. Certainly it seems unwarranted in this connection to ascribe specific properties to haloperidol. A potentially high risk of interaction should be recognised between lithium and natriuretic diuretics, and other drugs and therapeutic measures affecting sodium balance. Such interactions may disturb stable treatment monitoring and give rise to the start of self-increasing lithium intoxication. The practical clinical importance of lithium interactions with neuromuscular blocking agents, phenytoin, carbamazepine, iodide salts and methyldopa is only weakly supported by the data available at this time. However, if simple prophylactic measures are available when such drugs are to be used in patients receiving lithium, for example temporary withdrawal of lithium, it may be prudent to take such steps.
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PMID:Lithium and drug interactions. 612 49

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16