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)

The serotonin(5-HT) syndrome(SS) is a condition of both the central and peripheral 5-HTergic hyperstimulation, characterized by a constellation of 5-HT-related side effects(confusion, agitation, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering or tremor in the setting of the recent addition of 5-HTergic agents. The SS is produced most often by the concurrent use of monoamine oxidase inhibitors and other 5-HTergic agents. However, more recent reports suggest that the tricyclic antidepressant or selective serotonin reuptake inhibitor(SSRI) monotherapy induces the SS. Recently, for the operationalized assessment of both the presence and the severity of the core symptoms of the SS, Hegerl et al. developed the Serotonin Syndrome Scale(SSS) as a modification of the diagnostic criteria of the SS proposed by Sternbach. Since, in Japan, some novel 5-HTergic agents have been, and will be in use, recognition of the SS is quite important. Therefore, for clinical application of SSS, we prepared the Japanese-language version (JSSS).
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PMID:[The Japanese version of the serotonin syndrome scale (JSSS)]. 1087 22

A 68-year-old woman had a deep brain-stimulating electrode placed for worsening of a long-standing essential tremor. There is currently no data available on the use of electroconvulsive therapy (ECT) in the presence of the deep brain stimulator (DBS). We report here the successful use of ECT in this patient with no adverse effects to the patient or to the DBS. No special provisions were made with the ECT administration except to ensure that the stimulator was turned off prior to administration of the ECT series, and remained off through the eight treatments administered to this patient. Following the course of treatment, her mood was markedly improved, and she displayed only minor postictal confusion.
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PMID:ECT in a patient with a deep brain-stimulating electrode in place. 1100 51

Five individuals are described who had participated in a study of former dockyard painters. All had worked between 16 years and 45 years as industrial painters, much of the time inside ships. All underwent structured neurological examination, colour vision testing (allowing calculation of a colour confusion index corrected for age and alcohol), and detailed psychometric testing. An occupational history sufficient to allow estimation of past exposure to solvents was taken. All gave a history of exposure to high concentrations of solvents at work, and several described episodes of acute narcosis. All showed neurological deficits and some had overt neurological disease, although in no case had this previously been linked to their work. The most striking features, sufficient to constitute a syndrome, were acquired blue-yellow colour vision deficits, coarse tremor, impaired vibration sensation in the legs and cognitive impairment. Their estimated cumulative exposures to solvents ranged between the equivalent of 13 and 37 calendar years working at the Occupational Exposure Standard concentration (OES years). This study for the first time gives an indication of the concentrations of solvents likely to lead to serious neurological disease in humans. It serves as a reminder to physicians to take an occupational history from patients with obscure neurological or psychological impairment.
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PMID:Neurological deficits in solvent-exposed painters: a syndrome including impaired colour vision, cognitive defects, tremor and loss of vibration sensation. 1102 75

Hashimoto's encephalopathy is a poor understood neurological disorder associated with thyroid disease. We describe a 12 years old woman with a relapsing clinical picture characterized by acute onset confusion, tremor, convulsive seizures and a stroke-like episode associated with autoimmune thyroid disease. High titers of antithyroid antibodies were detected in her serum. Neurologic investigation showed a marked slowing of the basic activity in EEG, diminished perfusion of left hemisphere in brain SPECT, mild CSF protein level without pleocytosis, and normal brain CT and cerebral angiogram. The clinical course was favorable without corticosteroid therapy. Antithyroid antibodies and EEG were normal after one-year follow-up. We suggest that antithyroid antibody levels should be checked in any unexplained acute or subacute encephalopathy, especially when a relapsing course, stroke-like exacerbation, seizures, tremor or elevation of the CSF protein are found.
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PMID:[Hashimoto's encephalitis: a new case with spontaneous remission]. 1107 81

We report an unusual case of probable progressive multifocal leukoencephalopathy (PML), who initially presented with a right-sided movement disorder, including upper limb dystonia, tremor, and dyspraxia, reminiscent of corticobasal degeneration. In the further course, the patient developed disorientation, confusion, and bradyphrenia. The appearance of white matter MRI lesions as well as a positive PCR test result for JC-virus in the cerebrospinal fluid finally led to the correct diagnosis.
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PMID:A "cortico-basal degeneration"-like syndrome as first sign of progressive multifocal leukoencephalopathy. 1123 80

Psychiatric manifestations are infrequent or rarely described in Hashimoto's encephalopathy. It usually begins like a subacute diffuse encephalopathy with confusion, tremor and other neurologic symptoms. A relapsing course is characteristic. Neither biologic nor clinical symptoms are specific but high antithyroid antibodies levels are characteristic. The diagnosis can be seriously delayed by the fact that the different symptoms implicate approaches by psychiatrists, neurologists or endocrinologists. There are two clinical types. The one presented here evaluates progressively to dementia with psychotic episodes, confusion and seizures. An early steroid treatment makes the symptoms regress without aftereffects. We have analysed the clinical and biological findings of a woman who has been admitted to different neurologic and psychiatric departments before her diagnosis was made. First clinical presentation and evolution were that of a depression. Each time the antidepressive treatment was stopped, depression relapsed in spite of an appropriate steroid treatment. Literature shows that a close link exists between depression and antithyroid antibodies whatever thyroid status. This link does still exist after adjustment of psycho-social determinants of depression. The decrease of those antibodies only reflects the decrease of inflammation. So, for the psychiatrist it is important to diagnose Hashimoto's encephalopathy without delay, especially when psychiatric manifestations are in the foreground. Furthermore, a psychiatric report should systematically be added to the clinical and biological findings in order to make a better approach of the existing links between depression and other manifestations of the disease.
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PMID:[Depression, anti-thyroid antibodies and Hashimoto encephalopathy]. 1140 65

Since James Parkinson (1817) first characterized the shaking palsy as a unique condition, significant confusion has remained concerning the causes and treatments of Parkinson's disease (PD). Through the 19th century, a wide variety of approaches were attempted in an effort to reduce its cardinal signs--rigidity, tremor, and bradykinesia--but to little effect. Today, approaching 200 years after Parkinson's seminal work, this disorder is commonly treated by surgical means, inducing a lesion in one specific portion of a small nucleus in the central nervous system (Desaloms et al., 1998, Lang et al., 1999). The notion of providing a lesion to the nervous system as a therapy for PD, however, began in earnest at the beginning of the 20th century. The first attempt to alleviate the symptoms of PD through surgical means involved a section of the dorsal roots of the spinal cord supplying the affected limb (also known as dorsal rhizotomy). Although ultimately resulting in disastrous effects, these early surgical attempts proceeded from a firm body of clinical and experimental research on both the central and peripheral nervous systems. After briefly reviewing the use and failure of dorsal rhizotomy as a treatment for parkinsonian rigidity, this paper will examine the manner in which clinicians and scientists justified the procedure.
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PMID:Lesions as therapy: rigidity and Parkinson's disease. 1144 68

Besides the classic motor swings, many non motor fluctuations may occur in Parkinson's disease, but the clinical spectrum and the frequency of these symptoms are not well recognized. A total of 47 parkinsonian outpatients were questioned about any symptoms associated with off state. Nine patients had no fluctuations, 16 referred only to motor fluctuations and 22 to motor fluctuations associated with non motor symptoms. Overall, these patients referred to 54 symptoms (average 2.3/patients, range 1-6). These symptoms were classified as: autonomic (3 difficulty in swallowing, 7 hot, 11 sweat, 2 cold, 1 pallor, 1 abdominal bloating, 1 abdominal pain, 1 abdominal and genital pain, 5 bladder dysfunction, 2 feet oedema); sensory (7 sensory dyspnoea, 1 pain in lower limbs, 1 internal tremor); cognitive (3 depression, 4 anxiety, 2 panic, 1 drowsiness, 1 confusion). In patients without off periods, the length, severity and the average dosages of levodopa were fewer than in patients with fluctuations. No significant differences were found between patients with motor off and patients with associated non motor off regarding age (71.2+/-9.6 years vs 71.6+/-10.7 years), length of the disease (83.2+/-38.5 months vs 95.9+/-58.1 months), the Hoehn-Yahr (3.06+/-0.96 vs 3.02+/-0.96) and Webster (15.5+/-6.99 vs 15.1+/-5.9) scale, the dosages of levodopa (680.9+/-238.9 mg/die vs 679.7+/-289.6 mg/die), the number (2.3+/-1.7 vs 2.8+/-1.5) and length (6.8+/-5.2 h vs 7.2+/-7.1 h) of motor off. The non motor fluctuations were recognized in about 60% of patients with motor fluctuations: usually they were mild and less important than motor off, but sometimes these problems were disabling and led to unnecessary tests and therapies.
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PMID:Non motor off in Parkinson's disease. 1169 27

The clinical profile of neurotoxicity caused by immunosuppression has changed. When toxic levels are reached, both cyclosporine and tacrolimus may produce a clinical spectrum that varies from tremor and acute confusional state to status epilepticus and major speech or language abnormalities. Coma has become an unusual manifestation. Magnetic resonance imaging has been better defined, and abnormalities may be more widespread than those in the posterior lobes. These white matter lesions are caused by vasogenic edema, but may lead to apoptosis and cytotoxic edema if exposure is prolonged. Recent evidence suggests inhibition of a drug-efflux pump and dysfunction of the blood-brain barrier by enhanced nitric oxide production.
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PMID:Neurotoxicity of immunosuppressive drugs. 1169 28

We report a case of nefopam intoxication in a severely malnourished postoperative intensive care patient with profound hypoprotidemia. Nefopam induced agitation and confusion associated with anticholinergic symptoms such as tremor, hypertonia, mydriasis, and tachycardia. All these symptoms disappeared after withdrawal of the drug. Nefopam should be considered as a possible cause of confusion in postoperative patients.
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PMID:[A new cause of postoperative confusion syndrome: nefopam]. 1213 1


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