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)

beta-blockers have been accepted as a reasonable adjunct therapy for the treatment of hyperthyroidism. They lessen the sympathetic symptoms such as tachycardia and finger tremor. On the other hand, many studies have demonstrated a decrease in 3, 3', 5-triiodothyronine (T3) during treatment with beta-blockers (especially propranolol). The purpose of this study is to clarify the effect of arotinolol (alpha 1, beta-blocker) on the thyroid functions and autonomic nerve systems (ANS) of patients with Graves' disease. Arotinolol 20mg a day p.o. was given to untreated patients with Graves' disease (n = 16) for 2 weeks. Blood sampling and the ANS function-tests were done before and after the treatment. In addition, the in vitro effects of arotinolol on the cAMP production and the radioactive iodine uptake (RAIU) using rat thyroid cell line FRTL5 were evaluated to examine the direct influence on thyroid cells. Arotinolol improved hyperthyroid symptoms including tachycardia, but had no effect on ANS function-tests. It is of interest that not only T3 but also T4 decreased after the arotinolol treatment. We therefore suspected the direct suppressive effects of arotinolol on the thyroid. There were, however, no in vitro inhibitory effects on the cAMP production and the RAIU in TSH-stimulated FRTL5 cells. The reason why serum T4 levels in patients with untreated Graves' disease have decreased after the treatment of arotinolol could not be clarified. In conclusion, arotinolol is a very useful drug for the initial therapy of patients with Graves' disease to reduce the serum thyroid hormone levels and symptoms of hyperthyroidism when combined with antithyroid drugs.
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PMID:[The effect of arotinolol on the thyroid function and the autonomic nerve systems]. 768 Jun 18

A case of hyperthyroidism occurring in a 68 year old man receiving lithium carbonate (1 g/day) for 5 years is reported. The clinical history of the patient, treated for bipolar affective disorder, was remarkable for transient hypothyroidism followed several months later by tremor, increased free thyroxine and triiodothyronine, and decreased TSH levels which led to lithium withdrawal. Two months later, clinical and biological signs were unchanged, Tc99m-scan displayed a homogeneous and increased isotope uptake. In this setting, high levels of autoantibodies against TSH-receptor, and grade I exophthalmos and slightly ocular muscle enlargement at CT-scan favored the diagnosis of Graves' disease (perhaps facilitated by lithium therapy). Carbimazole treatment was effective in controlling hyperthyroidism. Review of the literature disclosed 44 cases of hyperthyroidism occurring in lithium-treated patients. Most of these cases concerned specific thyroid diseases, particularly with an autoimmune mechanism. There is also evidence for an actual role of lithium in increasing intrathyroid iodide pool and for an impact of lithium on the immune system. Thus, the hypothesis that lithium may trigger the development of an autoimmune thyroid disease in predisposed patients deserves further investigation.
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PMID:[Lithium therapy and hyperthyroidism: disease caused or facilitated by lithium? Review of the literature apropos of a case of hyperthyroidism preceded by transient hypothyroidism]. 808 84

Intracerebroventricular (icv) injection of propidium iodide (PI) in the rat results in a transient movement disorder characterized by nystagmus, ataxia, and shaking. In the present study we used c-Fos as a marker for neuronal activation to investigate the neural substrate underlying this movement disorder. PI was injected into the lateral cerebral ventricle of freely moving rats through a previously implanted cannula. Animals were perfused 3 h after the injection and the brains were processed for c-Fos immunocytochemistry. Paired control animals were injected with saline. After PI injection, a significant Fos expression was seen in the cerebral cortex, thalamic midline nuclei, thalamic intralaminar nuclei, hypothalamus, central gray, pontine nuclei, locus coeruleus, vestibular complex, inferior olive, ventrolateral medulla, nucleus of solitary tract, and deep cerebellar nuclei. Few or no Fos immunoreactive cells were seen in the above structures of the control animals. The present study indicates that a large number of neurons located in many different neural structures are activated following icv injection of PI. Second, consistent with the cerebellar feature of the movement disorder, a major Fos expression was found in the cerebellar circuitry (deep cerebellar nuclei, pontine nuclei, vestibular complex, and inferior olive). It reinforces further the assumption that the movement disorder is due to cerebellar dysfunction caused by PI.
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PMID:Neural substrate of a cerebellar movement disorder induced by intracerebroventricular injection of propidium iodide in the rat: a Fos immunocytochemical study. 830 26

The effects of nicotinic and beta-adrenergic receptor antagonists on tail-tremor induced by repeated nicotine administration were investigated in rats. The daily administration of nicotine (0.5 mg/kg/day, s.c.) for 8 days resulted in an augmentation of tail-tremor. However, repeated administration of dimethyl phenyl piperazinium iodide (1 mg/kg/day, s.c.) for 8 days did not cause tail-tremor. Mecamylamine (0.5 mg/kg, i.p), administered before the nicotine injection on each day, abolished the tail-tremor. After discontinuation of the mecamylamine treatment, nicotine injections caused tail-tremor augmentation. Propranolol (20 mg/kg, i.p.), administered before the nicotine on each day, suppressed the appearance of tail-tremor. After the discontinuation of propranolol treatment, the degree of tail-tremor induced by a single injection of nicotine on day 9 was much greater in the propranolol-treated group than in the saline-treated control group. Neither carteolol (20 mg/kg, i.p.) nor metoprolol (20 mg/kg, i.p.) treatment showed such effects. Intraspinal injection of 6-hydroxydopamine markedly enhanced the tail-tremor induced on the first day of nicotine injection. This effect became more intense on subsequent administration of nicotine. The enhanced tail-tremor following 6-hydroxydopamine treatment was abolished by mecamylamine (0.5 and 1 mg/kg, i.p.), and was suppressed by propranolol (5-20 mg/kg, s.c.) in a dose-dependent manner. These results suggest that central nicotinic receptors are essential for the onset and for the further development of tail-tremor induced by the repeated administration of nicotine, and that beta 2-adrenoceptors are associated with the tremor mechanism. Moreover, spinal noradrenergic mechanisms may be involved in the manifestation of this phenomenon.
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PMID:Role of central nicotinic and beta-adrenergic receptors in the onset and further development of tail-tremor induced by repeated nicotine administration to rats. 915 Dec 94

Stereotactic surgery for Parkinson's disease can be performed using different neuroimaging methods. Ventriculography has been used to locate the coordinates of the structures close to the third ventricle. Although it has several potential disadvantages related to the intraventricular injection of iodine contrast, it is considered a precise method. Computed tomography and magnetic resonance imaging have been used in some centers. In order to compare their efficacy, 50 stereotactic thalamotomies for Parkinson's disease were performed using either ventriculography (VE) (25) or magnetic resonance imaging (MRI) (25). In 14 out of 25 VE procedures, computed tomography (CT-scan) was also used and showed a significant mean difference of coordinate Y and Z. The clinical results employing either VE or MRI were similar, with 80% abolition of tremor in the VE group, and 84% in the MRI group, after a follow up period of at least 3 months. Another 12% of VE and 16% of MRI group showed significant improvement of tremor. Complication rate was 4% in both groups. MRI-guided stereotactic thalamotomy in Parkinson's disease has shown good clinical results, comparable to VE-guided stereotaxis.
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PMID:Comparison of MRI-guided and ventriculography-based stereotactic surgery for Parkinson's disease. 962 3

Iodine-123-beta-CIT (2 beta-carbomethoxy-3 beta-(4-iodophenyl)tropane) binds with high affinity to dopamine (DA) and serotonin (5-HT) transporters. This study examined the correlation of single-photon emission computed tomographic (SPECT) measures of [123I]beta-CIT binding to DA and 5-HT transporters with symptom severity in Parkinson's disease (PD). Forty-six L-dopa-responsive PD patients (Hoehn-Yahr stage 1-3) had SPECT scans at 20-24 h after injection of [123I]beta-CIT. Specific to nondisplaceable uptake ratios (designated V"3) were calculated in the striatum and hypothalamic/midbrain region, where the binding of [123I]beta-CIT is associated primarily with DA and 5-HT transporters, respectively. Striatal V"3 was significantly correlated with Hoehn-Yahr stage and total, motor and activities of daily living scores of Unified Parkinson's Disease Rating Scale (UPDRS). There was a significant correlation between the sum of lateralizing motor UPDRS subscores (tremor, rigidity, bradykinesia) calculated for each side of limbs and V"3 values in the contralateral striatum. No significant correlation was found between striatal V"3 and UPDRS rating of mentation, behavior, and mood. Hypothalamic/midbrain V"3 was not significantly correlated with either Hoehn-Yahr stage or UPDRS scores including both motor and nonmotor measures. The significant correlation of SPECT measures of striatal [123I]beta-CIT binding with motor severity suggests that [123I]beta-CIT binding to striatal DA transporters can serve as an in vivo indicator of disease severity in PD, with potential utility in the serial monitoring of disease progression.
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PMID:SPECT measurement of iodine-123-beta-CIT binding to dopamine and serotonin transporters in Parkinson's disease: correlation with symptom severity. 1031 33

Between January 1996 and September 1997 we treated 4 patients with iodine-induced thyrotoxic storm (2 females, 2 men; age 54-77 years). Iodine contamination was due to iodine-containing contrast media in 3 patients and iodine-containing disinfectant in 1 patient. Thyroid storm with tachycardia, hypertension, sweating, tremor, weight loss and coma occured 3-10 weeks after iodine contamination. These symptoms were accompanied by raised fT4- and fT3-values. All 4 patients were initially treated with antithyroid drugs for 7 days, whereas 2 patients with coronary artery disease, demonstrated by coronary angio-graphy, were treated with antithyroid drugs for 2 weeks. Because of unsuccessful antithyroid drug treatment, all 4 patients underwent subtotal thyroidectomy. There were no perioperative complications. We conclude that early thyroidectomy is the appropriate treatment for iodine-induced thyrotoxicosis even in patients with severe accompanying diseases.
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PMID:Thyroidectomy in iodine induced thyrotoxic storm. 1059

In a previous study, we speculated that some of the high mercury levels observed in head hair from a total of 14 subjects who resided around Lake Victoria, Tanzania, might be attributable to the habitual use of toilet soap containing considerable amounts of mercury (Harada et al. Sci Total Environ 1999;227:249-256). In August 1998, the current study was conducted to investigate if such mercury-containing soap was also available in the surroundings of Lake Victoria, Kenya, and if so, its toxic effects. A total of nine goldminers, 44 fishermen and their families, and 12 residents of Kisumu City, Kenya, volunteered for the study. Fourteen types of toilet soap were collected in Kisumu. Total mercury content was very significantly higher than in European-made soap (0.47-1.7%, as mercury iodide) compared with Kenya-made soap (0.41 x 10(-4)-6.2 x 10(-4)%). Indeed, all the subjects with a high hair mercury level (> 36.1 ppm) had made habitual use of European-made soap, accompanied by various symptoms, such as tremor, lassitude, vertigo, neurosthenia, and black and white blots, suggesting inorganic-mercury poisoning. On the other hand, any subject who had used soap other than the European-made soap, did not exceed a mercury level of 10 ppm in hair that is well within normal limits (Harada et al. Sci Total Environ 1999:227:249-256). The findings obtained suggest that the mercury-containing soap must be barred from circulation without delay, and that the residents' health in addition to the environmental pollution in Lake Victoria (Kenya as well as Tanzania) should be kept under close observation.
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PMID:Wide use of skin-lightening soap may cause mercury poisoning in Kenya. 1130 39

Iometopane [(123)I beta-CIT, GPI 200, RTI 55], a tropane derivative labelled with iodine-123, is a dopamine imaging agent that was under development with Guilford Pharmaceuticals (as Dopascan Injection) for the early diagnosis of Parkinson's disease. Neurochemical imaging with iometopane using conventional single photon emission computerised tomography (SPECT) provided images of the brain for the distinguished diagnosis of Parkinson's disease. The ability of iometopane to bind to the dopamine transporter on presynaptic dopaminergic nerve terminal in the striatum (caudate nucleus and putamen) has been used to differentiate the uptake of the agent by the neurons in the striatum in patients with a Parkinsonian disorder (Parkinson's disease and progressive supranuclear palsy) from patients without a Parkinsonian disorder (essential tremor and healthy controls) with high sensitivity and specificity. The diminished uptake of iometopane in the striatum on the SPECT images of patients with a Parkinsonian disorder can be applied to assess both disease trait and disease state (severity) reflected by the severity of the brain dopamine neuron loss. The rate of clinical progression of Parkinson's disease varies greatly and is currently unpredictable. Imaging with iometopane provides the opportunity to evaluate patients longitudinally from early to late disease using an objective biomarker for dopamine nerve cell degeneration. Diagnostic imaging with Dopascan Injection is thought to differentiate Parkinson's disease from other forms of tremor, eliminate tests such as MRI and CT scans, unnecessary and inappropriate medications (psychotropics), and significantly reduce the number of people remaining on Parkinson's disease medications for life, despite not having Parkinson's disease. Guilford Pharmaceuticals acquired the licence for iometopane from the Research Triangle Institute, US, and sub-licensed it to Daiichi Radioisotope Laboratories for marketing, sales and distribution in Japan, Korea and Taiwan. In July 2003, Daiichi Radioisotope Laboratories paid a milestone payment of $0.55 million to Guilford after filing an application for approval in Japan. In January 2002, Guilford signed an exclusive European development, marketing and sales and distribution agreement for iometopane with MAP Medical Technologies of Finland. Under the terms of the agreement, MAP Medical Technologies will assume responsibility for regulatory approvals, manufacturing, marketing and selling the agent in all member states of the EU and other selected markets. In return, Guilford will receive an upfront payment, milestone payments and royalties on future sales in these territories. In July 2002, MAP Medical Technologies become a subsidiary of Schering AG. In March 2002, Guilford Pharmaceuticals sublicensed iometopane to Molecular Neuroimaging LLC (MNI) of Connecticut, USA. Under the terms of the agreement, MNI will pay a royalty for each administration of iometopane, and also provide Guilford Pharmaceuticals with favourable pricing for the services (including administration of iometopane) for any clinical trials of Guilford's product candidates. This agreement will be terminated upon the US FDA's approval of the product candidate for marketing and sale in the US. Guilford has retained commercial rights to Dopascan Injection in the US. MAP Medical Technologies (Schering AG) submitted a Marketing Authorisation Application (MAA) in Finland for European approval of iometopane for the diagnosis of Parkinson's disease in April 2002. Daiichi Radioisotope Laboratories filed an application for approval of iometopane (Dopascan Injection) for the diagnosis of Parkinson's disease in Japan in July 2003. Guilford Pharmaceuticals is conducting a phase II clinical trial in 200 patients with Parkinson's disease where iometopane imaging is used to assess the effectiveness of GPI 1485, an investigational drug candidate, at baseline and at one year and two years after treatment with either GPI 1485 or placebo. The enrolment is expected to be completed in Q3 of 2003. Guint with either GPI 1485 or placebo. The enrolment is expected to be completed in Q3 of 2003. Guilford Pharmaceuticals decided not to proceed with phase III clinical trials and further development of iometopane due to its inability to contract a suitable manufacturer for the clinical and commercial supply of iometopane on acceptable conditions in the US. Guilford Pharmaceuticals obtained the patent coverage for iometopane in the US, Australia and Europe (Austria, Belgium, Switzerland, Liechtenstein, Germany, Denmark, Spain, France, the United Kingdom, Italy, Luxembourg, the Netherlands, Sweden and Greece). Separate filings were made in Finland, Norway, Japan, Canada and Korea. The manufacturing methods of Dopascan are protected by patents in the US and Europe. Dopascan is a registered trademark in the US, Canada, Europe and Asia.
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PMID:Iometopane: (123)I beta-CIT, dopascan injection, GPI 200, RTI 55. 1295 3

The effects of four organophosphorous compounds, three oximes and atropine sulphate, injected through an indwelling cannula into the third ventricle of unanaesthetized dogs were examined. The effects of 200 mug of dyflos were involuntary micturition, defaecation, akinesia of hind limbs and pronounced disturbances of awareness; those of 100 mug of ethyl pyrophosphate were tremor, restlessness and signs of fear; 500 mug to 5 mg of dyflos and 250 mug to 500 mug of ethyl pyrophosphate caused vomiting, salivation, twitches of facial muscles and recurrent epileptiform seizures. The injection of 40 to 80 mg of dimefox and of 50 mg of schradan elicited involuntary micturition, vomiting, salivation and defaecation. These effects occur probably after these substances have passed into the blood stream and have been converted in the liver to potent anticholinesterases. This view is supported by the finding of reduced blood cholinesterase activity. At a dose level of 12.5 mg, 1,1'-trimethylenebis(4-hydroxyiminomethylpyridinium bromide) produced strong convulsions. At this dose level pralidoxime iodide and diacetyl monoxime produced no observable effects. Atropine sulphate in a dose of 1 mg caused disturbances in consciousness and behaviour followed by convulsions. Intraventricular atropine and to a minor extent intraventricular oximes were able to antagonize the effects of intraventricular ethyl pyrophosphate. Pralidoxime iodide exerted a strong antagonistic effect also on intravenous injection.
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PMID:Effects of organophosphorous compounds, oximes and atropine injected into the third ventricle of unanaesthetized dogs. 1388 82


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