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)

Lorcainide hydrochloride or N-(4-chlorophenyl)-N-[1-(1-methyl-ethyl)-4-piperidinyl]benzeneacetamide mono-hydrochloride (R 15889) is a new anti-arrhythmic drug. Studies in dogs show that lorcainide is effective against post-infarction and ouabain-induced ventricular arrhythmias, and abolishes acetylcholine and aconitine-induced atrial fibrillation; it elevates the threshold of electrically induced ventricular fibrillation. In isolated dog and cow Purkinje fibers, in dog ventricular and in guinea-pig auricular muscle preparations, lorcainide decreases the rate of rise of the transmembrane action potential, the conduction velocity and spontaneous activity. It prolongs the refractory period of isolated Purkpinje and ventricular muscle preparations, and the functional refractory period of the AV node in the guinea-pig heart. It has no effect on Ca mediated electrical activity. Isometric force measurements in isolated cat papillary muscles and hemodynamic studies in anaesthetized and unanaesthetized dogs indicate that lorcainide moderately decreases myocardial contractility. Side effects observed at large doses are of central origin and include salivation, tremor and vomiting. Intravenous injection induces transient peripheral vasodilatation. Lorcainide is an antiarrhythmic of the local anaesthetic type. It is characterized by a good oral absorption, a long duration of action and a large safety factor.
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PMID:Antiarrhythmic, electrophysiologic and hemodynamic effects of lorcainide. 63 16

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
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PMID:Frequent neurologic toxicity associated with amiodarone therapy. 653 58

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.
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PMID:Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation. 663 51

Amiodarone was used to treat cardiac arrhythmias that had been refractory to conventional medical therapy. The first 70 consecutive patients treated with amiodarone in this study had at least 6 months of follow-up (range 6 to 24, mean 11) and form the basis for this report. Sixty-six patients were treated for ventricular arrhythmias and four for supraventricular tachycardias. Amiodarone therapy consisted of a loading dose of 600 mg orally twice a day for 7 days, and 600 mg daily thereafter. Doses were reduced only if side effects occurred. Because of frequent side effects, the dose was reduced from 572 +/- 283 mg per day (mean +/- standard deviation) at 45 days to 372 +/- 174 mg per day at 6 months. With a mean follow-up of 11 months in the 54 patients who continued to take amiodarone, only 4 patients had ventricular fibrillation. Three additional patients experienced recurrent sustained ventricular tachycardia in long-term follow-up. All 70 patients had extensive clinical and laboratory evaluation in follow-up. Side effects were common, occurring in 93% of patients. Thirteen patients (19%) had to discontinue the medication because of severe side effects. Fifty-six patients had gastrointestinal side effects, most commonly constipation. All patients but 1 eventually developed corneal microdeposits, and 43 patients were symptomatic. Cardiovascular side effects were uncommon. Symptomatic pulmonary side effects occurred in seven patients, with unequivocal pulmonary toxicity occurring in five. Neurologic side effects, most commonly tremor and ataxia, occurred in 52 patients. Thyroid dysfunction occurred in 3 patients, and 32 patients had cutaneous abnormalities. Miscellaneous other side effects occurred in 32 patients. Amiodarone appears to be useful in the management of refractory arrhythmias. Because virtually all patients develop side effects when given a maintenance daily dose of 600 mg, lower maintenance doses should be used. It is unknown if the more severe side effects are dose-related. Amiodarone is difficult to administer because of its narrow toxic-therapeutic range and prolonged loading phase. More importantly, the first sign of antiarrhythmic failure may be manifest as sudden cardiac death.
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PMID:Toxic and therapeutic effects of amiodarone in the treatment of cardiac arrhythmias. 668 51

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

Mutations of eag, first identified in Drosophila on the basis of their leg-shaking phenotype, cause repetitive firing and enhanced transmitter release in motor neurons. The encoded EAG polypeptide is related both to voltage-gated K+ channels and to cyclic nucleotide-gated cation channels. Homology screens identified a family of eag-related channel polypeptides, highly conserved from nematodes to humans, comprising three subfamilies: EAG, ELK, and ERG. When expressed in frog oocytes, EAG channels behave as voltage-dependent, outwardly rectifying K(+)-selective channels. Mutations of the human eag-related gene (HERG) result in a form of cardiac arrhythmia that can lead to ventricular fibrillation and sudden death. Electrophysiological and pharmacological studies have provided evidence that HERG channels specify one component of the delayed rectifier, IKr, that contributes to the repolarization phase of cardiac action potentials. An important role for HERG channels in neuronal excitability is also suggested by the expression of these channels in brain tissue. Moreover, mutations of ERG-type channels in the Drosophila sei mutant cause temperature-induced convulsive seizures associated with aberrant bursting activity in the flight motor pathway. The in vivo function of ELK channels has not yet been established, but when these channels are expressed in frog oocytes, they display properties intermediate between those of EAG- and ERG-type channels. Coexpression of the K(+)-channel beta subunit encoded by Hk with EAG in oocytes dramatically increases current amplitude and also affects the gating and modulation of these currents. Biochemical evidence indicates a direct physical interaction between EAG and HK proteins. Overall, these studies highlight the diverse properties of the eag family of K+ channels, which are likely to subserve diverse functions in vivo.
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PMID:The eag family of K+ channels in Drosophila and mammals. 1041 5

Prevalence of minor and major complications, side effects of stress echocardiography (stress-echoCG) was studied in a group of 1359 patients with suspected ischemic heart disease (IHD). Dipyridamole/atropine test was carried out in 184, dobutamine/atropine test - in 231, transesophageal atrial pacing (TEAP) - in 154, veloergometry (VEM) in half sitting position - in 122, and combination stress-echoCG - in 668 patients (dipyridamole/TEAP, n=151; dipyridamole/dobutamine, n=162; dipyridamole/paired TAP, n=112). We classified ventricular and supraventricular extrasystoles, head ache, nausea, muscular tremor as side effects, short paroxysms (less than 2 min) of hemodynamically insignificant supraventricular and ventricular tachycardia - as minor complications, and development of acute coronary syndrome, ventricular fibrillation - as major complications. Most frequent side effects during stress-echoCG were rare ventricular extrasystoles (26.0% during dobutamine, 18.9% during VEM test), and head ache (16,7% in dipyridamole tests). Major complications occurred in 2 cases (0,147%). One patient during standard dipyridamole test developed acute coronary syndrome requiring urgent coronary angiography and angioplasty of the right coronary artery. Another patient after administration of 0.25 ml of 0.1% atropine solution at the background of dobutamine infusion (40 mcg/kg/min) had ventricular fibrillation requiring resuscitative measures. Although stress-echoCG in general is a safe and highly informative method of diagnosis of IHD it can be accompanied with side effects during action of stress-agents, minor and major complications during conduction of tests. This dictates necessity of obtainment of compulsory informed consent from patients.
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PMID:[Complications of stress-echocardiography used for diagnosis of ischemic heart disease]. 1826 Sep 91

We report 2 cases of metastatic rectal cancer patients who received chemotherapy with FOLFOXIRI plus bevacizumab(Bev). Case 1: A 54-year-old woman diagnosed with advanced rectal cancer with synchronous liver metastasis underwent a laparoscopic low anterior resection. After the operation, she received FOLFOXIRI plus Bev treatment, and experienced Grade 4 adverse events, including dyspnea and ventricular fibrillation(Vf). After chemotherapy, no other metastasis was detected except a liver metastasis, and partial resection of the liver was performed. Histopathological evaluation revealed that the effect of the chemotherapy was Grade 1a. After liver resection, FOLFOXIRI plus Bev was administered, and a recurrence of the rectal cancer was not detected. Case 2: A 44-year-old woman was diagnosed with advanced rectal cancer with synchronous liver metastasis, distant lymph nodes metastasis, and vaginal invasion. First a colostomy was performed and FOLFOXIRI plus Bev treatment was administered. Grade 3 adverse events, including tremor, neuralgia, and anemia occurred, and chemotherapy was stopped for 3 months. Her adverse events were not under control when progression of the disease was detected, and her treatment was changed to another chemotherapy regimen.
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PMID:[Two Cases of Metastatic Rectal Cancer Patients Who Received Chemotherapy with FOLFOXIRI plus Bevacizumab]. 2813 5


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