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)

One hundred patients with Parkinson's disease (PD) and five patients with progressive supranuclear palsy were questioned about the frequency, circumstances, and consequences of falling. Parkinsonian symptoms were scored using the unified rating scale. Thirty-eight percent of parkinsonian patients fell, and 13% fell more than once a week. Broken bones (13%), hospitalization (18%), confinement to wheelchair (3%), and fear of walking occurred. Postural hypotension was uncommon and did not correlate to falling. Sensory loss, dementia, heart disease, and the use of antihypertensive medications were not related to falling. Falling did correlate with postural instability, bradykinesia, and rigidity but not with tremor. Falling was also related to age and duration of disease. The frequency of falling was correlated only to the severity of one parkinsonian symptom, postural instability. Progressive supranuclear palsy patients fell often and had marked postural instability. Factor analysis of parkinsonian characteristics yielded three groups, with tremor being an independent symptom. Frequent fallers and postural instability were not changed by dopaminergic therapy. Some fallers with gait difficulties and bradykinesia were improved with levodopa. Physical therapy was also of benefit to some patients. It is concluded that falling is a common problem in PD and may cause serious disability. Falling may be related to all the major motor signs except for tremor. Frequent falling is caused by postural instability, which is not reversible with dopaminergic therapy.
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PMID:Falls and Parkinson's disease. 272 Jul

A data base of 1,245 patients treated for ventricular arrhythmias, most of whom had serious cardiac disease, was reviewed. Only 2.9% of these patients had benign ventricular arrhythmias without structural heart disease. The overall incidence of proarrhythmia in this population was 9.2% (115/1,245), but was as frequent as 16% in patients with a history of cardiomyopathy. The proarrhythmic form was new sustained ventricular tachycardia in 22 patients (1.8%). Only 2 of 71 patients (2.8%) with primary arrhythmia had a proarrhythmic event. The incidence has decreased markedly over the past years as reduced doses and gradual titration have been used. There were 137 deaths in the data base of which 82 were sudden, all in patients with advanced (79) or moderately severe (3) cardiac disease. High initial doses, prior myocardial infarction and congestive heart failure (CHF) were positively associated with sudden cardiac death. There were no deaths among the 71 patients with benign arrhythmias. Death rates were related to the severity of the arrhythmia being treated. Comparisons with published survival curves indicated modest improvement; in no case was survival decreased. Invasive and noninvasive measures of left ventricular function indicated no adverse hemodynamic effects. There was only 1 case of new and 3 cases of worsened CHF probably related to encainide. Only 5 patients discontinued for CHF or related signs and symptoms. The most frequent drug-related noncardiac adverse reactions were dizziness (26%), abnormal or blurred vision (19%), QRS interval prolongation (5%), taste perversion (4%) and tremor (3%). In conclusion, the use of reduced doses and gradual titration of encainide has markedly decreased the incidence of proarrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of encainide for the treatment of ventricular arrhythmias. 309 26

The most frequent clinical manifestations in 100 elderly hyperthyroid patients entered in our study were: weight loss (83%), palpitations (85%), nodular goiter (71%) and tremor (74%). Association of weight loss with anorexia and constipation was found in 6% of the patients. The apathetic form of thyrotoxicosis was present in 2% of our patients. Thyrotoxic atrial fibrillation and thyrotoxic heart disease were found in 42% and 51% respectively.
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PMID:Hyperthyroidism in the elderly. I. Clinical manifestations. 383 36

We studied 51 patients with symptomatic unilateral watershed (WS) cerebral infarct on CT. In 22 patients, the infarct was between the superficial territory of the anterior and middle cerebral arteries, 20 had an infarct between the superficial territory of the middle and posterior cerebral arteries, and 9 had an infarct between the superficial and deep territory of the middle cerebral arteries. Each type had a characteristic neurologic picture. Syncope at onset (37%) and focal limb shaking (12%) were frequent. Thirty-eight patients (75%) had internal carotid artery occlusion or tight stenosis associated with a hemodynamically significant cardiopathy, increased hematocrit, or acute hypotension. Embolic infarction was probable in only two patients (4%) who had only atrial fibrillation.
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PMID:Unilateral watershed cerebral infarcts. 395 5

The role of pindolol in treating ventricular arrhythmia was studied in 43 patients with this disorder. Of these patients, 23 had coronary heart disease, 5 had valvular disease, and 15 had no demonstrable heart disease. patients underwent acute drug testing with 20 mg pindolol (phase 1) followed by maintenance therapy (phase 2) for 3 days (20 to 80 mg daily). Efficacy during both phases was evaluated by ambulatory monitoring and treadmill exercise testing. During acute drug testing, 50% of te patients responded. A concordant response between acute drug testing and phase 2 monitoring was seen in 81% (p less than 0.005) of patients and between acute drug testing and phase 2 exercise testing in 88% (p less than 0.005). Arrhythmia was suppressed during the phase 2 exercise test in 53% of patients; these included 80% of the patients without heart disease and 50% of those with coronary heart disease (not significant). During phase 2 monitoring, 60% of patients without heart disease responded vs. 25% with coronary heart disease (not significant). Side effects occurred in 12 patients (28%). These included congestive heart failure (3 patients); fatigue, lightheadedness, and insomnia (2 patients each); nausea, tremor, urinary retention, and bronchospasm (1 patient each); and aggravation of arrhythmia (7 patients). It is concluded that although pindolol alone is marginally effective for treating ventricular arrhythmia in patients with coronary heart disease, it appears to be more valuable in those without heart disease, especially when arrhythmia is provided by exercise. Acute drug testing proved highly predictive of the results with maintenance therapy and is a valuable rapid-screening procedure for identifying potential responders to pindolol.
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PMID:Pindolol for ventricular arrhythmia. 710 35

Serotonin reuptake inhibitors, used as antidepressants, may cause hyponatremia due to a syndrome of inappropriate antidiuretic hormone, specially in elders. Thirty cases with such complication have been reported in the last six years. We report a 76 years old female with a hypertensive cardiopathy and paroxysmal atrial fibrillation treated with amlodipine and sotalol. Five days after starting fluoxetine, the patient presented with a confusional state, gait instability and tremor. Laboratory assessment disclosed a plasma sodium of 115 meq/L. Fluoxetine was discontinued and fluids were restricted. The clinical condition of the patient improved and hyponatremia abated. Hyponatremia must be born in mind as a potential side effect of serotonin reuptake inhibitors.
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PMID:[Severe hyponatremia during treatment with fluoxetine]. 1043 20

Vascular parkinsonism has not been well defined and the clinical correlation of vascular parkinsonism is still not clear. The aim of the study was to estimate prevalence of occurrence of vascular parkinsonism, analysis of risk factors leading to its development and to identify clinical features that suggest a vascular origin. 214 patients with Parkinson's disease were examined. Their ages ranged from 37 to 88 years (median 66.4 years). Evidence of vascular parkinsonism was assessed using a vascular rating scale previously described by Winikates and Jankovic. Statistical analysis was performed with Mann-Whitney U test, chi 2 Pearson test, chi 2 Yates test, Spearman rank correlation and Student's t test. Out of 214 patients 8 were proved to have developed Parkinson's disease due to vascular disease, what gave 3.74%. Out of risk factors for stroke 5 patients had hypertension, 3 had diabetes mellitus, 2 suffered from heart disease, 2 had infarctus myocardii, 1 had hyperlipidemia, 1 had atrial fibrillation. Additionally, those patients had neuroimaging (CT or MRI) evidence of vascular disease in one or more vascular territories. Patients with vascular parkinsonism were older, had shorter duration of disease, were more likely to present rigidity rather than tremor. Dementia and incontinence were more common in vascular group than in Parkinson's disease group. Patients with vascular parkinsonism were also significantly more likely to have corticospinal findings. Proving that Parkinson's disease had vascular etiology is extremely difficult. The test results are inconclusive.
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PMID:[Clinical correlation of vascular parkinsonism]. 1509 42

(1) When people who are physically dependent on alcohol stop drinking, they experience an alcohol withdrawal syndrome. The symptoms generally resolve spontaneously within a week, but more severe forms may be associated with generalised seizures, hallucinations and delirium tremens, which can be fatal. (2) We carried out a literature review in order to obtain answers to the following questions: how to predict or rapidly diagnose a severe alcohol withdrawal syndrome; how to prevent and treat this syndrome; how to manage severe forms; and how to deal with the risk of vitamin B1 deficiency. (3) The main risk factors for severe withdrawal syndrome are: chronic heavy drinking; a history of generalised seizures; and a history of delirium tremens. (4) Anxiety, agitation, tremor, excessive sweating, altered consciousness and hallucinations are signs of a severe withdrawal syndrome. (5) Individual support and effective communication seem to reduce the risk of severe withdrawal syndrome. (6) Oral benzodiazepines are the best-assessed drugs for preventing a severe alcohol withdrawal syndrome, particularly the risk of seizures. When given for a maximum of 7 days, the adverse effects are usually mild. (7) Clinical trials of other antiepileptics suggest they are less effective than benzodiazepines, and their addition to benzodiazepine therapy offers no tangible advantage. (8) Betablockers increase the risk of hallucinations, and clonidine increases the risk of nightmares, and the efficacy of these two drugs is not well documented. Neuroleptics increase the risk of seizures. There are no convincing data to support the use of magnesium sulphate or meprobamate (the latter carries a risk of serious adverse effects). Acamprosate, naltrexone and disulfiram are not beneficial in alcohol withdrawal. (9) Gradual withdrawal, i.e. ingestion of decreasing amounts of alcohol, has not been compared with other methods but is generally not recommended. (10) There are no specific recommendations on hydration. Note that excessive water-sodium intake carries a risk of pulmonary oedema in patients with heart disease. (11) As vitamin B1 deficiency is frequent and can lead to serious complications in alcohol-dependent patients, oral vitamin B1 supplementation is widely recommended, despite the absence of comparative trials. High doses must be used to compensate for poor absorption. Intravenous administration is best if patients have very poor nutritional status or severe complications such as Gayet-Wernicke encephalopathy (a medical emergency), even though rare anaphylactic reactions have been reported after vitamin B1 injection. (12) Planned alcohol withdrawal in specialised hospital units has been extensively studied. Outpatient withdrawal may be more appropriate for patients who are at low risk of developing severe withdrawal syndrome. (13) A large proportion of alcohol-dependent patients were excluded from trials of withdrawal strategies. These include elderly patients, patients with serious psychiatric or somatic disorders, and patients who are also dependent on other substances. (14) An oral benzodiazepine is the best-assessed treatment for a single episode of generalised seizures or hallucinations during alcohol withdrawal. (15) In randomised comparative trials benzodiazepines were more effective than neuroleptics in preventing delirium-related mortality. Currently, with appropriate fluid-electrolyte support, continuous monitoring of vital signs, and respiratory support if necessary, the mortality rate for delirium tremens is under 3%. (16) In practice, patients who are attempting to stop drinking alcohol need close personal support and communication, and a reassuring environment, as well as regular monitoring for early signs of a withdrawal syndrome; the latter may require benzodiazepine therapy.
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PMID:Alcohol withdrawal syndrome: how to predict, prevent, diagnose and treat it. 1732 38

The use of MDMA (ecstasy) in Australia is a widespread and growing problem, promoting acute toxicity and disease which can lead to premature death in users. We report four cases of fatal serotonin toxicity caused by the combination of MDMA and moclobemide, a reversible MAO-A inhibitor with potent serotonergic activity. Despite the highly reported toxicity of this drug combination, there are very few reports of fatalities attributed to a MDMA and moclobemide interaction. Pathology and toxicology reports, initial police reports and coroners' findings were examined to determine the circumstances of the deaths. Symptoms of some of the four cases as reported by paramedics and medical staff included hyperthermia, hyperkalemia, profuse sweating, twitching and shaking. Two cases involved moclobemide concentrations consistent with common prescribed doses, while the other two cases involved much higher concentrations often associated with toxicity. Three of these cases presented with some form of heart disease.
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PMID:Serotonin toxicity involving MDMA (ecstasy) and moclobemide. 2157 Jul 86

The original descriptions of chorea date from the Middle Ages, when an epidemic of "dancing mania" swept throughout Europe. The condition was initially considered a curse sent by a saint, but was named "Saint Vitus's dance" because afflicted individuals were cured if they touched churches storing Saint Vitus's relics. Paracelsus coined the term chorea Sancti Viti and recognized different forms of chorea (imaginativa, lasciva, and naturalis). In the 17th century, Thomas Sydenham provided an accurate description of what he termed chorea minor. He also described rheumatic fever but did not associate it with chorea. It was only in 1850 that See established a relationship between chorea and rheumatic disease. A connection with cardiac involvement was soon recognized and in 1866 Roger postulated that chorea, arthritis, and heart disease had a common cause. The last quarter of the 19th century is marked by the works of Jean-Martin Charcot, Silas Weir Mitchell, William Osler, and William Richard Gowers, all of paramount importance in the refinement of the definition of chorea, its causes, and differential diagnosis. In 1841, Charles Oscar Waters gave a concise account of a syndrome, likely to be Huntington's disease (HD), later described further by George Huntington and named after him. In 1955, the Venezuelan physician Americo Negrette published a book describing communities in the State of Zulia in Venezuela, with unusual numbers of individuals with chorea. Negrette's works culminated in the creation of the Venezuela project and the subsequent discovery of seminal findings in HD. We review the historical facts and outstanding physicians that mark both HD and Sydenham's chorea's history in various sections.
Tremor Other Hyperkinet Mov (N Y) 2015
PMID:Chorea: A Journey through History. 2605 9


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