Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Choice of an antidepressant medication is, in part, based on the side effects produced by a drug and the desire to avoid certain reactions in a particular patient. The clinician needs a reliable method of predicting which medications are most likely to produce specific untoward effects. Understanding the synaptic pharmacology of the most commonly used agents could serve as a tool for predicting possible side effects and drug-drug interactions. Antidepressant drugs alter neurotransmitter effects at nerve synapses, probably by blocking norepinephrine and serotonin reuptake, and blockade of neurotransmitter receptor sites - primarily the histamine H1 receptor, the muscarinic receptor, and the alpha-1-adrenoceptor. Possible clinical side effects related to some of these interactions include tachycardia, tremor, and (possibly) male sexual dysfunction (associated with norepinephrine reuptake blockade); sedation (associated with histamine H1 blockade); orthostatic hypotension, dizziness, and reflex tachycardia (associated with alpha-1-adrenoceptor blockade), and blurred vision, dry mouth, and memory dysfunction (associated with muscarinic receptor blockade). Pharmacologic data that demonstrate the potencies and selectivities of the antidepressant drugs for reuptake blockade and receptor site antagonism might allow the clinician to make an informed, rational choice of antidepressant therapy. This paper presents data on drug potencies and selectivities, and attempts to relate these data to anticipated side effects and drug-drug interactions.
 ...
PMID:Pharmacology of antidepressants. 289 25

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)
 ...
PMID:Safety of encainide for the treatment of ventricular arrhythmias. 309 26

The chemistry, electrophysiology, pharmacokinetics, clinical use and efficacy, adverse effects, drug interactions, and dosage of encainide hydrochloride and flecainide acetate are reviewed. Encainide and flecainide are class 1c antiarrhythmic agents that slow myocardial conduction and mildly prolong the duration of repolarization. Both agents block anterograde conduction over accessory pathways and prolong the effective refractory period of the accessory pathway. Bioavailability of encainide ranges from 7% to 82%, whereas that of flecainide is 90% to 95%. Encainide is metabolized by the liver to two major active metabolites that are slowly eliminated in the urine. About 23% of flecainide's total body clearance is dependent on renal elimination, and drug excretion is slowed in patients with renal dysfunction, requiring dosage adjustments. Both agents are effective in the suppression and prevention of ventricular arrhythmias, including premature ventricular contractions and sustained and nonsustained ventricular tachycardia. These agents may also be valuable in controlling supraventricular arrhythmias. The most common adverse effects of both agents involve the central nervous system and include dizziness, blurred vision, and headache. The potential for proarrhythmic effects is a concern with these agents. The risk is greater in patients with more severe arrhythmias, poor ventricular function, or high serum concentrations of drug. The usual initial oral dosage of encainide hydrochloride is 25 mg three times a day, with a usual dosage range of 100-200 mg/day. Flecainide acetate should be initiated at 100 mg every 12 hours and may be increased up to 400 mg/day. Encainide and flecainide could become useful therapeutic options in the treatment of a variety of arrhythmias.
 ...
PMID:Encainide hydrochloride and flecainide acetate: two class 1c antiarrhythmic agents. 311 76

Encainide is an antiarrhythmic drug with class IC activity which has been used in the treatment of life-threatening ventricular arrhythmias, symptomatic ventricular arrhythmias and supraventricular arrhythmias. The antiarrhythmic activity is due to the parent drug and its two principal active metabolites, and in the extensive metabolising phenotype (90% of patients), metabolites are present in plasma at higher concentrations than encainide itself. Encainide produces little haemodynamic change in patients with left ventricular dysfunction and thus has considerable therapeutic potential in view of its efficacy in patients with ventricular tachycardia, premature ventricular complexes and the Wolff-Parkinson-White syndrome. However, this potential is reduced by a tendency for encainide to aggravate arrhythmia in a proportion of patients. At present there is no reliable method of identifying patients at risk for this potentially serious side effect. The most common non-cardiac side effects are dizziness and blurred vision which seldom necessitate withdrawal of treatment. Thus, encainide has proved effective in controlling ventricular tachyarrhythmias including those which have not been controlled by other antiarrhythmic drugs.
 ...
PMID:Encainide. A review of its pharmacological properties and therapeutic efficacy. 312 Dec 75

The electrophysiologic effects and antiarrhythmic efficacy of flecainide were evaluated by electrophysiologic study (EPS) in 20 patients with ventricular tachycardia (VT) refractory to an average 2.9 drugs. In 19 patients EPSs were performed with patients not receiving antiarrhythmic medications and receiving oral flecainide therapy at steady state (mean dose, 235 +/- 67 mg/day). Flecainide significantly increased the QRS complex duration (27%, P less than .001), PR interval (17%, P less than .001), and right ventricular effective refractory periods 8.5% and 21.1% (P less than .01) for the first and second extrastimuli, respectively. During baseline EPS, 17 patients were induced into VT and two were noninducible. Flecainide prevented EPS-induced VT in five patients and the induced VT became slow and hemodynamically stable in three. Two patients who failed flecainide monotherapy were induced into slow hemodynamically stable VT with flecainide in combination with amiodarone. The two noninducible patients, during baseline EPS, had suppression of spontaneous VT with flecainide. Overall, 13 of 20 patients received flecainide either alone or in combination with amiodarone for chronic therapy. Side effects encountered during the study consisted of blurred vision, dizziness, weakness, lethargy, nausea, worsened heart failure and bradyarrhythmias. After a mean 9-month follow-up (3 to 16 months) nine patients remain on flecainide therapy. There were three recurrences of slow, hemodynamically stable VT and no episodes of sudden death. Low-dose flecainide, either alone or in combination with other agents, is effective therapy for certain patients with refractory VT but heart failure remains a significant concern in patients with depressed left ventricular function.
 ...
PMID:Clinical and electrophysiologic effects of flecainide in patients with refractory ventricular tachycardia. 312 56

During May and June of 1985 the Health Protection Branch and several other agencies were involved in the investigation of over 300 reports of illness reported in the Vancouver area of British Columbia, Canada. Symptoms reported included nausea, vomiting, dizziness, muscle fasciculation and blurred vision. A review of the onset of symptoms and food consumed suggested that at least 140 people had become ill from eating cucumbers adulterated with a carbamate pesticide. The presence of residues of aldicarb in cucumbers from one particular producer was confirmed by laboratory analysis.
 ...
PMID:Report of illnesses caused by aldicarb-contaminated cucumbers. 336 Feb 4

Crisnatol is a novel lipophilic arylmethylaminopropanediol with significant antineoplastic activity in a variety of murine and human tumor models which functions as a DNA intercalator. In this Phase I trial, a 6-h infusion of the drug was administered i.v. in 700 to 1500 ml of 5% dextrose in water every 28 days. Eighty-five courses at doses of 7.5 to 516 mg/m2 were administered to 43 patients with refractory solid tumors. Reversible neurological toxicity was dose limiting at 516 mg/m2 and was manifested as somnolence, dizziness, blurred vision, unsteady gait, and alpha-slowing on electroencephalogram at the end of infusion. All neurological signs and symptoms were reversible. No hematological toxicity was observed. Other toxicities included phlebitis, mild to moderate nausea and vomiting, reversible sinus node arrest in one patient, and hypertension. Crisnatol plasma concentrations were determined by high-pressure liquid chromatography. After infusion, plasma concentrations declined biexponentially with a terminal t1/2 of 2.9 h. Using a two-compartment model, the mean apparent volume of distribution at steady state and total-body clearance were 58.8 liters/m2 and 18.3 liters/h/m2, respectively, indicative of extensive tissue distribution and rapid hepatic clearance. Peak plasma levels occurred at the end of infusion and correlated with the onset of neurological toxicity. The recommended Phase II dose for this schedule is 388 mg/m2.
 ...
PMID:Phase I and clinical pharmacology trial of crisnatol (BWA770U mesylate) using a monthly single-dose schedule. 339 16

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
 ...
PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

The main criteria of "cervicogenic headache" are considered to be as follows: relatively rare and long-lasting unilateral attacks of severe headache, although seemingly of a non-excruciating character, signs of neck involvement, and lack of "cluster pattern". In the present communication, the clinical manifestations in 11 patients fulfilling these criteria are described. All 11 patients selected in accordance with these criteria proved to be females, the age at onset ranging from 6 to 40 years (mean, 30 years). The mean duration of symptoms was 13 years. Six patients had had previous head/neck injuries. All patients had pain periorbitally, in the temporal region, and in the low occipital region (nape of the neck); less frequent were frontal, parietal, and facial pain and pain in the upper part of the occipital region. The duration of attacks was from 3 h to 3 weeks, and the interval between attacks lasted from 2 days to 2 months. The commonest accompanying phenomena were phonophobia, dizziness, ipsilateral eyelid edema, ipsilaterally blurred vision, and irritability. Some of the patients also had nausea (n = 7) and vomiting (n = 6). On physical examination, slight to moderate reduction of movements in the neck was noted, and five patients had ipsilaterally reduced sensation for touch in the trigeminal area. All the patients except one were severely afflicted. Attacks could, in addition to occurring spontaneously, be precipitated in all patients by head movements or by pressure at specific points in the neck.
 ...
PMID:"Cervicogenic headache": clinical manifestation. 360 68

A case of intravenous labetalol in the treatment of a resistant hypertensive emergency is reported. Although there have been several reports of the use of oral labetalol in resistant hypertension, no intravenous administration in hypertensive emergency resistant to other drugs has been reported to date. A 36-year-old black female with BP of 270/160 mm Hg with complaints greater than one month's duration of dizziness, severe headaches, blurred vision, shortness of breath, vomiting, palpitations, flushing, agitation, diarrhea, weakness, and weight loss, was treated successfully with intravenous labetalol after she failed to respond to other established parenteral antihypertensive drugs. The patient received labetalol 20 mg iv bolus, and then 20 mg every ten minutes until a cumulative dose of 200 mg was attained. Labetalol produced a prompt but smooth reduction in BP without any reflex tachycardia or other adverse effects. Intravenous labetalol may be safe and effective for the management of rapid BP control in hypertensive emergencies resistant to other parenteral antihypertensive agents.
 ...
PMID:Intravenous labetalol in the management of resistant hypertensive emergency. 360 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>