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

The single dose test was performed on 100 various cases of glaucoma, with prolonged use t.i.d. for 1 month in 30 cases, for 3 months in 50 cases, for 6 months in 30 cases, and for 1 year in 20 cases. The IOP was lowered by an average 20%, the effect being similar to that of timolol. Clonidine lowered the blood pressure by less than 10%, and the papillary perfusion index was increased rather than decreased. The discomforts, such as thirst, somnolence and dizziness were tolerable and diminished with continued use. The author recommends its wide application in treatment of glaucoma.
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PMID:[The ocular hypotensive effect and side reactions of domestic clonidine eyedrops]. 191 3

In a prospective, double-blind comparison, we assessed the efficacy of transdermal clonidine with that of chlordiazepoxide in the treatment of moderately severe acute alcohol withdrawal syndrome. While having significant withdrawal symptoms, 50 hospitalized men were randomly assigned to receive either transdermal clonidine or chlordiazepoxide over a 4-day study period. Outcome was evaluated daily, medically and psychiatrically, using both objective and subjective measurements for dependent variables. No patient in either study group had seizures or progression to delirium tremens. The group receiving transdermal clonidine had a more significant response globally for the signs and symptoms of alcohol withdrawal, as measured by the Alcohol Withdrawal Assessment Scale. Also, clonidine more effectively lowered elevated systolic and diastolic blood pressure and heart rate. The core target symptom, anxiety, decreased significantly more in the patients receiving transdermal clonidine when measured by the Hamilton Anxiety Rating Scale and its subscale for somatic anxiety. Cognitive function responded equally in both study populations. Clonidine-treated patients reported less diarrhea, dizziness, headache and fatigue, and the chlordiazepoxide-treated patients reported less nausea and vomiting. We conclude that transdermal clonidine is effective treatment for the acute alcohol withdrawal syndrome.
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PMID:Transdermal clonidine versus chlordiazepoxide in alcohol withdrawal: a randomized, controlled clinical trial. 200 May 17

In a randomized, double-blind crossover study, 40 patients with postherpetic neuralgia were given single oral doses of clonidine, 0.2 mg, codeine, 120 mg, ibuprofen, 800 mg, or inert placebo. Pain relief and side effects were recorded for 6 hours. Patients reported significantly more relief after clonidine than after the other three treatments. Codeine and ibuprofen were ineffective. Sedation, dizziness, and other side effects were more frequent after clonidine (74%) or codeine (69%) than after placebo (36%) or ibuprofen (28%). Reported pain relief was greater during trials in which side effects were present. A single, mild side effect was associated with as much additional pain relief as multiple, severe side effects. Clonidine's superiority to codeine, which had a similar incidence of side effects, argues for a specific analgesic effect. In addition, side effects may have contributed to clonidine analgesia, perhaps by suggesting to patients that they had received a potent drug.
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PMID:Association of pain relief with drug side effects in postherpetic neuralgia: a single-dose study of clonidine, codeine, ibuprofen, and placebo. 328 74

Clonidine was used as an adjunct to baclofen in 55 patients with spasticity due to spinal cord injury. Dosage was held at the minimum effect amount for those who responded. No effect was seen in 24 patients (44%), although 31 (56%) benefitted from the drug. Patients were grouped as quadriplegics or paraplegics, having complete or incomplete lesions. Of all quadriplegics, seven of 11 complete (64%) and 17 of 25 incomplete patients (68%) responded; among the paraplegics, six of 15 complete (40%) and one of four incomplete patients (25%) improved. Side effects were limited to postural hypotension necessitating reduction in dosage in three patients that were successfully treated; in the unsuccessfully treated group, one patient had insomnia, one had dizziness, and one had drowsiness.
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PMID:Clonidine effect on spasticity: a clinical trial. 334 19

A number of clinical observations have suggested that clonidine may be responsible for dizziness and even syncope. The aim of this study was to assess the effects of this drug on normal and pathological sinus and AV nodes and on carotid sinus sensitivity. 19 patients were investigated (average age: 73 years). 14 patients complained of dizziness or syncope, including 3 patients with spontaneous sinus node dysfunction. 5 patients were asymptomatic; 3 were investigated for severe sinus bradycardia (1 on clonidine); 1 patient had sinoatrial block and 1 patient underwent pre-operative assessment for intraventricular block. The sinus node was studied using Mandel's method at 100, 120 and 150/min; the AV node was studied by the extrastimulus method with fixed atrial cycle of 600 ms. The following parameters were measured: Wenckebach point, AH interval in spontaneous and paced cycle length of 600 ms, effective refractory periods. Carotid sinus sensitivity was tested by right and left carotid sinus massage. These parameters were measured under basal conditions and 15 and 30 minutes after IV injection of 0.150 mg of clonidine. Two groups of patients were identified from the results under basal conditions: group 1:11 patients with corrected post-stimulation pauses less than 525 ms, and group 2:8 patients with at least one corrected post-stimulation pause of over 525 ms. Clonidine influenced the post-stimulation pauses significantly in both groups. However, the number of pathological pauses increased much more in group 2 than in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of intravenous clonidine on normal and pathological sinus and atrioventricular nodes and carotid sinus sensitivity]. 392 89

Clonidine (Dixarit), 0.025 mg three times daily, was given to 15 patients with menopausal, predominantly vasomotor symptoms. Both the number and the subjectively judged intensity of flushes and sweating decreased continually and in a statistically significant manner during the nine-week time of observation. Additionally, frequency and intensity of headaches, dizziness and paraesthesias decreased, while the other symptoms such as irritability, weak memory and depression remained unchanged. Clonidine in the stated dosage had no significant effect on blood pressure and heart rate. Mild side effects, especially dry mouth and slight sleepiness, were evident only in the first three weeks.
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PMID:[Treatment of menopausal symptoms with low doses of clonidine (author's transl)]. 706 Apr 97

The prevalence of attention-deficit hyperactivity disorder (ADHD) in the USA is estimated at approximately 4-9% in children and 4% in adults. It is estimated that prescriptions for ADHD medications are written for more than 2.7 million children per year. In 2010, US poison centers reported 17,000 human exposures to ADHD medications, with 80% occurring in children <19 years old and 20% in adults. The drugs used for the treatment of ADHD are diverse but can be roughly separated into two groups: the stimulants such as amphetamine, methylphenidate, and modafinil; and the non-stimulants such as atomoxetine, guanfacine, and clonidine. This review focuses on mechanisms of toxicity after overdose with ADHD medications, clinical effects from overdose, and management. Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin. The primary clinical syndrome involves prominent neurological and cardiovascular effects, but secondary complications can involve renal, muscle, pulmonary, and gastrointestinal (GI) effects. In overdose, the patient may present with mydriasis, tremor, agitation, hyperreflexia, combative behavior, confusion, hallucinations, delirium, anxiety, paranoia, movement disorders, and seizures. The management of amphetamine, dextroamphetamine, and methylphenidate overdose is largely supportive, with a focus on interruption of the sympathomimetic syndrome with judicious use of benzodiazepines. In cases where agitation, delirium, and movement disorders are unresponsive to benzodiazepines, second-line therapies include antipsychotics such as ziprasidone or haloperidol, central alpha-adrenoreceptor agonists such as dexmedetomidine, or propofol. Modafinil is not US FDA approved for treatment of ADHD; however, it has been shown to improve ADHD signs and symptoms and has been used as an off-label pharmaceutical for this diagnosis in both adults and children. The mechanism of action of modafinil is complex and not fully understood. It is known to cause an increase in extracellular concentrations of dopamine, norepinephrine, and serotonin in the neocortex. Overdose with modafinil is generally of moderate severity, with reported ingestions of doses up to 8 g. The most common neurological effects include increased anxiety, agitation, headache, dizziness, insomnia, tremors, and dystonia. The management of modafinil overdose is largely supportive, with a focus on sedation, and control of dyskinesias and blood pressure. Atomoxetine is a selective presynaptic norepinephrine transporter inhibitor. The clinical presentation after overdose with atomoxetine has generally been mild. The primary effects have been drowsiness, agitation, hyperactivity, GI upset, tremor, hyperreflexia, tachycardia hypertension, and seizure. The management of atomoxetine overdose is largely supportive, with a focus on sedation, and control of dyskinesias and seizures. Clonidine is a synthetic imidazole derivative with both central and peripheral alpha-adrenergic agonist actions. The primary clinical syndrome involves prominent neurological and cardiovascular effects, with the most commonly reported features of depressed sensorium, bradycardia, and hypotension. While clonidine is an anti-hypertensive medication, a paradoxical hypertension may occur early with overdose. The clinical syndrome after overdose of guanfacine may be mixed depending on central or peripheral alpha-adrenoreceptor effects. Initial clinical effects may be drowsiness, lethargy, dry mouth, and diaphoresis. Cardiovascular effects may depend on time post-ingestion and may present as hypotension or hypertension. The management of guanfacine overdose is largely supportive, with a focus on support of blood pressure. Overdose with ADHD medications can produce major morbidity, with many cases requiring intensive care medicine and prolonged hospital stays. However, fatalities are rare with appropriate care.
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PMID:Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management. 2375 86