Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the newer antihypertensive agents are the beta-blocking drugs, such as propranolol. These agents are useful as second-step drugs to be used if diuretic therapy alone is not effective. In mild to moderately severe hypertension, propranolol, in does of up to 480 mg/day in combination with a thiazide diuretic, has been found to be effective in over 80% of patients on long-term therapy. This degree of response is essentially similar to that noted with a combination of reserpine and a diuretic agent. Although some observers believe that propranolol produces many fewer side effects than the other step 2 drugs (reserpine and alpha-methyldopa), there are some patients who do experience restlessness, insomnia, and depression. Clonidine may be substituted for another step 2 drug, is of moderate potency, but may not be tolerated by a large number of patients because of the severe dry mouth and drowsiness that it produces. Prazosin appears to be a suitable substitute for hydralazine as an effective vasodialator if thiazides plus propranolol or thiazides plus reserpine or alpha-methyldopa are not effective. In some instances, it many be an acceptable second-step drug because of its alpha-adrenoreceptor-blocking properties. The angiotensin II competitive inhibitors or converting enzyme inhibitors may in the future have some place in the management of hypertension.
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PMID:Propranolol and newer antihypertensive drugs in the management of hypertension. 42 60

Clonidine therapy was discontinued abruptly in seven patients. Blood pressure was recorded every hour or two hours throughout the study. Clonidine therapy was reinstituted 48 hours after its discontinuation in all except two patients, in whom it was reinstituted at 36 hours. During the withdrawal phase, blood pressure tended to return rapidly to nontreatment levels, but there was no "overshoot" in blood pressure. Apprehension, insomnia, palpitations, and sweating were experienced by two patients. These symptoms were relieved promptly by reinstituting clonidine therapy. In this prospective study, no blood pressure overshoot was noted with abrupt discontinuation of clonidine.
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PMID:Abrupt discontinuation of clonidine therapy. 49 Jul 93

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

Combined clonidine and naltrexone treatment allowed 38 of 40 patients addicted to methadone to withdraw completely in 4-5 days. For most patients naltrexone was gradually increased from 1 mg/day to 50 mg/day over 4 days. Clonidine reduced the intensity of naltrexone-induced withdrawal symptoms. Clonidine significantly decreased blood pressure without producing syncope and caused sedation but no other clinical problems. The withdrawal symptoms of anxiety, anorexia, insomnia, restlessness, and muscular aching were most resistant but were mild or nonexistent at discharge. Clonidine-naltrexone treatment should succeed with patients receiving methadone doses up to 50 mg/day, facilitate naltrexone maintenance, and apply to many clinical settings.
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PMID:The combined use of clonidine and naltrexone as a rapid, safe, and effective treatment of abrupt withdrawal from methadone. 371 21

A severe rebound rise in blood pressure with agitation and insomnia had been noted in five patients when they had previously ceased clonidine (Catapres) This has been shown to be reproducible in these patients and to be associated with a significant increase in urinary catecholamine excretion. The blood pressure can be controlled and the symptoms alleviated promptly by alpha and beta adrenergic receptor blockade using intravenous phentolamine and propranolol.
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PMID:Effects of clonidine withdrawal: possible mechanisms and suggestions for management. 470 9

Neuroleptic withdrawal reactions have significant clinical and medicolegal implications for individuals with developmental disabilities. Behavioral deterioration following neuroleptic taper can represent (a) relapse of a mental illness, (b) and anticholinergic rebound reaction, (c) tardive akathisia, and (d) possibly a supersensitivity psychosis. Such reactions may preclude the discontinuation of neuroleptic drug therapy, even in the absence of a drug-responsive psychiatric illness. In this report, the case histories of two individuals who experienced a thioridazine (Mellaril) withdrawal-induced behavioral deterioration were presented. Both reactions were characterized by anxiety and insomnia, and the patients' symptoms were relieved by uncontrolled treatment with clonidine (Catapres) therapy. Evidence for adrenergic hyperactivity as a mediating event was presented.
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PMID:Thioridazine withdrawal-induced behavioral deterioration treated with clonidine: two case reports. 756 44

There are few reports of the behavioral manifestations in the pediatric population infected with human immunodeficiency virus type 1 (HIV-1). We report a case of a 4-year-old child with acquired immunodeficiency syndrome, whose initial manifestation of central nervous system involvement consisted of sudden onset of impulsivity, hyperactivity, initial insomnia, and aggressive behavior. This clinical picture may suggest an initial presentation of HIV-1 encephalopathy. Clonidine was helpful in ameliorating these behaviors.
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PMID:Case study: behavioral symptoms of pediatric HIV-1 encephalopathy successfully treated with clonidine. 789 70

Children with autism spectrum disorders (ASD) often exhibit sleep and behavioral disorders. Treatment of sleep disorders can be difficult in these children. Clonidine, an alpha2-adrenergic receptor agonist, has been shown to be effective in reducing impulsivity, inattention, and hyperactivity, as well as in serving as a sedative for medial procedures. An open labeled retrospective study of clonidine in treatment of insomnia, and/or hyperactivity, inattention, mood disorder, and aggressive behaviors was conducted using parent reports of sleep initiation and maintenance, as well as behaviors prior and during clonidine treatment. Clonidine was effective in reducing sleep initiation latency and night awakening, to a less degree in improving attention deficits hyperactivity, mood instability and aggressiveness in this cohort of 19 children with ASD. The side effects were largely tolerable. Further evaluation with placebo-controlled double-blind clinical trial of clonidine use in ASD will provide more insight into the clinical efficacy and safety of the medicine in ASD.
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PMID:Use of clonidine in children with autism spectrum disorders. 1828 Jun 81

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

Dextromethorphan has been reported to ameliorate opioid withdrawal symptoms in both animal and human subjects. In the present study, we investigated the efficacy of dextromethorphan as an add-on medication in heroin detoxification treatment in a double-blind, placebo-controlled design. Sixty-five heroin-dependent patients (male, 63; female, 2) participated in this inpatient detoxification trial after giving informed consent. Clonidine 0.075 mg 4 times a day was given as an antiwithdrawal medication at baseline. Each patient was then randomly assigned to treatment with either dextromethorphan 60 mg or placebo 4 times a day as additional medication. Flurazepam 30 mg was given before bedtime for insomnia. Other medications that were allowed included loperamide for diarrhea and lorazepam for agitation. Participants were monitored using the Objective Opioid Withdrawal Scale 3 times a day as the primary outcome to compare drug efficacy between groups. Generalized estimating equation model analysis revealed that the Objective Opioid Withdrawal Scale had no group difference between dextromethorphan and placebo group overall (P = 0.29), whereas a significant difference between groups was found during day 3 to day 6 (P = 0.04) by post hoc analysis. There was no difference in the Clinical Global Impression Scale, patient's impression of treatment, and use of ancillary medications between groups. No severe adverse effects were noticed. We suggest that dextromethorphan has some beneficial effect in attenuating the severity of opioid withdrawal symptoms and can be used as an adjunction medication in the treatment of opioid withdrawal, whereas the exact efficacy needs further investigation.
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PMID:A double-blind, placebo-controlled trial of dextromethorphan combined with clonidine in the treatment of heroin withdrawal. 3010 85


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