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Restless legs syndrome (RLS) is a common disorder that can have a considerable impact on a patient's functioning and quality of life. The pharmacologic armamentarium for RLS contains dopamine agonists, a-2d ligands, and opioids, among other agents. Each of these types of drugs has strengths and limitations, and treatment selection should be based on the frequency of RLS symptoms and any accompanying pain. Dopaminergic augmentation, which exacerbates RLS symptoms, is the most common and challenging side effect of long-term RLS treatment with dopamine agonists and requires special clinical consideration. Iron status is also important to the effective management of RLS.
Restless legs syndrome (RLS) is a common sensory motor disorder characterized by the urge to move a leg, which worsens with physical and cognitive inactivity, particularly in the evening and at night, but transiently improves with activity. A number of diseases have symptoms that are often confused with those of RLS, and other conditions are associated with higher rates of RLS. RLS can also be exacerbated by certain medications. Because RLS lacks biomarkers and established tests to aid in its diagnosis, clinicians should be aware of the other disorders that can be confused with or accompany RLS.
Restless legs syndrome (RLS) is a common sensorimotor condition with symptoms ranging from mild discomfort to severe pain. Patients with RLS are likely to experience sleep disturbances and have a reduced quality of life. Several misconceptions related to its name, symptoms, and prevalence can hinder the correct diagnosis of RLS. Clinicians should use diagnostic criteria and associated symptom features such as sleep disturbance and family history to confirm the diagnosis and rule out other medical and psychiatric conditions. Several validated tools may assist clinicians by providing sample questions to recognize the symptoms and severity of RLS.
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Sir: Vagus nerve stimulation (VNS) has shown effects in treatment-resistant epilepsy1 and major depressive episode.2 Epidemiologic studies have described restless legs syndrome (RLS) to exist in varying degrees of severity in 2.5% to 10% of the population.3 Treatment of first choice is dopamine agonists, but agents that enhance inhibitory mechanisms in the way that anticonvulsive drugs do are effective, too.' ‹
Letter to the Editor
Fluoxetine-Mirtazapine Interaction May Induce Restless Legs Syndrome: Report of 3 Cases From a Clinical Trial
Sir: Mirtazapine is a novel antidepressant, known as a noradrenergic and specific serotonergic antidepressant (NaSSA). It is an antagonist of presynaptic α2-autoreceptors and α2- heteroreceptors, resulting in an increased release of both norepinephrine and serotonin, and it also enhances noradrenergic and serotonergic neurotransmission. However, mirtazapine potently blocks 5-HT2 and 5-HT3 receptors. Although there are several studies in the literature that examine the effects of mirtazapine on sleep parameters, further study of larger groups of depressed patients is clearly needed.
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Background: Antidepressant-inducedperiodic limb movement disorder (PLMD) may limit the tolerabilityof some antidepressant medications and interfere with treatmentresponse. Given the role of dopamine in PLMD and the effects ofbupropion sustained-release (SR) on central dopaminergicfunction, we hypothesized that bupropion SR would not beassociated with antidepressant-induced PLMD.
Method: In an expanded case-seriesdesign, we compared the effects of bupropion SR, after about 10weeks of treatment, on measures of PLMD, depression, and sleep in5 depressed (Research Diagnostic Criteria) patients who also metcriteria for having pretreatment PLMD. Depression was measuredusing the Beck Depression Inventory and the Hamilton Rating Scalefor Depression. Patients were considered to have PLMD ifpolysomnographic recordings showed > 5 periodic limbmovements/hour of sleep that were associated with arousals fromsleep.
Results: Bupropion SR treatment wasassociated with a reduction in measures of PLMD and animprovement in depression.
Conclusion: These results show thatbupropion SR is not associated with antidepressant-induced PLMD.Rather, bupropion SR treatment reduces objective measures of PLMDin depressed patients with the disorder.
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