ABSTRACT
OBJECTIVE: To evaluate prevalence and risk factors of restless legs syndrome (RLS) in secondary-care patients maintained on tricyclic and serotonin reuptake inhibiting antidepressants. METHOD: A total of 243 subjects with affective and anxiety disorders were interviewed for symptoms of RLS before and after at least 6 months of antidepressant pharmacotherapy within a naturalistic study. Logistic regression analysis was applied to adjust for the effects of age, gender, comorbidities, and the most frequent co-medications. RESULTS: The overall prevalence of RLS was 27%. In the RLS-affected patients, regular use or overuse of non-opioid analgesics frequently combined with caffeine was the major risk factor which significantly correlated with psychiatric and medical comorbidity. In a subsample of 172 patients who had seldom taken analgesics the prevalence of RLS was 9%, which corresponds with its prevalence in the general population. CONCLUSION: Neither antidepressants nor neuroleptics but non-opioid analgesics appear to be a major risk factor of RLS. Their regular use should be considered in studies of RLS-patients on psychotropic or other drugs. In this sample of secondary-care patients, ICD-10 classified depression or anxiety per se did not appear to be a risk factor of RLS.
Subject(s)
Analgesics, Non-Narcotic/therapeutic use , Antidepressive Agents, Tricyclic/therapeutic use , Restless Legs Syndrome/drug therapy , Restless Legs Syndrome/epidemiology , Adrenergic beta-Antagonists/therapeutic use , Adult , Antipsychotic Agents/therapeutic use , Anxiety/drug therapy , Anxiety/epidemiology , Caffeine , Coffee , Depression/drug therapy , Depression/epidemiology , Dopamine Antagonists/therapeutic use , Estrogen Replacement Therapy , Histamine H2 Antagonists/therapeutic use , Humans , Male , Middle Aged , Pain/drug therapy , Phosphodiesterase Inhibitors , Prevalence , Risk FactorsABSTRACT
Controlled studies in 1990-1992 with Danish, Sardinian, and Hongkong-Chinese patients consistently revealed a prevalence of goiter of about 50% in lithium treated patients. This is far beyond the frequency generally assumed for Germany, the whole country still known to be an endemic goiter area. Hypothyroidism as a side effect of lithium occurs in a clearly different group of patients and is much less frequent, the overall incidence being not substantially different from the incidence in the general population. But the risk of becoming hypothyroid as well as hyperparathyroid during lithium prophylaxis is markedly higher in women over 45 years of age, who in the general population are also prone to both endocrine dysfunctions. Lithium is considered to have a provoking role. Lithium is known to be accumulated in the bone and an impact on bone metabolism was shown in animal studies. The data reviewed prohibit the use of lithium during lactation and enforce strict indication in children. In adults the effect of lithium on bone should be considered only in osteomalacia and severe osteoporosis. This review is illustrated by the case of a 60-year-old woman, who after 4 years of successful treatment with lithiumcarbonate because of schizoaffective psychosis, developed a syndrome of hypercalcemia. Exstirpation of a parathyroid adenoma rendered her normocalcemic. Moreover, a pre-existing diffuse goiter had grown to a large nodular goiter within the course of her 5-year treatment. As she finally became paraparetic, she was admitted to our rehabilitation center for the diseases of the spinal cord. Her paraparesis may have been caused not only by the lithium-induced primary HPT, but in part by lithium itself. There are a few reports on lithium causing peripheral neuropathy at toxic levels. A transient deterioration of a pre-existing neuropathy, as in our case study, may have happened at lithium serum levels not far beyond the upper limit of 0.8 mmol/l.