Restless Legs Syndrome and Schizophrenia: A Case Report

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To the Editors
Restless legs syndrome (RLS), with a prevalence of 10% of the general population,1 is characterized by an urge to move the legs that is usually accompanied by or occurs in response to uncomfortable and unpleasant sensations in the legs. It may be idiopathic or secondary to pregnancy, low ferritin levels, uremia, and neurological disorders.1 Because RLS is associated with a dopaminergic dysregulation,2 dopamine agonists can treat RLS, whereas antipsychotic drugs, which are dopamine antagonists, can worsen it.2 Hence, the treatment of RLS in patients with schizophrenia is a matter of concern.
We report a case of complete recovery of idiopathic RLS in a patient with schizophrenia, after treatment with the antipsychotic drug amisulpride. The patient provided written informed consent for anonymized publication of her data.
A 36-year-old woman was admitted for the first time in the psychiatry department for positive and negative psychotic symptoms (PANSS total score = 112: positive score = 29, negative score = 33, general psychopathology score = 50), leading to a diagnosis of schizophrenia (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) that was never treated before. An idiopathic RLS was also diagnosed based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, criteria and an International Restless Legs Syndrome scale (IRLS) score of 31. She described uncomfortable and unpleasant sensations in the legs like burning feelings. Moreover, she had imperious need to move legs in the evening that was relieved by movements and associated sleep disturbances. These symptoms were present since the end of adolescence and were stable over time. Akathisia, a frequent symptom in patients with schizophrenia treated with antipsychotics, was excluded here because the symptoms had begun before antipsychotic treatment and were present only in the evening (Barnes Akathisia Rating Scale global score = 0). The RLS was considered idiopathic because no neurological disorder, uremia (4.2 mmol/L; reference range, 2.6-8.1), and pregnancy (beta-hCG < 2UI/L) were evidenced; ferritin (160 μg/L; reference range, 20–200) and renal function (glomerular filtration rate CKD-EPI = 111 mL/min/1.73 m2; reference range, 90-120) were in the reference range. The RLS had never been treated before. No abnormal involuntary movement was evidenced.
Risperidone (3 mg/d) was prescribed but discontinued after 2 weeks because of worsening of RLS. Indeed, after risperidone treatment, the uncomfortable sensations increased in intensity and frequency and extended to the arms. Thus, liquid haloperidol (11 mg/d) was introduced. This compound was chosen because the hallucinations were severe and because oral solution is available and could facilitate adequate dose management. However, haloperidol was stopped after 3 weeks because of extrapyramidal symptoms (Simpson Angus Scale score = 0.9) and akathisia (Barnes Akathisia Rating Scale global score = 4). Thus, amisulpride, a benzamide antipsychotic with a low risk of neurological symptoms, was chosen (dose up to 600 mg/d). A substantial recovery of RLS was observed after 2 weeks (IRLS score = 16), along with improvement of psychotic symptoms (PANSS total score = 40: positive score = 7, negative score = 14, general psychopathology score = 19). Interestingly, the patient stopped amisulpride for 3 days (because of bacterial conjunctivitis that she attributed to her treatment), leading to a worsening of RLS (IRLS score = 31). Restless legs syndrome improved after the reintroduction of amisulpride (400 mg/d) and recovered completely after one more week of treatment (IRLS score = 1).
Of note, the anticholinergic drug tropatepine (20 mg/d) was prescribed during 4 days to treat acute dystonia related to risperidone treatment. No effect on RLS was observed. Benzodiazepine treatments were also used during hospitalization to treat acute anxiety symptoms.
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