Relevance of the restless legs syndrome (willisekbom disease) for daily clinical practice with patients with psychiatric disorders

• Autor(a) principal: Tavares, Almir
• Data de Publicação: 2017
• Outros Autores: Dutra, Tatiana Leal, Daker, Maurício Viotti
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Debates em Psiquiatria (Online)
• DOI: 10.25118/2236-918x-7-4-4
• Texto Completo: https://revistardp.org.br/revista/article/view/86
• topic: Síndrome das pernas inquietas; doença de Willis-Ekbom; transtorno do sono; movimentos periódicos dos membros; metabolismo do ferro cerebral; dopamina; Restless legs syndrome; Willis-Ekbom disease; sleep disorder; periodic limb movements; brain iron metabolism; dopamine

In the past, the restless legs syndrome (RLS) was conceptualized as a sensitivity neurosis and tibial anxiety. The objective of the present study is to demonstrate, to physicians in general and psychiatrists in particular, that today, RLS is a complex and chronic, common and treatable, neuropsychiatric disorder with sensorimotor involvement, alterations of the dopaminergic system, and brain iron homeostasis disorders. Symptoms are exclusively subjective and can be chronic-persistent or intermittent. There is an urge to move the legs, accompanied by limb dysesthesias, which worsens with rest or inactivity and improves with movement. Diagnosis is exclusively clinical. Some medications have to be reduced or discontinued because they may worsen RLS, e.g., some antidepressants (particularly selective serotonin reuptake inhibitors, serotonin and noradrenalin reuptake inhibitors, and mirtazapine), neuroleptics, antiemetics, antihistamines,among others. It is relevant to observe that no worsening is observed with the anti depressant bupropion. Nonpharmacological treatment includes sleep hygiene and physical acti viti es. The drugs used in the treatment of RLS belong to four groups: dopaminergics (direct agonists and precursors of dopamine); α2δ-ligands; benzodiazepines; and opioids. Augmentati on is the main complicati on of long-term treatment: earlier initi ati on of symptoms in the course of the day; faster start when at rest; sprading of symptoms to the upper limbs and trunk; and shortening of treatment eff ects. Dopaminergic hypersti mulati on is the supposed cause of augmentation.