Dr Sher Mohammad and other authors discuss the anaesthetic implications and management of Restless Leg Syndrome, a chronic neurological sensory disorder that interferes with rest and sleep.
History and background
The first case report of Restless Leg Syndrome(RLS) was published in 1685 by Thomas Willis[1]. Karl Ekbom’s doctoral thesis “Restless Legs Syndrome: A Clinical Study of a Hitherto Overlooked Disease in the Legs Characterized by Peculiar paraesthesia (“anxietas Tibiarum”), Pain and Weakness and Occurring In Two Main Forms, asthenia Crurum Paraesthetica and asthenia Crurum Dolorosa”[1,2,3] was published in 1945. He was awarded with the Swedish Lennmalms Prize[4] for his work in 1949. For obvious reason, RLS has also been referred to as Willis-Ekbom syndrome.
Incidence and prevalence
RLS is a chronic neurological sensory disorder that interferes with rest and sleep. The prevalence of RLS is typically low in Asian countries and approximately 1-4% in Japan. It has a higher prevalence in women versus men. Early onset RLS has a peak incidence at 20-40 years of age, and a prevalence of 1.9% among children age 8-11 years.
Chemical disturbances leading to RLS
Although it is only partly understood, the pathophysiology of restless legs syndrome may involve dopamine and iron system perturbations. The interactions between impaired neuronal iron uptake and the functions of the neuromelanin-containing and dopamine-producing cells have roles in RLS development, indicating that iron deficiency might affect the brain dopaminergic transmissions in different ways (iron is a co-factor for L-DOPA which is a precursor of dopamine). Medial thalamic nuclei may also have a role in RLS as part of the limbic system modulated by the dopaminergic system which may affect pain perception. Improvement of RLS symptoms occurs in people receiving low-dose dopamine agonists(no longer first line of therapy though).
Primary and secondary RLS
Primary RLS is considered idiopathic and usually begins slowly, before approximately 40 years of age, and may disappear for months or even years. But it is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains.
Secondary RLS often has a sudden onset after age 40. It is mostly associated with specific medical conditions such as trauma, surgery, pregnancy or certain diet/drugs.
Causes of and conditions associated with RLS
While the cause is generally elusive, it is believed to be caused by changes in the neurotransmitter dopamine resulting from an abnormal use of iron by the nervous system. Total body iron deficiency results in RLS which could be due to underlying anaemia caused by internal bleeding (e.g. menstrual) or bone marrow issues. Other associated conditions may include end-stage kidney disease and haemodialysis, folate deficiency, magnesium deficiency, sleep apnoea, diabetes/impaired glucose tolerance, peripheral neuropathy, Parkinson’s disease, and certain autoimmune diseases (multiple sclerosis). RLS can worsen in pregnancy, possibly due to high oestrogen levels. Use of alcohol, nicotine products, and caffeine may be associated with RLS. A 2014 study from the American Academy of Neurology also found that reduced leg oxygen levels were strongly associated with restless legs syndrome symptom severity in untreated patients. Genetics also play a role as more than 60%