The COVID-19 pandemic introduced a wide spectrum of health challenges, extending far beyond the initial respiratory illness to include many neurological effects. This includes a notable link between SARS-CoV-2 infection and the onset or worsening of a specific neurological sleep disorder. Restless Legs Syndrome (RLS) is a condition characterized by a powerful, irresistible urge to move the legs, often accompanied by unpleasant sensations. Clinical observations now suggest a connection between a prior COVID-19 infection and the development of this syndrome.
Defining Restless Legs Syndrome
Restless Legs Syndrome (RLS), also known as Willis-Ekbom Disease, is defined by an overwhelming urge to move the limbs, typically the legs. This compulsion is frequently accompanied by uncomfortable sensations deep within the limbs, such as crawling, tingling, or burning feelings. Symptoms characteristically begin or worsen during periods of rest or inactivity, like sitting or lying down, making the condition disruptive to sleep.
Movement, such as walking or stretching, provides temporary relief from the sensations and the urge. RLS symptoms exhibit a distinct circadian pattern, becoming worse in the evening or night than during the day. RLS is classified as either primary (cause unknown or idiopathic) or secondary, resulting from another medical condition. Well-established secondary causes include kidney failure, pregnancy, and iron deficiency.
Evidence of Post-COVID RLS Onset
A growing body of evidence documents the development of new RLS symptoms following an acute COVID-19 infection. Studies indicate that RLS prevalence significantly increased during the pandemic, with some data suggesting a nearly triple rate in women with Long COVID compared to before their infection. This new-onset RLS is often seen as a component of Long COVID.
The RLS symptoms frequently manifest in a distinct post-infectious timeline, appearing weeks to months after the respiratory symptoms have resolved. The severity of the initial COVID-19 infection does not necessarily predict the later onset or severity of RLS. Individuals who experienced mild or moderate acute illness have also developed RLS during their recovery phase. This pattern suggests the underlying mechanism relates to the body’s prolonged response to the infection, rather than solely the acute viral load.
Underlying Biological Drivers
The connection between SARS-CoV-2 and RLS points toward several biological mechanisms that disrupt the central nervous system. One prominent proposed driver is the systemic inflammation and “cytokine storm” triggered by the viral infection. The release of inflammatory molecules, such as IL-6 and TNFα, can compromise the blood-brain barrier. This allows substances to enter the central nervous system, causing microglial activation and interfering with the brain’s signaling processes that regulate RLS.
Another significant factor is the virus’s impact on iron metabolism, a known driver of RLS. COVID-19 infection frequently leads to iron dysregulation, often resulting in a functional iron deficiency in the brain, even if blood iron levels appear normal. Inflammation causes the body to sequester iron away from the bloodstream, which can lead to low serum iron. Since iron is necessary for the production of dopamine—a neurotransmitter implicated in RLS—this functional deficiency directly contributes to the onset of symptoms.
There is also the possibility of a direct neurological impact, including potential viral neurotropism or the activation of autoimmune responses. The immune system’s reaction to the virus may mistakenly target and damage parts of the nervous system, including the dopaminergic pathways in the brain. Damage to these pathways, which control movement and sensation, would directly lead to the characteristic sensorimotor symptoms of RLS. Research also suggests a link through the renin-angiotensin-aldosterone system, which the virus utilizes for cell entry and which has been previously implicated in RLS in other disease states.
Treatment Approaches
Management of RLS following a COVID-19 infection begins with non-pharmacological interventions aimed at improving sleep quality and reducing symptom triggers. Maintaining consistent sleep hygiene is important, involving going to bed and waking up at consistent times. Avoiding common RLS triggers such as caffeine, alcohol, and nicotine, particularly in the evening, can also reduce symptoms.
Moderate, regular exercise, like walking or gentle stretching, improves circulation and reduces leg discomfort. Caution is advised for Long COVID patients with post-exertional malaise. Other supportive therapies, such as warm baths, leg massage, or applying heat, can provide temporary relief.
A targeted approach involves a thorough medical evaluation to check for underlying factors, particularly iron deficiency. If blood tests reveal low iron levels or low ferritin, iron supplementation is often a first-line treatment, sometimes combined with Vitamin C to enhance absorption. For more persistent or severe symptoms, healthcare providers may prescribe pharmacological options. These include:
- Gabapentinoids (e.g., gabapentin or pregabalin), which are effective for patients experiencing anxiety, pain, or sleep disturbances.
- Dopamine agonists, which act on the brain’s dopamine pathways to alleviate RLS symptoms.