Evie Summers
Sleep is crucial for promoting a healthy recovery after a stroke, but excessive sleep can be a sign of more serious underlying problems. Many stroke survivors experience fatigue and excessive sleepiness during the initial phases of stroke recovery. This condition is known as excessive daytime sleepiness (EDS) or hypersomnia, and it affects between 18% and 72% of stroke survivors. EDS can negatively impact a person's quality of life, cognitive functioning, and daytime functional performance. While the brain normally uses 20% of the body's total energy, that percentage increases during the first few weeks to months following a stroke, as the brain requires extra energy to heal. This can leave stroke survivors feeling exhausted and struggling to stay awake during the day.
| Characteristics | Values |
|---|---|
| Prevalence of EDS in stroke survivors | 18% to 72% |
| Excessive daytime sleepiness (EDS) | A syndrome that causes fatigue and excessive napping following a stroke |
| EDS as a primary disorder | EDS may develop as a complication of stroke, head injury, or cancer |
| EDS as a secondary disorder | EDS may occur secondarily to medications, behaviours, or other sleep disorders |
| Factors associated with EDS | Sleep-related breathing disorders, Reversed Robin Hood Syndrome, Depression |
| EDS persistence | EDS usually decreases after a few weeks but can last for over six months in about 30% of stroke survivors |
| Impact of EDS | Interference with stroke rehabilitation, recovery, mood, relationships, and daily activities |
| Treatment options | Address underlying conditions, pharmacological treatments, improve sleep hygiene, lifestyle changes |
| Sleep-related breathing disorders | Obstructive sleep apnea is the most common type |
| Reversed Robin Hood Syndrome | The brain attempts to redirect blood flow from damaged areas to healthy ones |
| Depression | Mental health disorders such as depression are common after a stroke |
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What You'll Learn
Excessive daytime sleepiness (EDS) and hypersomnia
EDS is often caused by chronic partial sleep deprivation, disorders of the central nervous system, psychological conditions, and neurological disorders. Sleep-disordered breathing, particularly obstructive sleep apnea (OSA), is another independent risk factor for stroke and a common cause of fragmented sleep, which may also cause EDS.
The following are some factors that can contribute to EDS in stroke survivors:
- Sleep-disordered breathing: This includes conditions such as OSA, which cause partial or complete cessation of breathing during sleep, resulting in excessive daytime sleepiness.
- Reversed Robin Hood Syndrome: This syndrome occurs when the brain redirects blood flow from damaged areas to healthy ones, which may lead to excessive sleeping after a stroke.
- Depression: Mental health disorders such as depression are common after a stroke and can cause fatigue and drowsiness, leading to excessive daytime sleep.
- Physical disability: Reduced physical activity levels due to physical disability can also contribute to EDS in stroke survivors.
The outcomes associated with EDS in stroke survivors can be serious and negative, including neurocognitive, functional, and health-related consequences. Some of the potential outcomes include:
- Neurological decline: EDS can lead to a decrease in alertness and cognitive functioning.
- Learning and memory deficits: EDS may impact a person's ability to learn and process memories.
- Physical function decline: EDS can interfere with rehabilitation and recovery, affecting a person's physical function.
- Mood instability: EDS has been linked to anxiety and depression.
- Increased risk of recurring stroke: EDS is an independent risk factor for stroke.
Addressing underlying conditions, such as sleep apnea or depression, is an important step in managing EDS. Stimulant medications, improving sleep hygiene, and cognitive-behavioral therapy are also recommended approaches to treat and manage EDS.
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Sleep-related breathing disorders
Obstructive Sleep Apnea (OSA)
OSA is a common disorder that is often encountered in family medicine. It is characterised by recurrent episodes of partial or complete closure of the upper airway, resulting in disturbed breathing during sleep. This can lead to decreased quality of life and significant medical complications if left untreated. OSA is associated with cardiovascular issues such as high blood pressure, coronary artery disease, stroke, and atrial fibrillation. Risk factors for OSA include obesity, age, and gender, as it is more common in men than women.
Central Sleep Apnea
Central sleep apnea occurs when there is a lack of effort to breathe during sleep. This can be due to the brain not sending the proper signals to the respiratory muscles, or the respiratory muscles not responding to the brain's signals. Central sleep apnea is less common than OSA, affecting just under 1% of people over 40 and is more common in males.
Sleep-Related Hypoventilation
Sleep-related hypoventilation disorders involve elevated blood levels of carbon dioxide during sleep due to a lack of air moving in and out of the lungs. This can be caused by lung conditions such as chronic obstructive pulmonary disease (COPD) or pulmonary hypertension, as well as disorders that affect the nervous system and certain types of medications. Obesity hypoventilation syndrome (OHS) is a specific type of sleep-related hypoventilation disorder that occurs in obese patients and often co-occurs with OSA.
Sleep-Related Hypoxemia Disorder
Sleep-related hypoxemia disorder is characterised by low levels of oxygen in the blood without a significant increase in carbon dioxide levels. This is often the result of another health problem that affects breathing, such as lung conditions.
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Reversed Robin Hood Syndrome
The redirection of blood flow is thought to be the brain's way of compensating for the damage caused by the stroke. While the exact mechanisms are not yet fully understood, this syndrome may be a contributing factor to the excessive sleepiness experienced by many stroke survivors.
Excessive daytime sleepiness (EDS) is a common symptom among stroke survivors, with an estimated prevalence rate ranging from 18% to 72%. EDS can have a significant impact on the quality of life, cognitive functioning, and daytime functional performance of those affected. It can also increase the risk of driving and industrial accidents.
The causes of EDS in stroke survivors are multifaceted and may include factors such as sleep-disordered breathing, depression, and the underlying stroke itself. Additionally, the use of certain medications and physical disability have also been implicated as potential contributors to EDS.
The outcomes associated with EDS in stroke survivors can be negative and far-reaching. These can include neurological decline, reduced alertness, learning deficits, memory problems, physical function decline, and impaired driving ability. Furthermore, EDS has been linked to increased mortality rates and elevated risk for recurring stroke.
Treating EDS in stroke survivors may involve addressing underlying conditions such as sleep apnea or depression. Stimulant medications, such as modafinil, may also be prescribed to help improve alertness and reduce tiredness during the day. Additionally, improving sleep hygiene and engaging in regular physical activity can also help to manage EDS.
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Depression
The number of patients currently being examined for PSD is over 7,000, and the prevalence of PSD is about 30% in stroke survivors. The percentage varies with the research population, depression severity, and follow-up durations enrolled by researchers.
Treatments for PSD include the use of antidepressants such as SSRIs (selective serotonin reuptake inhibitors), nortriptyline, and reboxetine. CBT (cognitive-behavioral therapy), electroconvulsive therapy, and psychological treatments are also promising but require more evidence.
Early treatment of PSD is beneficial for improving physical activities and stroke recovery. Patients with PSD who took antidepressants from the first month of their stroke presented more improvement in daily living activities than those who took antidepressants after one month.
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Medication and stimulants
Stimulants such as amphetamines, modafinil, and Ritalin (methylphenidate) can be used to help stroke patients boost alertness and reduce tiredness throughout the day. However, it is important to note that these stimulants can also have serious side effects, including increased heart rate and blood pressure, which may increase the risk of another stroke. Therefore, careful monitoring of heart rate and blood pressure is necessary for patients taking these stimulants. Additionally, individuals can develop a tolerance to these drugs, making them unsuitable for long-term use. However, in cases where timing is crucial for rehabilitation, short-term use of stimulants may be beneficial for optimising recovery speed.
Ritalin, for example, is a medication that increases neurotransmitter activity in the brain and is primarily used to manage cognitive and behavioural difficulties in individuals with ADHD. It works by blocking the reuptake of the neurotransmitters dopamine and norepinephrine, resulting in increased levels of these "feel-good" neurotransmitters in the brain, which can help boost mood and concentration. Due to its effects on motivation and mood, Ritalin is also used off-label as an alternative to antidepressants. This can be especially helpful for stroke survivors who develop post-stroke depression, which affects over 40% of stroke survivors. Ritalin can help enhance their ability to focus, act, and perceive a brighter future, thus improving their quality of life after stroke.
Another stimulant, amphetamine, has shown promising results in small initial studies for enhancing post-stroke motor and language recovery. However, a subsequent larger randomised, double-blind, placebo-controlled trial of amphetamine in 71 patients with sub-acute stroke did not show a drug-related benefit. More research is needed to determine the optimal dose and administration schedule for amphetamine in stroke patients.
Selective serotonin reuptake inhibitor (SSRI) drugs, such as fluoxetine, have also shown potential for promoting improved motor outcome after stroke. The FLAME study, a double-blind, placebo-controlled trial, found that non-depressed hemiplegic/hemiparetic patients who were randomised to 3 months of oral fluoxetine (20 mg/day) showed significantly greater gains in motor recovery compared to the placebo group. This improvement in motor function is clinically meaningful and adds to the substantial clinical experience with SSRIs, which have a generally strong safety record.
Dopaminergic drugs, such as L-Dopa, have also been studied for their potential to enhance motor recovery after stroke. A randomised, double-blind, placebo-controlled study found that 100 mg of L-Dopa per day, given as Sinemet and combined with physical therapy, was significantly better than placebo plus physical therapy on motor recovery after three weeks. However, more large-scale studies are needed to confirm these results.
Noradrenergic drugs have also shown promising results in small studies for promoting stroke recovery. For example, a pilot study of reboxetine, a noradrenergic drug, found improvements in motor function in chronic stroke patients.
It is important to note that the effectiveness of these drugs may depend on the timing of administration after the stroke. Recovery after stroke focuses on maximising the effects of neuroplasticity, and the brain's potential for increased plasticity may be highest in the early months after the stroke. Therefore, the window for therapeutic effectiveness is typically measured in days or weeks after the stroke, and rehabilitation should be most intensely pursued during this critical time.
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Frequently asked questions
EDS, also known as hypersomnia, is a condition that causes fatigue and excessive napping following a stroke. People with EDS feel compelled to sleep throughout the day, even after a full night's rest. Between 18% and 72% of stroke survivors experience EDS.
The most common symptoms of EDS include feeling overly drowsy throughout the day, difficulty staying awake during activities, excessive napping, slow response time, and difficulty concentrating.
EDS in stroke patients can be caused by various factors, including fatigue, medication, sleep-related breathing problems such as sleep apnea, depression, and Reversed Robin Hood Syndrome (where the brain favours sleep over other processes).
There are several treatment options for EDS, including stimulants to boost alertness, improving sleep quality through lifestyle changes, exercise, cognitive-behavioural therapy, and addressing underlying causes such as depression, brain damage, or medication side effects.
