Posts Tagged Sleep disorders

[BLOG POST] Mozart and epilepsy: the rhythm beats on

 

I can’t seem to get away from the theme of Mozart and epilepsy. When I first looked at this, in a blog post titled Mozart and seizures? The links between epilepsy and music, I took the topic rather lightly, more a subscript than a headline you may say. But I have since learnt to take the links between epilepsy and music more seriously.

By Barbara Krafft – The Bridgeman Art Library, Object 574471, Public Domain, Link

 

The major trigger for my ‘road to Damascus’ conversion is a 2018 paper titled Study of the Mozart effect in children with epileptic electroencephalograms, published in the journal Seizure. The paper was an eye-opener because it gave a very helpful comprehensive context to the broader beneficial effect of music…not just in epilepsy, but in other neurological disorders such as Parkinson’s diseasedementia and sleep disordersThe authors, Elyza Grylls and colleagues, started on the established premise that Mozart’s music has a beneficial effect on epilepsy. What they wanted to know was if other forms of music have a similar settling effect on epilepsy, or if only Mozart’s music carries the magic touch. The authors therefore played Mozart’s Sonata for two pianos in D major (K448) to 40 children with epilepsy who were undergoing an EEG (electroencephalogram, or electrical brain wave test). They then compared this with the effect of playing other types of music. Remarkably, they found that only Mozart’s Sonata led to a significant reduction in EEG epileptic discharges.

Public Domain, Link

The authors concluded that there was indeed an anti-epileptic effect of Mozart’s music, the so-called  ‘Mozart therapy’. But what is so special about K448? They speculate that it has to do with the structure of Mozart’s music, containing as it does, long periodicities. Interestingly, the music of Yanni, which is similarly structured, has somewhat a similar effect on brain wave activity. On the contrary, and sorry to Beethoven fans, Fur Elise doesn’t have this effect.

By W.J. Baker (held the expired copyright on the photograph) – Library of Congress[1]Contrairement à une erreur fréquemment répandue le buste a été réalisé par Hugo Hagen, non pas à partir du masque mortuaire mais, comme de nombreux autres, d’après le masque réalisé en 1812 par Franz Klein pour un buste qu’il devait réaliser ensuite., Public Domain, Link

So what does the structure of Mozart’s music do to the brain? One suggestion is that Mozart’s music enhances the body’s parasympathetic drive; this reduces the heart rate, and thereby inhibits the brain’s propensity to epileptic seizures. The suppression of this parasympathetic drive is of course the theory behind using vagus nerve stimulation (VNS) to treat drug-resistant epilepsy. For more on VNS, see my previous blog, Vagus nerve stimulation: from neurology and beyond!

By Bionerd – MRI at Charite Mitte, Berlin (used with permission), CC BY 3.0Link

You have surely wondered by now if K448 is the only one of Mozart’s compositions to have an anti-epileptic effect. It doesn’t matter if you have not, because the authors of another interesting paper did. They titled their study, published in 2018, Mozart’s music in children with drug-refractory epileptic encephalopathies: comparison of two protocols. Published in the journal Epilepsy and Behaviour, the authors, Giangennaro Coppola and colleagues, compared the effect of K448 with a set of his other compositions. Intriguingly they found that the composition set actually had a greater effect in epilepsy than K448…by a wide margin of 70% to 20%! Furthermore, the set was better tolerated by the children; they were less irritable and had a better nighttime sleep quality.   

https://www.publicdomainpictures.net/en/view-image.php?image=76907&picture=dog-amp-child-painting

It therefore appears as if it all rosy in the garden of music and the brain. But it is not! As every rose grows on a thorny tree, so do some forms of music trigger epileptic seizures. This so-called musicogenic epilepsy is well-recognised, and two recent culprits are the music of Sean Paul, discussed in the journal Scientific American , and the music of Ne Yo, explored by NME. Therefore you should craft your playlist wisely.

By CLASSICNEYO – Own workCC BY-SA 4.0Link

So, is it time for neurologists to start prescribing music?

Or is it too much of a double-edged sword?

Music is #SimplyIrresistible. Luca Florio on Flickr. https://www.flickr.com/photos/elle_florio/29516744480

via Mozart and epilepsy: the rhythm beats on – The Neurology Lounge

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[BLOG POST] Sleep Disorders After Brain Injury, PTSD, TBI

Why Do So Many Survivors Have Sleep Disorders After Brain Injury?

January 2018,  Written by Bill Herrin

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January’s Brain Injury Journey Bulletin dives into the new year with a topic that often keeps people up at night…sleep disorders after TBI.

Sleep. It can be elusive, and one of the most frustrating things to accomplish after brain injury – especially on a consistent basis. Quite often, sleep disorders can take hold after brain injury – and cause everything from anxiousness to feeling depressed, tired, irritable, and more. In this issue of the Brain Injury Journey Bulletin, we’re going to take a look at all the things that sleep can affect, and some ways to conquer a sleep disorder after TBI.

Tossing and Turning

When your quality of life is being affected by lack of sleep, the desperation of wanting to rest can actually hinder you from getting the rest you need. Here are some changes in sleep patterns after TBI that are quite common:

  • difficulty falling asleep easily
  • trouble staying asleep throughout the night
  • waking up very early in the morning and not falling back to sleep
  • falling asleep and awakening far later than desired
  • purposely staying up late at night to get things done

Examples are:

  • You get into bed around 10 but it takes you several hours to fall asleep.
  • You wake up frequently during the night for no major reason.
  • You wake up at 4 in the morning and cannot fall back to sleep.
  • You’re up late every night working on the computer and your partner keeps asking
    you to come to bed.

Sleep Disorders and Other Factors

There are lots of different sleep disorders, and they can involve many different parts of the brain. Here are some of the more well-known sleep disorders that people encounter: Insomnia, extreme drowsiness, altered sleep patterns and Narcolepsy. Other disorders that can directly contribute to lack of sleep are Restless Leg Syndrome, teeth grinding or clenching, involuntary movements of your arms/legs during sleep, sleepwalking, sleep apnea, etc. Other factors that can deprive you from sleep are pain, alcohol, caffeine and nicotine, depression…and naps. A poorly timed nap (late in the day) obviously can end up backfiring on you later that night! It’s best to limit the length of naps so they help you get through the day, but don’t keep you up at night.

When PTSD is involved, especially in military veterans, sleep disorders can disturb sleep to the point of a person dreading bedtime, and efforts to quiet the symptoms with drugs or alcohol can make symptoms worse in the long run. Hyper-alertness, flashbacks, or nightmares can play a big part in keeping PTSD survivors up at night.

Research has found that sleep disorders are 3 times more common in persons with TBI than the general population, that about 60% of TBI survivors have ongoing problems with sleeping, that women are more affected than men…and that aging increases the likelihood of sleep problems.

This group has been researching how people sleep, and they have collected some great information about how drug addiction and recovery can affect a person’s ability to have healthy, restorative sleep….along with addressing other sleep disorders. You can read the full guide at this link.

Better sleep?

Sleep, when achieved regularly, brings a bevy of positive side-effects, and is an essential component of mental and physical well-being. It can affect healing of the brain and body, improve short-term memory and attention, improvement of your mood, and it can even reduce physical pain. The main thing that sleep obviously provides is that you feel rested and more alert!

How You Sleep Also Matters

Being uncomfortable can affect your sleep more than you realize, too. Here’s a link to an article on WebMD.com that covers different sleep positions, and how they can help (or hinder) sleep, or even cause pain in your back, neck, etc.  Here’s the link.

Talk It Over With Your Doctor

There are plenty of over-the-counter and off-the-shelf medications specifically made to help you “catch some ZZZZZ’s” – but it’s very important that persons with brain injury talk to their doctor about the side effects of sleep medications before using any of them.

Brain injury presents a variety of issues that can cause stress, and the stress can easily parlay itself into loss of sleep. If loss of sleep is wearing you down, or slowing your recovery after TBI, you should speak with a physician right away. Once you seek medical advice, the doctor can help you discover the causes and effects of your sleep issues, and discuss all possibilities of easing the loss of sleep. From sleep labs to prescription medications, to discussing techniques for easing your mind before bedtime, your doctor will hopefully help you resolve the sleep deprivation to some degree.

Suggested Reading

The person you are with little or no sleep, versus the one you are when well rested can be like the difference in…well, like night and day! Tips for managing your sleep schedule, and how to improve it, are available in this easy-to-read tip card – available on our website. It’s titled “Sleep after brain injury”, and if you go to this link, you can get a free tip card and catalog.  Here’s the link. for the catalog & tip card. Here’s more info on the SLEEP tip card.

New Year, New Sleep Habits?

With a new year started, you can reference any issues imaginable that relate to PTSD, TBI, ABI, brain injury, concussion, and more, on Lash & Associates’ blog page. Specifically relating to the new year, realistic resolutions after TBI, here is a blog article by Donna O’Donnell Figurski that talks all about it. Here’s the link.

Knowing that stress and anxiety (after TBI) can take its toll, this blog post by Marilyn Lash and Taryn Stejskal, discusses managing stress, and the symptoms of stress that become evident when they’re taking their toll on your health and well-being. Here’s the link.

Blog Posts Galore On A Wide Range of TBI Issues

Feel free to keyword search our entire collection of blog posts, many written by well-known experts, clinicians in the field of brain injury, and also people who have survived brain injury, had family members that have a TBI, and much more. It’s a treasure trove of information that is available for FREE, 24/7/365. It’s all for you at this link!

Resolution of sleeping issues is a “2018 Resolution” for the new year that many have added to their lists to  achieve. We hope that you have a great new year, and that you rest assured…and sleep well!

 

 

 

 

via Sleep Disorders After Brain Injury, PTSD, TBI

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[WEB SITE] The Relationship Between Epilepsy and Sleep

The Thomas Haydn Trust in an aid to understanding Epilepsy and Sleep has published this mobile article. This article is not extensive and should not be used as medical advice; it’s intended for information purposes only. This dictionary is also available for download from http://www.thomashaydntrust.com/publications.htm in .pdf format. [Please note that this is version 1 and further updates may be availalbe]

Written by

M C Walker, S M Sisodiya

Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, Queen Square, London, and National Society for Epilepsy, Chalfont St Peter, Bucks. London, and National Society for Epilepsy, Chalfont St Peter, Bucks. September 2005. This article can be reproduced for educational purposes.

Introduction

Epilepsy has a complex association with sleep. Certain seizures are more common during sleep, and may show prominent diurnal variation. Rarely, nocturnal seizures are the only manifestation of an epileptic disorder and these can be confused with a parasomnia. Conversely, certain sleep disorders are not uncommonly misdiagnosed as epilepsy. Lastly, sleep disorders can exacerbate epilepsy and epilepsy can exacerbate certain sleep disorders. This chapter is thus divided into four sections: normal sleep physiology and the relationship to seizures; the interaction of sleep disorders and epilepsy; and the importance of sleep disorders in diagnosis.

Normal sleep physiology and the relationship to seizures

Adults require on average 7 – 8 hours sleep a night. This sleep is divided into two distinct states – rapid eye movement (REM) sleep and non-REM sleep. These two sleep states cycle over approximately 90 minutes throughout the night with the REM periods becoming progressively longer as sleep continues. Thus there is a greater proportion of REM sleep late on in the sleep cycles. REM sleep accounts for about a quarter of sleep time. During REM sleep, dreams occur; hypotonia or atonia of major muscles prevents dream enactment. REM sleep is also associated with irregular breathing and increased variability in blood pressure and heart rate. Non-REM sleep is divided into four stages (stages I – IV) defined by specific EEG criteria. Stages I/II represent light sleep, while stages III/IV represent deep, slow-wave sleep.

Gowers noted that in some patients, epileptic seizures occurred mainly in sleep. Sleep influences cortical excitability and neuronal synchrony. Surveys have suggested that 10 – 45% of patients have seizures that occur predominantly or exclusively during sleep or occur with sleep deprivation. EEG activation in epilepsy commonly occurs during sleep, so that sleep recordings are much more likely to demonstrate epileptiform abnormalities. These are usually most frequent during non-REM sleep and often have a propensity to spread so that the epileptiform discharges are frequently observed over a wider field than is seen during the wake state. Sleep deprivation (especially in generalised epilepsies) can also ‘activate’ the EEG, but can induce seizures in some patients. Thus many units perform sleep EEGs with only moderate sleep deprivation (late night, early morning), avoidance of stimulants (e.g. caffeine-containing drinks) and EEG recording in the afternoon. Sleep-induced EEGs in which the patient is given a mild sedative (e.g. chloral hydrate) are also useful.

Sleep and generalised seizures

Thalamocortical rhythms are activated during non-REM sleep giving rise to sleep spindles. Since similar circuits are involved in the generation of spike-wave discharges in primary generalised epilepsy, it is perhaps not surprising that non-REM sleep often promotes spike-wave discharges. Epileptiform discharges and seizures in primary generalised epilepsies are both commonly promoted by sleep deprivation. Furthermore, primary generalised seizures often occur within a couple of hours of waking, whether from overnight sleep or daytime naps. This is most notable with juvenile myoclonic epilepsy in which both myoclonus and tonic-clonic seizures occur shortly after waking, and the

Διαφήμιση

syndrome of tonic-clonic seizures on awakening described by Janz. Seizure onset in this syndrome is from 6 – 35 years and the prognosis for eventual remission is good.

Certain epileptic encephalopathies show marked diurnal variation in seizure manifestation and electrographic activity. An example is the generalised repetitive fast discharge during slow-wave sleep occurring in Lennox-Gastaut syndrome. Another example is electrical status epilepticus during sleep (ESES). This is characterised by spike and wave discharges in 85 – 100% of non-REM sleep. This phenomenon is associated with certain epilepsy syndromes, including Landau-Kleffner, Lennox-Gastaut syndrome, continuous spikes and waves during sleep and benign epilepsy of childhood with rolandic spikes. ESES can thus be a component of a number of different epilepsy syndromes with agedependent onset, many seizure types, and varying degrees of neuropsychological deterioration. Indeed, ESES has been described in the setting of an autistic syndrome alone with no other

manifestation of epilepsy.

Sleep and partial epilepsies

Inter-ictal epileptiform abnormalities on the EEG occur more frequently during sleep, especially stage III/IV sleep (slow-wave sleep). The discharges have a greater propensity to spread during sleep, and thus are often seen over a wider field than discharges occurring during wakefulness. Temporal lobe seizures are relatively uncommon during sleep, while frontal lobe seizures occur often predominantly (sometimes exclusively) during sleep. Nocturnal frontal lobe seizures can be manifest as: brief stereotypical, abrupt arousals; complex stereotypical, nocturnal movements; or episodic nocturnal wanderings with confusion. Inherited frontal lobe epilepsies can manifest with only nocturnal events that can be confused with parasomnias (see below). Autosomal dominant nocturnal frontal lobe epilepsy is such an epilepsy. This has been associated with mutations in alpha-4 and beta-2 subunits of the neuronal nicotinic acetylcholine receptor. Onset is usually in adolescence with seizures occurring frequently, sometimes every night. The seizures are provoked by stress, sleep deprivation and menstruation, and often respond well to carbamazepine.

The interaction of sleep disorders and epilepsy

Seizures can disrupt sleep architecture. Complex partial seizures at night disrupt normal sleep patterns, decrease REM sleep and increase daytime drowsiness. Daytime complex partial seizures can also decrease subsequent REM sleep, which may contribute to impaired function. Antiepileptic drugs (AEDs) can also disrupt normal sleep patterns, although there are conflicting data (this is partially due to drugs having different short-term and long-term effects). Carbamazepine, for example, given acutely reduces and fragments REM sleep, but these effects are reversed after a month of treatment. The GABAergic drugs can have a profound effect on sleep; phenobarbitone and benzodiazepines prolong non-REM sleep and shorten REM sleep, while tiagabine increases slow-wave sleep and sleep efficiency. Gabapentin and lamotrigine may both increase REM sleep.

Certain sleep disorders are more common in patients with epilepsy. This is particularly so with obstructive sleep apnoea which is more common in patients with epilepsy and can also exacerbate seizures. Indeed, sleep apnoea is approximately twice as common in those with refractory epilepsy than in the general population. The reasons why this is so are unknown, but may relate to increased body weight, use of AEDs, underlying seizure aetiology or the epilepsy syndrome itself.

Patients with obstructive sleep apnoea often find that seizure control improves with treatment of the sleep apnoea. Topiramate may also be a particularly useful drug in these cases.

The importance of sleep disorders in differential diagnosis

On occasions nocturnal seizures can be misdiagnosed as a primary sleep disorder (see above). Conversely, certain sleep disorders can be misdiagnosed as epilepsy and the more common of these will be discussed below. Sleep disorders tend to occur during specific sleep phases and thus usually occur at specific times during the night, while seizures usually occur at any time during the night. There may also be other clues in the history, including age of onset, association with other symptoms (see below) and the stereotypy of the episodes (seizures are usually stereotypical).

In cases where there is some uncertainty, video-EEG polysomnography is the investigation of choice. There are, however, instances in which the diagnosis can be difficult even after overnight video-EEG telemetry as frontal lobe seizures can be brief with any EEG change obscured by movement artefact, and it is often the stereotypy of the episodes that confirms the diagnosis.

Abnormalities of sleep are divided into three main categories: 1) dysomnias or disorders of the sleepwake cycle; 2) parasomnias or disordered behaviour that intrudes into sleep, and 3) sleep disorders associated with medical or psychiatric conditions. Although there is an extensive list of conditions within each of these categories, we will confine ourselves to the clinical features of the more common conditions that can be confused with epilepsy.

Narcolepsy

Narcolepsy is a specific, well-defined disorder with a prevalence of approximately one in 2000. It is a life-long condition usually presenting in late teens or early 20s. Narcolepsy is a disorder of REM sleep and has as its main symptom excessive daytime sleepiness. This is manifest as uncontrollable urges to sleep, not only at times of relaxation (e.g. reading a book, watching television), but also at inappropriate times (e.g. eating a meal or while talking). The sleep is itself usually refreshing. The other typical symptoms are cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations. These represent REM sleep phenomena such as hypotonia/atonia, and dreams occurring at inappropriate times. Cataplexy is a sudden decrease in voluntary muscle tone (especially jaw, neck and limbs) that occurs with sudden emotion like laughter, elation, surprise or anger. This can manifest as jaw dropping, head nods or a feeling of weakness or, in more extreme cases, as falls with ‘paralysis’ lasting sometimes minutes. Consciousness is preserved. Cataplexy is a specific symptom of narcolepsy, although narcolepsy can occur without cataplexy. Sleep paralysis and hypnagogic hallucinations are not particularly specific and can occur in other sleep disorders and with sleep deprivation (especially in the young). Both these phenomena occur shortly after going to sleep or on waking.

Sleep paralysis is a feeling of being awake, but unable to move. This can last minutes and is often very frightening, so can be associated with a feeling of panic. Hypnagogic/hypnopompic hallucinations are visual or auditory hallucinations occurring while dozing/falling asleep or on waking; often the hallucinations are frightening, especially if associated with sleep paralysis.

Narcolepsy is associated with HLA type. Approximately 90% of all narcoleptic patients with definite cataplexy have the HLA allele HLA DQB1*0602 (often in combination with HLA DR2), compared with approximately 25% of the general population. The sensitivity of this test is decreased to 70% if cataplexy is not present. The strong association with HLA type has raised the possibility that narcolepsy is an autoimmune disorder. Recently loss of hypocretin-containing neurons in the hypothalamus has been associated with narcolepsy, and it is likely that narcolepsy is due to deficiency in hypocretin (orexin).

Since narcolepsy is a life-long condition with possibly addictive treatment, the diagnosis should always be confirmed with multiple sleep latency tests (MSLT). During this test five episodes of sleep are permitted during a day; rapid onset of sleep and REM sleep within 15 minutes in the absence of sleep deprivation are indicative of narcolepsy.

The excessive sleepiness of narcolepsy can be treated with modafinil, methylphenidate or dexamphetamine and regulated daytime naps. The cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations respond to antidepressants (fluoxetine or clomipramine are the most frequently prescribed). People with narcolepsy often have fragmented, poor sleep at night, and good sleep hygiene can be helpful.

Sleep apnoea

Sleep apnoea can be divided into the relatively common obstructive sleep apnoea and the rarer central sleep apnoea. Obstructive sleep apnoea is more common in men than women and is associated with obesity, micrognathia and large neck size. The prevalence may be as high as 4% in men, and 2% in women. The symptoms suggestive of obstructive sleep apnoea are loud snoring, observed nocturnal apnoeic spells, waking at night fighting for breath or with a feeling of choking, morning headache, daytime somnolence, personality change and decreased libido. Although the daytime somnolence can be as severe as narcolepsy, the naps are not usually refreshing and are longer. Obstructive sleep apnoea and central sleep apnoea can be associated with neurological disease, but central sleep apnoea can also occur as an idiopathic syndrome. The correct diagnosis requires polysomnography with measures of oxygen saturations and nasal airflow or chest movements. To be pathological a sleep apnoea or hypopnoea (a 50% reduction in airflow) has to last ten seconds and there need to be more than five apnoeas/hypopnoeas per hour (the precise number to make a diagnosis varies from sleep laboratory to sleep laboratory).

Uncontrolled sleep apnoea can lead to hypertension, cardiac failure, pulmonary hypertension and stroke. In addition, sleep apnoea has been reported to worsen other sleep conditions, such as narcolepsy, and to worsen seizure control.

Treatment of sleep apnoea should include avoidance of alcohol and sedatives and weight reduction. Pharmacological treatment is not particularly effective, although REM suppressants such as protriptyline can be helpful. The mainstays of treatment are surgical and include tonsillectomies, adenoidectomy and procedures to widen the airway, and the use of mechanical devices. Dental appliances to pull the bottom jaw forward can be effective in mild cases, but continuous positive airway pressure administered by a nasal mask has become largely the treatment of choice for moderate/severe obstructive sleep apnoea. In cases associated with neuromuscular weakness intermittent positive pressure ventilation is often necessary.

Restless legs syndrome/periodic limb movements in sleep

Restless legs syndrome (RLS) and periodic limb movements in sleep (PLMS) can occur in association or separately. Most people with RLS also have PLMS, but the converse is not true and most people with PLMS do not have RLS. RLS is characterised by an unpleasant sensation in the legs, often described as tingling, cramping or crawling, and an associated overwhelming urge to move the legs. These sensations are usually worse in the evening, and movement only provides temporary relief. RLS affects about 5% of the population. Periodic limb movements in sleep are brief, repetitive jerking of usually the legs that occur every 20 – 40 seconds. These occur in non-REM sleep and can cause frequent arousals. PLMS occurs in about 50% of people over 65 years. These conditions can also be associated with daytime jerks. Both RLS and PLMS can be familial, but can be secondary to peripheral neuropathy (especially diabetic, uraemic and alcoholic neuropathies), iron deficiency, pregnancy and rarely spinal cord lesions.

Symptomatic relief can be achieved with benzodiazepines, gabapentin and opioids, but L-DOPA and dopamine agonists are the mainstay of treatment.

Sleep-wake transition disorders

The most common of these are hypnic jerks or myoclonic jerks that occur on going to sleep or on waking. They are entirely benign in nature, and require no treatment. They can occur in association with other sleep disorders. Rhythmic movement disorder is a collection of conditions occurring in infancy and childhood characterised by repetitive movements occurring immediately prior to sleep onset that can continue into light sleep. One of the most dramatic is headbanging or jactatio capitis nocturna. Persistence of these rhythmic movements beyond the age of ten years is often associated with learning difficulties, autism or emotional disturbance. Sleep-talking can occur during non-REM and REM sleep, but is often seen with wake-sleep transition and is a common and entirely benign phenomenon.

Nocturnal enuresis

Nocturnal enuresis is a common disorder that can occur throughout the night. Although diagnosis is straightforward, it can recur in childhood, and also occurs in the elderly, with approximately 3% of women and 1% of men over the age of 65 years having the disorder. Thus, on occasions, it can be misdiagnosed as nocturnal epilepsy.

Non-REM parasomnias

Non-REM parasomnias usually occur in slow-wave (stage III/IV) sleep. These conditions are often termed arousal disorders and indeed can be induced by forced arousal from slow-wave sleep. There are three main non-REM parasomnias – sleepwalking, night terrors and confusional arousal. These disorders often have a familial basis, but can be brought on by sleep deprivation, alcohol and some drugs. They can also be triggered by other sleep disorders such as sleep apnoea, medical and psychiatric illness. Patients are invariably confused during the event, and are also amnesic for the event. These conditions are most common in children, but do occur in adults.

Sleepwalking may occur in up to 25% of children, with the peak incidence occurring from age 11 – 12 years. The condition is characterised by wanderings often with associated complex behaviours such as carrying objects, and eating. Although speech does occur, communication is usually impossible. The episode usually lasts a matter of minutes. Aggressive and injurious behaviour is uncommon, and should it occur then polysomnography may be indicated to exclude an REM sleep parasomnia (see below), and to confirm the diagnosis. Night terrors are less common and are characterised by screaming, and prominent sympathetic nervous system activity – tachycardia, mydriasis and excessive sweating. Both these conditions are usually benign and rarely need treatment. If dangerous behaviour occurs, then treatment may be indicated. Benzodiazepines, especially clonazepam, are usually very effective.

REM parasomnias

Nightmares are REM phenomena that can occur following sleep deprivation, with certain drugs (e.g. L-DOPA) and in association with psychological and neurological disease. Sleep paralysis (see narcolepsy) is also an REM parasomnia, and may be familial.

Of more concern are REM sleep behaviour disorders. These consist of dream enactment. They are often violent, and tend to occur later in sleep when there is more REM sleep. These are rare and tend to occur in the elderly. In over one-third of cases, REM sleep behaviour disorders are symptomatic of an underlying neurological disease such as dementia, multisystem atrophy, Parkinson’s disease, brainstem tumours, multiple sclerosis, subarachnoid haemorrhage and cerebrovascular disease. In view of this, a history of possible REM sleep behaviour disorder needs to be investigated by polysomnography, and if confirmed, then possible aetiologies need to be investigated. REM sleep behaviour disorders respond very well to clonazepam.

Further reading

• BAZIL CW (2002) Sleep and epilepsy. Semin Neurol 22(3) , 321-327.

• FOLDVARY-SCHAEFER NJ (2002) Sleep complaints and epilepsy: the role of seizures,

antiepileptic drugs and sleep disorders. Clin Neurophysiol 19(6) , 514-521.

• MALOW BA (2002) Paroxysmal events in sleep. J Clin Neurophysiol 19(6) , 522-534.

• SCHNEERSON J. Handbook of Sleep Medicine . Blackwell Science, Oxford.

[END]

Source: The Relationship Between Epilepsy and Sleep – Wattpad

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[WEB SITE] The Evaluation and Management of Fatigue – Medscape

What Is Fatigue?

The Annals of Internal Medicine recently published two systematic reviews on the diagnosis and treatment of the chronic fatigue syndrome (CFS).[1,2] The reviews use the term “myalgic encephalomyelitis/chronic fatigue syndrome” (ME/CFS) to define this condition, and as the accompanying editorial points out,[3] an expert panel convened by the Institute of Medicine (IOM) recently found that ME/CFS is a disease with a physiologic basis.[4] It is not a purely psychological problem.

As a sleep physician, I am often asked to evaluate patients with a complaint of fatigue—which raises the question, how does a physician differentiate ME/CFS from other common causes of fatigue? Regardless of etiology, how do we manage fatigue?

Any discussion of fatigue must begin by defining the term. Max Hirshkowitz, PhD, a professor and renowned sleep researcher at Baylor College of Medicine, provided a complete definition that will serve as a reference for the remainder of this review.[5] He stressed the following points:

  1. Fatigue is perceived as a sense of tiredness, exhaustion, or lack of energy.
  2. Fatigue that is nonpathologic will improve with rest.
  3. Fatigue can be provoked by exceeding capacity in terms of time-on-task or stress load.
  4. Stress load can be altered by external (environmental) or internal (genetic predisposition, medical or behavioral illness) factors.
  5. Sleep duration, quality, and timing are significant mediators of the manifestations of fatigue.

In a global sense, then, fatigue occurs when circumstances require some combination of physical and cognitive work that exceeds the capacity of the individual. The point at which this will occur varies by genetics, training, and sleep.

Diagnostic Challenges

There is value in characterizing the patient’s fatigue complaint. Sleep physicians attempt to do this for a living, and it’s a messy business at best. Some will use the term “fatigue” to describe sleepiness, whereas others will not. It is often equated with a central perception, including “lack of energy,” “no motivation,” “difficulty concentrating,” or a perceived deficit in some other aspect of executive function.

Still other patients are using the term “fatigue” to mean exercise intolerance or the inability to push through a difficult workday. Oftentimes, the patient comes to physician attention owing to poor performance in a particular setting—such as on the job, in the classroom, or on the playing field. Clarifying the circumstances under which the perception of fatigue becomes a problem is critical to identifying the cause and designing the mitigation strategy.[5,6]

An appropriate review of the possible contributors to fatigue is also important. Because sleep plays such a pivotal role, a proper sleep history is mandatory. Any discussion of sleep disorders should start with a review of total sleep time. Current data show that cognitive, behavioral, and metabolic changes consistently occur with chronic sleep restriction to less than 6 hours per night.[7-9]

Continue —> The Evaluation and Management of Fatigue

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[ARTICLE] Impact of sleep duration on seizure frequency in adults with epilepsy: A sleep diary study

Highlights

•We studied the effect of partial sleep deprivation on seizure occurrence.

•Adults with epilepsy recorded 237 seizures and sleep and wake periods for 1 month.

•Sleep time was not different between preseizure and seizure-free periods.

•Napping, sleepiness, fatigue, and insomnia symptoms were commonly reported.

•Small degrees of sleep loss were not associated with seizures in our sample.

Abstract

Background

Prolonged sleep deprivation activates epileptiform EEG abnormalities and seizures in people with epilepsy. Few studies have addressed the effect of chronic partial sleep deprivation on seizure occurrence in populations with epilepsy. We tested the primary hypothesis that partial sleep deprivation over 24- and 72-hour periods increases seizure occurrence in adults with epilepsy.

Methods

Forty-four subjects completed a series of self-reported instruments, as well as 1-month sleep and seizure diaries, to characterize their sleep and quality of life. Diaries were used to determine the relationship between seizure occurrence and total sleep time 24 and 72 h before seizure occurrence using random effects models and a logistic regression model fit by generalized estimating equations.

Results

A total of 237 seizures were recorded during 1295 diary days, representing 5.5 ± 7.0 (mean ± SD) seizures per month. Random effects models for 24- and 72-hour total sleep times showed no clinically or statistically significant differences in the total sleep time between preseizure periods and seizure-free periods. The average 24-hour total sleep time during preseizure 24-hour periods was 8 min shorter than that during seizure-free periods (p = 0.51). The average 72-hour total sleep time during preseizure periods was 20 min longer than that during seizure-free periods (p = 0.86). The presence of triggers was a significant predictor of seizure occurrence, with stress/anxiety noted most often as a trigger. Mean total sleep time was 9 h, and subjects took an average of 12 ± 10 naps per month, having a mean duration of 1.9 ± 1.2 h. Daytime sleepiness, fatigue, and insomnia symptoms were commonly reported.

Conclusions

Small degrees of sleep loss were not associated with seizure occurrence in our sample of adults with epilepsy. Our results also include valuable observations of the altered sleep times and frequent napping habits of adults with refractory epilepsy and the potential contribution of these habits to quality of life and seizure control.

via Impact of sleep duration on seizure frequency in adults with epilepsy: A sleep diary study – Epilepsy & Behavior.

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[WEB SITE] Sleep and Traumatic Brain Injury

Every year about 1.7 million Americans sustain a Traumatic Brain Injury (TBI). 80 to 90 percent of these are considered mild, with the majority classified as concussions. In fact, the annual incidence of sports-related concussion alone has been estimated at over one million a year. In football, it is estimated that 10 percent of college and 20 percent of high school players sustain concussions.

We also see a high incidence of traumatic brain injury associated with falls, motor vehicle accidents, and in our returning veterans. In fact, in a survey of 2,525 Army infantry soldiers returning from Iraq, 15% reported injuries consistent with traumatic brain injury.

What do all of these people have in common? They have a very high incidence of sleep disorders, with as many as 70% complaining of insomnia, excessive daytime sleepiness, or severely fragmented sleep. These sleep disorders are usually noted in the first few weeks and may persist for years. As a result, they contribute to moodiness, cognitive dysfunction such as memory impairment, and lack of sustained attention.

What is most interesting is the very high incidence of sleep apnea that is found in these individuals. In several studies, the proportion of persons with TBI who are found to have sleep apnea is 30 to 50 percent. In all of these studies, patients with TBI and sleep apnea performed much worse when it came to mood and memory. They were also much more likely to be excessively sleepy and/or fatigued during the day.

Unfortunately, sleep disorders are frequently overlooked or discounted after TBI. I have had numerous patients over the years whose sleep problems began with a frequently forgotten concussion. One particular case was that of a 27-year-old man who had sustained a concussion when playing college football. Afterwards, he had had trouble with fatigue and moodiness and had complained of disrupted sleep. His new girlfriend noted that he snored and urged him to come see me. We tested him and found that he had sleep apnea. Several months later, after treatment, he was no longer fatigued and irritable and he was sleeping through the night.

The point here is that TBI in America is at an all time high, with an estimated 3.5 million suffering from chronic symptoms such as fatigue, sleepiness, cognitive dysfunction, moodiness, and anxiety. In many of these individuals, an underlying sleep disorder may be the cause. Given the very high incidence of sleep complaints, people with TBI should be thoroughly evaluated for underlying sleep disorders.

via Sleep and Traumatic Brain InjuryDr. Robert S. Rosenberg | Dr. Robert S. Rosenberg.

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[ARTICLE] Endocrine and Non-Endocrine factors Contributing to Chronic Fatigue After Traumatic Brain Injury

…Conclusions

Endocrine disorders did not appear to play a major role in Chronic fatigue after TBI. Vitamin D deficiency, poor sleep and anxiety were identified as the most important factors associated with pTBI-CF. Appropriate treatment for these disorders may help to reduce fatigue in pTBI patients…

via Endocrine and Non-Endocrine factors Contributing to Chronic Fatigue After Traumatic Brain Injury – Archives of Physical Medicine and Rehabilitation.

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[POSTER] Endocrine and Non-Endocrine factors Contributing to Chronic Fatigue After Traumatic Brain Injury

…Endocrine disorders did not appear to play a major role in Chronic fatigue after TBI. Vitamin D deficiency, poor sleep and anxiety were identified as the most important factors associated with pTBI-CF. Appropriate treatment for these disorders may help to reduce fatigue in pTBI patients…

via Endocrine and Non-Endocrine factors Contributing to Chronic Fatigue After Traumatic Brain Injury – Archives of Physical Medicine and Rehabilitation.

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