Posts Tagged sleep

[BLOG POST] Sleep Evaluation and Treatment Support Patient Outcome

(Note:  In this guest blog from Grace Griesbach, Ph.D., and CNS’ National Director of Clinical Research, she explains that proper sleep is a vital component in the rehabilitation of brain injury).

Historically, quotes referring to sleep have been associated with well-being. This is not without substance. The importance of sleep is appreciated when one considers that it is observed across the vast majority of animal species. In humans and other higher mammals, lack of sleep has been demonstrated to impact physical, cognitive and emotional functions negatively. Physical consequences of sleep deprivation include compromised immune responses, as well as hormonal and metabolic alterations that in turn will impact overall health. Sleep also promotes emotional and psychological well-being. As for cognitive functions, sleep has been shown to facilitate learning and memory.

Moreover, animal studies have shown that neural plasticity changes allow for better memory to occur during sleep. Sleep driven neural plasticity is also evident during brain development and during times when healing is necessary. Given the multiple functions of sleep, it is evident that sleep-related problems should not be ignored.

Unfortunately, the prevalence of sleep disorders following brain injury is notably higher compared to the general population. Many of those that have endured a traumatic brain injury or stroke have difficulty initiating or maintaining sleep. Daytime sleepiness (hypersomnia) and fatigue are frequently reported complaints that are associated with insomnia. Apnea, a common breathing-related sleep disorder, is frequently observed during the chronic brain injury period. Apnea is defined as breathing cessation for fixed periods during sleep and contributes to arousals throughout the night; promoting fragmented sleep.

Sleep follows a particular overnight pattern consisting of repeated sleep cycles. Each cycle is comprised of one rapid eye movement (REM) stage and three non-REM stages. These stages are defined by different brain activity patterns that have been associated with particular physiological and neural plasticity processes.

Studies focused on proper sleep closely examine brain wave activity and body physiology throughout the various sleep stages. Some stages are particularly important for memory, emotional well-being, and cognitive function, and may be compromised by interrupted sleep. The golden standard of evaluating sleep is with an overnight polysomnography study performed by a certified sleep technologist. The technologist places electrodes on the scalp of the patient to record brain activity. Breathing, heart rate, oxygen levels, and limb movement are also recorded during sleep. Results from these recordings are sent to a board-certified sleep medicine physician, who creates a report on the diagnosis and a treatment plan.

Centre for Neuro Skills (CNS) offers a comprehensive multidisciplinary approach to rehabilitation. This entails addressing key factors that impact recovery such as sleep. CNS has opened sleep laboratories within the residential buildings of our programs in Dallas, Texas and Bakersfield, California. All CNS facilities can arrange for a sleep evaluation at one of the labs, based on a patient’s needs and treatment plan. Sleep evaluations of CNS patients allow for the detection of sleep-related issues that are likely to hinder recovery. CNS sleep facilities also provide research opportunities to deepen understanding of sleep-related issues after brain injury. Findings from these studies will help improve treatment and develop new therapeutic strategies.

 

via Sleep Evaluation and Treatment Support Patient Outcome – Neuro Landscape

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[ARTICLE] Sleep Related Epilepsy and Pharmacotherapy: An Insight – Full Text

In the last several decades, sleep-related epilepsy has drawn considerable attention among epileptologists and neuroscientists in the interest of new paradigms of the disease etiology, pathogenesis and management. Sleep-related epilepsy is nocturnal seizures that manifest solely during the sleep state. Sleep comprises two distinct stages i.e., non-rapid eye movement (NREM) and rapid eye movement (REM) that alternate every 90 min with NREM preceding REM. Current findings indicate that the sleep-related epilepsy manifests predominantly during the synchronized stages of sleep; NREM over REM stage. Sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes or benign rolandic epilepsy (BECTS), and Panayiotopoulos Syndrome (PS) are three of the most frequently implicated epilepsies occurring during the sleep state. Although some familial types are described, others are seemingly sporadic occurrences. In the present review, we aim to discuss the predominance of sleep-related epilepsy during NREM, established familial links to the pathogenesis of SHE, BECTS and PS, and highlight the present available pharmacotherapy options.

Introduction

Epilepsy is characterized by frequent and unpredictable disruptions of brain functions resulting in “epileptic seizures.” Epilepsy has a great impact on the quality of life through increased incidence of injury and death, unemployment rates, lower monthly incomes, higher household costs and high absenteeism at work and schools (Jennum et al., 2017Trinka et al., 2018Wibecan et al., 2018). An epileptic seizure is considered as a transient episode of signs or symptoms, including transitory confusion, staring speech, irrepressible jerking movements, loss of consciousness, psychic symptoms such as fear and anxiety, due to the abnormal synchronous neuronal activity of the brain. The International League Against Epilepsy (ILAE) published a recent clinical definition of epilepsy in which a patient with any of the following conditions is considered to be an epileptic i.e., (i) two or more unprovoked seizures within more than 24 h apart; (ii) one unprovoked seizure and a probability of further seizures similar to the general recurrence risk, occurring over the next 10 years; (iii) definite diagnosis of an epilepsy syndrome (Fisher et al., 2014). Genesis of epilepsy is attributed to various predispositions that include neurological, perceptive, psychological, and social factors, which could either stimulate or worsen the syndrome. In early 2017, the point prevalence of active epilepsy was found to be 6.38/1,000 individuals, while the lifetime prevalence was 7.60/1,000 persons. Meanwhile, the annual cumulative incidence of epilepsy was 67.77/100,000 persons and the incidence rate was 61.44/100,000 person-years. The active annual prevalence, prevalence during lifetime and the incidence of epilepsy were found to be higher in the developing countries (Fiest et al., 2017).

A systematic review revealed that epilepsies of unknown etiology had the highest prevalence compared to the epilepsies of known origin (Fiest et al., 2017). These were due to known underlying factors that cause seizures such as brain damage (Sizemore et al., 2018), metabolic diseases (Tumiene et al., 2018), infections (Bartolini et al., 2018), hemorrhagic stroke (Zhao et al., 2018), and gene mutations (Leonardi et al., 2018). These precipitating factors tilt the balance between excitatory and inhibitory neurotransmissions which has been established in different types of epilepsy. Physical and psychological comorbidities are usually accompanied with epilepsy, such as depression (Jamal-Omidi et al., 2018), sleep disorders (Castro et al., 2018), and body injuries (Mahler et al., 2018). Advanced cases may suffer from memory loss (Reyes et al., 2018), behavioral disorders (Jalihal et al., 2018), and disturbance of autonomic functions (Fialho et al., 2018). The rate of sudden death in epileptic patients was reported to be three times higher than non-epileptic individuals (Kothare and Trevathan, 2018Pati et al., 2018).

Sleep deprivation is very common among the epileptic patients and lack of sleep could worsen the seizure expressions (Neto et al., 2016). In animal models, sleep deprivation was shown to heighten the propensity to seizures (McDermott et al., 2003). Sleep deprivation has been correlated with decline in various aspects of brain functional connectivity (Nilsonne et al., 2017). Generally, sleep deprivation is secondary to other factors such as illness, emotional or psychological stress, and alcohol use. Hence, lack of sleep alone may not be sufficient to cause seizures (Razavi and Fisher, 2017). A large body of literature on the effects of epilepsy on sleep and/or sleep-deprivation on the epileptic state has been collated (St Louis, 2011Unterberger et al., 2015).

Sleep-related epilepsy represents nocturnal seizures that manifest solely during the sleep state (Tchopev et al., 2018). Approximately 12% epileptic patients are affected by sleep-related epilepsy with the majority suffering from focal epilepsy (Derry and Duncan, 2013Losurdo et al., 2014). In a recent case report, focal epilepsies were anatomically linked to epileptogenic origins at the right frontal lobe, using white matter tractography MRI (Tchopev et al., 2018). In a separate study, ambulatory electroencephalogram (EEG) measurement in outpatient setting reported frontal lobe seizures to manifest more readily between 12 a.m. and 12 p.m., particularly around 6:30 a.m., whereas temporal lobe seizures expressed more frequently between 12 p.m. and 12 a.m., specifically around 8:50 p.m. (Pavlova et al., 2012). In addition to seizure onset, few seizures seem to propagate more readily during sleep, based on anatomical locus. Medial temporal lobe regions were shown more likely to manifest spike production or propagation during NREM sleep stage compared to other brain regions (Lambert et al., 2018). Sleep-related epilepsy is often misdiagnosed as sleep disorders (Tinuper and Bisulli, 2017), especially in cases where the seizures manifest exclusively during sleep. Over the past decade, the discovery of numerous pre-disposing genes and availability of advanced diagnostic tools have shed more light in understanding the nature of sleep-related epilepsy.

In the present review, we discuss sleep-related epilepsy with particular emphasis on three of the most frequently implicated epilepsies during the sleep state which include sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes (BECTS), and Panayiotopoulos Syndrome (PS).[…]

 

Continue —-> Frontiers | Sleep Related Epilepsy and Pharmacotherapy: An Insight | Pharmacology

Figure 1. Pathogenesis of sleep-related epilepsy. Mutations of genes associated with channelopathy and non-channelopathy origin of sleep related epilepsy could disrupt the balance between inhibitory and excitatory neurotransmissions in central nervous system, leading to manifestation of seizure. Various anti-epileptic drugs alleviate seizure by restoring chemical balance in brain. TPM, topiramate; VPA, valproic acid; CBZ, carbamazepine; OXC, oxcarbazepine; LTC, levetiracetam; LCS, lacosamide.

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[WEB PAGE] Study offers possibility of squelching a focal epilepsy seizure before symptoms appear

Patients with focal epilepsy that does not respond to medications badly need alternative treatments.

In a first-in-humans pilot study, researchers at the University of Alabama at Birmingham have identified a sentinel area of the brain that may give an early warning before clinical seizure manifestations appear. They have also validated an algorithm that can automatically detect that early warning.

These two findings offer the possibility of squelching a focal epilepsy seizure — before the patient feels any symptoms — through neurostimulation of the sentinel area of the brain. This is somewhat akin to the way an implantable defibrillator in the heart can staunch heart arrhythmias before they injure the heart.

In the pilot study, three epilepsy patients undergoing brain surgery to map the source of their focal epilepsy seizures also gave consent to add an investigational aspect to their planned surgeries.

As neurosurgeons inserted long, thin, needle-like electrodes into the brain to map the location of the electrical storm that initiates an epileptic seizure, they also carefully positioned the electrodes to add one more task — simultaneously record the electrical activity at the anterior nucleus of the thalamus.

The thalamus is a structure sitting deep in the brain that is well connected with other parts of the brain. The thalamus controls sleep and wakefulness, so it often is called the “pacemaker” of the brain. Importantly, preclinical studies have shown that focal sources of seizures in the cortex can recruit other parts of the brain to help generate a seizure. One of these recruited areas is the anterior thalamic nucleus.

The UAB team led by Sandipan Pati, M.D., assistant professor of neurology, found that nearly all of the epileptic seizures detected in the three patients — which began in focal areas of the cortex outside of the thalamus — also recruited seizure-like electrical activity in the anterior thalamic nucleus after a very short time lag. Importantly, both of these initial electrical activities appeared before any clinical manifestations of the seizures.

The UAB researchers also used electroencelphalography, or EEG, brain recordings from the patients to develop and validate an algorithm that was able to automatically detect initiation of that seizure-like electrical activity in the anterior thalamic nucleus.

“This exciting finding opens up an avenue to develop brain stimulation therapy that can alter activities in the cortex by stimulating the thalamus in response to a seizure,” Pati said. “Neurostimulation of the thalamus, instead of the cortex, would avoid interference with cognition, in particular, memory.”

“In epilepsy, different aspects of memory go down,” Pati explained. “Particularly long-term memory, like remembering names, or remembering events. The common cause is that epilepsy affects the hippocampus, the structure that is the brain’s memory box.”

Pati said these first three patients were a feasibility study, and none of the patients had complications from their surgeries. The UAB team is now extending the study to another dozen patients to confirm the findings.

“Hopefully, after the bigger group is done, we can consider stimulating the thalamus,” Pati said. That next step would have the goals of improved control of seizures and improved cognition, vigilance and memory for patients.

For epilepsy patients where medications have failed, the surgery to map the source of focal seizures is a prelude to two current treatment options — epilepsy surgery to remove part of the brain or continuous, deep-brain stimulation. If the UAB research is successful, deep brain stimulation would be given automatically, only as the seizure initiates, and it would be targeted at the thalamus, where the stimulation might interfere less with memory.

 

via Study offers possibility of squelching a focal epilepsy seizure before symptoms appear

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[WEB SITE] Learning stress-reducing techniques may benefit people with epilepsy

Learning techniques to help manage stress may help people with epilepsy reduce how often they have seizures, according to a study published in the February 14, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Despite all the advances we have made with new drugs for epilepsy, at least one-third of people continue to have seizures, so new options are greatly needed,” said study author Sheryl R. Haut, MD, of Montefiore Medical Center and the Albert Einstein College of Medicine in the Bronx, NY, and member of the American Academy of Neurology. “Since stress is the most common seizure trigger reported by patients, research into reducing stress could be valuable.”

The study involved people with seizures that did not respond well to medication. While all of the 66 participants were taking drugs for seizures, all continued to have at least four seizures during about two months before the study started.

During the three-month treatment period all of the participants met with a psychologist for training on a behavioral technique that they were then asked to practice twice a day, following an audio recording. If they had a day where they had signs that they were likely to have a seizure soon, they were asked to practice the technique another time that day. The participants filled out daily electronic diaries on any seizures, their stress level, and other factors such as sleep and mood.

Half of the participants learned the progressive muscle relaxation technique, a stress reduction method where each muscle set is tensed and relaxed, along with breathing techniques. The other participants were the control group-;they took part in a technique called focused attention. They did similar movements as the other group, but without the muscle relaxation, plus other tasks focusing on attention, such as writing down their activities from the day before. The study was conducted in a blinded fashion so that participants and evaluators were not aware of treatment group assignment.

Before the study, the researchers had hypothesized that the people doing the muscle relaxing exercises would show more benefits from the study than the people doing the focused attention exercises, but instead they found that both groups showed a benefit-;and the amount of benefit was the same.

The group doing the muscle relaxing exercises had 29 percent fewer seizures during the study than they did before it started, while the focused attention group had 25 percent fewer seizures, which is not a significant difference, Haut said. She added that study participants were highly motivated as was shown by the nearly 85 percent diary completion rate over a five-month period.

“It’s possible that the control group received some of the benefits of treatment in the same way as the ‘active’ group, since they both met with a psychologist and every day monitored their mood, stress levels and other factors, so they may have been better able to recognize symptoms and respond to stress,” said Haut. “Either way, the study showed that using stress-reducing techniques can be beneficial for people with difficult-to-treat epilepsy, which is good news.”

Haut said more research is needed with larger numbers of people and testing other stress reducing techniques like mindfulness based cognitive therapy to determine how these techniques could help improve quality of life for people with epilepsy.

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[VIDEO] A/Prof Danny Eckert: Sleep Your Way to Good Mental Health – NeuRA Talks

What does sleep have to do with mental health? Everything!

To see more seminars like this, visit: neuratalks.org

The focus of Neuroscience Research Australia, or NeuRA, has always been on neuroscience. We conduct clinical and laboratory research into neurological, psychiatric and psychological disorders.

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via NeuRA Talks – A/Prof Danny Eckert: Sleep Your Way to Good Mental Health – YouTube

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[Abstract+References] A pilot randomized controlled trial of on-line interventions to improve sleep quality in adults after mild or moderate traumatic brain injury.

To explore feasibility and potential efficacy of on-line interventions for sleep quality following a traumatic brain injury (TBI).

A two parallel-group, randomized controlled pilot study.

Community-based.

In all, 24 participants (mean age: 35.9 ± 11.8 years) who reported experiencing sleep difficulties between 3 and 36 months after a mild or moderate TBI.

Participants were randomized to receive either a cognitive behaviour therapy or an education intervention on-line. Both interventions were self-completed for 20–30 minutes per week over a six-week period.

The Pittsburgh Sleep Quality Index assessed self-reported sleep quality with actigraphy used as an objective measure of sleep quality. The CNS Vital Signs on-line neuropsychological test assessed cognitive functioning and the Rivermead Post-concussion Symptoms and Quality of Life after Brain Injury questionnaires were completed pre and post intervention.

Both programmes demonstrated feasibility for use post TBI, with 83.3% of participants completing the interventions. The cognitive behaviour therapy group experienced significant reductions (F = 5.47, p = 0.04) in sleep disturbance (mean individual change = −4.00) in comparison to controls post intervention (mean individual change = −1.50) with a moderate effect size of 1.17. There were no significant group differences on objective sleep quality, cognitive functioning, post-concussion symptoms or quality of life.

On-line programmes designed to improve sleep are feasible for use for adults following mild-to-moderate TBI. Based on the effect size identified in this pilot study, 128 people (64 per group) would be needed to determine clinical effectiveness.

 

1. Lundin, A, De Boussard, C, Edman, G. Symptoms and disability until 3 months after mild TBI. Brain Inj 2006; 20: 799806Google ScholarCrossrefMedline
2. Mathias, JL, Alvaro, PK. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep Med 2012; 13: 898905Google ScholarCrossrefMedline
3. Theadom, A, Cropley, M, Parmar, P. Sleep difficulties one year following mild traumatic brain injury in a population-based study. Sleep Med 2016; 16: 926932Google ScholarCrossref
4. Ouellet, MC, Savard, J, Morin, CM. Insomnia following traumatic brain injury: a review. Neurorehabil Neural Repair 2004; 18: 187198Google ScholarLink
5. Morin, CM, Belanger, L, Bastien, C. Long-term outcome after discontinuation of benzodiazepines for insomnia: a survival analysis of relapse. Behav Res Ther 2005; 43: 114Google ScholarCrossrefMedline
6. Buscemi, N, Vandermeer, B, Friesen, C. The efficacy and safety of drug treatments for chronic insomnia in adults: a meta-analysis of RCTs. J Gen Intern Med 2007; 22: 13351350Google ScholarCrossrefMedline
7. Sivertsen, B, Omvik, S, Pallesen, S. Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial. JAMA 2006; 295: 28512858Google ScholarCrossrefMedline
8. Vincent, N, Lewycky, S. Logging on for better sleep: RCT of the effectiveness of online treatment for insomnia. Sleep 2009; 32: 807815Google ScholarCrossrefMedline
9. Ponsford, J, Willmott1, C, Rothwell, A. Impact of early intervention on outcome following mild head injury in adults. J Neurol Neurosurg Psychiatr 2002; 73: 330332Google ScholarCrossrefMedline
10. Stepanski, EJ, Wyatt, JK. Use of sleep hygiene in the treatment of insomnia. Sleep Med Rev 2003; 7: 215225Google ScholarCrossrefMedline
11. Menon, DK, Schwab, K, Wright, DW. Position statement: definition of traumatic brain injury. Arch Phys Med Rehabil 2010; 91(110): 16371640Google ScholarCrossrefMedline
12. Teasdale, G., Jennett, B. Assessment of coma and impaired consciousness: a practical scale. Lancet 1974; 2(7872): 8184Google ScholarCrossrefMedline
13. Ohayon, MM, Carskadon, MA, Guilleminault, C. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep 2004; 27: 12551273Google ScholarCrossrefMedline
14. Kempf, J, Werth, E, Kaiser, PR. Sleep-wake disturbances 3 years after traumatic brain injury. J Neurol Neurosurg Psychiatr 2010; 81: 14021405Google ScholarCrossrefMedline
15. Fictenberg, NL, Putnam, SH, Mann, NR. Insomnia screening in postacute traumatic brain injury: utility and validity of the Pittsburgh Sleep Quality Index. Am J Phys Med Rehabil 2001; 80: 339345Google ScholarCrossrefMedline
16. Fogelberg, DJ, Hoffman, JM, Dikmen, S. Association of sleep and co-occurring psychological conditions at 1 year after traumatic brain injury. Arch Phys Med Rehabil 2012; 93: 13131318Google ScholarCrossrefMedline
17. Chung, F, Elsaid, H. Screening for obstructive sleep apnea before surgery: why is it important? Curr Opin Anaesthesiol 2009; 22: 405411Google ScholarCrossrefMedline
18. Ferri, R, Lanuzza, B, Cosentino, FI. A single question for the rapid screening of restless legs syndrome in the neurological clinical practice. Eur J Neurol 2007; 14: 10161021Google ScholarCrossrefMedline
19. Vincent, N, Walsh, K. Stepped care for insomnia: an evaluation of implementation in routine practice. J Clin Sleep Med 2013; 9: 227234Google ScholarMedline
20. Buysse, DJ, Reynolds, CF, Monk, TH. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res 1989; 28: 193213Google ScholarCrossrefMedline
21. Babor, TF, Higgins-Biddle, JC, Saunders, JB. AUDIT: alcohol use disorders identification test, guidelines for use in primary care. 2nd ed. GenevaWorld Health Organization2001Google Scholar
22. Zollman, FS, Cyborski, C, Duraski, SA. Actigraphy for assessment of sleep in traumatic brain injury: case series, review of the literature and proposed criteria for use. Brain Inj 2010; 24: 748754Google ScholarCrossrefMedline
23. Ayalon, L, Borodkin, L, Dishon, L. Circadian rhythm sleep disorders following mild traumatic brain injury. Neurology 2007; 68: 11361140Google ScholarCrossrefMedline
24. King, NS, Crawford, S, Wenden, FJ. The Rivermead Post-concussion Symptoms Questionnaire: a measure of symptoms commonly experienced after head injury and its reliability. J Neurol 1995; 242: 587592Google ScholarCrossrefMedline
25. Lannsjo, M, af Geijerstam, JL, Johansson, U. Prevalence and structure of symptoms at 3 months after mild traumatic brain injury in a national cohort. Brain Inj 2009; 23: 213219Google ScholarCrossrefMedline
26. Gualtieri, CT, Johnson, LG. A computerized test battery sensitive to mild and severe brain injury. Medscape J Med 2008; 10: 90Google ScholarMedline
27. Gualtieri, CT, Johnson, LG, Benedict, KB. Psychometric and clinical properties of a new, computerized neurocognitive assessment battery. Bal Harbor, FLAmerican Neuro-psychiatric Association Annual Meeting2004Google Scholar
28. Bullinger, M, Azouvi, P, Brooks, N. Quality of life in patients with traumatic brain injury-basic issues, assessment and recommendations. Restor Neurol Neurosci 2002; 20: 111124Google ScholarMedline
29. Saghaei, M, Saghaei, S. Implementation of an open-source customizable minimization program for allocation of patients to parallel groups in clinical trials. J Biomed Sci Eng 2011; 4: 734739Google ScholarCrossref
30. Hopkins, WG. A scale of magnitudes for effect statistics (In A New View of Statistics)2002http://www.sportsci.org/resource/stats/effectmag.html Google Scholar
31. Ponsford, JL, Parcell, DL, Sinclair, KL. Changes in sleep patterns following traumatic brain injury: a controlled study. Neurorehabil Neural Repair 2013; 27: 613621Google ScholarLink
32. Ouellet, MC, Morin, CM. Efficacy of cognitive-behavioral therapy for insomnia associated with traumatic brain injury: a single-case experimental design. Arch Phys Med Rehabil 2007; 88: 15811592Google ScholarCrossrefMedline
33. McPherson, K, Fadyl, J, Theadom, A. Living life after traumatic brain injury (TBI): phase 1 of a longitudinal qualitative study. J Head Traum Rehabil. Epub ahead of print 17 May 2017. DOI: 10.1097/HTR.0000000000000321 Google ScholarCrossref

 

via A pilot randomized controlled trial of on-line interventions to improve sleep quality in adults after mild or moderate traumatic brain injuryClinical Rehabilitation – Alice Theadom, Suzanne Barker-Collo, Kelly Jones, Margaret Dudley, Norah Vincent, Valery Feigin, 2017

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[Poster] Sleep Experiences Following Traumatic Brain Injury: A Qualitative Descriptive Study

First page of article

To describe the sleep experiences of adults living with moderate or severe traumatic brain injury (TBI).

via Sleep Experiences Following Traumatic Brain Injury: A Qualitative Descriptive Study – Archives of Physical Medicine and Rehabilitation

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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

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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.

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ABOUT THE THOMAS HAYDN TRUST

The Thomas Haydn Trust is The Paediatric Epilepsy Charity that aims to serve the needs of Young People, Parents, Carers and Medical Professionals. But to know who we are you need to know why we are.

Providing local services and sharing the rewards globally is the core of THT’s work, weather newly diagnosed or not, you will find THT a valuable source of support, knowledge and news for the epilepsies.

The Thomas Haydn Trust was set up in the wake of Thomas Haydn Smith’s diagnosis of Lennox-Gastaut Syndrome – One of the Most severe forms of Childhood Onset Epilepsies, affecting 1 in 1,000,000 epilepsy sufferer’s worldwide.

In setting up THT our aim was to combat many of the hurdles that Thomas and his family come across while living with LGS. THT strives to ‘Give Something Back’ to organisations that help families and children with severe epilepsies.

We work towards our goals in the following manner:

Research

Raising the need profile for both basic and clinical research into Lennox-Gastaut Syndrome and other childhood Epilepsies.

Support

By providing a free and open forum for sufferers, family and carers’, allowing them to share experiences, build relationships and facilitate peer learning. THT also provides details of leading specialist support organisations of specific Epilepsy conditions – Supporting the specific needs of the child.

Education

Developing an ever-expending resource of research findings and educational materials for the public and medical professionals.

Funding

Where possible, fund individuals and organisations involved in support, development and care of families with sick children.

Awareness

Raising awareness of childhood Epilepsies through various mediums including the internet, press, radio and television. Highlighting the effects of LGS and other childhood onset Epilepsies through our live events – Raising awareness is the key principle on which THT works.

Empowerment

Promoting the advancement of individuals with Epilepsy to speak out against ignorance, predjudice and bigotry that still surrounds conditions of Epilepsy.

Networking

Developing links with other national and international organisations to create a coalition of information sharing networks.

via The Relationship Between Epilepsy and Sleep – Wattpad

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[ARTICLE] Electroencephalography in the Diagnosis of Genetic Generalized Epilepsy Syndromes – Full Text

Genetic generalized epilepsy (GGE) consists of several syndromes diagnosed and classified on the basis of clinical features and electroencephalographic (EEG) abnormalities. The main EEG feature of GGE is bilateral, synchronous, symmetric, and generalized spike-wave complex. Other classic EEG abnormalities are polyspikes, epileptiform K-complexes and sleep spindles, polyspike-wave discharges, occipital intermittent rhythmic delta activity, eye-closure sensitivity, fixation-off sensitivity, and photoparoxysmal response. However, admixed with typical changes, atypical epileptiform discharges are also commonly seen in GGE. There are circadian variations of generalized epileptiform discharges. Sleep, sleep deprivation, hyperventilation, intermittent photic stimulation, eye closure, and fixation-off are often used as activation techniques to increase the diagnostic yield of EEG recordings. Reflex seizure-related EEG abnormalities can be elicited by the use of triggers such as cognitive tasks and pattern stimulation during the EEG recording in selected patients. Distinct electrographic abnormalities to help classification can be identified among different electroclinical syndromes.

Introduction

Genetic generalized epilepsy (GGE) encompasses several electroclinical syndromes diagnosed and classified according to clinical features and electroencephalographic (EEG) characteristics (13). The EEG hallmark of GGE is bilateral synchronous, symmetrical, and generalized spike-wave (GSW) discharges. Polyspikes and polyspike-wave discharges are also commonly seen in GGE. Fixation-off sensitivity (FOS), eye-closure sensitivity, photoparoxysmal response (PPR), epileptiform K-complexes/sleep spindles, and occipital intermittent rhythmic delta activity (OIRDA) are among the spectrum of abnormalities described in GGE (4).

In this review, we will be discussing the ictal and the interictal EEG abnormalities in GGE. We will also focus on the electrographic differences among different GGE syndromes, factors affecting the yield of EEG, and diagnostic pitfalls.[…]

Continue —> Frontiers | Electroencephalography in the Diagnosis of Genetic Generalized Epilepsy Syndromes | Neurology

 

Figure 1. Typical interictal epileptiform discharges in genetic generalized epilepsy. Note bilateral, symmetrical, and synchronous spike-wave discharges (A), polyspike-wave discharges (B), and polyspikes (C).

 

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[WEB SITE] Monitor stress, seizures, activity, sleep

Embrace it’s wearable device designed to improve the lives of the people with epilepsy.

 

“Embrace is glorious in design, very sleek and attractive. Living in a world of seizure helmets and wheelchairs it is nice to have such an unobtrusive and attractive device.

 

A gorgeous smart watch for you

The case is made of strong, polished metal with either an elegant leather or an elastic fabric band. Embrace is the thinnest smart watch of this kind ever made. It snaps on, then tightens with a magnet for perfect fit. […]

Source: Monitor stress, seizures, activity, sleep

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