Non-pharmacologic therapies for sleep disturbances after traumatic brain injury: a systematic review and meta-analysis.

Introduction: Restless Legs Syndrome (RLS) is a common sensorimotor neurological disorder, observed in individuals with Type 2 Diabetes Mellitus (T2DM), especially with diabetic neuropathy.It causes discomfort, impaired sleep, and reduced quality of life.While exercise improves RLS symptoms, few studies directly compared aerobic and strength training in this population.To compare effects of aerobic and resistance training on RLS severity, sleep quality, and daytime sleepiness in adults with T2DM.Material and methods: A single-blinded randomized controlled trial recruited 42 adults (aged 40-60 years) with T2DM, 5 years and RLS based on International Restless Legs Syndrome Study Group (IRLSSG) criteria.Eligibility included lower limb strength 3+/5 and oral hypoglycemic therapy.Exclusions were severe comorbidities, insulin therapy, injuries, or other sleep disorders.Participants were randomized via sealed envelopes into aerobic (n = 21) or resistance (n = 21) training groups.Both underwent supervised exercise thrice weekly for six weeks.Outcomes were assessed using the International RLS Rating Scale (IRLS), Pittsburgh Sleep Quality Index (PSQI), and Epworth Sleepiness Scale (ESS).Paired and independent t-tests were used for analysis Results: Data from 30 participants were analyzed.Groups were comparable at baseline (p > 0.05).Both groups showed significant within-group improvements in IRLS, PSQI, and ESS scores (p 0.05), changes in IRLS and ESS exceeded minimal clinically important difference (MCID) thresholds, supporting clinical relevance.Conclusions: Aerobic and resistance training improved RLS symptoms, sleep quality, and daytime sleepiness in adults with T2DM, supporting exercise as beneficial nonpharmacological strategy.

Objectives: We aimed to examine the relationship between alexithymia and sleep, independent of depression and anxiety.Methods: This cross-sectional study included participants who visited our sleep clinic between 2016 and 2022. In total, 142 participants (98 males and 44 females) were included, and they completed the Toronto Alexithymia Scale-20 (TAS-20). Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), and Insomnia Severity Index (ISI) scores were also recorded. The relationship between alexithymia and sleep (PSQI, ISI, and ESS scores) was determined after controlling for demographic and psychological (Beck Depression Inventory and State Trait Anxiety Inventory-Trait) variables.Results: Individuals with alexithymia had significantly higher PSQI, ESS, and ISI scores than those without alexithymia. Correlation analysis showed significant correlations between the total TAS-20 score and ISI (r=0.321) and ESS (r=0.253) scores. In multivariate linear regression analysis, the total TAS-20 score (β=0.201; <i>p</i>=0.022) was significantly associated with the ESS score.Conclusions: Alexithymia was associated with the severity of insomnia and daytime sleepiness in adults. However, when considering depression and anxiety in multivariate analysis, alexithymia was significantly associated with daytime sleepiness; however, its relationship with the severity of insomnia was not significant.

Poor sleep quality, often resulting from poor sleep hygiene, is common among medical students. Educational interventions aimed at improving sleep knowledge are beneficial for sleep quality in healthy populations. However, sleep education is often given minimal attention in medical school curriculums. The aim of the study was to explore whether a short educational intervention could improve sleep knowledge, and consequently sleep quality, among medical students. We recruited preclinical- and clinical-stage medical students during the 2017-2018 academic year. Students completed a demographic survey, the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), and the Assessment of Sleep Knowledge in Medical Education (ASKME) questionnaire. Students then attended a lecture on the physiology and importance of sleep. To assess the efficacy of the intervention, questionnaires were repeated 4 months thereafter. A total of 87 students (31 preclinical) with a mean age of 25.86 years (standard deviation [SD], 3.33), 51 of whom were women, participated in the study. At baseline, students had poor sleep quality with a PSQI mean score of 5.9 (SD, 2.37), without significant sleepiness, and a mean ESS score of 8.86 (SD, 4.32). The mean ASKME scores were consistent with poor sleep knowledge at 11.87 (SD, 4.32). After the intervention, the mean ASKME results improved to 14.15 (SD, 4.5; P < .001), whereas sleep quality did not. The effect was similar in preclinical and clinical medical students. Sleep knowledge was inadequate among medical students, who also experienced poor sleep quality. A short educational intervention improved sleep knowledge but was insufficient at improving sleep quality. Further studies are needed to determine which interventions may provide benefit in both sleep knowledge and sleep quality.

Sleep problems are common and disabling after traumatic brain injury (TBI). They negatively affect cognitive recovery, emotions, and overall quality of life. Fatigue and excessive daytime sleepiness are also frequent and significantly impair daily functioning. Although trazodone and melatonin are used off-label, we still do not know which works better or if they are more effective together for improving sleep quality, fatigue, and daytime sleepiness in TBI patients. This randomized, double-blind clinical trial aims to compare the effectiveness of trazodone, melatonin, and their combination for improving sleep quality, fatigue severity, and daytime sleepiness in adults with moderate to severe TBI. Forty-eight adults with moderate to severe TBI (Glascow Coma Scale (GCS) score of 3-12) and insomnia (insomnia severity index score (ISI) ≥ 8) will be randomly assigned (1:1:1) to receive nightly trazodone (25-100 mg), melatonin (3-5 mg), or both for 4 weeks. Changes in sleep quality (Insomnia Severity Index, ISI), fatigue severity (fatigue severity scale, FSS), and daytime sleepiness (Epworth sleepiness scale, ESS) will be assessed before and after treatment. Recruitment is ongoing. The data will be analyzed via mixed-design ANOVA, with suitable post hoc tests and nonparametric alternatives if the assumptions are not met. This study is one of the first to compare trazodone and melatonin alone and in combination for insomnia, fatigue, and daytime sleepiness in TBI patients. The results will help improve treatment strategies for managing sleep problems, fatigue, and daytime sleepiness in individuals with traumatic brain injury. Iranian Registry of Clinical Trials (IRCT) IRCT20241121063793N1. Registered on December 28, 2024.

BackgroundThis study aimed to investigate sleep quality, restless legs syndrome (RLS), and excessive daytime sleepiness in adults with spinal muscular atrophy (SMA) and their relationships with motor function, quality of life (QoL), fatigue, and depression.MethodsWe included 43 adults with SMA (31 non-ambulatory; 11 using non-invasive ventilation) and 43 age- and sex-matched healthy controls (HC). Subjective sleep quality and daytime sleepiness were assessed using the Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS). RLS was diagnosed using the International RLS Study Group diagnostic criteria. Revised Upper Limb Module (RULM), Hammersmith Functional Motor Scale Expanded (HFMSE) and respiratory function, as well as, 36-Item Short Form Health Survey (SF-36), Beck Depression Inventory (BDI) and Fatigue Severity Scale (FSS) were recorded.ResultsSMA patients had significantly worse scores in sleep efficiency domain of the PSQI (0.7 ± 1.0 vs. 0.3 ± 0.6, p = 0.04) as well as in global PSQI score compared to HC (5.5 ± 3.5 vs. 4.0 ± 2.6, p = 0.029). Patients classified as poor sleepers (PSQI > 5) had a higher body mass index (BMI), greater BDI, and ESS scores. No association between global PSQI score and HFMSE or RULM score was observed. Patients classified as poor sleepers had lower total SF-36 score in comparison to good sleepers (53.2 ± 15.4 vs. 69.6 ± 12.3, p < 0.001). RLS was present in five SMA patients (11.6%).ConclusionPoor sleep quality is common in adults with SMA. It contributes to a lower QoL and should be addressed as a part of the standard of care in adults with SMA.

TMS and CBT-I for comorbid depression and insomnia. Exploring feasibility and tolerability of transcranial magnetic stimulation (TMS) and cognitive behavioral therapy for insomnia (CBT-I) for comorbid major depressive disorder and insomnia during the COVID-19 pandemic

INTRODUCTION Psychiatric disorders are common after stroke and traumatic brain injury (TBI) both in the short term and long term. They can be caused by regional disruption of neuronal network, impairment of regional cerebral blood flow, impaired cerebral metabolism, axonal injury, and pressure effect of intracranial bleed. Around 16 million people each year experience first ever stroke. Of these patients, 5 million become disabled and 5.7 million dies.[1] Traumatic brain injuries are also common and pose an enormous burden on families and caregivers because of the associated neuropsychiatric complications.[2] However, these neuropsychiatric complications are often remained unaddressed or not adequately treated because of the treating doctor's preoccupation with other severe physical disabilities, whereas treating these neuropsychiatric complications can improve the overall outcome of the patients to a considerable extent. In this clinical practice guideline (CPG), the assessment of psychiatric disorders following stroke and TBI is discussed together, while the management of psychiatric disorders following stroke and TBI is discussed separately under the two broad subheadings. This CPG mostly focused on the most common neuropsychiatric consequences of stroke and TBI, namely depression, psychosis, anxiety, posttraumatic stress disorders (PTSD), mania, emotional lability, fatigue, apathy, and personality changes. There is substantial overlap between neuropsychiatric disorders following stroke and TBI and repetitions will be avoided. This CPG does not include the cognitive consequences of stroke and TBI. We included researches both on ischemic stroke and intracerebral hemorrhage. However, we did not include dementia. CATEGORIES OF EVIDENCE AND STRENGTH OF RECOMMENDATIONS While writing this CPG, we ensured compliance with AGREE II instrument. We marked available evidences from Ia to IV and strengths of recommendations from A to D as per the prevailing norms.[3] Categories of evidence Ia: Evidence from meta-analysis of randomized controlled trials (RCTs) Ib: Evidence from at least one RCT IIa: Evidence from at least one controlled study without randomization IIb: Evidence from at least one quasi-experimental study III: Evidence from nonexperimental descriptive studies, such as correlation studies comparative studies, and case − control studies IV: Evidence from opinions and/or clinical experience of respected authorities or expert committee reports. Strength of recommendations A: Directly based on Category I evidence B: Directly based on Category II evidence or extrapolated recommendation from Category I evidence C: Directly based on Category III evidence or extrapolated recommendation from category I or II evidence D: Directly based on Category IV evidence or extrapolated recommendation from Category I, II or III evidence S: Standard of care. GENERAL ASSESSMENT OF PSYCHIATRIC DISORDERS FOLLOWING STROKE AND TRAUMATIC BRAIN INJURY As a referral physician, psychiatrists have the role to make thorough assessment of a patient following stroke and TBI to rule in/out the presence of any psychiatric disorders in a busy emergency room or inpatient department or intensive care unit (ICU). To assess the consciousness level of the patient, Glasgow Come Scale still remains the gold standard. It is usually very difficult to conduct a psychiatric assessment on a semi-comatose patient or a patient who is uncooperative. In that case, one can use Kirby's pro forma for examining uncooperative patients. The attending psychiatrist should examine the patient in a calm environment with not too many people around. However, the presence of primary caregiver can be allowed if the patient cannot give reliable and valid information which is more often the case. The demeanor of the treating doctor should be nonthreatening. He should talk in a clear voice with every word being uttered with due stress to reach the patient who usually have some or the other sensory impairment. If in delirium, psychiatrist should revisit the patient at a later date and time. Psychiatrist should also take the pain to bring forth the history of substance use disorders which are commonly associated with road traffic accidents and resultant TBI [Box 1].Box 1: Checklist for treating psychiatrist while evaluating post stoke and posttraumatic brain injury psychiatric disordersThe treating psychiatrist should go through the clinical records very carefully and if needed should corroborate the clinical history from the primary caregiver or the eye witnesses. Patient's past psychiatric history is of immense importance as it has some correlation with development of poststroke depression (PSD) and other psychiatric disorders. Psychiatrist should also go through the laboratory reports carefully and look for underlying infection, blood loss, electrolyte disturbances, endocrine dysfunction, and other systemic comorbid conditions which are reflected in complete blood count, urine culture and sensitivity, cerebrospinal fluid study, hemoglobin level, serum sodium, serum potassium, serum chloride, serum thyroid-stimulating hormone, serum parathyroid hormone, fasting blood sugar, liver function test, serum creatinine, etc. If needed and when in doubt, the referral psychiatrist should order for more biochemical investigation to rule out organic condition. The psychiatrist should also pay attention to the neuroimaging reports (computed tomography scan, magnetic resonance imaging, etc.,) to decipher a possible connection between the neurological insult and psychiatric disorder. Electroencephalography should be ordered to rule out subconvulsive status epilepticus which can mimic a psychiatric disorder. A detailed scrutiny of the medications already received should be done to rule out any iatrogenic psychiatric disorder. If needed, the psychiatrist should talk to treating neurologist or the neurosurgeon regarding stoppage of medicine, replacing the offending drug, or possible dose adjustment. A detailed mental status examination should be done with particular focus on obtaining an adequate speech sample, looking for the predominant affect, presence of any delusion or hallucination, and assessment of cognitive function, particularly judgment, abstract thinking, and lobar functions. There are provisions to diagnose various psychiatric disorders following stroke, transient ischemic attack (TIA), and brain injury in DSM 5 and ICD10. The diagnosis of poststroke and post-TBI psychiatric disorders depends on structured clinical interview and using of a screening instrument. There is no universally accepted screening instrument for diagnosing psychiatric disorders following stroke or TBI. For the diagnosis of PSD, Beck Depression Inventory, Hamilton Depression Rating Scale, Nine-item Patient Health Questionnaire-9, Hospital Anxiety Depression Scale, Geriatric Depression Scale, and the Center for Epidemiological Studies Depression (CES-D) Scale have been used. Anxiety disorders can be screened by Hospital Anxiety and Depression Scale-Anxiety Subscale and Hamilton Anxiety Scale. For screening of PTSD, psychiatrist can use clinician administered PTSD Scale, PTSD checklist for a stressor, TIA or stroke as stressor; Post-Traumatic Stress Diagnostic Scale; Impact of Events Scale-Revised. Brief Psychiatric Rating Scale can be used for screening of psychosis and Young's Mania Rating Scale can be used for screening of mania. For the assessment of personality disorders or personality changes, a detailed psychological evaluation with Eysenck's Personality Questionnaire, Minnesota Multiphasic Personality Inventory, International Personality Disorder Examination, or Iowa Personality Disorder Screen may be needed [Table 1].Table 1: Screening tools and management of various psychiatric disorders following stroke/traumatic brain injuryMANAGEMENT OF POSTSTROKE PSYCHIATRIC DISORDERS Poststroke depression PSD is the one of the most commonly reported neuropsychiatric conditions following stroke. Often undiagnosed, PSD is a treatable condition. PSD can occur within 1–18 months following stroke and its prevalence vary considerably over time (reported prevalence at 1, 3, 6, 12, and 18 months were 24.5%, 27.1%, 28.3%, 19.8%, and 26.3%, respectively).[4] PSD is believed to be associated with worse functional outcome following stroke. A meta-analysis showed that, PSD had a adverse impact on survival rates following stroke and it affected short-term mortality more than long-term mortality.[5] Various meta-analysis and systematic review have looked into the role of prophylactic antidepressant treatment to reduce the chance of developing PSD.[6789] Many of them found that, selective serotonin reuptake inhibitors (SSRIs), cognitive behavioral therapy (CBT), and physical exercise improved mood symptoms in PSD. A Cochrane review which included 63 RCTs and over 9000 participants and specifically looked into the role of SSRIs in PSD found that, SSRIs should not be used routinely to promote recovery after stroke as they do not improve recovery after stroke (A).[10] In the Effect of fluoxetine on functional outcomes after acute stroke trial, eligible patients with stroke were recruited and randomly given fluoxetine (20 mg daily) or placebo for 6 months, starting after 2 − 15 days of stroke. After 12 months of follow-up, fluoxetine was found to improve the neuropsychological scale score but not other variables. Therefore, it did not support the routine use of prophylactic fluoxetine in PSD (A).[11] Similar was the finding from the efficacy of citalopram treatment in acute stroke (TALOS study) (A).[12] The efficacy of CBT on PSD remains undetermined due to low quality of the studies and high degree of heterogeneity among them as found by one meta-analysis (A).[13] Neuromodulation techniques such as transcranial direct current stimulation and transcranial magnetic stimulation can offer some benefit, but there are the lack of high quality RCTs (B).[14] SSRIs and SNRIs are often used in conjunction with anti-platelet medication such as clopidogrel in PSD. Fluoxetine and fluvoxamine (CYP2C19 inhibiters) can reduce the efficacy of clopidogrel and can increase the risk of ischemic disease.[15] There have been concerns regarding intracranial bleed following the use of SSRIs also. Studies have suggested that, if given before stroke, SSRIs were associated with severity and mortality in patients with hemorrhagic stroke.[16] However, one recent review pointed out the lack of evidence in support of SSRIs alone increasing the risk of spontaneous intracranial bleed. Therefore, it can be concluded that, SSRIs should not be prescribed prophylactically in all poststroke patients. Rather, they should be screened for PSD and if diagnosed, then only SSRIs and SNRIs can be prescribed as needed (S) with some sort psychological intervention (CBT) (B). Both neurologists and psychiatrists need to be aware of drug-drug interaction which can be potentially life threatening in such group of patients (S). Poststroke psychosis The symptoms of PSP include delusions, hallucinations, psychomotor agitation, irrelevant and incoherent speech, catatonic symptoms, and sleep cycle disturbances. These symptoms usually manifest within a week following stroke but may manifest several weeks later also. Studies form the early 90s indicated that PSP is relatively rare and after 9 years' follow-up only 5 patients developed PSP.[17] A recent meta-analysis found the prevalence of PSP to be around 4.86%.[18] Literature on the management of PSP is sparse compared to PSD or poststroke anxiety (PSA). RCTs on the management of PSP are lacking. The treatment usually follows same principles which are followed for the management and treatment of primary psychotic disorders. Secondgenerationantipsychotics(SGAs), for example, quetiapine, risperidone, andolanzapinearemostcommonlyusedtotreatPSP (D). However, their safety in patients with stroke is highly debatable. Olanzapine can have deleterious effect of plasma glucose and lipids which are not welcome in patients with stroke. Quetiapine can cause postural hypotension, whereas risperidone can cause extra-pyramidal side effects. The concern of anti-psychotics being associated with high incidences stroke has been refuted by a large case − control study.[192021] TheusualpracticeistostartlowandgoslowincaseoftreatmentofPSP(S). However, incertaincases(agitatedandviolentpatients)injectablesmightberequiredandinthatcaseinjectableolanzapineorinjectablehaloperidolcanbeused(D). Asinpatientswithprimarypsychoticdisorders, CBTforhallucinationordelusioncanbebeneficialinPSP(S).[22] Poststroke anxiety disorders PSA is common and only second to PSD in terms of prevalence. All kind of anxiety disorders can be seen following stroke but the core symptoms remain the same – palpitation, psychic and physical restlessness, excessive worry and fear, feeling of nervousness, pseudo neurological symptoms, for example, dizziness, blurring of vision, tingling and numbness of hands and feet, fine tremors, etc. Sensory impairment, ICU admission, painful physical conditions, communication difficulties, and sleep disturbance can lead to the development of PSA. A meta-analysis found the prevalence of PSA to vary between 20% to 24% depending on the time elapsed following stroke.[23] SSRIs, SNRIs, Tri-CyclicAntidepressants(TCAs), Mirtazapine, Buspirone, Benzodiazepines, and Z-drugsallhavebeenusedinthetreatmentofPSAintheabsenceofanydefiniteguideline(D).[24] Meta-analyses conducted by Chun etal. reported beneficial effect of pharmacotherapy (paroxetine, imipramine, and buspirone) and psychotherapy compared to control. However, the studies were of low quality and highly heterogeneous, and therefore, the positive conclusion could be due to bias.[25] Cochrane review in this area also highlighted lack of quality studies and emphasized the need of large scale RCTs.[24] Nonpharmacologicalmanagements, for example, Yoga, Tai-Chi, Self-helpmindfulness, andrelaxationtechniquescanoffersomebenefitinthemanagementofPSA(C).[2627] Therefore, SSRIs, SNRIs, andevenTCAscanbeusedinthetreatmentofPSA(S, D)alongwithnon-pharmacologicalinterventions(C). However, as in case of PSD, psychiatrists and neurologists should be aware of potential drug-drug interactions. Posttraumatic stress disorder following stroke PTSD develops following an event which pose actual or imagined threat to physical and psychological integrity of an individual and stroke is no less than a catastrophe. Symptoms of PTSD include intrusive flashbacks/memories, autonomic arousal, emotional numbness, and avoidance behavior. Poststroke PTSD often has associated PSD and PSA (in up to 40% of the cases).[28] A meta-analysis reported 1-year prevalence of poststroke PTSD to be around 23%.[29] Furthermore, persons with PTSD have higher risk of developing stroke compared to people without PTSD.[30] There is dearth of RCTs in treatment of PTSD. SSRIs, SNRIs, andTCAscanbetried(D). Othermedications, e.g., antipsychotics, anticonvulsants, andanxiolyticshavealsobeentried(D).[31] Psychotherapeutic approaches, e.g., trauma-focused therapies, CBT, and exposure therapy appears to be helpful in resolution of symptoms but they need to be tested in large scale studies (D).[32] Poststroke mania Prevalence of poststroke mania (PSM) is rather low (<2%).[33] Most of the data in this area are in the form of case report or case series.[33] Majority of the subject developed PSM between 1 day to 24 months after stroke.[34] In 1978, Kraut-hammer and Klerman gave the concept of secondary mania in which a manic episode is produced by metabolic, neurological, or toxic disorder.[34] The criteria of secondary mania (PSM in this case) are as follows: (1) symptoms lasting for at least 1 week; (2) presence of elevated or irritable mood; and (3) presence of at least two symptoms out of the followings: Pressured speech, grandiosity, hyperactivity, flight of ideas, distractibility, lack of judgment, and decreased sleep; and (4) no history of affective illness or delirium co-occurring with the mania. Lesions responsible for PSM are usually found in the caudate nucleus, parietal, temporal, and frontal lobes and thalamus. Mania is more common with right-sided lesions, although left sided lesions have also been reported.[3536] Treatment of PSM is in line with treatment of an acute manic episode. Moodstabilizers, e.g., valproate, carbamazepine, oxcarbazepine, etc.;antipsychotics, e.g., olanzapine, quetiapine, risperidone, etc.;andbenzodiazepinesarethemainstayoftreatment(S. D). It is better to avoid lithium in this population because of the presence of multiple comorbidities and potential drug-drug interactions. Furthermore, choosing a mood stabilizer which allows antiepileptic coverage is beneficial. Poststroke emotional lability Poststroke emotional lability is also known by various other names, for example, pathological laughter/crying, emotional incontinence, hyperemotionality, pseudobulbar affect, etc. The symptoms appeared to be dramatic but transient. Patients can present with sudden onset laughter or crying while speaking on a rather inconspicuous matter. Sometimes, it may be difficult to differentiate it from depression. If symptoms are long-lasting, it may result in distress, depression, social avoidance, and embarrassment. The prevalence of poststroke emotional lability varies between 8% to 32%.[37] Quality research in the management of poststroke emotional lability is lacking, thereby precluding any meaningful recommendation. ACochranereviewwithtotal293participantsreported, antidepressantsreducedthefrequencyoflaughingandcryingepisodesbutthequalityofevidencewaslow(A). The effect was not specific to any particular drug or class of drugs. The review pointed our several methodological deficiencies.[38] Poststroke fatigue Poststroke fatigue (PSF) is common sequalae of both ischemic and hemorrhagic stroke. Nearly half of the stroke survivors suffer from PSF. A systematic review put the prevalence of PSF between 25% and 85%.[39] Uniform definition of PSF is lacking. Most commonly PSF is described as, subject lack of mental and physical energy which interferes with individual's day to day activities. PSF has been found to be associated with old age, neurological deficits, diabetes, hypertension, heart failure, kidney disease, pain, anxiety, depression, sleep disturbances, prestroke fatigue, and cognitive impairment.[40] Few studies have pointed to a link between PSF and subcortical and infra-tentorial infarcts.[40] Considering the multifactorial causation of PSF, any one particular pharmacological agent is unlikely to provide any benefit. Modafinil, amoodawakenerhasbeenfoundtobeusefulinPSFfollowingbrainstem-diencephalicstrokebecauseofitseffectonreticularactivatingsystem(C).[41] A small RCT also favoured the use of Modafinil up to a dose of 400 mg/day (B).[42] SSRIs including fluoxetine, escitalopram, sertraline and SNRI, duloxetine has been studied in PSF but none were proven beneficial except for anxiety symptoms.[4344] Clinicians often try vitamin supplementations in PSF. Vitamin B12, Vitamin B1, and idebenone, a synthetic coenzyme Q10 analog have all been studied, but results are inconclusive (C).[454647] JointAmericanStrokeAssociationandAmericanHeartAssociationstatementencouragesregularphysicalexercisetoreducePSF(D, S).[48] A Cochrane review which included two nonpharmacological interventions, mindfulness-based stress reduction program and a fatigue education program found no conclusive evidence of any intervention having any efficacy to treat PSF (A).[49] Poststroke apathy Post-stroke apathy is of stroke. It is by a lack of with and criteria for poststroke apathy for weeks or and two other symptoms cognitive or and functional There are conditions, particularly depression, which can mimic poststroke In that case, should be put on of cognitive symptoms of depression, for example, low lack of attention and ideas, etc. prevalence of poststroke apathy was in a large Poststroke apathy is more common in less and in of and depression in 40% of Patients with poststroke apathy have been found to have higher risk of depression and worse functional Quality evidence for the treatment of poststroke apathy is lacking. There is one RCT with mg and mg which in in Scale score and more There are Poststroke personality disorders There can be of personality or patient can personality after a stroke. There are that patient and/or Personality are more in case of frontal Studies have put the prevalence of and at and The in the prevalence was because of the in which the study was population of stroke, and used to assess personality changes. There are very RCTs which have looked into the treatment of poststroke personality disorders have been extrapolated from studies conducted in SSRIs, for example, in this group of patients OF PSYCHIATRIC DISORDERS FOLLOWING TRAUMATIC BRAIN INJURY For management of psychiatric disorders following TBI, we are not to the same for stroke for of this Rather, we will management and treatment evidences as The first report of psychiatric disorder following TBI was of a who an in when an and frontal which personality form a responsible to and not to take A of psychiatric disorders can be seen following TBI. Posttraumatic agitation, and are common in Posttraumatic has been to posttraumatic consciousness and in cognitive The of posttraumatic varies between to sleep and underlying delirium can promote can be physical and and often than not is sudden and in The of is the severity of injury and of The of in TBI varies between 25% to is although a rather form compared to and it is common in post-TBI patients which as excessive with The of post-TBI varies between to as per the of the studies consequences of TBI are apathy, and We have discussed apathy in in the of psychiatric disorders following stroke. The prevalence of post-TBI apathy varies between 20% to As discussed it may be difficult to differentiate apathy from depression. Furthermore, apathy can to available pharmacological anxiety, and psychosis are other common psychiatric disorders following TBI. The prevalence of depression after TBI was higher compared to population and was put at having depression at the time of injury, cognitive deficits, of left and and pain was associated with depression in TBI All of anxiety for example, anxiety social anxiety and PTSD are common in TBI patients. The prevalence of anxiety disorders varies between and following between psychosis and TBI is less A meta-analysis suggested that, risk of was in TBI group as compared to the control but of studies included any meaningful and are higher in TBI group as compared to the population and some have found it to be as high as Around 20% participants with TBI all of for example, mood antipsychotics, and have been used in the treatment of psychiatric disorders following TBI [Table but in the of study and large of the studies recommendations are difficult to In clinical many of these alone or in There is evidence in of nonpharmacological Cochrane review did not any evidence in of any nonpharmacological for example, mindfulness-based cognitive therapy or CBT for depression following There are a psychiatrist should be aware while such patients, for example, level of cognitive function, neuroimaging done or presence or of clinical subconvulsive status medications received by the patient, drug-drug etc. [Box of medications for should be prescribed to improve patient compliance (S). or should be used because of risk of and cognitive (S). but not the attending psychiatrist should also use depending on of comorbid physical conditions 1].Table used to treat psychiatric disorders following traumatic brain injury and their of to for treating psychiatrist in patients with traumatic brain 1: of psychiatric management of a patient with traumatic brain Psychiatric disorders following stroke and TBI present for the treating a who is with brain psychiatrists of should in of brain and its the other being a behavioral should be the of the patient, the need of the and the emotional need of The link between psychiatric disorders following stroke and TBI is not an Therefore, treatment also to be one drug for Psychiatrist often has to do and before the As already been there is dearth of large scale RCTs for most of the conditions and treatment recommendations are often extrapolated from primary disorders. However, that may not a or brain may not function in the same as a or However, this guideline an to of the available evidences in this area and recommendations were based on has to while this is in a particular clinical support and of There are no of

The purpose of this study was to describe objective sleep-wake characteristics and glycemia over 7-14 days in young adults with type 1 diabetes. In addition, person-level associations among objective sleep-wake characteristics (total sleep time, sleep variability, and sleep fragmentation index), daytime sleepiness, and glycemia (glycemic control and glucose variability) were examined. In this cross-sectional study, objective sleep-wake characteristics were measured via actigraphy and glucose variability via continuous glucose monitoring over 6-14 days. At baseline, participants completed the Psychomotor Vigilance Test, the Trail Making Test, and questionnaires on daytime sleepiness, sleep quality, and sleep disturbance including sleep diaries. Forty-six participants (mean age, 22.3 ± 3.2 years) wore a wrist actigraph and underwent continuous glucose monitoring concurrently for 6-14 days. Greater sleep variability was directly associated with greater glucose variability (mean of daily differences; r = .33, P = .036). Higher daytime sleepiness was directly associated with greater glucose variability (mean of daily differences; r = .50, P = .001). The association between sleep variability and glucose variability (mean of daily differences) was no longer significant when accounting for daytime sleepiness and controlling for type 1 diabetes duration (P > .05). A higher sleep fragmentation index was associated with greater glucose variability (B = 1.27, P = .010, pr2 = 0.40) after controlling for type 1 diabetes duration and accounting for higher daytime sleepiness. Sleep-wake variability, sleep fragmentation, daytime sleepiness, and the associations with glycemia are new dimensions to consider in young adults with type 1 diabetes. Sleep habits in this population may explain higher glucose variability, and optimizing sleep may improve overall diabetes management. Griggs S, Hickman RL Jr, Strohl KP, Redeker NS, Crawford SL, Grey M. Sleep-wake characteristics, daytime sleepiness, and glycemia in young adults with type 1 diabetes. J Clin Sleep Med. 2021;17(9):1865-1874.

Objective To investigate the correlation between insomnia and sleep quality in adolescents. Methods According to Insomnia Severity Index (ISI) Chinese Version, 3342 students technician training in school were divided into non insomnia group (N = 2345) and insomnia group (N = 997). Sleep and emotional state were assessed by ISI Chinese Version, Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), Self?Rating Anxiety Scale (SAS) and Beck Depression Inventory (BDI). The social demographic data were collected simultaneously. Results The number of insomnia, daytime sleepiness, anxiety and depression in the population was 997 (29.83%), 568 (17.00%), 243 (7.27%) and 1287 (38.51%), respectively. The comparison of social demographic data between 2 groups showed that the proportion of female ( P = 0.000), poor physical condition ( P = 0.000), non?only child ( P = 0.006), high learning pressure ( P = 0.000) and smoking ( P = 0.027) in insomnia group were significantly higher than those in non insomnia group. The total scores of ISI Chinese Version ( P = 0.000), ESS ( P = 0.000), SAS ( P = 0.000) and BDI ( P = 0.000) in insomnia group were significantly higher than those in non insomnia group. Pearson correlation analysis showed that ISI Chinese Version and PSQI scores were positively correlated with ESS score ( r = 0.361, P = 0.000; r = 0.064, P = 0.000), SAS score ( r = 0.326, P = 0.000; r = 0.069, P = 0.000) and BDI score ( r = 0.529, P = 0.000; r = 0.067, P = 0.000), and ISI Chinese Version had higher correlation ( r = 0.300-0.600) with the above scores than PSQI ( r < 0.100). Further partial correlation analysis showed that ISI Chinese Version score was negatively correlated with PSQI score ( r = ? 0.056, P = 0.001). Conclusions Higher proportion of female, worse physical condition, more non?only child, greater learning pressure and higher smoking rate were observed in insomnia group. Daytime sleepiness, anxiety and depression in insomnia group were more serious than those in non insomnia group, but PSQI score can not distinguish the above differences. Compared with PSQI, ISI Chinese Version is more closely related to daytime sleepiness, anxiety and depression, and might be more suitable for assessing insomnia in adolescents. DOI: 10.3969/j.issn.1672-6731.2017.09.007

ObjectiveInsufficient sleep duration and quality has negative effects on athletic performance, injury susceptibility and athlete development. This study aimed to assess the sleep characteristics of professional Qatar Stars League (QSL)...

Study Objectives: We conducted a meta-analysis to assess the effects of different regular exercise (lasting at least 2 months on a regular basis) on self-reported and physiological sleep quality in adults. Varied exercise interventions contained traditional physical exercise (e.g., walking, cycling) and mind–body exercise characterized by gentle exercise with coordination of the body (e.g., yoga).Methods: Procedures followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Systematical searches were conducted in three electronic databases (PubMed, Embase, and Web of Science) for relevant research that involved adult participants without pathological diseases receiving exercise intervention. The search strategy was based on the population, intervention, comparison, and outcome study design (PICOS) framework. The self-reported outcomes included varied rating scales of Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), and Epworth Sleepiness Scale (ESS). Subgroup meta-analyses of PSQI scores were conducted based on type of exercise, duration of intervention, and participants' age and gender. The physiological outcomes were measured by Actigraph. All meta-analyses were performed in a fixed or random statistic model using Revman software.Results: Twenty-two randomized controlled trials were included in the analysis. The overall analysis on subjective outcomes suggests that exercise interventions significantly improved sleep quality in adults compared with control interventions with lower PSQI (MD −2.19; 95% CI −2.96 to −1.41), ISI (MD −1.52; 95% CI −2.63 to −0.41), and ESS (MD −2.55; 95% CI −3.32 to −1.78) scores. Subgroup analyses of PSQI scores showed both physical and mind–body exercise interventions resulted in improvements of subjective sleep to the same extent. Interestingly, short-term interventions (≤3 months) had a significantly greater reduction in sleep disturbance vs. long-term interventions (>3 months). Regarding physiological sleep, few significant effects were found in various sleep parameters except the increased sleep efficiency in the exercise group vs. control group.Conclusions: Results of this systematic review suggest that regular physical as well as mind–body exercise primarily improved subjective sleep quality rather than physiological sleep quality in adults. Specifically, self-reported sleep quality, insomnia severity, and daytime sleepiness could be improved or ameliorated with treatment of exercise, respectively, evaluated by PSQI, ISI, and ESS sleep rating scales.

Poor sleep quality has been associated with poor cognitive performance, anxiety, stress, fatigue, and overall poor health.The present study aimed to assess the quality of sleep and daytime sleepiness in adults aged between 21 and 55 years living in the Mumbai metropolitan region (MMR), India.They were interviewed regarding their quality of sleep using a pretested, semistructured questionnaires -Pittsburgh sleep quality index (PSQI) and the Epworth sleepiness scale (ESS).Out of 758 adults, 49.9% of them had poor sleep quality (PSQI > 5).Excessive daytime sleepiness was reported by 30%.Only 18.3% of the participants slept for more than 7 hours at night, and 20% of participants reported a sleep latency of over 30 min every night.Sleep efficiency was more than 85% in almost 66% (n = 500) of the participants, however, it was observed that the duration of sleep was not adequate in 197 participants who reported less than 6 hours of sleep every night.Adults aged 21-32 years had a poor sleep quality with a significantly higher PSQI and ESS scores, increased sleep latency, and lower sleep efficiency compared to older adults.Sleep quality in young adults is compromised and it is important to intervene them correctly to address the specific determinants of the sleep problems.

The primary objective of this study was to describe characteristics of sleep across the three domains of sleep quality, daytime sleepiness, and behavioral alertness in community-dwelling adults with heart failure. The secondary objective was to identify modifiable factors associated with behavioral alertness. A sample of 280 adults with chronic heart failure was enrolled. Widely used, validated, and sensitive measures of sleep quality (Pittsburgh Sleep Quality Index), daytime sleepiness (Epworth Sleepiness Scale, Stanford Sleepiness Scale), and behavioral alertness (Psychomotor Vigilance Test [PVT]) were collected at baseline, 3 and 6 months. Sociodemographic and clinical characteristics, including exercise, were measured at baseline. Participants were primarily male and functionally compromised with a mean left ventricular ejection fraction of 35 percent. The majority of the sample (73%) reported poor sleep quality. The mean (± SD) Epworth Sleepiness Scale score was low (7.0 ± 4.6), indicating they did not perceive daytime sleepiness. In contrast, behavioral alertness was relatively poor as evidenced by a slow PVT mean response time (3.09 ± 0.76). Participants who reported exercising at least one hour in the past week were more alert and had faster response times than those reporting no exercise. Although sleep quality was poor and behavioral alertness was compromised, these heart failure patients did not feel sleepy. Exercise may help to promote behavioral alertness and reduce daytime sleepiness in adults with heart failure.

Primary objective: To characterize sleep architecture and self-reported sleep quality, fatigue and daytime sleepiness in individuals with TBI. Possible relationships between sleep architecture and self-reported sleep quality, fatigue and daytime sleepiness were examined.Methods: Forty-four community-dwelling adults with TBI completed the Pittsburgh Sleep Quality Index (PSQI), Multidimensional Assessment of Fatigue (MAF) and Epworth Sleepiness Scale (ESS). They underwent two nights of in-laboratory nocturnal polysomnography (NPSG). Pearson product-moment correlation coefficients and hierarchical linear regression was used to analyse the data.Results: Based on the PSQI cut-off score of ≥ 10, 22 participants were characterized as poor sleepers. Twenty-seven participants met criteria for clinically significant fatigue as measured by the GFI of the MAF. Fourteen participants met criteria for excessive daytime sleepiness as measured by the ESS. Poor sleep quality was associated with poor sleep efficiency, short duration of stage 2 sleep and long duration of rapid eye movement sleep. There was little-to-no association between high levels of fatigue or daytime sleepiness with NPSG sleep parameters.Conclusions: A high proportion of the sample endorsed poor sleep quality, fatigue and daytime sleepiness. Those who reported poorer sleep quality evidenced a shorter proportion of time spent in stage 2 sleep. These findings suggest that disruptions in stage 2 sleep might underlie the symptoms of sleep disturbance experienced following TBI.

To evaluate the relations between sleep characteristics and cardiovascular risk factors and napping behavior, and to assess whether daytime napping leads to subsequent better or worse sleep. The sample consisted of 224 (African American, Caucasian, and Asian) middle-aged men and women. Sleep measures included nine nights of actigraphy and sleep diaries, sleep questionnaires, and one night of polysomnography to measure sleep disordered breathing. More frequent napping was associated with shorter nighttime sleep duration averaged across the nine nights of actigraphy (especially among African Americans), more daytime sleepiness, more pain and fatigue by diary, and increased body mass index and waist circumference. Shorter nighttime sleep duration was associated with taking a nap during the next day and taking a nap was associated with less efficient sleep the next night. Napping in middle-aged men and women is associated with overall less nighttime sleep in African Americans and lower sleep efficiency as measured by actigraphy, and increased BMI and central adiposity. These findings point to the importance of measuring of napping in understanding associations of sleep with cardiovascular risk.