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Departments of Rehabilitation Medicine (Drs Flanagan and Greenwald) and Medicine (Dr Wieber), Mount Sinai School of Medicine, New York, NY.
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Latest citations:
J Head Trauma Rehabil. ;25 (1):61-7
20051895
Department of Physical Medicine and Rehabilitation, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. elarson@ric.org
OBJECTIVE: To summarize the literature on the available pharmacotherapy for insomnia and the adverse cognitive effects of those options in persons with traumatic brain injury (TBI). DESIGN: Ovid/MEDLINE databases were searched by using the following key words:"brain injury,""sleep initiation and maintenance disorders,""hypnotics and sedatives,""benzodiazepines,""trazodone," and "neuronal plasticity." RESULTS: The reviewed literature consistently reported that benzodiazepines and atypical gamma-aminobutyric acid (GABA) agonists result in cognitive impairment when plasma levels are at their peak. Evidence of residual effects on cognition was reported for benzodiazepines but was seen less often in atypical GABA agonists. However, evidence has also been presented that GABA agonists have adverse effects on neuroplasticity, raising concerns about their use in patients recovering from TBI. CONCLUSIONS: Use of benzodiazepines in TBI has been discouraged and some authors also advocate caution in prescribing atypical GABA agonists. Alternate treatments including trazodone and a newer class of agents, melatonin agonists, are highlighted, along with the limited data available addressing the use of these medications in TBI. Finally, suggestions are offered for further research, especially on topic related to neural plasticity and functional recovery.
Department of Psychiatry, University of Vermont, Burlington, VY, USA.
Since deleterious effects of m-CPP, the primary catabolic metabolite of trazodone, were last reviewed 2 years ago, research data continue to accrue showing that clinically significant levels of m-CPP (a) are generated in patients using trazodone for sleep and (b) are present 24 h a day and (c) have potentially serious ill effects. This commentary argues that the documented potential for harm and multiple risks of m-CPP outweigh potential benefits of trazodone, given the development and marketing of many safer alternatives since trazodone's introduction in the 1980s.
Mark T. Keegan, MD Department of Anesthesiology, Mayo Clinic, Charlton 1145, 200 First Street SW, Rochester, MN 55905, USA. keegan.mark@mayo.edu.
Providing adequate sedation in the neurologic intensive care unit (ICU) depends on determination of proper goals for sedation, adequate assessment of the level of sedation, and appropriate choice of drug based on the patient's physiology. The management of sedation in the ICU will influence long-term outcome. Delirium, anxiety, and pain must be identified and treated separately. The use of protocols can improve compliance with published evidence-based recommendations. Propofol and dexmedetomidine may be used for rapidly titratable sedation, benzodiazepines for anxiolysis, neuroleptics for treatment of delirium, and opiates for analgesia. Unique aspects of patients with acute brain disease, such as elevated intracranial pressure or status epilepticus, require adaptation of sedative regimens. Processed EEG monitoring and volatile anesthetic agents have not yet proven beneficial or practical for use in the ICU.
OBJECTIVE: To test the efficacy of a cognitive-behavioral therapy (CBT) for insomnia in persons having sustained traumatic brain injury (TBI). DESIGN: Single-case design with multiple baselines across participants. SETTING: Outpatient rehabilitation center. PARTICIPANTS: Eleven subjects having sustained mild to severe TBI who developed insomnia after the injury. INTERVENTION: Eight-week CBT for insomnia including stimulus control, sleep restriction, cognitive restructuring, sleep hygiene education, and fatigue management. MAIN OUTCOME MEASURES: Total wake time, sleep efficiency, and diagnostic criteria. RESULTS: Visual analyses, corroborated by intervention time series analyses and t tests, revealed clinically and statistically significant reductions in total wake time and sleep efficiency for 8 (73%) of 11 participants. An average reduction of 53.9% in total wake time was observed across participants from pre- to post-treatment. Progress was in general well maintained at the 1-month and 3-month follow-ups. The average sleep efficiency augmented significantly from pretreatment (77.2%) to post-treatment (87.9%), and also by the 3-month follow-up (90.9%). Improvements in sleep were accompanied by a reduction in symptoms of general and physical fatigue. CONCLUSIONS: The results of this study show that psychologic interventions for insomnia are a promising therapeutic avenue for TBI survivors.
Other papers by authors:
PM R. 2010 Jun ;2 (6):485-7
20630433
Rusk Institute of Rehabilitative Medicine, 400 E 34th St, Ste 600, New York, NY 10016().
PM R. 2009 Jan ;1 (1):76-80
19627876
Rusk Institute of Rehabilitation Medicine, New York, NY 10016().
Teresa A Ashman,
Joshua B Cantor,
Wayne A Gordon,
Lisa Spielman,
Steve Flanagan,
Annika Ginsberg,
Clara Engmann,
Matthew Egan,
Felicia Ambrose,
Brian Greenwald
Department of Rehabilitation Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. teresa.ashman@mssm.edu
OBJECTIVE: To examine the efficacy of sertraline in the treatment of depression after traumatic brain injury (TBI). DESIGN: Double-blind, randomized controlled trial. SETTING: Research center at a major urban medical center. PARTICIPANTS: Subjects were a referred and volunteer sample of 52 participants with TBI, a diagnosis of major depression disorder (MDD), and a score on the Hamilton Rating Scale for Depression (HAM-D) of 18 or greater. The majority of the sample was male (58%), had less than 14 years of education (73%), had incomes below $20,000 (82%), and were from minority backgrounds (75%). Approximately one third of the sample had mild brain injuries, and two thirds had moderate to severe brain injuries. The mean age was 47+/-11, and the mean time since injury was 17+/-14 years. One participant withdrew from the study because of side effects. INTERVENTION: Daily oral sertraline in doses starting at 25mg and increasing to therapeutic levels (up to 200mg) or placebo for 10 weeks. MAIN OUTCOME MEASURES: The HAM-D, the Beck Anxiety Inventory, and the Life-3 quality of life (QOL). RESULTS: No statistically significant differences were found at baseline between drug and placebo groups on baseline measures of depression (24.8+/-7.3 vs 27.7+/-7.0), anxiety (16.4+/-12.3 vs 24.0+/-14.9), or QOL (2.96+/-1.0 vs 2.9+/-0.9). The income level of those receiving placebo was significantly lower than those participants receiving medication. Analyses of covariance revealed significant changes from preintervention to posttreatment for all 3 outcome measures (P<.001) but no group effects. Random-effects modeling did not find any significant difference in patterns of scores of the outcome measures between the placebo and medication groups. CONCLUSIONS: Both groups showed improvements in mood, anxiety, and QOL, with 59% of the experimental group and 32% of the placebo group responding to the treatment, defined as a reduction of a person's HAM-D score by 50%.
New York University School of Medicine, The Rusk Institute of Rehabilitation, New York, NY, USA.
Traumatic brain injury (TBI) is widespread and leads to death and disability in millions of individuals around the world each year. Overall incidence and prevalence of TBI are likely to increase in absolute terms in the future. Tackling the problem of treating TBI successfully will require improvements in the understanding of normal cerebral anatomy, physiology, and function throughout the lifespan, as well as the pathological and recuperative responses that result from trauma. New treatment approaches and combinations will need to be targeted to the heterogeneous needs of TBI populations. This article explores and evaluates the research evidence in areas that will likely lead to a reduction in TBI-related morbidity and improved outcomes. These include emerging assessment instruments and techniques in areas of structural/chemical and functional neuroimaging and neuropsychology, advances in the realms of cell-based therapies and genetics, promising cognitive rehabilitation techniques including cognitive remediation and the use of electronic technologies including assistive devices and virtual reality, and the emerging field of complementary and alternative medicine.
Stroke. 2008 Apr 3;:
18388345
Rajiv R Shah,
Sepideh Haghpanah,
Elie P Elovic,
Steven R Flanagan,
Anousheh Behnegar,
Vu Nguyen,
Stephen J Page,
Zi-Ping Fang,
John Chae
From the Departments of Radiology, and Physical Medicine and Rehabilitation, Case Western Reserve University at MetroHealth Medical Center, Cleveland, Ohio; Kessler Medical Rehabilitation Research and Education Center, West Orange, NJ; the Department of Rehabilitation Medicine, Mt Sinai School of Medicine, New York, NY; the Department of Physical Medicine and Rehabilitation, Carolina Rehabilitation, Charlotte, NC; the Department of Rehabilitation Sciences, University of Cincinnati, Cincinnati, Ohio; and NeuroControl Corporation, North Ridgeville, Ohio, Z.P.F. is now affiliated with NBI Development, San Francisco, Calif.
BACKGROUND AND PURPOSE: We describe the structural abnormalities in the painful shoulder of stroke survivors and their relationships to clinical characteristics. Method-Eighty-nine chronic stroke survivors with poststroke shoulder pain underwent T1- and T2-weighted multiplanar, multisequence MRI of the painful paretic shoulder. All scans were reviewed by one radiologist for the following abnormalities: rotator cuff, biceps and deltoid tears, tendinopathies and atrophy, subacromial bursa fluid, labral ligamentous complex abnormalities, and acromioclavicular capsular hypertrophy. Clinical variables included subject demographics, stroke characteristics, and the Brief Pain Inventory Questions 12. The relationship between MRI findings and clinical characteristics was assessed through logistic regression. RESULTS: Thirty-five percent of subjects exhibited a tear of at least one rotator cuff, biceps or deltoid muscle. Fifty-three percent of subjects exhibited tendinopathy of at least one rotator cuff, bicep or deltoid muscle. The prevalence of rotator cuff tears increased with age. However, rotator cuff tears and rotator cuff and deltoid tendinopathies were not related to severity of poststroke shoulder pain. In approximately 20% of cases, rotator cuff and deltoid muscles exhibited evidence of atrophy. Atrophy was associated with reduced motor strength and reduced severity of shoulder pain. CONCLUSIONS: Rotator cuff tears and rotator cuff and deltoid tendinopathies are highly prevalent in poststroke shoulder pain. However, their relationship to shoulder pain is uncertain. Atrophy is less common but is associated with less severe shoulder pain.
Mount Sinai Hospital, New York, NY 10029-6504, USA. steve.flanagan@mssm.edu
This self-directed learning module reviews common clinical problems and issues pertaining to early management of persons with traumatic brain injury (TBI). It is part of the study guide on brain injury medicine in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. Acute TBI is frequently complicated by agitation, dystonia, and numerous orthopedic and neurologic comorbidities, often causing a decrement in function, which requires careful assessment and treatment. Individuals with acute brain injury typically receive rehabilitation in a setting determined by numerous factors, including medical stability and tolerance to rehabilitation interventions. OVERALL ARTICLE OBJECTIVES: To describe (a) common traumatic brain injury-related comorbidities and treatment strategies,(b) potential causes of declining patient performance, and (c) appropriate settings for rehabilitation interventions.
Department of Physical Medicine and Rehabilitation, Rochester, MN, USA. brown.allen@mayo.edu.
This self-directed learning module reviews the current epidemiology of traumatic brain injury (TBI), its pathophysiology, prognostication after injury, currently available innovative early approaches to diagnosis and treatment, and effective methods of prevention. It is intended to provide the rehabilitation clinician with current knowledge to accurately inform patients, families, significant others, referring physicians, and payers and to aid in clinical decision making while caring for patients after TBI. OVERALL ARTICLE OBJECTIVE: To describe current knowledge in traumatic brain injury epidemiology, pathophysiology, prognostication, acute treatment, and prevention.
Institute for Rehabilitation and Research, Houston, TX 77030, USA. Sunil.Kothari@memorialhermann.org
This self-directed learning module describes recent developments in the field of traumatic brain injury (TBI) rehabilitation. In particular, it focuses on the implications of recent technological advances for evaluation, prognostication, and treatment. It is part of the chapter on TBI medicine in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article specifically focuses on neuroplasticity and its implications for rehabilitation interventions, the role of innovative neuroimaging modalities, improvements in our ability to prognosticate made possible by newer technologies, technologically based enhancement of motor rehabilitation, and the role of alternative and complementary medicine in TBI rehabilitation. OVERALL ARTICLE OBJECTIVE: To describe recent advances in our ability to evaluate, prognosticate, and treat traumatic brain injury.
Kessler Medical Rehabilitation Research and Education Center, West Orange, NJ 07052, USA. eelovic@kmrrec.org
This self-directed learning module highlights the rehabilitation aspects of care for people with traumatic brain injury (TBI) after the acute phase. It focuses on issues important to community reentry, outpatient care, and return to work. It is part of the chapter on TBI medicine in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article specifically focuses on the formulation of rehabilitation plans to address the issues of cognitive dysfunction, behavioral disturbances, and community reintegration. Topics covered include pharmacologic and nonpharmacologic approaches to cognitive and affective disorders, intimacy, social isolation, mobility, and return to work. Finally, the critical issues of legal competency and obtaining informed consent in the population with cognitive impairment are discussed. OVERALL ARTICLE OBJECTIVE: To summarize the issues that affect outpatient care, independence, and community reentry after traumatic brain injury.
Barrow Neurological Institute, Phoenix, AZ 85013-4405, USA. ckwasnica@chw.edu
This self-directed learning module highlights the subpopulations of traumatic brain injury (TBI) that are treated by the rehabilitation practitioner. It is part of the chapter on TBI in the self-directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. Specifically, this article focuses on the management of patients with mild TBI, children, and individuals with acquired brain injury from other etiologies, such as anoxic events or neoplastic lesions. The clinical spectrum of TBI, from the most severe presentation to the mildest, requires similar clinical skills to evaluate and manage. OVERALL ARTICLE OBJECTIVE: To describe the spectrum of brain injury populations based on age, severity, and etiology.
Latest similar papers:We reviewed the pharmacological efficacies and side effects of antidepressants. Selective serotonin reuptake inhibitors (SSRIs) and serotonin noradrenaline reuptake inhibitors (SNRIs) are most popularly prescribed for anxiety disorders as well as mild or moderate depression. These drugs have less orthostatic, cognitive, cardiovascular, and anticholinergic side effects. Tricyclic antidepressants are still important for treating severe depression, and mianserin and trazodone are useful for treating delirium. Clinicians should select antidepressants considering their pharmacologic profiles and avoiding adverse effects.
This paper is a review of the use of drugs in sleep and wakefulness disorders. Insomnia is more often a symptom than an autonomic disorder. Good knowledge of the clinical facts is required before prescribing hypnotics. Sedative drugs are potentially hypnotics; yet, melatonin is not sedative and may be considered to resynchronise of sleep phases. Stimulant drugs are prescribed in attention disorders; methylphenidate is the more frequently used. Narcolepsy, which is characterized by daytime sleepiness and irresistible episodes of sleep, is treated by an alpha1 noradrenergic stimulant modafinil which has no amphetaminic properties.
About 90% of neurodegenerative diseases with parkinsonism are associated with sleep disorders including daytime sleepiness, sleep-related breathing disorders and parasomnias. It is hard to define what ratio of insomnia and daytime hypersomnia is caused by the antiparkinsonian treatment, by the somatic and mental-emotional symptoms of the neurodegenerative disease and by the neurodegenerative brain process itself. Recent research suggests that the latter group is more important than expected. In Parkinson syndromes the structures included in sleep regulation--mainly within the brainstem--are also affected resulting in specific sleep disorders being the primary biological symptoms of these diseases. The recently described parasomnia--REM sleep behavior disorder--has a specific significance in this respect: it may prevent by several years a high ratio of the parkinsonian disorders--especially synucleinopathies--offering the possibility of prevention by identifying the affected individuals. There seems to exist a similar although less clarified association between daytime sleepiness and Parkinson disease. Analysing the behavior of the orexin system in neurodegenerative diseases may help to learn more about this, recently described neurohumoral system and may clear the association of narcolepsy with neurodegeneration. By understanding the associations of parkinsonian disorders and sleep disorders new therapeutical strategies may be invented and may offer new aspects to understand the mechanism of them.
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