[3], With advances in the management of head trauma, an increasing number of patients are surviving with residual neurological impairments. The complex nature of traumatic brain injury outcomes and possible accompanying injuries might require the neurological physiotherapist to use core skills like facilitation, therapeutic exercises or physical activity prescription, but also to clinically reason and apply the knowledge of therapeutic interventions and strategies from other specialities, eg. There is, however, growing evidence that medications may speed recovery by enhancing some neurological functions without impacting others. Neurology 1995;45:865-872. Passler M, Riggs R. Positive outcomes in traumatic brain injury-vegetative state: Patients treated with bromocriptine. The aim of this systematic review was to critically evaluate the evidence regarding efficacy of pharmacological interventions for anxiety after TBI. Data extracted included participant characteristics, TBI severity, study design, pharmacological interventions, and outcomes. The highest concentration of serotonergic and adrenergic fibres is located near the frontal lobes, the most common site of traumatic contusion.[24]. Searches were conducted with Medline, Embase, PsycINFO, Web of Science, PubMed. Mayo Clin Proc 2000;75:711-721. Karli D, Burke D, Kim H, et al. 2003;15:359-370. NIH The review will also summarize existing literature on these conditions, in addition to describing clinical experience. 36. Mild TBI was included in 3% of the SRs. There are, however, a number of agents that inspire optimism. [12], Two separate studies have suggested methylphenidate is effective in the treatment of agitation and seizures,[16,17] while another demonstrated no neurobehavioral benefit.[18]. Cochrane Database Syst Rev. Curr Opin Neurol 1997;10:52-57. HHS Investigations utilizing 600 to 2250 mg of valproic acid daily (resulting in serum levels of 40 to 100 µg/mL), have demonstrated positive neurocognitive effects, including improved recent memory and problem-solving, as well as ameliorating neuropsychiatric and neurobehavioral symptoms such as depression, mania, destructive and aggressive behavior, restlessness, disinhibition, impulsivity, lability, and alertness. Hasuike A, Ueno D, Nagashima H, Kubota T, Tsukune N, Watanabe N, Sato S. J Periodontal Res. Saletu B, Saletu M, Grunberger J, et al. Selecting the most appropriate agent requires careful analysis of the neurological disabilities present, the nature of the underlying lesion, and the time elapsed since the injury. Meythaler J, Lawrence D, Devivo M, et al. An alternate version of ICMJE style is to additionally list the month an issue number, but since most journals use continuous After a traumatic brain injury (TBI), many persons experience significant and debilitating problems with anxiety. [26] It is also a noncompetitive NMDA receptor antagonist and may provide protection against possible glutamate-mediated excitotoxicity in the context of TBI. However early intervention is needed in the course of AD at Mild Cognitive Impairment (MCI) or mild dementia stages to help prevent decline and maintain good quality of life. Future studies will undoubtedly add to the clinician’s armamentarium for the care of TBI patients. Despite potentially severe consequences, post-TBI psychiatric sequelae are underdiagnosed and undertreated. Fortunately, a number of pharmacological interventions show promise in helping patients cope with these losses and deficits. In acutely ill patients, one recent single-centre study ( n = 195 patients) reported antipsychotic use in 26.7% of patients within 7 days of TBI [ 26 ]. Most medications were administered during the acute stage. Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly Work in • Lee HB, Lyketsos CG, Rao V. Pharmacological management of the psychiatric aspects of traumatic brain injury. [2] In the US, approximately 2 million people will sustain a TBI each year, one-quarter of whom will require hospitalization, leading to a conservative estimate of direct and indirect costs of $50 billion to $100 billion annually. Despite the prevalence and cost of TBI-related disabilities there is a paucity of literature reviewing modern approaches to pharmacotherapy. 9. Common drugs may influence motor recovery after stroke. Recovery from vegetative state of six months’ duration associated with Sinemet (levodopa/carbidopa). Agitated symptom response to divalproex following acute brain injury. Objective. 18. J Neuropsychiatry Clin Neurosci 2000;12:395-397. Siddall OM, Use of methylphedinate in traumatic brain injury. Saniova B, Drobny M, Kneslova L, et al. 780 retrieved SRs underwent a two-level screening to determine inclusion. Brain Inj 2000;15:321-331. Halpern SD, Ubel PA, Caplan AL, Marion DW, Palmer AM, Schiding JK, et al. O’Dell MW, Riggs RV. eCollection 2018. doi: 10.1136/bmjopen-2019-036300. Arch Phys Med Rehabil 1996;77:536-540. Synnot A, Bragge P, Lunny C, Menon D, Clavisi O, Pattuwage L, Volovici V, Mondello S, Cnossen MC, Donoghue E, Gruen RL, Maas A. PLoS One. Hellawell DJ, Taylor RT, Pentland B. Cognitive and psychosocial outcome following moderate or severe traumatic brain injury. There are also a number of animal studies examining drugs that have the potential to adversely affect brain recovery following TBI. The antiparkinsonian drugs amantadine, bromocriptine, and levodopa combined with carbidopa (e.g., Sinemet) have varied mechanisms of action, but all ultimately serve to increase dopamine levels in the brain. There is no period after the journal name. Int Rev Psychiatry. Malden, MA: Blackwell Science; 2000:5-12. [27], Bromocriptine is a dopamine receptor agonist affecting primarily D2 receptors and to a lesser extent D1 receptors. Walker W, Seel R, Gibellato M, et al. J Head Trauma Rehabil 1987;2:29-33. Doctors usually need to assess the situation quickly. Those who survive traumatic brain injury may experience anxiety, agitation, memory impairments, and behavioral changes. Wroblewski B, Leary J, Phelan A, et al. Pharmacological intervention is frequently used to control aggression following TBI. [5-8], Depending on the location of injury, damage can occur to a variety of neurotransmitter networks critical to cognitive processes. When problematic TBI symptoms are identified, clinicians can use this information to determine pharmacological options and integrate them with nonpharmacological options such as physical therapy, occupational therapy, physiatry, and the patient’s support network. Keywords: Neuropsychiatric symptoms may present as mood disorders, posttraumatic stress disorder, and personality changes characterized by disinhibition and egocentricity. 2. Vancouver Group. Background. Psychostimulants Forsyth R, Jayamoni B. Noradrenergic agonists for acute traumatic brain injury. COVID-19 is an emerging, rapidly evolving situation. PROSPERO Registration: CRD42015017355. Psychostimulants such as methylphenidate are most commonly used to treat attention deficit hyperactivity disorder (ADHD), a condition that involves problems with executive functioning and can be characterized as similar to brain injury both in terms of symptoms and neurotransmitter aberrations.[10]. 53 , No. The aim of this systematic review was to critically evaluate the evidence regarding efficacy of pharmacological interventions for aggression following TBI in adults. Traumatic Brain Injury and PTSD: Focus on Veterans. in Medical Journals, visit www.icmje.org. [34], The evidence is similarly limited for levidopa and carbidopa medications where nonrandomized studies suggest that they might be useful in the chronic phase of TBI with diffuse injury and persistent vegetative state. Methylphenidate has a quick onset of action and relatively benign side effect profile, and we believe it to be useful in both the acute and chronic phase of TBI. However, it should be noted that there is some evidence that dopamine blockade may negatively affect recovery.[47,48]. Anticonvulsants have been used with varying results for treating symptoms of TBI. SRs were assessed for methodological quality by using the AMSTAR measurement tool. 54. Treatments for spasticity include a range of pharmacological and non-pharmacological interventions, often used in combination. Feeney DM, Gonzalez A, Law WA. Brain Inj 1993;7:333-338. Brain Injury 1999;13:863-872. Challman T, Lipsky J. Methylphenidate: Its pharmacology and uses. Crismon M, Childs A, Wilcox R, et al. Amantadine to improve neurorecovery in traumatic brain injury-associated diffuse axonal injury: A pilot double-blind randomized trial. When treating neurological deficits medically, there is evidence to support the tailored use of these agents for particular TBI clinical scenarios. J Neurotrauma. The ICMJE created the After removing duplicates, 166/780 SRs published between 1990-2017 were reviewed, 62 of which met inclusion criteria. Research for the effects of pharmacological intervention for managing agitation during this period is inconclusive. Try to use non-pharmacological interventions whenever they are indicated and appropriate. Fortunately, current evidence suggests that antidepressants can be used to manage both neuropsychiatric and additional neurological deficits persisting from brain injury. Ann Pharmacother 2005;39:1309-1313. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. 49. Gultekin R, Huang S, Clavisi O, Pattuwage L, König TC, Gruen R. Injury. 4. 30. BCMJ standard citation style is a slight modification of the ICMJE/NLM style, as follows: For more information on the ICMJE Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly Work Brain Inj 1999;13:808-811. 40. respiratory care, orthopaedic and trauma protocols, … Woo BH, Nesathurai S (eds). 22. If the decision is made to use medications to promote TBI recovery or treat its attendant disabilities, clinicians should thoroughly document the goals of pharmacotherapy and closely monitor for side effects. doi: 10.1002/14651858.CD009221.pub2. Summary The NLM now lists all authors. Zafonte R, Watanabe T, Mann N. Amantadine: A potential treatment for the minimally conscious state. Pharmacological interventions in traumatic brain injury: Can we rely on systematic reviews for evidence? [28] The use of levodopa and carbidopa in combination directly increases dopamine levels: levodopa becomes dopamine once decarboxylated, while carbidopa inhibits L-amino decarboxylase, allowing levodopa to reach the central nervous system.[28]. The group became known as the Kaelin C, Cifu D, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Anticonvulsants Schallert T, Hernandez T, Barth T. Recovery of function after brain damage: Severe and chronic disruption by diazepam. Pharmacological strategies under investigation are targeting sites involved in the secondary cascade that contribute to overall poor outcome following the primary injury. Thus, synthesis of the research for non-pharmacological interventions for reducing agitation during post-traumatic amnesia is essential for improving long … The impact of methylphenidate on chronic attention is more ambiguous: one study suggests improvement in long-term processing speed and attention to tasks but not increased sustained attention or decreased susceptibility to distraction. Mooney G, Haas L. Effect of methylphenidate on brain injury-related anger. 27. 2020 Nov 5;10(6):335-345. doi: 10.9740/mhc.2020.11.335. Pharmacological complications 1 management of moderate to moderately severe traumatic brain injury of clinical Amsterdam. The prevalence and cost of TBI-related disabilities. [ 25 ], Gibellato M Maki. 54 ( 4 ):374-387. doi: 10.1016/j.injury.2015.10.011 with these losses and.! Mci and mild AD dementia 37 ( 1 ): CD008929 are usually emergencies and consequences can worsen.. 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