Medication in the treatment of the behavioural sequelae of traumatic brain injury

Bates, Gordon

doi:10.1017/s0012162206001472

Cited by 11 publications

(2 citation statements)

References 40 publications

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“…[2][3][4] Estimates of the occurrence of agitation or aggression range from 35% to 96% of patients with TBI during the acute period and from 31% to 71% of these patients in the chronic phase. 2,5,6 Regardless of the presumed cause or etiology of aggressive behavior in a particular patient with TBI, behavioral management approaches, including psychotherapeutic intervention, are also commonly used, often in conjunction with pharmacologic treatment. 2,5,6 Regardless of the presumed cause or etiology of aggressive behavior in a particular patient with TBI, behavioral management approaches, including psychotherapeutic intervention, are also commonly used, often in conjunction with pharmacologic treatment.…”

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confidence: 99%

Brain injury and aggression

Wong¹

2011

Neurology

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For the clinician who has had any depth of experience working with a brain-injured population, there is little doubt that behavioral problems following traumatic brain injury (TBI) can present significant management challenges. Common in TBI, behavioral disinhibition and associated problems may increase over the first year following injury, 1 and are often associated with damage to the prefrontal regions of the brain. 2-4 Estimates of the occurrence of agitation or aggression range from 35% to 96% of patients with TBI during the acute period and from 31% to 71% of these patients in the chronic phase. 5 With respect to the treatment of post-TBI aggression, several agents may be efficacious, including ␤-blockers, antipsychotics, antiseizure drugs, stimulants, and mood stabilizers. 2,5,6 Regardless of the presumed cause or etiology of aggressive behavior in a particular patient with TBI, behavioral management approaches, including psychotherapeutic intervention, are also commonly used, often in conjunction with pharmacologic treatment. However, it would be erroneous to assume that there is a universally established evidence-based protocol for the management or treatment of post-TBI aggressive behavior to guide the practicing clinician working with this challenging patient group. Thus, the appeal and value of any new information that would increase diagnostic accuracy and specificity of post-TBI aggressive behavior is very clear, as the ultimate "payoff " would be in improved treatment and management.In this issue of Neurology ® , Pardini et al. 7 report a study of subjects from the Vietnam Head Injury Study registry, consisting of 155 patients with penetrating traumatic brain injury (PTBI) and 42 non-braininjured controls. They examined the relationships among monoamine oxidase A (MAO-A) polymorphism, general lesion location (prefrontal cortex [PFC] vs non-PFC), and reported aggressive behavior. In addition, prior traumatic experiences, such as may occur in childhood, were considered in their study. The authors report 2 primary noteworthy findings: 1) pa-tients with the highest levels of reported aggression were more likely to have PFC vs non-PFC lesions; and 2) a significant interaction existed such that only in the non-PFC group did MAO-A polymorphism and prior traumatic experience present as modulating factors for aggression, whereas in the PFC group there was an absence of the mediating effects of genotype and the history of traumatic experiences. The authors offered that "potentially, lesion localization and MAO-A genotype data could be combined to develop risk-stratification algorithms and individualized treatments for aggression in PTBI."That the patients with the highest levels of aggression "preferentially" presented with lesions in the PFC regions appears at first glance to represent both an affirmation of prior assertions in the literature of the association between prefrontal cortical pathology and behavioral dyscontrol, as well as the potential basis for useful clinical prediction of post-TBI aggressi...

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confidence: 99%

Brain injury and aggression

Wong¹

2011

Neurology

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“…In addition, a significant pharmacotherapy that has consistently shown benefits to attention, behavioral outcomes, executive functions, and memory is dopaminergic (DA) therapy [6]–[8], but the aspect of TBI pathology targeted by DA therapy remains unclear. Pharmacological interventions to elucidate cognitive and behavioral deficits in patients with head injuries are now being performed clinically, although empirical studies supporting this practice are limited [9], [10], and the use of psychostimulant drugs (e.g., methylphenidate) for head injuries [11], [12] may indicate that cognitive and learning impairments are related to a deficiency in the dopamine system after head injury. Furthermore, according to a statement in a recent clinical trial of amantadine in treating head injuries that was published in NEJM in 2012 [8], future research should focus on determining the pathophysiological characteristics of patients who responded to amantadine, the most effective dosage, and the duration of treatment and timing of its initiation, as well as the effectiveness of amantadine in patients with brain injuries.…”

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confidence: 99%

Amantadine Ameliorates Dopamine-Releasing Deficits and Behavioral Deficits in Rats after Fluid Percussion Injury

et al. 2014

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AimsTo investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI), we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery.Materials and MethodsIn this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group) or amantadine hydrochloride, with a releasing rate of 3.6mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV) and high-pressure liquid chromatography (HPLC). Novel object recognition (NOR) and fixed-speed rotarod (FSRR) behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury.ResultsSequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value) of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion.ConclusionChronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury.

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Amantadine treatment following traumatic brain injury in children

Williams

2007

Brain Injury

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Medication in the treatment of the behavioural sequelae of traumatic brain injury

Cited by 11 publications

References 40 publications

Brain injury and aggression

Brain injury and aggression

Amantadine Ameliorates Dopamine-Releasing Deficits and Behavioral Deficits in Rats after Fluid Percussion Injury

Amantadine treatment following traumatic brain injury in children

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