Pharmacotherapy of Posttraumatic Cognitive Impairments

Brain Injury Rehabilitation Unit, HealthONE Spalding Rehabilitation Hospital, Aurora, CO, USA.
Behavioural neurology (Impact Factor: 1.45). 02/2006; 17(1):25-42. DOI: 10.1155/2006/460592
Source: PubMed


Pharmacotherapy may contribute to the rehabilitation of persons with posttraumatic cognitive impairments. This article reviews first the neurobiological consequences of traumatic brain injury with a particular emphasis on acute and long-term posttraumatic neurochemical disturbances. Studies of pharmacotherapies for posttraumatic cognitive impairments are reviewed next, and are organized according to medication class and the neurotransmitter system they affect most. Based on the evidence provided by that review, augmentation of posttraumatic cerebral catecholaminergic and cholinergic function are suggested as potentially useful neurochemical targets for pharmacologic intervention in this population. More specifically, it is suggested that persons with posttraumatic impairments in arousal, speed of processing, and possibly attention may benefit most from treatment with an agent that augments cerebral catecholaminergic function, and that persons whose predominant posttraumatic impairment is in the domain of memory may benefit most from treatment with cholinesterase inhibitors. Practical considerations regarding the use of pharmacotherapies for posttraumatic cognitive impairments are offered, and the need for additional research in this area is highlighted.

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    • "Chronic primary or secondary dysfunction in dopaminergic , noradrenergic, and serotonergic systems seem to be relatively common consequences of TBI [Arciniegas and Silver, 2006; McAllister et al., 2006]. It is well established that these systems are also compromised in MD patients [Bennett, 2010; Drevets et al., 2000; Muller et al., 2011; Wagner et al., 2010]. "
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    ABSTRACT: Background: Many people with a traumatic brain injury (TBI), even mild to moderate, will develop major depression (MD). Recent studies of patients with MD suggest reduced fractional anisotropy (FA) in dorsolateral prefrontal cortex (DLPFC), temporal lobe tracts, midline, and capsule regions. Some of these pathways have also been found to have reduced FA in patients with TBI. It is unknown whether the pathways implicated in MD after TBI are similar to those with MD without TBI. This study sought to investigate whether there were specific pathways unique to TBI patients who develop MD. Methods: A sample of TBI-MD subjects (N = 14), TBI-no-MD subjects (N = 12), MD-no-TBI (N = 26), and control subjects (no TBI or MD, N = 23), using a strict measurement protocol underwent psychiatric assessments and diffusion tensor brain Magnetic Resonance Imaging (MRI). Results: The findings of this study indicate that (1) TBI patients who develop MD have reduced axial diffusivity in DLPFC, corpus callosum (CC), and nucleus accumbens white matter tracts compared to TBI patients who do not develop MD and (2) MD patients without a history of TBI have reduced FA along the CC. We also found that more severe MD relates to altered radial diffusivity. Conclusions: These findings suggest that compromise to specific white matter pathways, including both axonal and myelination aspects, after a mild TBI underlie the susceptibility of these patients developing MD.
    Human Brain Mapping 01/2014; 35(1). DOI:10.1002/hbm.22171 · 5.97 Impact Factor
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    • "Given that improvements were seen in multiple measures of working memory , and that we found moderate - to - large ef - fect sizes , we believe that these results are clinically sig - nificant . Working memory dysfunction is a commonly cited problem following TBI ( Arciniegas and Silver , 2006 ; Dikmen et al . , 2009 ; Eslinger et al . "
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    ABSTRACT: Acupressure is a complementary and alternative medicine (CAM) treatment using fingertips to stimulate acupoints on the skin. Although suggested to improve cognitive function, acupressure has not been previously investigated with a controlled design in traumatic brain injury (TBI) survivors, who could particularly benefit from a non-pharmacological intervention for cognitive impairment. A randomized, placebo-controlled, single-blind design assessed the effects of acupressure (eight treatments over 4 weeks) on cognitive impairment and state of being following TBI, including assessment of event-related potentials (ERPs) during Stroop and auditory oddball tasks. It was hypothesized that active acupressure treatments would confer greater cognitive improvement than placebo treatments, perhaps because of enhanced relaxation response induction and resulting stress reduction. Significant treatment effects were found comparing pre- to post-treatment change between groups. During the Stroop task, the active-treatment group showed greater reduction in both P300 latency (p = 0.010, partial η² = 0.26) and amplitude (p = 0.011, partial η² = 0.26), as well as a reduced Stroop effect on accuracy (p = 0.008, partial η² = 0.21) than did the placebo group. Additionally, the active-treatment group improved more than did the placebo group on the digit span test (p = 0.043, Cohen's d = 0.68). Together, these results suggest an enhancement in working memory function associated with active treatments. Because acupressure emphasizes self-care and can be taught to novice individuals, it warrants further study as an adjunct treatment for TBI.
    Journal of neurotrauma 10/2010; 28(1):21-34. DOI:10.1089/neu.2010.1515 · 3.71 Impact Factor
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    • "Finally, pharmacological intervention studies provide another hint of a dopaminergic component to TBI, in that administration of (dopaminergic) stimulants improves cognition in TBI patients (Arciniegas and Silver, 2006; Tenovuo, 2006). Therefore, just as schizophrenics are thought to smoke cigarettes to normalize neurotransmitter-mediated deficits in cognition, it is possible that exogenous enhancement of DA transmission by DAT blockers like cocaine or other stimulants might normalize this circuitry, providing a possible abuse risk with chronic administration. "
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    ABSTRACT: Wars in Afghanistan and Iraq have resulted in thousands of military personnel suffering traumatic brain injury (TBI), including closed-head injuries. Of interest is whether these individuals and other TBI survivors are at increased risk for substance use disorder (SUD). While it has been well established that drug or alcohol intoxication itself increases probability of suffering a TBI in accidents or acts of violence, little is known about whether the brain insult itself increases the likelihood that a previously non-drug-abusing individual would develop SUD. Might TBI survivors be unusually vulnerable to addiction to opiate analgesics compared to other pain patients? Similarly, it is not known if TBI increases the likelihood of relapse among persons with SUD in remission. We highlight challenges in answering these questions, and review neurochemical and behavioral evidence that supports a causal relationship between TBI and SUD. In this review, we conclude that little is known regarding the directionality of TBI increasing drug abuse, and that collaborative research in this area is critically needed.
    Journal of neurotrauma 03/2009; 26(7):1077-82. DOI:10.1089/neu.2008-0849 · 3.71 Impact Factor
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