A Pilot Study of Quetiapine Treatment of Aggression Due to Traumatic Brain Injury

Bristol-Myers Squibb, New York, New York, United States
Journal of Neuropsychiatry (Impact Factor: 2.82). 02/2006; 18(4):547-9. DOI: 10.1176/appi.neuropsych.18.4.547
Source: PubMed


In a 6-week open-label, flexible dose pilot study of quetiapine for treatment of aggression secondary to traumatic brain injury (TBI), seven subjects who were at least 3-months post-injury were enrolled. The Overt Aggression Scale - Modified (OAS-M) and Clinical Global Impression (CGI) were primary outcome measures. Administration of quetiapine at doses of 25 to 300 mg daily was efficacious and well-tolerated in reducing irritability and aggression resulting from TBI, with an associated improvement in cognitive functioning.

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    • "It is also safe regarding extrapyramidal side effects6,33,52,61). Clinical studies have revealed that quetiapine is also a suitable agent for the treatment of aggression and agitation due to traumatic cerebral damage39). Quetiapine causes blockage with its high binding affinity for serotonin 5-HT2 and 5-HT6 receptors and the more moderate affinity for dopamine D2 receptors. It also has affinity towards α1 and α2 receptors and H1 receptors like clozapine. "
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    ABSTRACT: This study was undertaken in the belief that the atypical antipsychotic drug quetiapine could prevent apoptosis in the penumbra region following ischemia, taking into account findings that show 5-hydroxytryptamine-2 receptor blockers can prevent apoptosis. We created 5 groups, each containing 6 animals. Nothing was done on the K-I group used for comparisons with the other groups to make sure adequate ischemia had been achieved. The K-II group was sacrificed on the 1st day after transient focal cerebral ischemia and the K-III group on the 3rd day. The D-I group was administered quetiapine following ischemia and sacrificed on the 1st day while the D-II group was administered quetiapine every day following the ischemia and sacrificed on the 3rd day. The samples were stained with the immunochemical TUNEL method and the number of apoptotic cells were counted. There was a significant difference between the first and third day control groups (K-II/K-III : p=0.004) and this indicates that apoptotic cell death increases with time. This increase was not encountered in the drug groups (D-I/D-II : p=1.00). Statistical analysis of immunohistochemical data revealed that quetiapine decreased the apoptotic cell death that normally increased with time. Quetiapine is already in clinical use and is a safe drug, in contrast to many substances that are used to prevent ischemia and are not normally used clinically. Our results and the literature data indicate that quetiapine could help both as a neuronal protector and to resolve neuropsychiatric problems caused by the ischemia in cerebral ischemia cases.
    Journal of Korean Neurosurgical Society 07/2013; 54(1):1-7. DOI:10.3340/jkns.2013.54.1.1 · 0.64 Impact Factor
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    • "Atypical antipsychotics seem as effective as haloperidol for the treatment of delirium in patients who are critically ill (including those who are mechanically ventilated), tend not to interfere strongly with cerebral dopaminergic function, and produce fewer adverse motor effects than haloperidol [141]. These agents also may facilitate, or at least not adversely affect, cognition when used for the treatment of posttraumatic delirium, although there currently are limited data with which to support this suggestion [142] [143]. "
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    ABSTRACT: Traumatic brain injury (TBI) results in approximately 230,000 hospitalizations annually in the United States. Advances in the acute management of TBI have improved survival after TBI. Many TBI survivors develop neurobehavioral disturbances in the acute post-injury period. Neurobehavioral sequelae present clinical management challenges for critical care professionals. This article defines and describes TBI and reviews its common neuroanatomic and neurobehavioral consequences. These disturbances are organized under the framework of posttraumatic encephalopathy, and the characteristic forms and stages of recovery of this condition are discussed. Recommendations regarding evaluation and management of posttraumatic neurobehavioral problems in the critical care setting are offered.
    Critical Care Clinics 11/2008; 24(4):737-65, viii. DOI:10.1016/j.ccc.2008.06.001 · 2.16 Impact Factor
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    ABSTRACT: In this review, the current evidence is examined regarding neuropharmacologic treatment for children and adolescents (under the age of 18 years) who sustained a traumatic brain injury (TBI). Although the focus is on the pediatric TBI population, there is a paucity of empirical data related to the role of medication with children and adolescents after brain injury. Therefore, findings from the adult TBI literature are incorporated where appropriate so as to identify potential agents that warrant further examination in pediatric populations. This review addresses specific sequelae of TBI from the earliest stages of neurologic recovery to long-term comorbidities, including disorders of impaired consciousness, post-TBI agitation, cognitive decline, and post-TBI depression. The evidence regarding the role of medication in neuroprotection and neurorecovery in this population is also explored. Medication classes reviewed include excitatory amino acids, antagonists to the N-methyl-D-aspartate receptor, dopamine agonists, benzodiazepines, β-blockers, anticonvulsants, and antidepressants. It is hoped that this review will guide future research, and ideas as to how this may be accomplished within a pediatric population are suggested.
    PM&R 12/2010; 2(12):1127-40. DOI:10.1016/j.pmrj.2010.07.007 · 1.53 Impact Factor
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