Eric B Larson1, Felise S Zollman. 1. Department of Physical Medicine and Rehabilitation, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. elarson@ric.org
Abstract
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.
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.
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