Cognitive rehabilitation for memory deficits following stroke

Background: Memory problems are a common cognitive complaint following stroke. Memory rehabilitation programmes either attempt to retrain lost or poor memory functions, or teach patients strategies to cope with them. Objectives: To determine the effectiveness of cognitive rehabilitation for memory problems following stroke. Search methods: We searched the Cochrane Stroke Group Trials Register (last searched September 2006). In addition, we searched the following electronic databases; the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2005), MEDLINE (1966 to June 2005), EMBASE (1980 to June 2005), CINAHL (1982 to June 2005), PsycINFO (1980 to July 2006), AMED (1985 to June 2005), British Nursing Index (1985 to June 2005), CAB Abstracts (1973 to May 2005) and the National Research Register (June 2006). We handsearched relevant journals and searched reference lists. Selection criteria: We selected controlled trials of memory retraining in stroke. We excluded studies with mixed aetiology groups unless 75% or more of the participants had a stroke or separate data were available for the stroke patients. Data collection and analysis: Two review authors selected trials for inclusion, assessed quality, and extracted data. Main results: Two trials, involving 18 participants, were included. One study compared the effectiveness of a mnemonic strategy treatment group with a 'drill and practice' control, while the other compared the effectiveness of an imagery mnemonics programme with a 'pragmatic' memory rehabilitation control programme. Formal meta‐analyses could not be performed due to a paucity of studies and lack of commonly‐employed outcome measures. The results do not show any significant effect of memory rehabilitation on performance of objective memory tests, and no significant effects of treatment on subjective and observer‐rated measures of memory. Authors' conclusions: There was no evidence to support or refute the effectiveness of memory rehabilitation on functional outcomes, and objective, subjective, and observer‐rated memory measures. There is a need for more robust, well‐designed and better‐reported trials of memory rehabilitation using common standardised outcome measures

Adrenoceptors in acoustically primed audiogenic seizures

Bibliography: pages [77]-86.The audiogenic seizure (AGS) is a convulsive seizure syndrome elicited through exposure to intense sound. Genetically AGS-resistant. C57BL/6J mice may be rendered seizure susceptible through an acoustic priming procedure. These experiments investigated a possible role for adrenoceptors in acoustically primed AGS. It was hypothesized that the sequelae of acoustic priming involve increases in the activity of excitatory alpha-1 and beta-1 adrenoceptors with a concurrent decrease in the activity of inhibitory alpha-2 receptors. These alterations in receptor activity may produce an imbalance between excitatory and inhibitory mechanisms which results in AGS susceptibility. These hypotheses were evaluated through the administration of selective adrenoceptor antagonists to primed C57BL/6J mice. Experiment 1 replicated the priming phenomenon. In Experiment 2, methoxyamine exerted proconvulsant effects across all stages of the seizure syndrome, and the higher doses resulted in diminished latencies to all stages. The alpha-1 antagonist prazosin exerted anticonvulsant effects on seizure incidence. The beta-1 antagonist atenolol also exerted anticonvulsant effects. The alpha-2 agonist yohimbine failed to exert proconvulsant effects and reduced seizure incidence to zero at higher doses. The results suggest that acoustically primed AGS in C57BL/6J mice may involve a significant increase in the activity of alpha-1 and beta-1 adrenoceptors. No support was found for a role of alpha-2 adrenoceptors in acoustically primed AGS.M.A. (Master of Arts

Selective Serotonin Reuptake Inhibitors for Treating Neurocognitive and Neuropsychiatric Disorders Following Traumatic Brain Injury: An Evaluation of Current Evidence

The prevalence of neuropsychiatric disorders following traumatic brain injury (TBI) is 20%–50%, and disorders of mood and cognition may remain even after recovery of neurologic function is achieved. Selective serotonin reuptake inhibitors (SSRI) block the reuptake of serotonin in presynaptic cells to lead to increased serotonergic activity in the synaptic cleft, constituting first-line treatment for a variety of neurocognitive and neuropsychiatric disorders. This review investigates the utility of SSRIs in treating post-TBI disorders. In total, 37 unique reports were consolidated from the Cochrane Central Register and PubMed (eight randomized-controlled trials (RCTs), nine open-label studies, 11 case reports, nine review articles). SSRIs are associated with improvement of depressive but not cognitive symptoms. Pooled analysis using the Hamilton Depression Rating Scale demonstrate a significant mean decrease of depression severity following sertraline compared to placebo—a result supported by several other RCTs with similar endpoints. Evidence from smaller studies demonstrates mood improvement following SSRI administration with absent or negative effects on cognitive and functional recovery. Notably, studies on SSRI treatment effects for post-traumatic stress disorder after TBI remain absent, and this represents an important direction of future research. Furthermore, placebo-controlled studies with extended follow-up periods and concurrent biomarker, neuroimaging and behavioral data are necessary to delineate the attributable pharmacological effects of SSRIs in the TBI population