MD; for the NEST-2 InvestigatorsBackground and Purpose-We hypothesized that transcranial laser therapy (TLT) can use near-infrared laser technology to treat acute ischemic stroke. The NeuroThera Effectiveness and Safety Trial-2 (NEST-2) tested the safety and efficacy of TLT in acute ischemic stroke. Methods-This double-blind, randomized study compared TLT treatment to sham control. Patients receiving tissue plasminogen activator and patients with evidence of hemorrhagic infarct were excluded. The primary efficacy end point was a favorable 90-day score of 0 to 2 assessed by the modified Rankin Scale. Other 90-day end points included the overall shift in modified Rankin Scale and assessments of change in the National Institutes of Health Stroke Scale score. Results-We randomized 660 patients: 331 received TLT and 327 received sham; 120 (36.3%) in the TLT group achieved favorable outcome versus 101 (30.9%), in the sham group (Pϭ0.094), odds ratio 1.38 (95% CI, 0.95 to 2.00).Comparable results were seen for the other outcome measures. Although no prespecified test achieved significance, a post hoc analysis of patients with a baseline National Institutes of Health Stroke Scale score of Ͻ16 showed a favorable outcome at 90 days on the primary end point (PϽ0.044). Mortality rates and serious adverse events did not differ between groups with 17.5% and 17.4% mortality, 37.8% and 41.8% serious adverse events for TLT and sham, respectively. Conclusions-TLT within 24 hours from stroke onset demonstrated safety but did not meet formal statistical significance for efficacy. However, all predefined analyses showed a favorable trend, consistent with the previous clinical trial (NEST-1). Both studies indicate that mortality and adverse event rates were not adversely affected by TLT. A definitive trial with refined baseline National Institutes of Health Stroke Scale exclusion criteria is planned.
The feasibility ofusing the endogenous P3 component of the auditory evoked potential as an objective means of evaluating cognitive function in aging and dementia was examined. A systematic increase in the latency of the P3 component was found as a function of increasing age in normal subjects. For patients with neurological diseases producing dementia, the latency of the P3 component substantially exceeded the normal age-matched value in 80% of the cases. The P3 latencies for neurological and psychiatric patients without dementia did not differ from normal, except for patients with a history of serious brain trauma. In those patients who were followed serially over periods of time during which there were changes in mental status, the P3 latency akd clinical status correlated. These results suggest that the P3 latency may provide a sensitive means for evaluating changes in cognitive function resulting from normal aging and neurological dysfunction.
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