An insomnia tablet could help people recover from a stroke, a study found.
Zolpidem is a new class of sleeping pills sold under the brands Stilnoct and Edluar in the UK and Ambien in the US.
It is handed out to 750,000 NHS patients each year and works by dampening the electrical activity of the brain.
But a Stanford University School of Medicine study found lab mice which had strokes rebounded significantly faster if they received low doses of the pill.
It is suggested the drug helps the brain rewire itself after the stroke repairing the damage caused.
A stroke is a life-threatening condition that occurs when the blood supply to part of the brain is cut off.
The faster someone is treated the less damage is caused to the body which can cause brain injury, disability and possibly death.
Every year, around 110,000 people have a stroke in England and it is the third largest cause of death, after heart disease and cancer.
If untreated after a few days tissue death continues to spread to adjacent brain regions due to repercussions from the initial damage but the brain begins slowly rewiring itself and substituting new neural connections for those destroyed by the stroke.
Within three to six months, at least 90 per cent of all the recovery a stroke patient is likely to experience takes place.
Until now no drug has been shown to improve recovery after the stroke
But zolpidem enhanced a type of nerve-cell signaling activity whose role in recovery unexpectedly appears beneficial.
This signaling was bolstered even though the drug was given at doses well below those at which it exerts its hallmark sedative effect.
Nerve cells signal to one another by means of substances called neurotransmitters.
Neurotransmitters can be excitatory, triggering propagation of an impulse in the receiving nerve cell.
Or they can be inhibitory, temporarily preventing the receiving nerve cell from propagating any impulses.
The roughly one-fifth of all nerve cells in the brain that are inhibitory mainly do their job by secreting a neurotransmitter called GABA.
The bulk of GABA signaling takes place at synapses, scientists have learned that nerve cells can also feature GABA receptors elsewhere on their outer surfaces.
These are called extrasynaptic receptors.
Previous research suggested that extrasynaptic GABA signaling impeded stroke recovery in an animal model.
But until the new study, published online in Brain, nobody had looked into the impact on stroke recovery of the far more common synaptic GABA signaling.
Professor in Neurosurgery and the Neurosciences Dr Gary Steinberg said: “Before this study, the thinking in the field was that GABA signaling after a stroke was detrimental
“But now we know that if it’s the right kind of GABA signaling, it’s beneficial. And we’ve identified an FDA-approved drug that decisively promotes the beneficial signaling.”
While zolpidem dramatically improved mice’s rate of recovery from stroke, its ability to increase the extent of their recovery couldn’t be determined because, unlike humans, mice naturally regain most of their pre-stroke function eventually.
Further experiments are planned to test the drug in other animal models, as well as to experiment with different dose sizes and timing, before proceeding to clinical trials
However he cautioned that the study’s results need to be independently replicated in other laboratories before clinical trials of the drug’s capacity as a stroke-recovery agent can begin.