Vagus nerve stimulation effective in inhibiting cortical spreading depression

A poster presentation at the International Headache Congress in Valencia, Spain reports that VNS inhibits cortical spreading depression (CSD), which is known to be the cause of migraine aura and a trigger for headache.

CSD is a local disturbance in the occipital cortex (a region of the brain), which is caused by a slowly propagating wave of depolarisation - suppression of electrical activity - spreading across the cortex.

The researchers determined that both surgically implanted and non-invasive VNS were just as effective at reducing CSD. They also found that VNS reduced CSD in 20 to 30 minutes as against the standard migraine prophylactic drugs, which took weeks to have a similar effect.

Professor Cenk Ayata commented:

What we have established is that VNS reduces the hyper excitability of the brain by suppressing CSD and that VNS is much quicker at achieving this than traditional migraine prophylactic agents such as topiramate and valproic acid. We were also able to establish that VNS was effective in reducing CSD for at least three hours after only four minutes of treatment. Our findings have opened up exciting possibilities for further research.

Reducing CSD is the validated platform for screening pharmacological therapies for migraine with aura. Many preventative migraine drugs, regardless of pharmacological class, inhibit CSD.

The preclinical study had four arms; non-invasive VNS; surgically implanted VNS; sham group – electrodes were implanted but never stimulated; and naive animals. CSD was elicited by either a continuous KCI application or by electrical stimulation.

CSD was then measured in all groups and it was found that VNS raised the electrical threshold to initiate CSD by more than threefold and reduced the frequency and speed of the continuous KCI-induced CSDs.

Blood pressure and heart rate were also continuously monitored and were only minimally and transiently affected by VNS.

The authors believe that VNS works by modification of specific brain pathways, neurotransmitters and cytokines.

A full paper on this research will be published in a scientific journal by the end of the year.

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