Migraine Headache Background
Migraine headaches are traditionally vasomotor or vascular headaches, that is, a headache bought on by changes in blood flow around the brain and neck. But recent research (Nardone, 2008) shows there is a strong neurological component with abnormalities occurring in the brain stem around the Trigemino-Cervical complex as well as neurogenic (neurological caused) inflammation of the meninges (a membrane which covers the brain and spinal cord).
Head pain and non vascular headaches arise from activation of the Trigemino-Cervical nucleus which resides in the spinal cord at the top of the neck. It is involvement of the Trigemino-Cervical nucleus during a migraine, that is responsible for the pain experienced during an attack.
Cervical Migraine Headaches
As the name suggests cervical migraines are migraine headaches that are triggered by dysfunction in the cervical (neck) joints and muscles. The difference between migraine suffers and those with cervical migraine syndrome is that in between migraine attacks patients with cervical migraine syndrome will experience dysfunction in the muscles and joints around the neck and head. This results in pain around the base of the skull and in the neck. It is thought that the stiff joints and muscle spasm in the neck may act as possible triggers for the vascular migraine headache.
It is postulated that spinal manipulation therapy (SMT) works by “loosening” up the stiff joints and muscle spasm in the neck which then “calms” the nocipetive (pain) fibers around the Trigemino-cervical nucleus. In such cases SMT removes a triggering mechanism, just like avoiding certain foods that are known to trigger a migraine. This postulation is supported by research that shows migraine suffers report significant improvements in migraines following SMT (Tuchin, 2000).
It is important to remember though that, SMT does not affect the vascular component of the headache, but acts on the neurological and musculoskeletal component, which in the case of cervical migraine syndrome is a trigger.
Schurks M and Diener HC, “Pathophysiology of migraine and clinical implications”, Schmerz, 2008, October, Vol 5, pg 523-6, 528-30