Author: Fred Kahn MD, FRCS (C)
Source: Meditech International Inc.
DEFINITION AND PATHOPHYSIOLOGY
Migraine is a chronic, episodic, primary headache1. It is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).2
Migraine can be viewed as an inherited disorder with episodic symptoms that arise in the brain. Given the emerging evidence that migraine is based on complex, heterogeneous genetics, migraine attacks may be initiated in several ways. All humans have a trigeminocervical pain system that governs the head and upper neck, serving as a type of early warning system to protect the brain and upper cervical spinal cord from real or threatened injury. Any alteration in the stability of pathways either directly involved in or modulating the trigeminocervical pain system is a potential cause of migraine. Some people may inherit a low activation threshold for migraine; others, one that is at the high end. The more often destabilizing triggering factors in the environment either separately or in combination meet this threshold, the more often the pain system is activated. This would explain why some people are headache prone and others are relatively resistant.
Aura is thought to be caused by a spreading wave of depolarization (cortical spreading depression). Aura is also associated with a localized reduction in blood flow followed by an increase in blood flow and characteristically affects the parieto-occipital cortex. Experimental evidence suggests that the cortical events underlying aura symptoms may be one of the ways that headaches are initiated in migraine patients. It is likely that the genes that make a person susceptible to aura are distinct from the ones that confer susceptibility to migraine headaches.
Symptoms typically last from 4 to 72 hours and may be excruciating. Pain is often, but not always, unilateral, throbbing, worse with exertion, and accompanied by autonomic symptoms (e.g., nausea; sensitivity to light, sound, odors, etc.) Fortification spectra and other transient focal neurologic deficits, aura occur in a few patients, usually just prior to onset of the headache.2 The diagnosis of migraine can usually be established on the basis of taking a thorough history.
CAUSES AND TRIGGERS
Many potential migraine triggers have been identified; these include the ingestion of red wine, hypoglycemia, excessive afferent stimuli (flashing lights, strong odors), weather changes, sleep deprivation, stress and hormonal factors. Cranial trauma, cervical pain and temporo-mandibular joint dysfunction may also trigger or exacerbate migraine headaches. Sensory input from the trigeminal nerve and cranial nerves IX and X have also been found to trigger migraines. Fluctuating estrogen levels are a potent migraine factor. Many females experience the onset of migraine headaches at menarche, severe attacks during menstruation (menstrual migraine) and increased severity during menopause. For most women, migraines are less frequent and severe during pregnancy, although they may become more pronounced during the 1st and occasionally the 2nd trimester. Oral contraceptives and other forms of hormone therapy occasionally increase the severity of the headache and have been associated with CVA type episodes in women who have attacks associated with a variety of aura.
CURRENT MODES OF TREATMENT
Many different medications have been specifically designed to treat migraines, with varying degrees of efficacy. In addition, some drugs commonly used to treat other conditions may also help to relieve or prevent migraines. Medications used to combat migraines include analgesics, triptans, antiemetics, and opioids, along with preventative medications such as beta-blockers, calcium channel blockers, serotonin receptor antagonists and OnabotulinumtoxinA. These medications all too frequently have many undesirable side-effects and limited efficacy. Lifestyle changes (diet, exercise, sleeping habits) and some alternative therapies such as acupuncture, biofeedback therapy, massage therapy and manipulation, have been found to be helpful for some patients.
LASER THERAPY FOR MIGRAINES
A number of clinical trials have been performed in order to determine the efficacy of Laser Therapy for Migraines, both in children and adults. Gottschling et al.4 examined the effect of laser acupuncture on children with migraines or tension-type headaches. Over a four month clinical trial, they found that the laser treated group had a significant decrease in the number of headaches per month, a reduction in the severity of the pain and duration as compared to the placebo treated group. Ebneshahidi et al. 5 also used laser acupuncture to show that adult patients suffering from tension-type headaches showed a significant decrease in headache intensity, the duration of attacks and number of days with headache per month, compared to the placebo treated group. For more than 40 years, Laser Therapy has been effectively used in the treatment of acute and chronic conditions, including degenerative disc disease, repetitive stress injuries, muscle strains, sprains and arthritis.6 Laser Therapy is a non-invasive, pain-free, light-based therapy that uses a combination of red and infrared light in the form of superluminous light-emitting diodes and laser diodes. The power output of these devices is below the level of surgical and other high-intensity lasers. Photon particles of light are absorbed by the mitochondria through cytochrome c oxidase and result in increased cellular ATP levels.6 Both Laser Therapy and acupuncture have been shown to increase endogenous opioid production and release, in addition to elevating the pain threshold levels.7, 8