Until recently, scientific literature on headaches did not seem to answer a myriad diagnostic questions related to caring for patients. Prior to the last five years, dedicated research yielded astonishingly little conclusive information. This information was often presented in such a fragmented way as to cause further confusion.
The pathophysiology is still so full of conflicting and complicated theories that even the most earnest researcher is tempted to give up seeking the answers. Despite the paucity of training most medical professionals received in college regarding headaches, most clinicians remain committed to helping patients. Headaches are a problem that medical specialists encounter every day.
Headaches are far and away the greatest cause of human suffering. Consider this:
- Most people do not seek care for their headaches and yet four per- cent of all patients claim headaches as their primary concern and al- most a third of all patients claim it as their secondary concern.1
- The estimated prevalence rate for all types of headaches is 93 percent of all males and 99 percent of all females.2
- Forty-five million Americans suffer a headache every day of their lives with the annual cost of migraine treatment topping one billion dol- lars in health care cost and 13 bil- lion in lost workdays.3
- The pediatric headache rate has in- creased from 14 percent in 1972 to 50 percent in 1992.4
- Still, more than 90 percent of peo- ple with headache problems have never seen a specialist for their pain.5
Of the many types of headaches, the tension headache is by far the most prevalent — with 38 percent of all males and 46 percent of all females suffering from this form.6 Seymour Diamond describes the tension headache in his chapter “Muscle Contraction Headache” in Practicing Physician Approach to Headache, as “chronic, nonpulsatile, tightness, band-like pain in the temporal area, unilateral or bilateral, associated with stress.”
The next most prevalent is the migraine — claimed by six percent of all males and 18 percent of all females.7 In the 1980s, the prevalence of migraines increased by 60 percent. Stephen Silberstein describes the migraine headache as “a severe episodic unilateral throbbing headache with genetic inheritance aggravated by exercise and associated with nausea, phonophobia, and photophobia.”8
Other less frequent but still important forms of headaches are a result of sinus infections, aneurysms, tumors or growths, temporal arteritis and trigeminal autonomic cephalgia’s (CPH, cluster, etc). This miscellaneous headache group is too complex to fully define, has less probability of occurring, and is too diffuse a group to review for the purposes of this article. Still, all forms must be considered in any headache differentiation.
This diagnostic picture is painful and depressing. With suffering all this time, why has science been so unfruitful on such a plague to society? The good news is much has been accomplished in the last five years.
Early Headache Management Theories
Thankfully, the management of head-aches has come a long way since the days of leeches, bloodletting, and spirit removal. The early scientific management ideas resulting from the anecdotal evidence of single practitioners yielded many of the treatments used today.
Pharmacies are now full of migraine treatments. Much of the first effective migraine management came with the introduction of ergotoamines DHE. This was followed by heart medicine beta-blockers and calcium channel blockers, and later the tryptans. Unfortunately, hard science has had little to offer tension headache sufferers. Tension headaches have failed the polypharmacy, imaging, dental, and blood tests.
Oddly enough, up till now, practitioners have largely ignored the behavioral sciences as a means of managing headaches — especially migraines. Now, with the emergence of the most recent scientific literature, medicine has begun to embrace behavior modification techniques for use with both the tension headache and migraine therapies.
The complex pathophysiology of the tension headache and migraine has long challenged researchers seeking an etiology. The discovery of the etiology lies in the identification of the complex set of initiators, aggravators, and perpetuators — not a single-cause viewpoint.
Headache and Inflammation
The latest research on neurogenic inflammation in migraine and tension headaches provides a better understanding of the patho-physiology of both diseases. At last, there are the necessary tools to relieve headache suffering.
One of the most intriguing areas of headache research concerns the effects of neurogenic inflammation. In his presentation at the AHS headache symposium in Scottsdale Arizona in 1999, Michael Cutrer of the Harvard Medical School stated that, “under steady-state conditions, the brain vigorously maintains the equilibrium of its extacellular environment.”
When an appropriate amount of inflammation chemicals travel to the brain, glial cells, neurons, lymphatics, and vascular system rapidly take up the neurogenic chemicals. When an overload of chemicals travel to the brain, a headache results. What causes the overload is an increase in neural transmission in the trigeminal afferent system, cervical afferents, and even the sympathetic system. Other inflammation chemicals like lactic acid, prostaglandins, cytokines, nerve growth factor, and other inflammation by-products are also to blame. These neurotransmitters can cause the nociceptors in the trigeminal vessel walls to become sensitive which lowers the stimulation threshold.
Two neurotransmitters, CGRP and SubP, stimulate mast cells to degranulate which in turn spurs a release of inflammation chemicals. According to Weiler’s analysis of PET scans, the neurogenic inflammatory chemicals seem to trigger the migraine generator in the corpus.9
The neuropeptide, Sub P, initiates a release of histamine from the mast cells, which activates H1 endothelial receptors inducing formation of nitric oxide (NO).10 The nitric oxide, a gaseous neurotransmitter, rapidly diffuses into the vascular smooth muscle which activates CGNP and relaxes the muscle thus causing vasodilatation.11
The neurotransmitter CGRP exhibits vasodilatation properties of its own. Sub P also initiates release of cytokine from monocytes. The neuro-transmitters CGRP and Sub P alter the function and chemotactic activity of immune cells. It is likely that the release of these neuropeptides in large quantities overrides the brain’s ability to manage the steady state of balance thereby initiating a cascade of biochemical changes.
Inflammation and the Central Nervous System
The classic analogy of the nervous system is a set system with simple transmission of signals. According to recent research, this analogy is far from correct.