Resolving Tension Headaches Part - 3

Biochemical Changes

If we review the literature on tension headaches there is no doubt that tension headaches are associated with changes in the levels of certain brain chemicals such as serotonin, bradykinins, and substance P.

• Serotonin acts as a chemical messenger that transmits nerve signals between nerve cells. It also causes blood vessels to narrow.
• Bradykinins mediates the inflammatory response, increases vasodilatation (expansion of arteries and veins), and causes contraction of smooth muscle.
• Substance P functions as a neurotransmitter, especially in the transmission of pain impulses from peripheral receptors to the central nervous system.

The question is, are these chemical the initial factor that created the headache or are they a secondary consequence of physical restrictions. In my opinion, the physical changes probably took place first; which in turn caused a cascade of events that eventually increased, or altered, the levels of these chemicals.

Support for my perspective comes from what is called central sensitization. Central sensitization has been hypothesized as one of the primary mechanisms of chronic pain conditions. Central sensitization occurs when pain receptors in your nervous system (nociceptive neurons) become sensitized by tissue damage or inflammation.

By damage, I am not just referring to some type of trauma like a motor vehicle accident. I am also referring to damage caused by:

• The micro trauma of repetitive strain injuries.
• Stress caused by muscle imbalances.
• Long-term stress placed on your body by poor posture.
• De-conditioned muscles.

All these causes can produce areas of hyper-tonicity (increased tension) in our bodies that become chronically restricted; such as that huge knot most people have in their shoulders or the one just under the base of their skull.

When these hypertonic tissues becomes irritated or inflamed it releases chemical mediators (bradykinin, serotonin, substance P), which cause a sensitization of nerve endings resulting in pain, tension, and the production of headaches. If we review the history of most patients who suffer from tension headache we will routinely find a source of initial tissue damage (accident, trauma, history of tension) and associated inflammation which causes biochemical changes that elicit headaches.

Myofascial trigger points and sensitization: an updated pain model for tension-type headache Fernandez-de-las-Penas C, Cuadrado ML, Arendt-Nielsen L, Simons DG, Pareja JA. Cephalalgia. 2007 May;27(5):383-93. Epub 2007 Mar 14. inDepartment of Physical Therapy, Occupational Therapy, Physical Medicine and Rehabilitation, Universidad Rey Juan Carlos, Madrid, Spain.

Stress-induced pain and muscle activity in patients with migraine and tension-type headache. Leistad RB, Sand T, Westgaard RH, Nilsen KB, Stovner LJ. Cephalalgia. 2006 Jan;26(1):64-73. Department of Neuroscience, Norwegian University of Technology and Science and Department of Neurology and Clinical Neurophysiology, St Olavs Hospital, Trondheim, Norway.

In part four of “Resolving Tension Headaches” we will cover some viable treatment options.

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