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Tension-Type Headache: Around and over our heads

By Yohyoh Wang

“There is an ache inside that Gordian knot, the brain, which wants to do so much in so many directions.”1

Headaches, now all too familiar to working Americans, have become an irritating symbol of a harried lifestyle. Of the many types of headaches, tension-type headaches (TTH) are the most frequently reported; a conservative estimate of headache prevalence is around 40% of the American population, with some sources reporting upwards of 78%2. Anecdotal evidence and scientific research alike identify psychological stress as a common trigger of TTH, suggesting that somehow one’s perception of stress is capable of inducing physical pain. Although TTH is extremely prevalent, the specific mechanisms that underlie headache formation are still, for the most part, unknown. This piece will explore research of headaches, current theories about the pathophysiology of TTH, and treatments of cranial pain with a wide range of success rates.

Most people, particularly those who work long hours or have stressful jobs, have experienced headache multiple times in their life. The term headache in general refers to any nociception in the head, including the face, neck, and skull. A tension-type headache is characterized by persistent feelings of tightness in bandlike patterns around the skull. This tension, as opposed to a sharp or twisting sensation, is a marked characteristic of TTH. Another distinguishing feature of TTH is its close association with psychosomatic triggers; that is, a patient’s emotional, rather than physical, state can influence their susceptibility to developing headache.

Although TTH is often triggered by psychological stress, some anatomical features of the brain and head may influence an individual’s susceptibility to headache. Tightness in the pericranial muscles, which surround the skull, have been shown to increase sensitivity to pain3. Individuals with denser muscles seem to have a lower threshold for nociception; since the pericranial muscle fibers are abnormally inelastic, the response to applied pressure can be incredibly painful. This pathophysiology has been invoked in explanations for the feelings of tightness associated with TTH. If a psychological stressor induces a reflexive physical response4 – clenching the jaw, grinding teeth, or wrinkling the brow, for example – that further tightens the already tight pericranial muscles, TTH pain can become further amplified.

After repeated reactivation of pain pathways, headache pain can even worsen and turn chronic. Individuals with chronic TTH, when compared to control individuals without chronic headache conditions, exhibited lower thresholds for pain when pressure was applied to myofascial areas associated with pericranial muscle tightness5. One proposed mechanism for sensitization involves interactions of the nociceptive pathways with the spinal cord. When a pain signal travels from the site of pain to the spinal cord, the increased signal firing of sensory neurons in the pathway could augment that particular pathway’s significance in sensory input. Exciting the nociceptive pathway from a particular muscle may strengthen its signaling and increase sensitivity to lower levels of stimulation. If an individual experiences multiple headaches in a short period of time, he or she could develop a chronic TTH condition due to the sensitization of the nociceptive pathway.

Despite the variety of theories surrounding the mechanisms of headache pain, the underlying causes of TTH are still nebulous. Physicians, thus, are faced with common cases of headache pain without access to treatments that have been successful across the board.

Historically, headache treatment falls into two broad categories: proactive and reactive. Proactive headache treatments attempt to minimize triggering psychological behaviors, while reactive treatments target the headache pain itself. These opposing fields of treatment are reflected in medications prescribed to sufferers of TTH. Most people who experience headache pain reach for aspirin, ibuprofen, and prescription analgesics as reactive treatment. Some others, particularly those with an awareness of their increased susceptibility on headache, use preventative treatment like antidepressants and muscle relaxants (including Botox, which in tranquilizing the pericranial muscles may lessen the physical triggers of headache pain).

 

Proactive versus reactive cognitive therapies have also been researched to combat psychological abnormalities that aggravate TTH. One theory, for example, posits that an individual has a large degree of cognitive control over their headache pain. This was tested by a study in which one experimental group of individuals with chronic TTH was subjected to a proactive stress-coping program6 designed to lower negative perceptions of stressful situations in an effort to curb the somatic response to psychological triggers. The other experimental group received reactive biofeedback training, which targeted relaxation of muscle tightness as a response to headache pain. After the experiment ended, the stress-coping group reported a significantly lower headache frequency than both the control group and the biofeedback training group. These results suggest that the psychological component of headache pain is more influential than the actual physical pain, even though the reactive group directly targeted the muscle tightness associated with nociception.

In the forty years since the stress coping study was published, chronic TTH treatment has shifted its focus to incremental care, with the goal of lessening headache frequency over time. Due to the lingering vagueness surrounding the biological mechanisms of headache, some physicians chose to consider each headache individually. A recently introduced ten-step process examines a headache in multiple ways; the headache disorder is first classified, then the immediate pain is treated, and the physician considers treatment options7. The medical frustration with the elusive cause of tension-type headaches is even reflected on the American Migraine Foundation’s website2, which states: “There is no one approach for all patients…[treatment] must be individualized for each patient, so be sure you explore your symptoms in detail with your doctor.” Given the inability of research to translate into broadly successful headache treatment, proactive treatment has taken a back seat to reactive pain relief medication, and the best proactive advice physicians give is to avoid psychological stressors, including stress and lack of sleep. Until the medical community can successfully cut its age-old Gordian knot, patients may only have access to a jumble of general analgesics, muscle relaxants, and motherly advice to curb headache pain.

Historically, headache treatment falls into two broad categories: proactive and reactive. Proactive headache treatments attempt to minimize triggering psychological behaviors, while reactive treatments target the headache pain itself. These opposing fields of treatment are reflected in medications prescribed to sufferers of TTH. Most people who experience headache pain reach for aspirin, ibuprofen, and prescription analgesics as reactive treatment. Some others, particularly those with an awareness of their increased susceptibility on headache, use preventative treatment like antidepressants and muscle relaxants (including Botox, which in tranquilizing the pericranial muscles may lessen the physical triggers of headache pain).

Proactive versus reactive cognitive therapies have also been researched to combat psychological abnormalities that aggravate TTH. One theory, for example, posits that an individual has a large degree of cognitive control over their headache pain. This was tested by a study in which one experimental group of individuals with chronic TTH was subjected to a proactive stress-coping program6 designed to lower negative perceptions of stressful situations in an effort to curb the somatic response to psychological triggers. The other experimental group received reactive biofeedback training, which targeted relaxation of muscle tightness as a response to headache pain. After the experiment ended, the stress-coping group reported a significantly lower headache frequency than both the control group and the biofeedback training group. These results suggest that the psychological component of headache pain is more influential than the actual physical pain, even though the reactive group directly targeted the muscle tightness associated with nociception.

In the forty years since the stress coping study was published, chronic TTH treatment has shifted its focus to incremental care, with the goal of lessening headache frequency over time. Due to the lingering vagueness surrounding the biological mechanisms of headache, some physicians chose to consider each headache individually. A recently introduced ten-step process examines a headache in multiple ways; the headache disorder is first classified, then the immediate pain is treated, and the physician considers treatment options7. The medical frustration with the elusive cause of tension-type headaches is even reflected on the American Migraine Foundation’s website2, which states: “There is no one approach for all patients…[treatment] must be individualized for each patient, so be sure you explore your symptoms in detail with your doctor.” Given the inability of research to translate into broadly successful headache treatment, proactive treatment has taken a back seat to reactive pain relief medication, and the best proactive advice physicians give is to avoid psychological stressors, including stress and lack of sleep. Until the medical community can successfully cut its age-old Gordian knot, patients may only have access to a jumble of general analgesics, muscle relaxants, and motherly advice to curb headache pain.

Works Cited

  1. Tranströmer, Tomas. 2011. “The House of Headache”, New Yorker 87 (October): 32.
  2. American Migraine Foundation. 2014. “Tension-Type Headache”. Accessed February 12, 2017. https://americanmigrainefoundation.org/living-with-migraines/types-of-headachemigraine/tension-type-headache/
  3. Ashina, M., L. Bendtsen, R. Jensen, J. Olesen, and F. Sakai. 1999. “Muscle hardness in patients with chronic tension-type headache: relation to actual headache state.” Pain 79 (2-3): 201-205. doi:10.1016/S0304-3959(98)00167-5.
  4. Jensen, R., and J. Olesen. 1996. “Initiating Mechanisms of Experimentally Induced Tension-Type Headache.” SAGE 16 (3): 175-182. doi:10.1046/j.1468-2982.1996.1603175.x.
  5. Bendtsen, L. 2000. “Central Sensitization in Tension-Type Headache—Possible Pathophysiological Mechanisms.” SAGE 20 (5): 486-508. doi: 10.1046/j.1468-2982.2000.00070.x.
  6. Andrasik, F., Kenneth A. Holroyd, and T. Westbrook. 1977. “Cognitive control of tension headache.” Cognitive Therapy and Research 1 (2): 121. doi:10.1007/BF01173633.
  7. Garza, Ivan, Angela O’Neil, Robert D. Sheeler, and Bert B. Vargas. 2016. “Chronic Daily Headache: Ten Steps for Primary Care Providers to Regain Control.” Headache 56 (10): 1675-1684. doi: 10.1111/head.12881.
  8. Image: Pavel Tchelitchew, Spiral Head Series, 1950. 
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