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==Overview==
The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive  pathways, environmental and genetic factors. It includes hypersensitivity of central and peripheral nociceptive  pathways: lack of habituation, Nitric oxide and combination of genetic and envirommental factors.
 
==Pathophysiology==
==Pathophysiology==
It is suggested that abnormalities in the peripheral and central nervous systems may be involved in the pathophysiology of TTH. It has long been believed that they are caused by [[muscle tension]] around the head and neck and the restriction of blood flow to those areas as a result, the cause of which is often the presence of an unresolved subconscious [[emotional conflict]] and [[anxiety]]. One of the theories says that the main cause for tension type headaches and [[migraine]] is teeth clenching which causes a chronic contraction of the [[temporalis muscle]]. Although muscle tension may be involved, scientists now believe there is not one single cause for this type of headache. Another theory is that the pain may be caused by a malfunctioning pain filter which is located in the brain stem. The view is that the brain misinterprets information, for example from the temporal muscle or other muscles, and interprets this signal as pain. One of the main molecules which is probably involved is [[serotonin]]. Evidence for this theory comes from the fact that chronic tension-type headaches may be successfully treated with certain antidepressants such as [[amitriptyline]]. However, the analgesic effect of amitriptyline in chronic tension-type headache is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved. Recent studies of [[nitric oxide]] (NO) mechanisms suggest that NO may play a key role in the pathophysiology of CTTH.<ref> Ashina M, Lassen LH, Bendtsen L, Jensen R, Olesen J. Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial. Lancet. 1999 Jan 23;353:287-9</ref>. The sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase (NOS) and the generation of NO. Patients with chronic tension-type headache have increased muscle and skin pain sensitivity, demonstrated by low mechanical, thermal and electrical pain thresholds. Hyperexcitability of central [[Pain and nociception|nociceptive]] neurons (in [[Trigeminal nucleus|trigeminal spinal nucleus]], [[thalamus]], and [[cerebral cortex]]) is believed to be involved in the pathophysiology of chronic tension-type headache.<ref>Ashina S, Bendtsen L, Ashina M. Pathophysiology of tension-type headache. Curr Pain Headache Rep, 2005 Dec; 9:415-22.</ref> Recent evidence for generalized increased pain sensitivity or [[hyperalgesia]] in CTTH strongly suggests that pain processing in the central nervous system is abnormal in this primary headache disorder. Moreover, a dysfunction in pain inhibitory systems may also play a role in the pathophysiology of chronic tension-type headache.<ref> Pielsticker A, Haag G, Zaudig M, Lautenbacher S.  Impairment of pain inhibition in chronic tension-type headache. Pain. 2005 Nov;118:215-23.</ref>
 
The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive  pathways, environmental and genetic factors.<ref name="pmid29368949">{{cite journal |vauthors= |title=Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition |journal=Cephalalgia |volume=38 |issue=1 |pages=1–211 |date=January 2018 |pmid=29368949 |doi=10.1177/0333102417738202 |url=}}</ref><ref name="pmid12699459">{{cite journal |vauthors=Jensen R |title=Peripheral and central mechanisms in tension-type headache: an update |journal=Cephalalgia |volume=23 Suppl 1 |issue= |pages=49–52 |date=2003 |pmid=12699459 |doi=10.1046/j.1468-2982.2003.00574.x |url=}}</ref><ref name="pmid15184615">{{cite journal |vauthors=Ulrich V, Gervil M, Olesen J |title=The relative influence of environment and genes in episodic tension-type headache |journal=Neurology |volume=62 |issue=11 |pages=2065–9 |date=June 2004 |pmid=15184615 |doi=10.1212/01.wnl.0000129498.50793.8a |url=}}</ref><ref name="pmid10376164">{{cite journal |vauthors=Russell MB, Ostergaard S, Bendtsen L, Olesen J |title=Familial occurrence of chronic tension-type headache |journal=Cephalalgia |volume=19 |issue=4 |pages=207–10 |date=May 1999 |pmid=10376164 |doi=10.1046/j.1468-2982.1999.019004207.x |url=}}</ref><ref name="pmid9521579">{{cite journal |vauthors=Russell MB, Iselius L, Ostergaard S, Olesen J |title=Inheritance of chronic tension-type headache investigated by complex segregation analysis |journal=Hum. Genet. |volume=102 |issue=2 |pages=138–40 |date=February 1998 |pmid=9521579 |doi=10.1007/s004390050666 |url=}}</ref>
 
=== Hypersensitivity of central and peripheral nociceptive  pathways: ===
 
* Increased sensitivity of central and peripheral nociceptive  pathways has a central role in the pathogenesis of tension type headache.<ref name="pmid12699459">{{cite journal |vauthors=Jensen R |title=Peripheral and central mechanisms in tension-type headache: an update |journal=Cephalalgia |volume=23 Suppl 1 |issue= |pages=49–52 |date=2003 |pmid=12699459 |doi=10.1046/j.1468-2982.2003.00574.x |url=}}</ref>
* Hypersensitivity of central nociceptive  pathways and central nervous system is more commonly involved with chronic type tension headache.<ref name="pmid21029081">{{cite journal |vauthors=Bezov D, Ashina S, Jensen R, Bendtsen L |title=Pain perception studies in tension-type headache |journal=Headache |volume=51 |issue=2 |pages=262–71 |date=February 2011 |pmid=21029081 |doi=10.1111/j.1526-4610.2010.01768.x |url=}}</ref>
* Hypersensitivity of peripheral nociceptive  pathways and peripheral nervous system is more commonly involved with episodic type tension headache.<ref name="pmid20816435">{{cite journal |vauthors=Bendtsen L, Fumal A, Schoenen J |title=Tension-type headache: mechanisms |journal=Handb Clin Neurol |volume=97 |issue= |pages=359–66 |date=2010 |pmid=20816435 |doi=10.1016/S0072-9752(10)97029-2 |url=}}</ref> <ref name="pmid16275843">{{cite journal |vauthors=Schmidt-Wilcke T, Leinisch E, Straube A, Kämpfe N, Draganski B, Diener HC, Bogdahn U, May A |title=Gray matter decrease in patients with chronic tension type headache |journal=Neurology |volume=65 |issue=9 |pages=1483–6 |date=November 2005 |pmid=16275843 |doi=10.1212/01.wnl.0000183067.94400.80 |url=}}</ref>
** Peripheral factors:<ref name="pmid11037746">{{cite journal |vauthors=Bendtsen L |title=Central sensitization in tension-type headache--possible pathophysiological mechanisms |journal=Cephalalgia |volume=20 |issue=5 |pages=486–508 |date=June 2000 |pmid=11037746 |doi=10.1046/j.1468-2982.2000.00070.x |url=}}</ref><ref name="pmid16282042">{{cite journal |vauthors=Ashina S, Bendtsen L, Ashina M |title=Pathophysiology of tension-type headache |journal=Curr Pain Headache Rep |volume=9 |issue=6 |pages=415–22 |date=December 2005 |pmid=16282042 |doi=10.1007/s11916-005-0021-8 |url=}}</ref>
*** Active and latent trigger points (Increased muscle tenderness)<ref name="pmid21735049">{{cite journal |vauthors=Bendtsen L, Fernández-de-la-Peñas C |title=The role of muscles in tension-type headache |journal=Curr Pain Headache Rep |volume=15 |issue=6 |pages=451–8 |date=December 2011 |pmid=21735049 |doi=10.1007/s11916-011-0216-0 |url=}}</ref>
*** Forward head posture<ref name="pmid17501847">{{cite journal |vauthors=Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA |title=Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache |journal=Headache |volume=47 |issue=5 |pages=662–72 |date=May 2007 |pmid=17501847 |doi=10.1111/j.1526-4610.2006.00632.x |url=}}</ref>
*** Decreased neck mobility<ref name="pmid16942471">{{cite journal |vauthors=Fernández-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA |title=Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache |journal=Headache |volume=46 |issue=8 |pages=1264–72 |date=September 2006 |pmid=16942471 |doi=10.1111/j.1526-4610.2006.00440.x |url=}}</ref><ref name="pmid16618263">{{cite journal |vauthors=Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA |title=Trigger points in the suboccipital muscles and forward head posture in tension-type headache |journal=Headache |volume=46 |issue=3 |pages=454–60 |date=March 2006 |pmid=16618263 |doi=10.1111/j.1526-4610.2006.00288.x |url=}}</ref>
*** Increased levels of interleukin-1 beta (inflammatory mediator)
 
==== Lack of Habituation: ====
 
* Lack of habituation is also observed to be an important pathogenetic factor in a subset population of tension type headache
* Low pain, electrical and thermal thresholds in patients with chronic tension type headache may suggest abnormal limbic-controlled descending pain pathways secondary to underlying deficient descending inhibition.<ref name="pmid14604505">{{cite journal |vauthors=Bendtsen L |title=Central and peripheral sensitization in tension-type headache |journal=Curr Pain Headache Rep |volume=7 |issue=6 |pages=460–5 |date=December 2003 |pmid=14604505 |doi=10.1007/s11916-003-0062-9 |url=}}</ref>
 
==== Nitric oxide: ====
 
* NO is one of the most importanr chemical mediator involved in the pathogenesis of tension type headache<ref name="pmid22527035">{{cite journal |vauthors=de Tommaso M, Ceci E, Pica C, Trojano M, Delussi M, Franco G, Livrea P, Ruggieri M |title=Serum levels of N-acetyl-aspartate in migraine and tension-type headache |journal=J Headache Pain |volume=13 |issue=5 |pages=389–94 |date=July 2012 |pmid=22527035 |pmc=3381063 |doi=10.1007/s10194-012-0448-3 |url=}}</ref>
* Nitric oxide synthase inhibitors have a potent antinociceotive effect<ref name="pmid22584531">{{cite journal |vauthors=Fischer M, Wille G, Klien S, Shanib H, Holle D, Gaul C, Broessner G |title=Brain-derived neurotrophic factor in primary headaches |journal=J Headache Pain |volume=13 |issue=6 |pages=469–75 |date=August 2012 |pmid=22584531 |pmc=3464472 |doi=10.1007/s10194-012-0454-5 |url=}}</ref>
 
=== Genetic factors: ===
 
* Genetic factors have a strong association in the pathogenesis of chronic tension headaches compared to episodic.<ref name="pmid15184615">{{cite journal |vauthors=Ulrich V, Gervil M, Olesen J |title=The relative influence of environment and genes in episodic tension-type headache |journal=Neurology |volume=62 |issue=11 |pages=2065–9 |date=June 2004 |pmid=15184615 |doi=10.1212/01.wnl.0000129498.50793.8a |url=}}</ref>
* First degree relatives of chronic TTH have 3 times higher risk of developing chronic TTH compared to the general population<ref name="pmid10376164">{{cite journal |vauthors=Russell MB, Ostergaard S, Bendtsen L, Olesen J |title=Familial occurrence of chronic tension-type headache |journal=Cephalalgia |volume=19 |issue=4 |pages=207–10 |date=May 1999 |pmid=10376164 |doi=10.1046/j.1468-2982.1999.019004207.x |url=}}</ref>
* Chronic TTH has a complex multifactorial inheritance<ref name="pmid9521579">{{cite journal |vauthors=Russell MB, Iselius L, Ostergaard S, Olesen J |title=Inheritance of chronic tension-type headache investigated by complex segregation analysis |journal=Hum. Genet. |volume=102 |issue=2 |pages=138–40 |date=February 1998 |pmid=9521579 |doi=10.1007/s004390050666 |url=}}</ref>
 
==== Environmental factors: ====
 
* Several studies have shown that episodic TTH may be caused by a variety of genes in combination with environmental factors.


== References ==
== References ==

Latest revision as of 17:44, 7 June 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors. It includes hypersensitivity of central and peripheral nociceptive pathways: lack of habituation, Nitric oxide and combination of genetic and envirommental factors.

Pathophysiology

The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors.[1][2][3][4][5]

Hypersensitivity of central and peripheral nociceptive pathways:

  • Increased sensitivity of central and peripheral nociceptive pathways has a central role in the pathogenesis of tension type headache.[2]
  • Hypersensitivity of central nociceptive pathways and central nervous system is more commonly involved with chronic type tension headache.[6]
  • Hypersensitivity of peripheral nociceptive pathways and peripheral nervous system is more commonly involved with episodic type tension headache.[7] [8]
    • Peripheral factors:[9][10]
      • Active and latent trigger points (Increased muscle tenderness)[11]
      • Forward head posture[12]
      • Decreased neck mobility[13][14]
      • Increased levels of interleukin-1 beta (inflammatory mediator)

Lack of Habituation:

  • Lack of habituation is also observed to be an important pathogenetic factor in a subset population of tension type headache
  • Low pain, electrical and thermal thresholds in patients with chronic tension type headache may suggest abnormal limbic-controlled descending pain pathways secondary to underlying deficient descending inhibition.[15]

Nitric oxide:

  • NO is one of the most importanr chemical mediator involved in the pathogenesis of tension type headache[16]
  • Nitric oxide synthase inhibitors have a potent antinociceotive effect[17]

Genetic factors:

  • Genetic factors have a strong association in the pathogenesis of chronic tension headaches compared to episodic.[3]
  • First degree relatives of chronic TTH have 3 times higher risk of developing chronic TTH compared to the general population[4]
  • Chronic TTH has a complex multifactorial inheritance[5]

Environmental factors:

  • Several studies have shown that episodic TTH may be caused by a variety of genes in combination with environmental factors.

References

  1. ↑ "Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition". Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. PMID 29368949.
  2. ↑ 2.0 2.1 Jensen R (2003). "Peripheral and central mechanisms in tension-type headache: an update". Cephalalgia. 23 Suppl 1: 49–52. doi:10.1046/j.1468-2982.2003.00574.x. PMID 12699459.
  3. ↑ 3.0 3.1 Ulrich V, Gervil M, Olesen J (June 2004). "The relative influence of environment and genes in episodic tension-type headache". Neurology. 62 (11): 2065–9. doi:10.1212/01.wnl.0000129498.50793.8a. PMID 15184615.
  4. ↑ 4.0 4.1 Russell MB, Ostergaard S, Bendtsen L, Olesen J (May 1999). "Familial occurrence of chronic tension-type headache". Cephalalgia. 19 (4): 207–10. doi:10.1046/j.1468-2982.1999.019004207.x. PMID 10376164.
  5. ↑ 5.0 5.1 Russell MB, Iselius L, Ostergaard S, Olesen J (February 1998). "Inheritance of chronic tension-type headache investigated by complex segregation analysis". Hum. Genet. 102 (2): 138–40. doi:10.1007/s004390050666. PMID 9521579.
  6. ↑ Bezov D, Ashina S, Jensen R, Bendtsen L (February 2011). "Pain perception studies in tension-type headache". Headache. 51 (2): 262–71. doi:10.1111/j.1526-4610.2010.01768.x. PMID 21029081.
  7. ↑ Bendtsen L, Fumal A, Schoenen J (2010). "Tension-type headache: mechanisms". Handb Clin Neurol. 97: 359–66. doi:10.1016/S0072-9752(10)97029-2. PMID 20816435.
  8. ↑ Schmidt-Wilcke T, Leinisch E, Straube A, Kämpfe N, Draganski B, Diener HC, Bogdahn U, May A (November 2005). "Gray matter decrease in patients with chronic tension type headache". Neurology. 65 (9): 1483–6. doi:10.1212/01.wnl.0000183067.94400.80. PMID 16275843.
  9. ↑ Bendtsen L (June 2000). "Central sensitization in tension-type headache--possible pathophysiological mechanisms". Cephalalgia. 20 (5): 486–508. doi:10.1046/j.1468-2982.2000.00070.x. PMID 11037746.
  10. ↑ Ashina S, Bendtsen L, Ashina M (December 2005). "Pathophysiology of tension-type headache". Curr Pain Headache Rep. 9 (6): 415–22. doi:10.1007/s11916-005-0021-8. PMID 16282042.
  11. ↑ Bendtsen L, Fernández-de-la-Peñas C (December 2011). "The role of muscles in tension-type headache". Curr Pain Headache Rep. 15 (6): 451–8. doi:10.1007/s11916-011-0216-0. PMID 21735049.
  12. ↑ Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA (May 2007). "Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache". Headache. 47 (5): 662–72. doi:10.1111/j.1526-4610.2006.00632.x. PMID 17501847.
  13. ↑ Fernández-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA (September 2006). "Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache". Headache. 46 (8): 1264–72. doi:10.1111/j.1526-4610.2006.00440.x. PMID 16942471.
  14. ↑ Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA (March 2006). "Trigger points in the suboccipital muscles and forward head posture in tension-type headache". Headache. 46 (3): 454–60. doi:10.1111/j.1526-4610.2006.00288.x. PMID 16618263.
  15. ↑ Bendtsen L (December 2003). "Central and peripheral sensitization in tension-type headache". Curr Pain Headache Rep. 7 (6): 460–5. doi:10.1007/s11916-003-0062-9. PMID 14604505.
  16. ↑ de Tommaso M, Ceci E, Pica C, Trojano M, Delussi M, Franco G, Livrea P, Ruggieri M (July 2012). "Serum levels of N-acetyl-aspartate in migraine and tension-type headache". J Headache Pain. 13 (5): 389–94. doi:10.1007/s10194-012-0448-3. PMC 3381063. PMID 22527035.
  17. ↑ Fischer M, Wille G, Klien S, Shanib H, Holle D, Gaul C, Broessner G (August 2012). "Brain-derived neurotrophic factor in primary headaches". J Headache Pain. 13 (6): 469–75. doi:10.1007/s10194-012-0454-5. PMC 3464472. PMID 22584531.


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