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| __NOTOC__ | | __NOTOC__ |
| {{Tension headache}} | | {{Tension headache}} |
| {{CMG}} | | {{CMG}} {{AE}} {{SAI}} |
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| | ==Overview== |
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| ==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>
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| == References == | | == References == |
Revision as of 00:22, 1 June 2020