Additionally, CTTH patients exhibit decreased thermal and pain thresholds which further bolsters support for central sensitization occurring in CTTH.The alterations in physiology that lead to overall process of central sensitization involve changes at the level of neural tracts, neurotransmitters and their receptors, the neural synapse, and the post-synaptic membrane. Evidence suggests dysfunction in supraspinal descending inhibitory pain pathways may contribute to the pathogenesis of central sensitization in CTTH. Neurotransmitters
Specific neuronal receptors and neurotransmitters thought to be most involved include NMDA and AMPA receptors, glutamate, serotonin (5-HT), β-endorphin, and nitric oxide (NO). Of the neurotransmitters, NO plays a major role in central pain pathways and likely contributes to the process of central sensitization. Briefly, the enzyme nitric oxide synthase (NOS) forms NO which ultimately results in vasodilatation and activation of central nervous system pain pathways. Serotonin may also be of significant importance and involved in malfunctioning pain filter 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. Evidence for this theory comes from the fact that chronic tension-type headaches may be successfully treated with certain antidepressants such as nortriptyline. However, the analgesic effect of nortriptyline, as well as amitriptyline in chronic tension-type headache, is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved. Synapses
Regarding synaptic level changes, homosynaptic facilitation and heterosynaptic facilitation are both likely to be involved in central sensitization.
It is important to note that large daily doses of paracetamol should be avoided as it may cause liver damage especially in those that consume 3 or more drinks/day and those with pre-existing liver disease. Ibuprofen, one of the NSAIDs listed above, is a common choice for pain relief but may also lead to gastrointestinal discomfort.Analgesic/caffeine combinations are popular such as the aspirin-caffeine combination or the aspirin, paracetamol and caffeine combinations. Frequent use (daily or skipping just one day in between use for 7–10 days) of any of the above analgesics may, however, lead to medication overuse headache.Analgesic/sedative combinations are widely used (e.g., analgesic/antihistamine combinations, analgesic/barbiturate combinations such as Fiorinal).Muscle relaxants are typically used for and are helpful with acute post-traumatic TTH rather than ETTH. Opioid medications are not utilized to treat ETTH. Botulinum toxin does not appear to be helpful. Chronic
Classes of medications involved in treatment of CTTH include tricyclic antidepressants (TCAs), SSRIs, benzodiazepine (Clonazepam in small evening dose), and muscle relaxants. The most commonly utilized TCA is amitriptyline due to the postulated role in decreasing central sensitization and analgesic relief. Another popular TCA used is Doxepine. SSRIs may also be utilized for management of CTTH. For patients with concurrent muscle spasm and CTTH, the muscle relaxant Tizanidine can be a helpful option.These medications however, are not effective if concurrent overuse of over the counter medications or other analgesics is occurring. Stopping overuse must occur prior to proceeding with other forms of treatment. Manual therapy
Current evidence for acupuncture is slight.