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Classification
The International Headache Society's (IHS) most current classification system for headache disorders is the International Classification of Headache Disorders 3rd edition (ICHD-3) as of 2018. This classification system separates tension-type headache (TTH) into two main groups: episodic and chronic. Chronic TTH is defined as fifteen days or more per month with headache for greater than three months or one-hundred eighty days or more with headache per year. Episodic TTH is less than fifteen days per month with headache or less than one-hundred eighty days with headache per year. However, episodic TTH is further sub-divided into frequent and infrequent TTH. Frequent TTH is defined as ten or more episodes of headache over the course of one to fourteen days per month for greater than three months or at least twelve days per year, but less than one-hundred eighty days per year. Infrequent TTH is defined as ten or more episodes of headache for less than one day per month or less than twelve days per year. Furthermore, all sub-classes of TTH can be classified as having presence or absence of pericranial tenderness, which is tenderness of the muscles of the head. Probable TTH is utilized for patients with overlapping characteristics of TTH and migraine without aura.

Tension Headache Cause
Although the musculature of the head and neck and psychological factors such as stress may play a role in the overall pathophysiology of TTH, neither is believed any longer to be the sole cause of the development of TTH.R The pathologic basis of TTH is most likely derived from a combination of personal factors, environmental factors, and alteration of both peripheral and central pain pathways.JA Peripheral pain pathways receive pain signals from pericranial (around the head) myofascial tissue (protective tissue of muscles) and alteration of this pathway like underlies episodic tension-type headache.JA It is over time that prolonged alterations in the peripheral pain pathways leads to increased excitability of the central nervous system pain pathways and the transition of episodic tension-type headache into chronic tension type headache.JA

The alterations in the central pain response are formally known as central sensitization, which manifests as allodynia and hyperalgesia.Chen

The sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase (NOS) and the generation of NO. Moreover, a dysfunction in pain inhibitory systems may also play a role in the pathophysiology of chronic tension-type headache.

Evidence also suggests dysfunction in supraspinal descending inhibitory pain pathways may contribute to the pathogenesis of central sensitization in CTTH. Chen

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).Chen Of the neurotransmitters, NO plays a major role in central pain pathways and likely contributes to the process of central sensitization.chen.

Regarding synaptic level changes, homosynaptic facilitation and heterosynaptic facilitation are both likely to be involved in central sensitization. Homosynaptic facilitation occurs when synapses normally involved in pain pathways undergo changes involving receptors on the post-synaptic membrane as well as the molecular pathways activated upon synaptic transmission. Lower pain thresholds of CTTH result from this homosynaptic facilitation. In contrast, heterosynaptic facilitation occurs when synapses not normally involved in pain pathways become involved. Once this occurs innocuous signals are interpreted as painful signals. Allodynia and hyperalgesia of CTTH represent this heterosynaptic facilitation clinically.

If other treatment is not working, a health care provider may use an MRI to confirm a more complicated diagnosis (e.g., new daily persistent headache).

Once this has occurred most effective approach to treatment is implementing a multidisciplinary plan that encompasses pharmacology, stress reduction, physical therapy and psychotherapy. Jay

In addition, pericranial tenderness, inflammation, and muscle ischemia have been postulated in headache literature to be part of the peripheral changes underlying TTH.Ashina, Chen. However, multiple studies have failed to illustrate evidence for a pathologic role of either ischemia or inflammation within the muscles. Ashina, Chen. Pericranial tenderness is also not likely a peripheral causal factor for TTH, but may instead act to trigger a chronic pain cycle in which the peripheral pain response is transformed over time into a centralized pain response. Ashina, Chen.