Tension-type headache

The aetiology and pathophysiology of tension-type headaches (TTHs) are not fully understood. However, there is evidence suggesting the involvement of peripheral factors, particularly the pericranial muscles. Studies have demonstrated the prominence of pericranial tenderness in patients with both episodic and chronic TTH. Moreover, experimental human models have shown that pericranial tenderness can precede the onset of headache symptoms.[3]

Genetic factors have been implicated in the aetiology of TTH, but the specific genes involved are unknown and difficult to identify due to multifactorial inheritance.[7] Data from twin studies suggest that migraine and TTH have partly shared aetiologies, raising the possibility of a shared genetic predisposition. Genetic factors seem to have a more important influence in frequent episodic and chronic TTH compared with episodic TTH.[8] One study found that first-degree relatives of probands with chronic TTH had a 2.1 to 3.9-fold significantly increased risk of chronic TTH compared with the general population, while spouses had no increased risk.[9] A twin study of episodic TTH concluded that environmental influence is of major importance for episodic TTH, and a genetic factor, if it exists, is minor.[10]

Psychological stress is a common trigger for TTH although it is more likely to trigger migraine than TTH. Extended periods of mental tension or psychological stress may play a role in central sensitisation and the development of chronic TTH. Disturbed sleep patterns can trigger episodic TTH and insomnia and other sleep disorders are associated with chronic TTH.[11] Anxiety and depression can be present in those with TTH, but they are comorbid without implying cause and effect.

The pathophysiology of TTH is not fully understood. It is thought that, as with migraine, the release and activation of inflammatory agents leads to sensitisation of peripheral trigeminal afferents and ultimately to central hypersensitivity.[12] It has been speculated that in TTH, the major nociceptor is the pericranial musculature, whereas in migraine, it is blood vessels and meningeal nociceptors. This concept helps explain why patients frequently report both migraine and TTH.[13] Those with chronic TTH have a state of generalised hyperalgesia, suggesting central sensitisation; stimuli that are normally painless are misinterpreted as pain.[14] In addition to peripheral and central sensitisation, impaired or altered descending pain modulation has been reported to play a significant role in chronic TTH. Peripheral factors such as increased tenderness, muscle hardness, possible local ischaemia, and inflammation have also been implicated. Furthermore, various neuropeptides, nitric oxide, and serotonin have been found to be involved in the pathophysiology. It is noteworthy that the infusion of nitric oxide has been shown to trigger TTH, further emphasising its potential role in the condition.[3]

The International Classification of Headache Disorders (ICHD): tension-type headache - ICHD-3 (adapted)[1]

2.1 Infrequent episodic tension-type headache
- Associated with pericranial tenderness
- Not associated with pericranial tenderness
2.2 Frequent episodic tension-type headache
- Associated with pericranial tenderness
- Not associated with pericranial tenderness
2.3 Chronic tension-type headache
- Associated with pericranial tenderness
- Not associated with pericranial tenderness
2.4 Probable tension-type headache
- Probable infrequent episodic tension-type headache
- Probable frequent episodic tension-type headache
- Probable chronic tension-type headache

Aetiology

Pathophysiology

Classification