Tension-type headache (TTH) represents one of the most costly diseases because of its very high prevalence. TTH is the most common type of headache, and it is classified as episodic (ETTH) or chronic (CTTH). It had various ill-defined names in the past including tension headache, stress headache, muscle contraction headache, psychomyogenic headache, ordinary headache, and psychogenic headache. See Medscape's Headache Resource Center for more information.
The International Headache Society (IHS) defines TTH more precisely and differentiates between the episodic and the chronic types.
The following is a modified outline of the IHS diagnostic criteria:
See the list below:
Pathogenesis of TTH is complex and multifactorial, with contributions from both central and peripheral factors. In the past, various mechanisms including vascular, muscular (ie, constant overcontraction of scalp muscles), and psychogenic factors were suggested. The more likely cause of these headaches is believed now to be abnormal neuronal sensitivity and pain facilitation, not abnormal muscle contraction.
Various evidence suggests that, like migraine, TTH is associated with exteroceptive suppression (ES2), abnormal platelet serotonin, and decreased cerebrospinal fluid beta-endorphin. In one study, plasma levels of substance P, neuropeptide Y, and vasoactive intestinal peptide were found to be normal in patients with CTTH and unrelated to the headache state.
Several concurrent pathophysiologic mechanisms may be responsible for TTH; according to Jensen, extracranial myofascial nociception is one of them. Headache is not related directly to muscle contraction, and possible hypersensitivity of neurons in the trigeminal nucleus caudalis has been suggested.
Bendtsen described central sensitization at the level of the spinal dorsal horn/trigeminal nucleus due to prolonged nociceptive inputs from pericranial myofascial tissues.[1] The central neuroplastic changes may affect regulation of peripheral mechanisms and can lead to increased pericranial muscle activity or release of neurotransmitters in myofascial tissues. This central sensitization may be maintained even after the initial eliciting factors have been normalized, resulting in conversion of ETTH into CTTH.
Further research is necessary to understand and clarify the mechanisms of TTH. Research may lead to the development of more specific and effective management in the future.
TTH is the most common primary headache syndrome.
Rasmussen et al reported a lifetime prevalence of TTH of 69% in men and 88% in women in the Danish population.[2] The patient may experience more than one primary headache syndrome. In one study by Ulrich et al, the 1-year prevalence of TTH was the same among individuals with and without migraine.[3]
Women are slightly more likely to be affected than men.
TTH can occur at any age, but onset during adolescence or young adulthood is common. It can begin in childhood.
Tension-type headaches (TTHs) are characterized by pain that is usually mild or moderate in severity and bilateral in distribution. Unilateral pain may be experienced by 10-20% of patients. Headache is a constant, tight, pressing, or bandlike sensation in the frontal, temporal, occipital, or parietal area (with frontal and temporal regions most common).
Patients with TTH have normal findings on general and neurologic examinations.
Some patients may have tender spots or taut bands in the pericranial or cervical muscles (trigger points).
Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor.
The diagnosis of tension-type headache (TTH) is clinical. As with the other primary headaches, no specific diagnostic test is available for TTH.
Occasionally, studies may be required to exclude secondary headache disorders.
Neuroimaging studies are important to rule out secondary causes of headache, including neoplasms and cerebral hemorrhage.
MRI imaging shows the greatest detail of cerebral structures and is especially useful in evaluating the posterior fossa.
CT scan with contrast is a viable alternative but is inferior to MRI for viewing structures in the posterior fossa.
Neuroimaging is indicated if the headaches are atypical in any way or if they are associated with abnormalities in the neurologic examination.
Management of TTH consists of pharmacotherapy, psychophysiologic therapy, and physical therapy.
Pharmacotherapy consists of abortive therapy (to stop or reduce severity of the individual attack) and long-term preventive therapy. Preventive drugs are the main therapy for CTTH, but they seldom are needed for ETTH.
Consider preventive medications if the headaches are frequent (>2 attacks per wk), of long duration (>3-4 h), or severe enough to cause significant disability or overuse of abortive medication.
Physical therapy techniques include hot or cold applications, positioning, stretching exercises, traction, massage, ultrasound therapy, transcutaneous electrical nerve stimulation (TENS), and manipulations.
Psychophysiologic therapy includes reassurance, counseling, relaxation therapy, stress management programs, and biofeedback techniques. With these modalities of treatment, both frequency and severity of chronic headache may be reduced.
Psychiatry consultations: CTTH can mask or be associated with comorbid conditions such as depression, anxiety, or other serious emotional disorders.
These nonpharmacologic methods have shown improvement of central nervous-system related symptoms:
The goals of pharmacotherapy for tension-type headaches (TTHs) are to relieve the headache, reduce morbidity, and prevent complications.
Clinical Context: First choice for treatment of headache, especially during pregnancy and breastfeeding.
Clinical Context: First choice for treatment of headache, especially during pregnancy and breastfeeding.
Clinical Context: First choice for treatment of headache, especially during pregnancy and breastfeeding.
These agents inhibit inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. They generally are used in mild to moderately severe headaches; however, they also may be effective for severe headaches.
Clinical Context: Has demonstrated effectiveness in treatment of pain.
Clinical Context: Has demonstrated effectiveness in treatment of pain.
These drugs increase the synaptic concentration of serotonin and/or norepinephrine in CNS by inhibiting their reuptake by the presynaptic neuronal membrane.
Cymbalta can also be helpful for patients who have coexisting depression.
Clinical Context: Has potent specific 5-HT uptake inhibition with fewer anticholinergic and cardiovascular adverse effects than TCAs.
Clinical Context: Atypical nontricyclic antidepressant with potent specific 5-HT uptake inhibition and fewer anticholinergic and cardiovascular adverse effects than TCAs.
Clinical Context: Atypical nontricyclic antidepressant with potent specific 5-HT uptake inhibition and fewer anticholinergic and cardiovascular adverse effects than TCAs.
These agents specifically inhibit presynaptic reuptake of serotonin. May be considered as an alternative to TCAs.
Clinical Context: Magnesium metabolism may have a significant role in both the etiology and the treatment of muscle contraction tension headache.
Electrolytes such as magnesium may help in the treatment of tension headache.
Advise the patient with tension-type headaches (TTHs) to take the following actions:
For excellent patient education resources, visit eMedicineHealth's Headache Center. Also, see eMedicineHealth's patient education articles Causes and Treatments of Migraine and Related Headaches, Tension Headache, and Chronic Pain.