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Tension-type headache (TTH) is an ill-defined and heterogeneous syndrome, with its diagnosis based mainly on the absence of features found in other types of headaches, such as migraine. It is thus above all a “featureless” headache characterized by nothing but pain in the head. The headaches formerly described as “muscular contraction,” “psychogenic,” “psychomyogenic,” “tension,” “stress,” and “essential or non-migrainous” are classified in this group. However, because of lack of specificity of the diagnostic criteria, there is evidence that some patients with migraine are erroneously included.
The term “tension type” was chosen by the first Classification Committee of the to offer a new heading underlining its uncertain pathogenesis but nevertheless indicating that some kind of mental or muscular tension may play a causative role. Because the exact pathogenesis remains unsolved, this term has been maintained in the second edition of the , although it is commonly translated into “tension headache” in many non–Anglo-Saxon countries.
TTH is the most common form of headache but receives much less attention from health authorities, clinical researchers, and industrial pharmacologists than migraine does. This may be due to the fact that most individuals with TTH never consult a doctor and treat themselves, if necessary, with over-the-counter analgesics. However, frequent and chronic TTH constitutes a major health problem with an enormous socioeconomic impact.
The exact causes of TTH are still unknown. Both peripheral myofascial mechanisms and central dysregulation of pain-processing structures have been found, but their relative weight in the pathogenesis of TTH varies with headache frequency and between patients. No ancillary investigations are diagnostic of this form of headache, and definition of the disease therefore relies exclusively on symptomatology, which as mentioned, is not as distinct as for migraine. Because of this lack of disease-specific features, a number of secondary headaches can be manifested as TTH. Despite the meager scientific foundations regarding both mechanisms and treatment of TTH, it is impossible to manage these patients with some success, even though no major therapeutic breakthrough has occurred in recent years.
The general diagnostic criteria for tension-type headache (TTH) in the second edition of the International Classification of Headache Disorders (ICHD-II) are the same as in the first International Headache Society (IHS) classification. The only change is the subdivision of TTH into three groups differing by headache frequency. The chronic subtype (CTTH) is a serious disease associated with greatly decreased quality of life, high disability, and substantial socio economic cost. Within the episodic subgroup (ETTH), however, disability and most likely pathophysiology differ among subjects, with occasional or frequent episodes of TTH. Therefore, in ICDH-II the authors decided to subdivide ETTH further into an infrequent subtype with headache episodes occurring less than once per month and a frequent subtype ( Box 59-1 ). The infrequent subtype has very little impact on the individual and does not deserve much attention from the medical profession. However, those with frequent episodes of TTH can encounter considerable disability that sometimes warrants expensive drugs and prophylactic medication.
At least 10 episodes occurring on <1 day per month (<12 days per year) and fulfilling criteria B–D
At least 10 episodes occurring on ≥1 but <15 days per month for at least 3 months (≥12 and <180 days per year) and fulfilling criteria B–D
Headache occurring on ≥15 days per month on average for >3 months (≥180 days per year) and fulfilling criteria B–D
Headache lasts hours or may be continuous
Both of the following:
No more than one of photophobia, phonophobia, or mild nausea
Neither moderate or severe nausea nor vomiting
Episodes fulfilling all but one of criteria A–D for 2.1, 2.2, or 2.3
Episodes do not fulfill criteria for 1.1 Migraine without aura
Not attributed to another disorder
Because tenderness on manual palpation is the most useful criterion ( , ) to distinguish subgroups of TTH, patients are now separated according to the presence or absence of “increased pericranial tenderness.” Pericranial tenderness is easily recorded by manual palpation consisting of small rotating movements and firm pressure (if possible aided by the use of a palpometer) with the second and third fingers on the frontal, temporal, masseter, pterygoid, sternocleidomastoid, splenius, and trapezius muscles. A local tenderness score of 0–3 on each muscle can be summed to yield a total tenderness score (TTS) for each individual ( ). This has proved to be a valid clinical subdivision, but the vast majority of disabled patients (i.e., those with frequent TTH or CTTH) have increased pericranial tenderness and thus qualify for 3rd digit code 1 ( ). This and the fact that the clinical features, pathophysiological abnormalities, and response to therapy seem to be similar between the two subgroups (Schoenen et al 1991b) leave open the question of the utility of such subdivision.
There is some reason to believe that with the diagnostic criteria used for TTH, patients coded for ETTH include some who have a mild form of migraine without aura. Clinical experience favors this suspicion, especially in patients who also have migraine attacks. Some patients may display pathophysiological features typical of migraine ( ). Moreover, among persons in the general population classified as having TTH, clinical features suggestive of migraine may occur in non-negligible proportions: aggravation by routine physical exercise, 27.7%; pulsating quality, 17.5%; anorexia, 18.2%; photophobia, 10.6%; unilateral headache, 10%; and nausea, 4.2% ( ). Since a substantial proportion of patients may have atypical symptoms, ETTH can be difficult to distinguish from migraine without aura (IHS code 1.1) or from organic brain disease ( , ). The diagnosis of CTTH, on the other hand, seems straightforward in most cases with a long clinical course, although some patients may have migrainous features (see above) ( ). Moreover, the introduction of category 1.5.1 ( Chronic migraine ) into ICHD-II creates a problem with respect to the differential diagnosis between this and category 2.3 ( Chronic tension-type headache ). Both diagnoses require headache (meeting the criteria for migraine or TTH, respectively) on at least 15 days per month. Therefore, it is theoretically possible that a patient can have both these diagnoses.
In view of the above, a proposal for new, stricter diagnostic criteria was published under A2 ( Tension-type headache ) in the appendix of ICHD-II. In future studies, comparison of patients in whom the diagnosis is made according to the explicit criteria and others in whom the diagnosis is made according to the appendix criteria is recommended. The latter includes three instead of two of the following pain characteristics—bilateral location, pressing non-pulsating quality, mild to moderate intensity, and no aggravation on physical exercise—as well as absence of nausea, vomiting, and phono- or photophobia. This pertains not only to the clinical features but also to the pathophysiological mechanisms and response to treatment.
Many patients with CTTH may overuse medication acutely, such as combination analgesics. When this fulfills criterion B (dose and duration of substance intake) for any of the subforms of ICHD-II 8.2 ( Medication-overuse headache ), the default rule is to code for 2.4.3 ( Probable chronic TTH ) plus 8.2.7 ( Probable medication-overuse headache ). When these criteria are still fulfilled 2 months after overuse of medication has ceased, 2.3 ( Chronic tension-type headache ) should be diagnosed and 8.2.7 discarded. If at any time sooner the criteria are no longer fulfilled because improvement has occurred, 8.2 ( Medication-overuse headache ) should be diagnosed and 2.4.3 discarded.
In most patients, TTH evolves over time from the episodic to the chronic form ( ). However, if the headache fulfills CTTH criteria A–E and, unambiguously, is daily and unremitting within 3 days of its first onset, the patient should receive the diagnostic ICHD-II code 4.8 ( New daily-persistent headache ), another heterogeneous entity.
In a population-based study the lifetime prevalence of TTH was 79%, with 3% having CTTH (i.e., headache present on more than 15 days per month) ( ). In a longitudinal study of a cohort of children in New Zealand, the 1-year prevalence at 26 years of age was 11.1% for TTH versus 3.2% for migraine and 4.3% for combined headache ( ). So-called chronic daily headache, in which patients have at least 15 headaches per month, may affect up to 4% of the general population. It includes a majority of patients with chronic migraine or TTH from overuse of medication, as well as patients with CTTH, chronic migraine (ICHD-II 1.5.1), and a puzzling minority of patients with new, daily persistent headache (ICHD-II 4.8). The prevalence of TTH seems to be higher in women than in men and declines with age. In specialized headache clinics the proportion of patients in whom TTH is diagnosed is variable, but in general it is around 25% ( ).
In a recent meta-analysis ( ) of 19 studies performed between 1991 and 2009, the prevalence of TTH in more than 66,000 adults was 62.6%, and 3.3% of the general population had CTTH. In children (>25,000), the respective prevalence rates were 15.9% and 0.9%.
It is still a matter of debate whether the pain with TTH originates from myofascial tissue or from central mechanisms in the brain. Progress in research is hampered by difficulty obtaining homogeneous populations of patients because of the lack of specificity of the clinical features and diagnostic criteria. The present consensus nonetheless is that peripheral pain mechanisms are most likely to play a role in codes 2.1 ( Infrequent episodic tension-type headache ) and 2.2 ( Frequent episodic tension-type headache ) whereas central pain mechanisms play a more important role in 2.3 ( Chronic tension-type headache ).
We previously published comprehensive reviews of the pathophysiology of TTH ( , , , , ). Below we summarize the known pathophysiological features, present the most recent data, and propose a pathogenic model.
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