CHAPTER 57 TENSION-TYPE HEADACHE
Tension-type headache, the most common of the primary headaches,1,2 has tremendous socioeconomic effects.2,3 For many years, various terms such as tension headache, muscle contraction headache, psychomyogenic headache, stress headache, ordinary headache, essential headache, idiopathic headache, and psychogenic headache were used to characterize this common headache disorder. In 1988, the International Headache Society, to avoid using terminology with a specific pathophysiological implication, introduced the term tension-type headache.4 The pathophysiology of tension-type headache is still far from clear, although advances in basic and clinical research have increased knowledge about the mechanisms underlying this disorder.5,6
DEFINITION
The second edition of The International Classification of Headache Disorders (ICHD-II)7 subdivides tension-type headache into three main forms:
All forms are subdivided further into headache associated or not associated with pericranial tenderness. Diagnostic criteria are shown in Table 57-1.
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At least 10 episodes occurring on <1 day per month on average (<12 days per year) and fulfilling the next three criteria:
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EPIDEMIOLOGY
The lifetime prevalence of tension-type headache is between 30% and 78%.1,2 Most affected patients (59%) reported tension-type headache one day each month or less; 24% to 37% had headache several times each month; 10% had it weekly; and 2% to 3% of the population had chronic tension-type headache (≥15 days per month).8 The global prevalence of chronic tension-type headache is uniform (i.e., 2% to 3%). Unlike migraine headache, women are only slightly more affected than men, with a male/female ratio of 4:5.1,2,6
CLINICAL FEATURES
Tension-type headache is diagnosed exclusively on the basis of the history and somatic and neurological examination findings. The infrequent subtype has very little effect on the individual and does not represent a clinical or treatment challenge. However, frequent and chronic subtypes are always associated with considerable disability and high personal and socioeconomic costs. Patients usually complain of mild to moderate pain of varying duration in both the infrequent and frequent episodic forms of tension-type headache or of constant mild or moderate pain in the chronic form. The headache is bilateral, pressing or tightening pain, often described as feeling like “a pressure bandage around the head.” It is never associated with typical migrainous characteristics, such as aggravation by routine physical activity, severe nausea, vomiting, and severe photophobia or phonophobia. According to the ICHD-II criteria (see Table 57-1), patients with infrequent and frequent episodic tension-type headache have no more than one of the associated symptoms of photophobia or phonophobia. Mild nausea, photophobia, or phonophobia (no more than one of these symptoms) may be present in chronic tension-type headache.
ETIOLOGY AND PATHOPHYSIOLOGY
Although there has been considerable progress in research on tension-type headache,5,6 the origin of pain in this prevalent primary headache is unknown. It has been suggested that both peripheral (nociception from myofascial tissue) and central (increased excitability of central nervous system) factors play a major role in the pathophysiology of tension-type headache. Epidemiological studies reported an increased familial risk in tension-type headache.9,10
Peripheral Factors
Individuals who have been exposed to static or repetitive work for long periods of time may develop pericranial muscle tenderness and tension-type headache. Therefore, for many years the research on the mechanisms that lead to tension-type headache focused on peripheral or muscular factors. Increased pericranial myofascial tissue tenderness to manual palpation is the most prominent abnormal finding in patients with chronic tension-type headache.11–13 Painful impulses from these tissues may be referred to the head and perceived as headache, and myofascial mechanisms may therefore play a major role in the pathophysiology of tension-type headache.14 Possible excessive pericranial muscle contraction, ischemia, and inflammation have been extensively studied in tension-type headache; however, electromyography with surface electrodes failed to demonstrate significantly increased activity.15–17
A microdialysis study reported altered blood flow regulation in tender skeletal muscles of patients with chronic tension-type headache during static work.18 The authors found no difference in locally increased interstitial lactate between patients and control subjects. This seems to rule out the presence of ischemia in the tender points of chronic tension-type headache patients during static exercise. It was hypothesized that increased excitability of neurons in the central nervous system may affect the regulation of muscle blood flow during static work.18 The microdialysis study also demonstrated that the interstitial concentration of inflammatory mediators in tender muscle did not differ between patients with chronic tension-type headache and healthy subjects.19 These data indicate that tender points are not sites of ongoing inflammation.
Central Factors
Since the mid-1990s, there has been increasing interest in the role of central factors in tension-type headache. It has been shown that pressure pain detection and thresholds of tolerance of mechanical stimuli were decreased in chronic tension-type headache sufferers.20,21 Furthermore, Bendtsen and colleagues22
