Hemodynamics and Muscle Metabolism of Tension-Type Headaches
Messoud Ashina
Michael Langemark
In spite of considerable progress in tension-type headache research in recent years (2), the origin of pain in this prevalent primary headache is unknown. Findings of increased myofascial tenderness (6,10,12,15) and muscle hardness (3,20) in patients with chronic tension-type headache suggest that tender pericranial muscles might be the sites of primary hyperalgesia. It has been hypothesized that disturbances in local muscle ischemia and metabolism in the tender areas may explain myofascial pain in tension-type headache and in other myofascial pain disorders such as trapezius myalgia (8). Various in vitro and in vivo methods, such as muscle biopsy, single-fiber laser Doppler, and magnetic resonance spectroscopy, have been used to explore the mechanisms responsible for myofascial pain. The results of these studies have been conflicting. Whereas open studies suggested abnormalities in microcirculation (13,14), controlled and blinded studies have failed to find firm evidence of peripheral abnormalities (21) in patients with chronic myofascial pain (25). In addition to myofascial factors in tension-type headache, it has also been suggested that nociceptive input from the cranial vasculature may contribute to a primary myofascial nociception in patients through mechanism of convergence of painful input from different compartments (16). In this chapter, we focus on various methods used to explore muscle blood flow and metabolism, as well as hemodynamics of cephalic nonmuscular compartments in patients with tension-type headache.
MUSCLE BLOOD FLOW AND METABOLISM
In an early study, blood flow in the splenius capitis muscle was measured by the sodium-24 clearance method in patients with muscle contraction headache (17). Mean muscle blood flow of patients during headache was found to be 33% higher than the mean blood flow in patients outside of headache. However, there were several methodologic shortcomings in this study, such as the tracer used not being freely diffusible, which introduces an important source of error. Furthermore, the electromyography level was not controlled.
Langemark et al. (11) studied temporal muscle blood flow by injecting 133Xe into the muscle and recording the washout curve (Fig. 72-1). The resting temporal muscle blood flow in patients with chronic tension-type headache was not significantly different from that of controls. Resting blood flows on the two sides were highly correlated, and no right-left differences could be demonstrated. During isometric work, blood flow increased approximately fivefold in both patients and controls (Fig. 72-2). A brief reactive hyperperfusion after isometric work was found in eight patients and one control subject. The cause and importance of the phenomenon remains unexplained. No trend toward correlation was found between the reported severity of headache and the main flow parameters (resting flow and relative flow increase during exercise). The authors could not demonstrate any difference in relative hypoperfusion or hyperperfusion on the headache and nonheadache side. No correlation was found between mechanical pressure pain thresholds and muscle blood flow values in either rest or in response to isometric work.
Microdialysis is a unique technique for investigating and monitoring local muscle blood flow and metabolism in vivo within a tissue volume of less than 1 cm3 (9). Using the microdialysis technique, Ashina et al. (4) estimated blood flow and interstitial lactate concentrations in the trapezius muscle at rest and in response to static exercise in patients with chronic tension-type headache. The major finding of that study was a decreased blood flow in response to static exercise in a tender point in patients. The increase in muscle blood flow from baseline to exercise
and postexercise periods was lower in patients than controls (Fig. 72-3). There was no difference in resting blood flow between patients and controls. It could be suggested that patients develop a relative ischemia in the tender point during static exercise. If so, one would expect that the increase of interstitial lactate concentration would be higher in patients than controls. However, the authors observed no difference in local increase of interstitial lactate between patients and controls (Fig. 72-4). This seems to rule out the presence of ischemia in the tender point of patients with chronic tension-type headache during rest and static exercise.
and postexercise periods was lower in patients than controls (Fig. 72-3). There was no difference in resting blood flow between patients and controls. It could be suggested that patients develop a relative ischemia in the tender point during static exercise. If so, one would expect that the increase of interstitial lactate concentration would be higher in patients than controls. However, the authors observed no difference in local increase of interstitial lactate between patients and controls (Fig. 72-4). This seems to rule out the presence of ischemia in the tender point of patients with chronic tension-type headache during rest and static exercise.
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