The aim of the present thesis was to investigate the pathophysiology of chronic
tension-type headache with special reference to central mechanisms. Increased tenderness to palpation of pericranial myofascial tissues is the most apparent abnormality in patients with
tension-type headache. A new piece of equipment, a so-called palpometer, that makes it possible to control the pressure intensity exerted during palpation, was developed. Thereafter, it was demonstrated that the measurement of tenderness could be compared between two observers if the palpation pressure was controlled, and that the Total Tenderness Scoring system was well suited for the scoring of tenderness during manual palpation. Subsequently, it was found that pressure
pain detection and tolerance thresholds were significantly decreased in the finger and tended to be decreased in the temporal region in chronic
tension-type headache patients compared with controls. In addition, the electrical pain threshold in the cephalic region was significantly decreased in patients. It was concluded that the central
pain sensitivity was increased in the patients probably due to sensitization of supraspinal neurones. The stimulus-response function for palpation pressure vs.
pain was found to be qualitatively altered in chronic
tension-type headache patients compared with controls. The abnormality was related to the degree of tenderness and not to the diagnosis of
tension-type headache. In support of this, the stimulus-response function was found to be qualitatively altered also in patients with
fibromyalgia. It was concluded that the qualitatively altered nociception was probably due to central sensitization at the level of the spinal dorsal horn/trigeminal nucleus. Thereafter, the prophylactic effect of
amitriptyline, a non-selective
serotonin (5-HT) reuptake inhibitor, and of
citalopram, a highly selective
5-HT reuptake inhibitor, was examined in patients with chronic
tension-type headache.
Amitriptyline reduced
headache significantly more than placebo, while
citalopram had only a slight and insignificant effect. It was concluded that the blockade of
5-HT reuptake could only partly explain the efficacy of
amitriptyline in
tension-type headache, and that also other actions of
amitriptyline, e.g. reduction of central sensitization, were involved. Finally, the plasma
5-HT level, the platelet
5-HT level and the number of platelet
5-HT transporters were found to be normal in chronic
tension-type headache. On the basis of the present and previous studies, a pathophysiological model for
tension-type headache is presented. According to the model, the main problem in chronic
tension-type headache is central sensitization at the level of the spinal dorsal horn/trigeminal nucleus due to prolonged nociceptive inputs from pericranial myofascial tissues. The increased nociceptive input to supraspinal structures may in turn result in supraspinal sensitization. The central neuroplastic changes may affect the regulation of peripheral mechanisms and thereby lead to, for example, increased pericranial muscle activity or release of
neurotransmitters in the myofascial tissues. By such mechanisms the central sensitization may be maintained even after the initial eliciting factors have been normalized, resulting in the conversion of episodic into chronic
tension-type headache. Future basic and clinical research should aim at identifying the source of peripheral nociception in order to prevent the development of central sensitization and at ways of reducing established sensitization. This may lead to a much needed improvement in the treatment of chronic
tension-type headache and other chronic myofascial
pain conditions.