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Related Experiment Videos

Central sensitization in tension-type headache--possible pathophysiological mechanisms.

L Bendtsen1

  • 1Department of Neurology, Glostrup Hospital, University of Copenhagen, Copenhagen, Denmark. bendtsen@dadlnet.dk

Cephalalgia : an International Journal of Headache
|October 19, 2000
PubMed
Summary

Chronic tension-type headache involves increased central pain sensitivity, likely due to central sensitization. Amitriptyline is effective, suggesting mechanisms beyond serotonin reuptake inhibition are involved in treating this headache disorder.

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Area of Science:

  • Neuroscience
  • Pain Research
  • Headache Medicine

Background:

  • Chronic tension-type headache (CTTH) is characterized by increased tenderness in pericranial myofascial tissues.
  • Central mechanisms, particularly pain sensitivity, are implicated in CTTH pathophysiology.
  • Existing diagnostic tools for tenderness assessment lacked controlled pressure application.

Purpose of the Study:

  • To investigate the pathophysiology of CTTH, focusing on central mechanisms.
  • To develop and validate a tool for objective tenderness measurement.
  • To explore the efficacy of specific medications and their mechanisms in CTTH.

Main Methods:

  • Development of a palpometer for controlled pressure during palpation.
  • Assessment of pressure pain detection and tolerance thresholds, and electrical pain thresholds.

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  • Evaluation of the stimulus-response function for palpation pressure versus pain.
  • Clinical trial examining the prophylactic effects of amitriptyline and citalopram.

    • Main Results:

    • Significantly decreased pressure pain thresholds and electrical pain thresholds in CTTH patients, indicating increased central pain sensitivity.
    • Qualitatively altered stimulus-response function for palpation pressure versus pain, linked to tenderness and observed in fibromyalgia as well.
    • Amitriptyline showed significant prophylactic effect compared to placebo, while citalopram had minimal effect.
    • Normal plasma and platelet serotonin levels in CTTH patients.

    Conclusions:

    • CTTH pathophysiology involves central sensitization at the spinal dorsal horn/trigeminal nucleus level, potentially leading to supraspinal sensitization.
    • The efficacy of amitriptyline may involve mechanisms beyond serotonin reuptake inhibition, such as reducing central sensitization.
    • A pathophysiological model for CTTH is proposed, highlighting the role of sustained nociceptive input and central neuroplastic changes.
    • Future research should focus on identifying peripheral nociception sources and developing strategies to reduce central sensitization for improved CTTH treatment.