Pain Mechanisms in Tension Headache
March 1, 2002 2 minutes read
Pain Mechanisms in Tension Headache
Abstract & Commentary
Source: Rollnik JD, et al. Botulinum toxin type A and EMG: A key to the understanding of chronic tension-type headaches? Headache. 2002;41:985-989.
Excessive pericranial muscle contraction has been speculated as a mechanism for pain generation in chronic tension headache (CTH). However, using surface EMG recordings, excessive contraction has never been demonstrated. Further evidence that muscle contraction plays no role in CTH is offered in this small (n = 8) randomized, placebo-controlled trial comparing pericranial injection of 500 MU botulinum toxin (Botox A) to isotonic saline. Patients satisfied International Headache Society criteria for CTH, had normal brain imaging, and were excluded if there was evidence of analgesic abuse, psychiatric disease, psychosocial factors (eg, workman’s compensation), or symptoms of nontension headaches. Examinations were performed at baseline, 6, and 12 weeks and included surface EMG recording of frontal and anterior temporal muscles bilaterally. Headache pain intensity and duration was the primary outcome target, measured as "area under the headache curve." T tests and chi-square tests supplied statistical analysis.
Despite a significant decrease at 12 weeks of temporalis muscle EMG activity in Botox treated patients, neither of the 2 groups at 6 or 12 weeks showed any change of intensity, duration, frequency, or use of analgesics. One must conclude that muscle contraction plays little or no role in pain generation in CTH.
Commentary
Inhibiting nitric oxide (NO) synthesis reduces headache and, conversely, glycerol trinitrate, an NO donor, increases headache in CTH sufferers moreso than in healthy controls. This suggests that NO central sensitization may play a role in the pathogenesis of CTH (Lancet. 1999;353:287-289; Brain. 2000;123: 1830-1837). Other evidence points to decreased peripheral sympathetic activity in CTH (Headache. 2001;41:157-163). Among 28 patients with CTH, transcranial Doppler ultrasonography of the middle cerebral artery demonstrated a lower Mayer wave coefficient of variation than normal controls. Mayer waves, spontaneous cerebral blood flow velocity oscillations at 4-7 cycles/minute, have no central generator but reflect arterial blood pressure. Decreased Mayer wave variability thus supports peripheral sympathetic autonomic dysfunction in CTH. Conversely, B waves that reflect cerebral blood flow velocity oscillations at 0.5-3 cycles/minute and generated by brain stem nuclei, varied more in 30 migraine patients compared to either 28 CTH patients or 30 normal controls. This observation suggests dysfunction of central monoaminergic/serotonergic systems in migraine. —Michael Rubin.
Rubin, MD, Associate Professor of Clinical Neurology, New York Presbyterian Hospital-Cornell Campus, is Assistant Editor of Neurology Alert.
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