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Triptans: Actions and Reactions
Nahas SJ, Silberstein SD.
Posted: June 2008  
Headache  2008;48:611-613

Subcutaneous sumatriptan is superior to placebo in achieving headache relief. Some commonly reported adverse events are paresthesias, tingling, and transient worsening of headache. Why do patients develop these symptoms? Our unique case may shed light on its actions.

Case:   A 40-year old woman with previously episodic and now continuous migraine headache accompanied by cutaneous allodynia has coincident recurrent, multidermatomal, painful herpetic skin outbreaks as well as post-herpetic neuralgia. In addition, she has right-sided oral lesions. Prior to developing the dermatologic herpetic manifestations, she treated migraine with sumatriptan 6 mg. SC without adverse advents. Following the herpetic outbreaks, she used sumatriptan 4 mg. SC and experienced paresthesias and tingling in both the acute herpetic lesions and the post-herpetic scars. This was followed immediately by dramatic worsening of the trigeminal and extratrigeminal burning and lancinating pain, which persisted for up to 60 minutes before returning to baseline. Her migraine headache was partially relieved, without initial worsening. The same phenomena were observed after treatment with eletriptan 40 mg. orally. Frovatriptan 2.5 mg. orally, almotriptan 12.5 mg. orally, and rizatriptan 10 mg. orally had no effect on either her migraine or her herpetic pain. DHE relieved her headache temporarily without exacerbating her herpetic pain. Repeated trials of the above medications at various times had the same results.

Often, triptans initially worsen migraine pain before ameliorating it, and once allodynia has occurred, efficacy is often partial or absent.

Why arenít triptans useful in other pain syndromes? One possibility is that a central mechanism of action of the triptans is most important in achieving pain relief, and in the absence of central inflammation, which disrupts the blood-brain barrier, triptans may not be able to penetrate the central nervous system sufficiently to exert their effects.

Why didnít DHE, which was effective in treating the patientís migraine, cause similar initial worsening of pain? Its widespread actions may also underlie our patientís lack of worsening of herpetic pain by a number of theoretical and currently improvable mechanisms.

Conclusion:   In the face of tissue injury and perpetuated sensitization, triptans may temporarily aggravate both trigeminal and extratrigeminal nonmigraine pain, without providing relief. This speculation, coupled with what is thus far known about migraine pathophysiology and triptan mechanisms, begs continued study to better understand the biology of pain generation and relief.