Exploding vs. imploding headache in migraine prophylaxis with Botulinum Toxin A

Abstract

Migraine headache is routinely managed using medications that abort attacks as they occur. An alternative approach to migraine management is based on prophylactic medications that reduce attack frequency. One approach has been based on local intramuscular injections of Botulinum Toxin Type A (BTX-A). Here, we explored for neurological markers that might distinguish migraine patients who benefit from BTX-A treatment (100 units divided into 21 injections sites across pericranial and neck muscles). Responders and non-responders to BTX-A treatment were compared prospectively (n=27) and retrospectively (n=36) for a host of neurological symptoms associated with their migraine. Data pooled from all 63 patients are summarized below. The number of migraine days per month dropped from 16.0+/-1.7 before BTX-A to 0.8+/-0.3 after BTX-A (down 95.3+/-1.0%) in 39 responders, and remained unchanged (11.3+/-1.9 vs. 11.7+/-1.8) in 24 non-responders. The prevalence of aura, photophobia, phonophobia, osmophobia, nausea, and throbbing was similar between responders and non-responders. However, the two groups offered different accounts of their pain. Among non-responders, 92% described a buildup of pressure inside their head (exploding headache). Among responders, 74% perceived their head to be crushed, clamped or stubbed by external forces (imploding headache), and 13% attested to an eye-popping pain (ocular headache). The finding that exploding headache was impervious to extracranial BTX-A injections is consistent with the prevailing view that migraine pain is mediated by intracranial innervation. The amenability of imploding and ocular headaches to BTX-A treatment suggests that these types of migraine pain involve extracranial innervation as well.

Fig. 1

Prospective study: effects of BTX-A on mean±SEM attack frequency, attack duration and pain intensity in responders and non-responders. Gray and black bars depict values before and after treatment, respectively.

Fig. 2

Illustrations of migraine pain and its directionality based on patients’ testimonies. A. exploding headache, B. Imploding (crushing and stabbing) headache, C. Ocular headache.

Fig. 3

Retrospective study: effects of BTX-A on mean±SEM attack frequency, attack duration and pain intensity in responders and non-responders. Gray and black bars depict values before and after treatment, respectively.

Fig. 4

Effects of BTX-A on mean±SEM number of days of migraine per month (attack frequency × attack duration) according to the type of headache in imploding (n=31), ocular (n=5) and exploding (n=27) headache patients pooled from the prospective and retrospective studies. Gray and black bars depict values before and after treatment, respectively.

Fig. 5

Effects of placebo injections on mean±SEM number of days of migraine per month (attack frequency × attack duration) according to the type of headache in imploding/ocular (n=6) and exploding (n=6) headache patients. Gray and black bars depict values before and after treatment, respectively.