Botulinum neurotoxin and chronic migraine: muscle fiber chemodenervation or nociceptic system modulation?

Abstract

The results of controlled investigations suggest that botulinumtoxin type A (BTA) leads to decrease headache intensity and prevent migraine attacks. The antinociceptive mechanisms of BTA action remain unclear. Modern and previous hypothesis of antinociceptive action BTA in chronic migraine (CM) are discussed in details. Recent experimental and clinical evidence strongly suggest that BTA has aspecific antinociceptive effect realized through inhibition of proinflammatory neurotransmitters release not only from the sensory terminals but from muscle nociceptors. The mechanism of the action of BTA in CM has more than one target and is considered to involve different pathophysiological levels CM: neurogenic inflammation, peripheral and central sensitization. The administration of BTA on the PREEMPT principle (paradigm) ensures optimal neurotoxin distribution in the anatomic areas in accordance with their sensory innervation by cervical segments and sensory fibers in the trigeminal system, the terminal branches which are the major target of BTA in the treatment of CM.

Keywords

• хроническая мигрень
• ботулинический токсин типа а
• оnabotulinumtoxina
• хемоденервация
• антиноцицептивное действие
• калицитонин-генсвязанный пептид
• нейрогенное воспаление
• периферическая сенситизация
• центральная сенситизация