Definition
Migraine Pain
Migraine pain is nociceptive pain arising from the activation of sensory nerve terminals innervating intracranial structures, principally the meninges and large cranial vessels.
The brain parenchyma itself is insensitive to pain; migraine pain originates extracerebrally.
Anatomical Source
Pain-producing structures
The principal structures capable of generating migraine pain are:
- The dura mater and its blood vessels
- Large cerebral arteries and venous sinuses
- The peripheral terminals of the trigeminal nerve that supply these structures
These tissues are densely innervated by meningeal nociceptors, which are activated during an attack.
Mechanism
Neurovascular cascade
The sequence producing pain is the trigeminovascular cascade:
- Trigeminal nerve terminals release neuropeptides, principally CGRP.
- CGRP produces meningeal vasodilation and neurogenic plasma extravasation.
- Inflammatory mediators sensitise and activate meningeal nociceptors.
- Afferent signals travel via the peripheral trigeminal pathway to the brainstem, thalamus, and cortex.
The pain is therefore a secondary consequence of an intrinsic neuronal event that activates vascular and inflammatory pathways. The brain feels no pain.
Why Pain Occurs
Protective but maladaptive signal
Pain in migraine is evolutionarily a protective signal indicating cranial homeostatic disturbance.
In the migraine brain, this signal becomes pathologically amplified: central sensitisation magnifies the pain beyond the peripheral stimulus, and the system loses its normal habituation, converting a transient warning into sustained, debilitating pain.