Pathophysiology

The pathophysiology of headache disorders is complex and multifactorial. For primary headaches such as migraine and tension-type, the underlying mechanisms are not entirely understood but likely involve interplay between the trigeminal nerve, cranial vasculature, and central pain pathways.

Migraine Pathophysiology:

• Trigeminovascular activation – Trigeminal nerves surrounding cranial vessels are activated, leading to release of vasoactive neuropeptides like CGRP that promote vasodilation. This results in throbbing head pain.
• Cortical spreading depression – Abnormal neuronal depolarization wave spreads across the cortex, which can produce neurological aura symptoms.
• Sensitization – Repeated migraine attacks lead to sensitization of trigeminal and central pain pathways, contributing to headache progression.

Tension-Type Headache Pathophysiology:

• Peripheral mechanisms – Sensitization of pain-sensitive nerve pathways surrounding extracerebral muscles and soft tissues of the head and neck. Can lead to sustained muscular contraction.
• Central mechanisms – Sensitization of nociceptive neurons in trigeminal nucleus caudalis and upper cervical spine.

Secondary headaches have varied mechanisms based on the underlying disorder:

• Vascular – Subarachnoid hemorrhage, arterial dissection, cerebral venous thrombosis
• Infection – Meningitis, encephalitis, brain abscess
• Intracranial pressure – Tumor, idiopathic intracranial hypertension
• Inflammation – Temporal arteritis, acute angle closure glaucoma
• Substance use – Medication overuse, illicit drugs, alcohol

Understanding the pathophysiologic basis of headaches guides optimal abortive therapy and vigilance for secondary causes requiring emergency diagnosis and management.