Headache - classification, etiology, and pathogenesis.
Headache is pain perceived in the head or upper neck, arising from pain-sensitive structures such as blood vessels, meninges, cranial nerves, and muscles.
Classification
- 1 Primary headaches (functional)
No identifiable structural or metabolic cause.
- 2 Secondary headaches (symptomatic)
Due to an underlying disease.
Etiology
Primary headaches
Migraine: Genetic predisposition, triggers like stress, certain foods, hormonal changes.
Tension-type: Stress, muscle tension, poor posture.
Cluster: Possibly hypothalamic dysfunction, circadian pattern.
Secondary headaches
Direct irritation or compression of pain-sensitive structures (meninges, vessels).
Inflammatory mediators from infections.
Increased or decreased intracranial pressure.
Hypoxia or metabolic disturbances.
Pathogenesis
Migraine
Neurovascular theory:
- Cortical spreading depression → transient neuronal depolarization → aura symptoms. (visual disturbances, sensory changes).
- Release of calcitonin gene-related peptide (CGRP) and other vasoactive peptides → vasodilation of intracranial vessels → pain.
Trigeminal nerve activation → further neurogenic inflammation.
Tension- type headache
Muscle contraction and tension in scalp and neck muscles → activation of myofascial nociceptors.
Possible central sensitization in chronic cases.
Cluster headache
Hypothalamic activation → triggers trigeminal- autonomic reflex.
Parasympathetic hyperactivity → lacrimation, nasal congestion.
Severe vasodilation in cavernous sinus area → intense periorbital pain.
Secondary headaches
Increased intracranial pressure (tumors, hemorrhage ) → stretch of meninges and large vessels.
Infection-induced inflammation (e.g., meningitis) → cytokine-mediated meningeal irritation.
Vascular headache (e.g., subarachnoid hemorrhage ) → blood in subarachnoid space irritates meninges.