Atlas of pathophysiology, 2 Edition
Part II - Disorders
Headache, although usually benign, can be a serious and commonly disabling disorder. The International Headache Society (IHS) identified a comprehensive classification system that includes more than 100 types of headaches, which are divided into 13 categories. Various processes may cause headache, and they range from benign to life-threatening.
Primary headaches are classified based on their symptom profiles and account for 90% to 98% of headaches. Primary headaches include migraines, tension-type, and cluster.
Acute and progressive, secondary headaches are the result of an identifiable structural or physiologic cause, including:
· head trauma
· vascular disorders
· nonvascular intracranial disorders
· substance abuse and substance withdrawal
· metabolic disorders
· disorders of the face and neck
· cranial neuralgias.
Primary headaches occur when pain-sensitive structures of the head, including the cerebral vasculature, musculature, and cranial or cervical nerves, are irritated. Vascular changes occur as follows:
· Stimulation of the trigeminal ganglion located in the midbrain causes releases of substance P and calcitonin gene-related peptide (CGRP).
· The release of substance P causes degranulation of mast cells.
· Mast cells release histamine, and platelets release serotonin.
· Vasodilation, plasma extravasation, and inflammation occur.
· Inflammation and release of substance P cause distention of cranial arteries and headache pain.
· Triggers either directly act on the vasomotor tone or mediate the neurochemical release of vasoactive substances.
· Vasoconstriction, platelet changes, and neurochemical mediators initiate cerebral ischemia and activate the trigeminal-vascular system.
Signs and symptoms
· Commonly preceded by temporary focal neurologic signs known as auras (auras are usually visual—scotomata, zigzag, flashing lights and colors, geometric shapes, jagged lines.)
· Unilateral in onset but may become generalized
· Begins as a dull ache that progressively worsens and develops into throbbing, pulsating pain
· Commonly associated with photophobia, nausea and vomiting, phonophobia, and paresthesia
· Gradual onset of bilateral bandlike pressure or tightening of mild to moderate intensity; usually doesn't prohibit daily activities
· Not aggravated by physical activity or accompanied by associated symptoms; may have phonophobia or photophobia
· May be triggered by stress, fatigue, loud noises, heat, or bright lights
· Chronic form possibly resembles depression or fibromyalgia syndrome
· Acute onset of excruciating severe unilateral orbital pain lasting 15 to 180 minutes
· Episodic clusters; one every other day to eight per day; commonly nocturnal
· Accompanied by ipsilateral lacrimation, conjunctival injection, rhinorrhea, miosis, ptosis, and nasal congestion
The presence of one or more of these factors is an indication for further evaluation:
· first-onset headache that begins after age 50
· sudden-onset headache
· accelerating pattern of headaches
· new-onset headache in a patient with cancer or human immunodeficiency virus
· headache with systemic illness (fever, stiff neck, or rash)
· presence of focal neurologic symptoms (not typical aura)
Diagnostic test results
· Skull X-rays identify skull fracture.
· Computed tomography scan shows tumor or subarachnoid hemorrhage or other intracranial pathology; reveals pathology of sinuses.
· Lumbar puncture shows increased intracranial pressure suggesting tumor, edema, or hemorrhage.
· EEG shows alterations in the brain's electrical activity, suggesting intracranial lesion, head injury, meningitis, or encephalitis.
· Sinus X-rays show sinusitis.
· Avoidance of trigger mechanisms
· Over-the-counter analgesics or anti-inflammatory agents
· Analgesics or combination analgesics
· Vasoconstrictors, such as ergotamine tartrate and dihydroergotamine
· Serotonin agonists, such as sumatriptan, naratriptan, rizatriptan, and zolmitriptan
· Opioid analgesics
· Sedatives or tranquilizers
· Intranasal lidocaine
· Lithium carbonate
· Preventive therapy with beta-adrenergic blockers, calcium antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin antagonists, monoamine oxidase inhibitors, anticonvulsants, or nonsteroidal anti-inflammatories
VASCULAR CHANGES IN HEADACHE