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Flashcards in Headaches Deck (22):



Increase in ICP
Intracranial inflammation
Inflammation of other cranial structures
Nerve and muscle disease
Decrease in ICP
Vascular or Migraine
Other (secondary to systemic disease)


Primary headaches



Tension-type headaches
Cluster headache and other trigeminal autonomic cephalalgias
Other primary headaches


Secondary headaches

List of etiologies

i) Headache attributed to head and neck trauma
ii) Headache attributed to cranial or cervical vascular disorder
iii) Headache attributed to non-vascular intracranial disorder
iv) Headache attributed to a substance or its withdrawal
v) Headache attributed to infection
vi) Headache attributed to disturbance of homoeostasis
vii) Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures
viii) Headache attributed to psychiatric disorder


Migraine without aura

Etiologies/clinical presentation

Common migraine, hemicrania simplex

Idiopathic, recurring headache disorder manifesting attacks lasting 4-72 hours. Typical characteristics of headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea, photo- and phonophobia.


Migraine without aura

IHS criteria

A. At least 5 attacks fulfilling B-D.
B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated).
C. Headache has at least two of:
Unilateral location
Pulsating quality
Moderate or severe intensity
Aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
D. During headache at least one of : Nausea and/or vomiting, Photophobia and phonophobia
E. Not attributed to another disorder


Typical aura with migraine headache

Clinical presentation

Typical aura consisting of visual and/or sensory and/or speech symptoms. Gradual development, duration no longer than one hour, a mix of positive and negative features and complete reversibility characterise the aura which is associated with a headache fulfilling criteria for 1.1 Migraine without aura.


Typical aura with migraine headache

Pg. 417

Do it


Warning signs in headache


First & worst headache comes to the ER: needs a CT & LP to rule out subarachnoid hemorrhage (SAH)
Headaches that awaken a patient at night or occur first thing in the morning suggest increased ICP
Palpable tender temporal arteries suggest GCA: check ESR
Cherry-red headache patients in winter: think CO
Virtually all headaches can cause nausea & vomiting


Cluster headache


Excrutiating, penetrating, non-throbbing pain unilaterally, usually in the trigeminal distribution
Associated conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, & ptosis
Peaks in 10-15 minutes, lasts 45-60 minutes
Occurs 1-3 times per day during cluster, often nocturnal
Typical cluster lasts 2-3 months and occurs every year or two
Affect men more often than women, 4-7:1


Tension type headache


Diffuse, bilateral, pressing or “tightening” quality, “like a band around the head”
Mild to moderate in severity
Usually episodic, may become chronic
Phonophobia, photophobia, or mild nausea occur rarely
Not really due to muscle tightness
Prevalence is 69% for men, 88% for women


Pathophysiology of headache

a. Migraine is a neurovascular disorder.
b. Genetic factors alter the response threshold to specific trigger factors in a migraineu
c. The exact nature of the central dysfunction is not clear
d. Spreading depression-like phenomena
e. Activation of brain stem monoaminergic nuclei that are part of the central autonomic, vascular and pain control centers
f. Local vasodilatation of intracranial extracerebral blood vessels occurs
g. There is consequent stimulation of surrounding trigeminal sensory nervous pain pathways
h. Activation of the 'trigeminovascular system' causes the release of vasoactive sensory neuropeptides, especially CGRP, that increase the pain response
i. The activated trigeminal nerves convey nociceptive information to central neurons in the brain stem trigeminal sensory nuclei


Serotonin in the pathophysiology of headache

The 'triptan' anti-migraine agents (e.g. sumatriptan, rizatriptan, zolmitriptan naratriptan) are serotonergic agonists

They cause vasoconstriction through 5-HT1B receptors that are expressed in human intracranial arteries

They inhibit nociceptive transmission through an action at 5-HT1D receptors on peripheral trigeminal sensory nerve terminals in the meninges and central terminals in brain stem sensory nuclei.


Migraine therapy


a. NSAIDs: ibuprofen, naproxen, ketorolac
b. Avoid narcotics except in ER
c. Sumatriptan IM or PO (up to 80% effective)
d. Ergotamine SL or PO
e. D.H.E. 45 (dihydroergotamine)
f. Isometheptene
g. 100% oxygen, ipsilateral intranasal 4% lidocaine for cluster headache


Migraine therapy


a. Dietary: find precipitants
i) Caffeine, chocolate, nuts, aged cheeses, processed meats, alcohol (especially red wine)
b. Beta blockers (especially propranolol)
c. Daily naproxen
d. Calcium channel blockers
e. Amitriptyline and other tricyclics
f. Valproic acid (Depakote)
g. Prednisone (short course) to break status migrainosus or cluster
h. Lithium for cluster headaches


Pesudotumor cerebri

Gen chars

a. Signs and symptoms of increased intracranial pressure without hydrocephalus
b. Usually small, slit-like ventricles
c. Mean age at onset 30 years, F:M 9:1
d. 90% of patients are obese, also associated with endocrinopathies, pregnancy, oral contraceptives, steroids, lithium, tetracycline, vitamin A intoxication


Pseudotumor cerebri


(1) Headache 94%
(2) Transient visual obscuration 68%
(3) Pulsatile intracranial noises 58%
(4) Photopsia 54%
(5) Retrobulbar pain 44%
(6) Diplopia 38%
(7) Vision loss 30%
(8) Pain on eye movement 22%


Pseudotumor Cerebri


(1) Papilledema 100%
(2) Vith nerve palsies 20%
(3) Contrast sensitivity deficit 50-70%
(4) Color vision loss 20%
(5) Visual field loss
(a) Symptomatic 30%
(b) On perimetry >90%


Pseudotumor cerebri


i) Weight loss
ii) Acetazolamide
iii) If there is progressive visual loss:
(1) Optic nerve sheath fenestration
(2) Lumbar-peritoneal shunting


Trigeminal neuralgia or tic doloreux


a. Paroxysmal, severe lancinating unilateral pain in the distribution of one or more branches of the trigeminal nerve
b. Episodes last 30-60 seconds
40 years in 90%, F:M 3:2
d. Examination is normal


Trigeminal neuralgia or tic doloreux


Carbemazepine and phenytoin each are effective in 70-80% of cases
Tricyclics, baclofen, clonazepam, valproic acid can also be effective
Surgical treatments include microvascular decompression, percutaneous radiofrequency ablation of the trigeminal ganglion, local neurolysis and trigeminal rhizotomy


Giant cell or temporal arteritis


Usually > 60 yo

Oral prednisone


Giant cell or temporal arteritis


headache, often in temporal or occipital areas
fever, malaise, weight loss
jaw claudication
sudden vision loss

Signs and findings
tenderness over the temporal arteries
elevated ESR
vasculitis on biopsy