Headaches Flashcards
Heachache
etiologies
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
Types
list
Migraine
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
list
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
chars
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
chars
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
abortive
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
prophylaxis
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
