Handler: Headaches Flashcards
4 primary types of headaches?
Migraine
Tension
Cluster
Chronic daily headache
4 secondary headaches?
Post-traumatic (post concussion)
Space occupying lesions (tumors)
Assocaited with cerebrovascular disease
Hypertensive encephalopathy
Patients present not only for the headaches, but back fear of _______
brain tumor
Triggers, aura, self-treatment, diet (food, caffeine, etoh), sleep, relation to menses, childhood assocaitions
OPQRSTA
HA diary
Headache history
BP
Head
Vision, visual fields, EOMs, funduscopic exam (papilledema)
Brief neuro exam (language, gait, motor, reflexes)
PE for HA
If history is characteristic, no focal neuro findings and gait is normal
It is unlikely a _________
brain tumor
Do patients with primary headache disorders that you were able to obtain a good history require imaging studies?
No!
___% have absence of aura
___% have presence of aura
with migraine headaches
85%
15%
Onset in adolescence and early adulthood
peak ages 30-45
Migraine headaches
Infantile colic
Motion sickness with nausea and vomiting
Menstrial headaches
HA that worsen with physical activity
HA post consumption of small amounts of colored wine or liquor
Caffeine withdrawal HA
Water diving HA
After certain foods (chocolate, peanuts, caffeine)
These are called?
“Migraineurs”
2nd most common headache disorder
Prevalence 12%
18% in women and 6% in men
Migraine headaches
Pathophys unclear
End pathway: activation of afferent sensory fibers that innervate meningeal/cerebral blood vessels
Fibers arise from Trigeminal nerve
Migraine headaches
Pathophys: mirgraines have ______ and ______ components
No identifiable cause
Infammatory, vascular
Vasodilators (NTG) can trigger migraine headaches
Substances that cause vasoconstriction (erotamine) abort headaches
This is the ________ theory
Vasogenic
brain activates or sensitizes trigeminal nerve fibers within the meninges initiating the headache via neurogenic inflammation. The vascular changes that occur during the attack are the result of vascular inflammation
_______ theory believed by most neurologists
Neurogenic
Sx: photophobia, phonophobia, nausea, vomiting cannot be explained by vasogenic theory alone
Aural sx: visual hallucincations that cannot be explained by vasoconstriction or vasodilation alone
Seen in the _____ theory
Neurogenic
Neurotransmitter which activates pain fibers in the brainstem and contributes to vasoconstrictiopn and inflammation
Release of peptides and neurotransmitter at trigeminal nerve branches leads to inflammation and vasodilation of meningeal and dural blood vessels
Serotonin
Drugs that are _____ for serotonin receptors abort headaches when taken early
Example: 5-hydroxy tryptamine analogs
agonists
Transient (15-30”) epiosodes of focal neurologic dysfunction that appear before the headache phase begins
Aura
Expanding scotoma (blind spot) with scintillating margin: visual hallucinations with stars, sparks, and zigzags of light
Visual field defects
Unilateral paresthesias
Numbness
Weakness
Dysphagia
Aura
_____ symptoms suggest decreased blood flow in the distribution of the internal carotid artery mimicking TIA’s
Uncommonly involve distribution of basilar artery leading to vertigo, ataxia, tinnitis, and hearing loss
Aural
activation of a wave of electrical activity that spreads throughout the brain, depressing cortical activity and resulting in visual and other symptoms; initiated by the CNS. “Spreading depression of Lao” seen on PET scans.
What does this contribute to?
Mirgraine Aura
Can be lateralized to one side or generalized
Usually throbbing (mod-severe) and worse with physical activity
Develop gradually and last several hours
Associated sx: nausea, photophobia, phonopobia
Spectrum can vary and is a continum that might include aura, lateralization, varying length
Headache phase
Prolonged aura with neurologic deficits lasting
1 hour –> week
Uncommon
What type of migraine?
Complex
Rarely there are permanent neuro deficits consistent with localized stroke (with defect on CT or MRI) in the distribution of the internal carotid but neuro-imaging or angiography do not show occlusion or fixed stenosis of intracerebral vessles
Seen with what type of mirgraine?
Complex
Avoid triggers if identifiable (foods, additives, caffeine, strong smells, response to stress, sleep cycles)
Preventative treatment for what?
Migraines
Bed rest in dark room
Mild attacks: ASA, NSAIDS effective if taken early but may need to be combined with other meds
Abortive therapy for ____?
Migraines
Older migraine medication
Potent serotonin agonist and vasoconstrictor
caution in patients with HTN, Hx of CAD or stroke
Less selective/ safe than the new agents
Ergotamine
Older treatment for migraines
Ergotamine 1mg and caffeine 100mg
Cafergot
One of the top 5 diagnosies that PCP’s see in the office
Headaches
Newer treatment for migraines
high affinity for serotonin receptors in trigeminal nerve branches with additional vasoconstrictive effects (see below): Sumatriptan (Imitrex), Zolmitriptan (Zomig) and others; similar efficacy.
Very few S/E and very safe
Avoid in patients with CHF
5-HT1 receptor agonists
5-HT1 receptors are the predominant serotonin receptors in the CNS. Many of them function as presynaptic autoreceptors whose activation inhibits the release of serotonin and related neurotransmitters that cause vasodilation, inflammation and pain.
Activation of these receptors in pial/dural vessels leads to __________
Vasoconstriction
Injected (auto-injector_ subcutaneous sumatriptan most effecti in aborting HA (oral meds poorly absorbed)
Also intra-nasal sumatriptan an alternative: less predictable
Used for acute _________?
severe headaches
Usually treated in the ED with injectable dihydroergotamine and effective hours into an attack. Essential to pre-treat with anti-nauseant/emetic agent like metoclopramide.
Injectable narcotic, often Meperidine, combined with an anti-emetic (ED only).
Treatment for what type of HA?
Severe intractable migraine headaches
What very potent NSAID can be used to prevent relapse of acute HA?
Indomethacin
What is another drug that can be used to treat migraines that is effect and is used for a short course?
Steroids (glucocorticoids)
HA’s limit work or daily activity 3 or more days/month
Sx of HA are severe or prolonged
Previous migraines were associated with a complication (complex migraine or stroke)
Treatment is empirical
Indication for migraine prophylaxis
Beta adrenergic blockers: propranolol, metoprolol and others that cross BBB
Tricyclic antidepressants: amitriptylene, nortriptylene
Calcium channel blockers: verapamil, others.
Anticonvulsants: gabapentin, valproic acid, topiramate (Topamax)
Botulinum toxin type A- local injection into scalp
Used for what?
Migraine prophylaxis
Most common type of HA
Females>males
Usually begin in 3rd decade
Tension HA
Poorly understood
includes vascular, muscular & myofascial components
Pathophys of ________?
Tension HA
Which type of HA has genetic predisposition?
Migraine HA
Episodic and chronic forms
Symmetric tightness/pressure
Mild/mod pain that lasts min-days
DO NOT worsen with PE
no nausea or vomiting or ofther neuro sx
Associated sx: poor concentration, stress, fatigue, noise, glare, depression
Tension headaches
Acetaminophen, NSAIDS
Meds for migraines may also be effective but NOT 1st line
Treatment for tension headaches
Relaxation techniques
Biofeedback
Prevention for what type of headache?
Tension headache
What is the other name for cluster headaches?
Migrainous neuralgias
Much less common than migraines or tension HA’s
Males 6x> females
3rd-6th decade
Cluster headaches
Poorly understood
Likely vascular with activation of trigeminal-vascular system
Pathogensis of what type of headaches?
Cluster headaches
Watery eye, dropping eyelid, runny nose
Horner’s syndrome
Seen with what type of HA?
cluster headaches
Recurrent episodes of intense unilateral orbital, supraorbital, or temporal head pain along with ipsilateral partial cervical sympathetic paralysis (conjunctival injection, lacrimation, rhinorrhea, nasal congestion, eyelid edema, loss of facial sweating); last 15” to 2 hrs and recur daily for days to weeks.
Triggers: ETOH, stress, glare, foods
Cluster HA’s
100% O2 x 15”- very effective for long duration (1-2 hrs) HA’s
Oral drugs often not as effective as other routes: nasal, rectal or injection.
Acute attacks: Ergotamine tartrate, Sumatriptan, butorphanol, others ).
Prophylaxis: Verapamil, Ergotamine.
Tx for what type of headache?
Cluster headaches
Any headache occurring > 15 days/month (often for 3 mos or more). Often develops over time in a patient with intermittent HA’s.
Includes tension, cluster, migraine, and other vascular headaches.
Chronic daily headaches
What is the most common contributing factor to chronic daily headaches?
Medication overuse
Often requires combination pharmacologic and behavioral interventions: biofeedback, massage, acupuncture, relaxation and physical therapy. Reduction of meds (if taking several) and caffeine often beneficial.
Often difficult
Treatment for what type of headache?
Chronic daily headaches
A variety of neoplasms (benign and malignant) can cause headaches related to displacement of vascular structures.
Intracranial mass lesions
Sx: usually dull bifrontal or occipital headaches that begin in the a.m., are worsened by exertion or postural changes and may be associated with N & V.
Clues: new onset HA’s in patients >45 y.o. Usually associated with other neurologic findings, focal or diffuse (generalized disturbance of cerebral function).
Intracranial mass lesions
___% of intracranial mass lesions are gliomas
remainder are meningiomas, astrocytomas, acoustic neuomas
50%
Signs: Neuro defects, papilledema, personality changes, intellectual decline, seizures and emotional lability.
Dangers: Brain Hernation through tentorial hiatus due to incrased pressure, leading to stupor and coma often followed by death.
Intracranial mass lesions
How do you diagnose a intracranial mass lesion?
CT or MRI scans
Treatment of intracranial mass lesions depends on ________?
pathology
