Neuro2: Headaches

Front 1

Secondary vs Primary Headaches and common causes

Back 1

Primary - no cause found. Tension-type (brief, mild), Migraines (prolonged, severe), others

Secondary - due to underlying cause (stroke, tumor, head injury, infection, etc)

Headache "clinics" see primary since secondary would resolve if treat underlying

Front 2

Tension-type Headache features

Back 2

Brief (minutes), mild to moderate, not disabling, NO other features (NO vomiting, nausea, etc.)

Stress can trigger

Front 3

Migraine headache epidemiology

Back 3

12% population gets. 3x more common for women, worse in "productive/reproductive years" (20s-50s)

Front 4

Most common migraine symptoms

Back 4

Pulsatile head pain > sensitivity to light (80%) > sensitivity to sound (76%) and occasionally vomiting, blurred vision, aura (rarely), etc.

May be unilateral as well

Front 5

Burden of migraines to pt

Back 5

Over 90% have severe pain, 3/4 reduced function and 1/3 require bed rest

Lots of direct and indirect costs in workforce

Front 6

Pediatric Migraine prevalence

Back 6

Half of all migraine pts (before 12 y/o MALES get more)

about 5% children get

after puberty more common in women

Front 7

Chronic migraine def

Back 7

15 or more in last 3 months

Front 8

Interictally status of migraine pts

Back 8

predisposed to attacks, abnormal cortical processing and impaired QOL.

Front 9

What causes chronification of migraines

Back 9

allodynia
central sensitization

Front 10

Pathogenesis of Migraines; Possible contributing factors; neurotransmitters implicated

Back 10

Possible causes: mitochondrial dysfunction, increased plasma MMP-9, somatosensory cortex abnormalities, higher insulin levels, increased white matter glucose uptake, vascular smooth muscle dysfunction (cGMP and NO response)

In attacks have high IL10, TNFa, IL1b

NTs: dopamine, glutatmate (excitatory and drug target), melatonin (sleep disorder pt more likely to get migraines)

Pathogenesis: NOT primary vascular condition but neurological dysfunction, but thought to be due to dysfunction of an ion channel in aminergic brainstem nuclei modulating cranial vessels (trigeminal cervical complex)

Aura of oligemia (depressed neuronal function) passes across cortex involving opthalamic division of CNV and pain comes from inflammation of dura mater

Front 11

Where do migraines start

Back 11

Trigeminal cervical complex (in brainstem)

Front 12

What causes pain in migraines

Back 12

sterile neurogenic inflammation of dura mater

Front 13

Dopamine antagonists use in migraines

Back 13

helps relieve nausea and vomiting

Front 14

Glutamate role in migraines

Back 14

excites trigeminal nucleus and levels rise following noxious stimuli in migraines

Released in cortical spreading depression and antagonists help relieve symptoms (topomax, zonegran, felbatol, remacemide)

Front 15

Substances that trigger trigeminal sensory nerves for migraines

Back 15

Calcitonin gene related peptide, substance P

Front 16

Pathophysiology of migraines; why do some patients cry, why do some vomit

Back 16

Trigeminal autonomic reflex (regulates pain) sends sensory input to trigeminocervical complex

Relayed to higher brain centers, processed, descending output to meningeal blood vessels via neurons of superior salivatory nucleus to pterygopalatine ganlion to meningeal vessels

This leads to pain of migraine

1 neuron (sensory) relays to brainstem, 2nd from there to thalamus, 3rd from there to cortex where pain is perceived

Vessels dilate BUT not main mechanism of pain

Cry - some neurons go to limbic system (emotion)

Vomit - some neurons to area postrema in floor of 4th ventricle

Front 17

Comorbidities of migraines/associations

Back 17

Epilepsy, sleep disorders, asthma, syncope, depression, persistent foramen ovale, CV illness, obesity, incomplete Circle of Willis

Front 18

Medicines associated with inducing migraines

Back 18

Ergot medications, triptans

Front 19

IHS diagnostic criteria for migraines in Adults, Pediatrics

Back 19

Adults: 5 or more episodes, 4-72 hr span,

MUST have 2 of (unilateral pain, throbbing, aggravation on movement, moderate to severe)

MUST have 1 of (nausea/vomitting, photophobia, phonophobia)

Ask for "headache days" and how many disabling

Pediatric - same as adult EXCEPT duration between 1-48 hours, pain can be bilateral

In pediatrics may not need 5 episodes if have an aura or can reverse aura etc.

Front 20

Diagnosing migraines

Back 20

Ask patient whats wrong, episodic pain, OK between episodes. headaches began between 7-10 years old

Front 21

Headache Questionnaire

Back 21

For how long, where, how (quality, not most useful), why (should have no cause if magraines), frequency, severity, duration, better worse, associations (aura, N/V)


If has been going on for 10 years less likely to be lifethreatening (tumor, infection, abscess, aneurysm etc). Ie. headaches suddenly for 3 weeks = BAD

frequency tailors therapy. more = aggressive

severity allows you to track progress

I

Front 22

Things improving headaches suggesting a migraine

Back 22

Pain made better by lying in a dark, quiet room

Front 23

Cluster Headache

Back 23

Uncommon primary headache where a pt wakes up about 90 minutes after go to sleep, pace around, pain lasts 15 minutes or so

NOT a migraine b/c migraines helped by sleep, quiet and movement makes worse

Front 24

When does migraine diagnosis require further workup than interview

Back 24

If patient has another clinical symptom (ie left sided weakness) or something can do imaging

If everything else normal can diagnose there

Front 25

Migraine variants

Back 25

Retinal migraine, confusional migraine, opthalmoplegic migraine, basilar type (aura)

Front 26

Childhood Periodic Syndromes

Back 26

Benign Paroxysmal Vertigo, Paroxysmal toricollis, alternating hemiplegia of childhood, CYCLIC VOMITING, etc. can signal a migraine but child can't tell you about headaches

Front 27

Why should migraines be treated

Back 27

Headaches associated with:

Stroke and CV disease

Silent white matter lesions - dementia

MORE headaches develop over time. PROGRESSIVE

Front 28

Goals of Treatment

Back 28

Decrease frequency, duration, severity, disability, improve QOL

Front 29

Nonpharmacologic and pharmacologic treatments of migraine

Back 29

Nonpharmacologic - AVOID triggers, exercise, less caffeine, eat healthy, improve sleep

Pharmacologic -
Prophylactic (offer if 6 headaches no impairment, 4 w impairment, 3 w severe imparment, NOT if just 1 time or if have just 3/month but no impaired) - use for 4-6 wks before declaring failure -

Drugs - TOPAMAX, B blockers, DIVALPROEX

Abortive - AS SOON as get pain take meds IMMEDIATELY and take a high enough dose to get rid of headache

Drugs - NSAIDs (excedrin), antiemetics, Ergots (inhaled DHE), triptans, Cgrp receptor antagonists

Front 30

CGRP receptor antagonists MOA and use

Back 30

abortive migraine therapy

Blocks release of CGRP via serotonic receptor action but lacks vasoconstriction at all

Prevents secretion at trigeminal nerve fibers and vasdilates peripherally

Front 31

Fasted acting abortive therapy, BEST to use

Back 31

Inhaled DHE (Ergot medicine)

BEST: TRIPTANS

Front 32

Triptans MOA and use

Back 32

VERY safe, orally or spray

Serotonin receptor agonists, causes vasoconstriction, inhibit peripheral and central trigeminocervical inhibition, inhibit NT release (CGRP, substance P) and inhibit inflammation