Headache

Question 1

most common type of headache and most common presentation in docs office

Answer 1

The most common type of primary headache are tension-type headaches

Migraine headaches are the most common presentation in the doctor’s office

Question 2

peripheral sensitization mechanism of a migraine

Answer 2

Peripheral sensitization: throbbing head pain that worsens with movement due to primary/first order sensitization of nociceptors of the meninges and dural vessels → normal pulsation activates the nociceptors

So, normal pulsation of intravascular pressure activates nociceptors of the dura inappropriately during migraine, whereas without migraine, normal pulsations or movements inside the head are painless.

Question 3

the cortex of the brain/brain parenchyma technically cannot feel pain. What structures are pain-sensitive?

Answer 3

Dura mater (mostly adjacent to vessels)

Dural arteries and large veins

Pial arteria

Falx cerebri, tentorium

Venous (dural) sinuses

Proximal portions of large intracerebral arteries

CN V, VII, IX, X

Question 4

central sensitzation mechanism of migraines

Answer 4

Central sensitization: sensitization of 2nd order nociceptive neurons in the caudal trigeminal nucleus where there is convergent input from dural nociceptors and nociceptors from the skin of the face (especially VII facial) → pain with shaving, touching skin, wearing glasses, putting the face on pillow

Trigeminovascular theory: why does the sensitization occur?

Trigeminal afferents on dural vessels release neuropeptides antidromically (CGRP, SubstP, Bradykinin)

These peptides act on dural vessels to cause neurogenic inflammation– vasodilation, extravasation of plasma proteins such as histamine → AKA NEUROGENIC INFLAMMATION

This is believed to cause sensitization of the nociceptors

Question 5

outline the trigeminovasculat theory of nociceptor sensitization in migraines

Answer 5

Trigeminovascular theory: why does the sensitization occur?

Trigeminal afferents on dural vessels release neuropeptides antidromically (CGRP, SubstP, Bradykinin)

These peptides act on dural vessels to cause neurogenic inflammation– vasodilation, extravasation of plasma proteins such as histamine → AKA NEUROGENIC INFLAMMATION

This is believed to cause sensitization of the nociceptors

Question 6

Outline how the aura is created in a migraine headahce

Answer 6

the aura mechanism is due to cortical spreading depression of Leao

neuronal excitation/depolarization→ increased blood flow via vasodilation→ decreased neuronal activity → decreased blood flow → spread through cortex.

CSD activates release of neuropeptides from trigeminovascular neurons and causes plasma protein extravasation leading to neurogenic inflammation.

Question 7

outline the diagnostic criteria for migraine without Aura (543210 rule)

Answer 7

Definition: duration for 4-72 hours, recurrent (at least 5 attacks), no secondary cause identified.

Symptoms: throbbing, worse with movement, skin sensitive to light touch, allodynia

Etiology: genetic– D2 neuron receptor changes, sodium ATPase mutations etc.

Diagnostic Criteria WITHOUT Aura (most common):

Pain criteria (2 of): throbbing, unilateral, moderate or severe, worse with routine activity/movement

Associated symptoms (1 of): photophobia and phonophobia, nausea and or vomiting

**Memorization technique: 5-4-3-2-1-0:

• At least 5 attacks
• 4 hours in duration
• 3 days in duration
• 2 pain features
• 1 associated feature
• 0 other causes identified.

Question 8

5 hints as to why aura from migraine is NOT a stroke:

Answer 8

Gradual onset of symptoms

Complete resolution

Spread of symptoms usually makes some anatomic sense with respect to cortical representation; doesn’t necessarily respect vascular territories

Often involves the tongue.

Usually more positive symptoms then negative.

Question 9

4 classes of medication for acute pharmacologic treatment for migraine management

Answer 9

1. NSAIDS
2. triptans
3. combo
4. Anti-emetics; metaclopramide

Question 10

when should you consider using prophylactic treatment in migraine management

Answer 10

• >8 headache attacks per month
• Recurrent migraine attacks causing disability despite optimal treatment
• Frequency of acute mediation use is >10 days/month for triptans, >15 days for NSAID, acetaminophen
• Recurrent attacks with prolonged aura

Betablockers and Antidepressants→ SSRIs not recommended, antiepileptics, riboflavin and citrate vitamins, CGRP receptor antagonists (monoclonal antibodies), botox injections

Question 11

management of medication overuse headache

Answer 11

• withdrawal of medications must be done, 10% make an improvement.

Question 12

definition and diagnostic criteria of a cluster headache

Answer 12

Definition: 5 attacks of severe or very severe unilateral, orbital, supraorbital and or temporal pain lasting 15-180 minutes.

• To diagnose episodic cluster, must have more than one cluster, lasting between 7 and 365 days, with a remission > 1 month.
• Most attacks last 2 wks to 3 months.
• Chronic cluster is diagnosed when attacks last >365 days without remission.

Frequency- 1 every other day to 8 per day, not attributed to another disorder and at least one of the following:

• Ipsilateral conjunctival injection/lacrimation
• Ipsilateral nasal congestion/rhinorrhea
• Ipsilateral eyelid edema
• Ipsilateral forehead and facial sweating
• Ipsilateral miosis/ptosis or a sense of restlessness/agitation

Question 13

common triggers for cluster headache

Answer 13

etOH, nitraaets, histamine, MSOKING

Question 14

abortive, transitional, preventatibe and surgical management of cluster headaches

Answer 14

Abortive: oxygen, triptans, nasal spray, occipital nerve block, intranasal lidocaine, possible non-invasive vagal nerve stimulation

Transitional: steroids (poor evidence), vitamin D and Ca

Preventative: verapamil, lithium, melatonin, topiramate

Surgery: deep brain stimulation (⅔ of patients benefit)

Question 15

diagnostic criteria for tension headache

Answer 15

Definition: at least 10 episodes occurring less than 1 day per month (infrequent) or between 1 and 14 days per month (frequent), and fulfilling:

• Duration 30 min to 7 days
• Has at least 2 of the following criteria:
  
  • Bilateral location– usually front and occipital
  • pressing/tightening quality
  • Mild or moderate intensity
  • Not aggravating by routine activity
• No nausea or vomiting
• No more than one of photophobia or phonophobia (or else consider migraine)
• May or may not be associated with increased pericranial tenderness with palpation of pericranial muscles.

Investigations: look for depression and MSK problems

Management; physio for postural training, acupuncture, venlafaxine, amitriptyline, treat depression.

Question 16

most common cause of headache in babys

Answer 16

Fever- meningitis, Red Reflex- retinoblastoma

Question 17

most common cause of headache in child

Answer 17

viral

Question 18

most common cause of head ache in teen

Answer 18

trauma/concussion

Question 19

most common cause of headaache in college

Answer 19

meningitis, tension headache, migraine

Question 20

common cause of headache in adult population

Answer 20

common cold, sinusitis, otitis, sinus thrombosis, dental pain, analgesic headache, shingles, trigeminal neuralgia, aneurysm

Question 21

common cause of headache in elderly population

Answer 21

acute glaucoma, temporal arteritis, trauma (subarachnoid hemorrhage), tumours/mets.

Question 22

SNOOP redflags of headache that may indicate a secondary headache type over a primary

Answer 22

S: systemic symptoms (myalgais, amalaise, fever, weightloss), sudden onset

N: neurological signs/symptoms (diplopia, RAPD)

O: older age over 40

O: onset (thunderclap)– trauma and neck stiffness

• Thunderclap headache is a medical emergency. Could be a subarachnoid hemorrhage

Remote history of cancer

P: progressive tempo

P: pressure (symptoms of raised ICP)

• Projectile vomiting
• Morning headache
• Supine headache
• Headache with valsalva

Question 23

investigations into subarachnoid hemorrahe

Answer 23

• emergent CTA
• lumbar puncture to look for xanthochromia from RBC breakdown
• vascular imaging with CTA or CTV

Question 24

investigations into vasculitis

Answer 24

giant cell/temporal arteritis can cause a secondary headache in the temrporal region.

• ESR and CRP elevated. Temperal artery biopsy will show granulation and inflammation.

tx with prednisone

Question 25

Epi; mostly in women who experience weight gain Symptoms: chronic daily headache, papilledema, transient visual obscurations, tinnitus, occasionally diplopia, raised CSF opening pressure in absence of other causes (ex/ tumor, dural sinus, thrombosis). May cause progressive visual field deficits **what disease could be causing this secondary headache and symptoms in this patient profile? How would you treat this?**

Answer 25

pseudotumor cerebri (idiopathic intracrnial hypertension) is a problem caused by elevated cerebrospinal fluid pressure in the brain. ## Footnote Management: Rule out structural cause of papilledema by brain imaging and venogram (CT, CTV) Measure ICP Counsel for weight loss Acetazolemide Humphrey Visual Test q3 months.