Headache & Pain

Question 1

3 Steps of Headache Dx

Answer 1

• 1- Rule out secondary headaches (1-3% presentations)
• 2- Recognize migraine (95% presentations)
• 3- Review other primary headaches (tension or cluster)

Question 2

Nasty 9 of Secondary Headache

Answer 2

• First/worst
• Abrupt onset headache (thunder clap)
• New onset or fundamental change in pattern of headache
• New headache if <5 yo and >50 yo (b/c inc incidence of brain tumors ann onset of 1st primary headache normally b/n 5-50)
• If cancer, immunosuppression or pregnancy
• Headache w/ syncope or seizure
• Triggered (not worsened) by exertion or sex
• Neurological symptoms >60 min in duration
• Abnormal physical exam or neuro exam (ex - fever and stiff neck)

Question 3

4 Stages of Migraine

Answer 3

• Prodrome (w/in 24 hrs b/f headache)
• Aura (5-60 min b/f headache)
• Headache (4-72 hrs)
• Postdrome (24-48 hrs after headache)

Question 4

Prodrome

Answer 4

• Occurs w/in 24 hrs b/f migraine; includes yawning, cravings, muscle pain, irritability, depression, euphoria
• Hypothalamus

Question 5

Aura

Answer 5

• Discrete episode of reversible neuro symptoms lasting 5-60 min
  
  • Most common complaint is visual (starts at occipital cortex)
  • Wave of excitation/depolarization due to hyper excitability —> compensatory vasodilation (auto regulation - brain increases blood flow to areas of high cortical activity)

Question 6

Headache Phase of Migraine

Answer 6

• Lasts 4-72 hrs
• Nociceptors in meninges, vessels and bone (periosteum) —> pain activates trigeminal nerve (especially V1 - ophthalmic branch) —> vasodilation/inflammatory chemicals (CGRP, substance P, neurokinin —> AA cascade)

Question 7

Postdrome

Answer 7

• For 24-48 hrs after migraine
• Body returns to homeostasis
• Fatigue, muscle aches, moodiness, malaise

Question 8

Migraine Pain Circuit

Answer 8

Trigeminal ganglion —> spinal trigeminal nucleus (gets pain & temp for face) —> VPM thalamus —> cortex

Question 9

2 Other Primary Headaches

Answer 9

• Tension = mild and common
  
  • Bilateral, not pulsatile, no sensitization or vomiting
• Cluster = severe and uncommon
  
  • Often leads to suicide
  • “trigeminal autonomic cephalalgias” - often associated w/ lacrimation, nasal congestion, rhinorrhea, mitosis, ptosis, eyelid edema, pacing/restlessness, forehead/face sweating

Question 10

Endogenous Opioids (3 types, uses, mechanism)

Answer 10

• 3 peptides ea act as agonist on different opioid receptors
  
  • Enkephalins - delta receptor
  • Dynorphins - kappa receptor
  • Endorphins - mu receptor
• Result = INHIBITION
  
  • Either by pre-synaptic blockade - inhibit pre-synaptic Ca++ channel
  • OR by post-synaptic hyper-polarization - enhance post-synaptic potassium conduction
• Uses/Effects
  
  • Suppress cough, analgesia, sedation, vasodilation, causes constipation, urinary retention and euphoria

Question 11

NSAIDs v Acetaminophen v Aspirin

Answer 11

Acetaminophen

• Analgesic & anti-pyretic
• NOT anti-inflammatory
• COX-3 inhibitor (some COX 2)
• Mainly central effects
• Liver toxicity- NAPQI

Aspirin

• Anti-inflammator, analgesic & anti-pyretic
• Also anti-thrombotic (may cause bruising)
• COX 1 & COX 2 irreversible inhibitor
• GI effects and Reyes so do not give kids

NSAIDs

• Anti-inflammatory, analgesic & anti-pyretic
• Somewhat anti-thrombotic
• COX 1 and COX 2 reversible inhibitor
• Sequesters to areas of inflammation
• Kidney toxicity

Question 12

Triptans Mechanism of Action

Answer 12

• Selective 5HT1 agonists
• Block transmission b/n 1st order trigeminal ganglia and its synapse on 2nd order spinal trigeminal nucleus (in paint circuit)
• NOT as effective once the 2nd order spinal trigeminal nucleus is already sensitized