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3153 > headache & migraine > Flashcards

headache & migraine Flashcards

1
Q

Headache pathophysiology

A

Nerves of muscle and blood vessels surround head, neck, face

○ Pain-sensing nerves set off by: stress, muscle tension, enlarged blood vessels, other triggers

○ Once activated, nerves send messages to brain –> sense pain (as if cmg from deep within head)

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2
Q

primary headaches (ICH3)

A

migraine
tension-type headache

trigeminal autonomic cephalagias (TACs)
other 1* HA disorders

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3
Q

2* headache

A

trauma/ injury to head/ neck
cranial or cervical vascular disorder
non-vascular IC disoder

infection
homeostasis disorder
psychiatric disorder
HA. facial pain – disorder of cranium, neck, eyes, ear, nose, sinus, teeth, mouth, facial/cervical struc

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4
Q

neuropathies, facial pains, other headaches

A

painful lesions of cranial neuropathies and other facial pain

other HA disorders

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5
Q

2nd headache red flags

SNNOOP10

A

systemic sx (fever)
neoplasm hx (cancer)
Neurologic deficit/ dysfunction
onset of headache SUDDEN
older age (>50yo)

pattern change, recent onset
positional headache (at certain posture)
ppt by sneeze, cough, exercise
papilledema (optic disc)
progressive w/ atypical presentation
preg
painful eye with autonomic features (HR, BP, RR)
post-traumatic HA
pathology of immune system – HIV/ immunocompromised
painkiller overuse / new drug at HA onset

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6
Q

** STROKE sx

A

FAST (Facial drooping, Arm weakness, Speech difficulties and Time)

weakness of face/arm/leg on 1 side of body
sudden, severe headache w/ no apparent cause
difficulty speaking, understand language

dizzy, loss of balance/ coordination
visual loss
sudden onset of HA, seizures, loss of consciousness

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7
Q

TTH features

A
  • bilateral
  • pressing/ tightening (non pulsatile)
  • mild-mod pain
  • not aggravated by routine activities
  • no other sx (pericranial/ cervical muscle tenderness)
  • no premonitory sx and aura

duration: 30mins- 7d
freq: infreq ~ daily

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8
Q

differential with cluster headache

A
  • unilateral
  • variable pain
  • severe - VERY SEVERE pain
  • restless, agitation
  • cranial autonomic sx SAME SIDE as HA (nasal congestion, swollen eye, sweat)

duration: 15-180mins
freq: freq during clusters

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9
Q

migraines features

A
  • unilateral (can be bilateral too)
  • pulsatile/ throbbing
  • mod-severe pain
  • aggravated by routine activities
  • NV, photophobia, phonophobia , aura, allodynia

duration: 4-72hrs
freq:recurrent with variable freq

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10
Q

types of TTH

A

Infrequent episodic

Freq episodic

Chronic TTH

Medication overuse headache

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11
Q

infreq TTH

A

<1 ep/ mnth
Duration: 30min - 7d

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12
Q

freq TTH

A

at least 10 eps occuring on 1-14d/mnth, for >3mnths
Duration: 30min - 7d

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13
Q

chronic TTH

A

> 15d/mnth average for 3mnths
Duration: hrs-days

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14
Q

MOH

A

Headache =/> 15 days/mnth in pt with pre-existing headache disorder

Regular overuse > 3mnths of =/>1 drug for acute/ sx tx of headache
* Ergotamines, opioids, triptans/ combi =/> 10 d/mnth
* Simple analgesic (paracetamol, NSAID) =/> 15d/mnth
* Any combi of above or one or more meds than above for =/> 10d/mnth

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15
Q

triggers for TTH

A

Physical/ emotional stress
Activities that cause head to be held at one position for long time (neck muscle locked, pain receptors triggered)

Alcohol - withdrawal
Caffeine - withdrawal
Cold/ flu or sinus infections
Dehydration
Hunger

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16
Q

mechanism of TTH

A

1) myofascial - incr tender, inflamm, local ischaemia

2) vascular - incr blood flow to cerebral artery.
Abnormal carotid artery blood flow/ extrcranial vascular resp

3) genetic

4) central - sensitisation, dysfunction in descending pain modulation

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17
Q

acute pain management for TTH

A
  • Paracetamol (w/ or w/o caffeine), aspirin
  • NSAID: ibuprofen, naproxen, diclofenac, ketoprofen
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18
Q

prophylactic management for TTH

A
  • Amitriptyline (1st line, tricyclic antidep)
  • Mirtazapine (antidep tetracyclic)
  • venlafaxine (SNRI)
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19
Q

non-pharm for TTH management

A
  • Avoid triggers
    • Stress management
    • Posture, neck strain
  • Cognitive behavioural therapy, biofeedback, relaxation
  • Physical, occupational therapy
  • Lifestyle and modification
    * sleep hygiene
  • headache diary (identify triggers)
  • medication use (prevent MOH)
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20
Q

how does MOH occur

A

medication to provide short term pain relief
rebound headache
higher med dose needed to provide relief

vicious cycle of med overuse

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21
Q

diagnose MOH

A

1) duration of acute HA drugs > 3mnths
2) freq (>/= 15days per mnth)
3) headache not other ICHD3 diagnosis

ergotamines, opioids, triptans/ combi =/> 10d
paract/ NSAID =/> 15d
any combi of above =/> 10d

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22
Q

migraine diagnosis ICHD3 criteria

at least 5 attacks that fulfil —-

A

1) Headache attack last 4-72hrs (when untx/ unsuccessful)

2) Headache characteristic (=/>2 of 4)

3) Non-headache sx (=/>1) if no aura
- NV
- Photophobia/ phonophobia

4) not accounted for another ICHD3 dx

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23
Q

headache characteristics =/>2 out of 4

A

Unilateral location
Pulsating quality
Mod-severe pain intensity

Aggravation by/ causing avoidance of routine physical activity (walk, climb stairs)

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24
Q

episodic migraine

A

over a lifetime
=/>5 migraine attacks lasting 4-72hrs

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25
Q

chronic migraine

A

> 3 mnths
=/>15 MHDs (mnthly headache day)

and

=/> 8MMDs (mnthly migraine day)

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26
Q

MHDS monthly headache day

A

a day with migraine-type or TTH

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27
Q

MMDs monthly migraine day (accompanying characteristics)

A

=/>2 migraine characteristics
* Unilateral
* pulsating
* moderate/ severe
* aggravation by, or causing avoidance of, routine physical activity

If no aura =/> 1 of the following migraine sx
* Photophobia/ phonophobia
* NV

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28
Q

migraine w/ aura

at least 2 attacks fulfilling:

A

=/> 1 of following reversible aura sx:
(visual/ sensory/ speech, lanaguge / motor/ retinal/ brainstem)

=/>3 of the characteristics
*1 aura sx spread gradually over >5mins
* 2 or more aura sx occur in succession
* each indiv aura sx lasts 5-60mins
* =/>1 sx unilateral
* =/>1 sx is positive
* HA follow/ accompanied by aura (within 60mins)

29
Q

migraine pathophysiology

A

prodrome

+/- aura

ictal

postdrome

30
Q

prodrome caused by

A

Activation of hypothalamus, neuropeptides (involved in homeostasis)

Regulate homeostasis : burdensome non-pain sx (prodrome, other phases): NV,LOA, fatigue (migraine)

Incr blood flow in early premonitory phase > nitroglycerin induced migraine

31
Q

neuropeptides like…

A

leptin, neuropeptide Y and Orexin A/B

32
Q

hypothalamus responsible for

A
  • Nociceptive processing
  • Control sleep-wake cycle
  • Feeding
  • Thirst
  • Arousal
  • Autonomic and endocrine regulation
33
Q

prodrome duration and sx

A

Few hrs - days

  • Fatigue
  • Cognitive difficulties
  • Mood changes
  • Food cravings
  • Neck pain
  • Yawning
34
Q

aura caused by

A

Cortical spreading depression in cortex

1) CSD = Large wave of slow spreading depolarisation within grey matter
a. Inhibits cortical activity
b. 2-6mm/min

2) Change in synaptic activity, EC ion conc, blood flow, metabolism
a. Inhibit cortical activity, reduced blood flow

3) CSD activate trigeminovascular system
Drive aura sx

35
Q

aura duration and sx

A

5-60mins

  • Visual aura
  • Sensory disturbances
  • Speech disturbances
  • Motor sx
36
Q

ictal (headache) causes

A

Neuropeptides (eg CGRP calcitonin-gene related peptide) cause sensitisation, inflammation in central and peripheral trigeminovascular system

lead to pain and non-pain sx in ictal phase

37
Q

CGRP involvement in migraine pain

A
  • Head pain and other, non-pain sx
  • its receptor expressed in multiple anatomic regions relevant to migraine
    □ Trigeminovascular
    □ Cranial parasympathetic systems

evidence:
- When infused, can induce migraine-like attacks
- CGRP lvls incr sig during migraine attack
- CGRP therapeutics effective

38
Q

sensitisation and sx (allodynia) in ictal phase

A
  • Sensitise 1* nociceptors and central trigeminovascular neurons
  • MRI shows struc abnormalities in brainstem
    □ Altered sensory processing and brainstem structure contribute to
    □ Severity of allodynia, hypersensitivity to migraine pain
39
Q

photophobia in migraine

A
  • Retinal and trigeminal nociceptive inputs –> converge in thalamus
    □ projects to nociceptive areas of cortex S1/S2
    □ exacerbate migraine by LIGHT
  • Hypersensitise visual cortex (V1/V2) can also contribute to the photosensitive effect
40
Q

headache duration and sx

A

4-72hrs

  • Headache
  • N, V
  • Photophobia
  • Phonophobia
41
Q

postdrome caused by

A
  • Region of brain remain activated after headache cessation, olfactory regions, midbrain, hypothalamus
42
Q

postdrome duration and sx

A
  • Fatigue, food cravings, cognitive sx
    Continue in attack but overshadowed by HA sx (pain, NV, aura)

Few hrs - days
* Fatigue
* Difficult conc
* Neck stiffness

43
Q

interictal

A

periods b. migraine attacks
hrs - days after attack

  • regions remain abnormally active (olfactory, midbrain, hypothalamus)

+ light, - pain
○ Activate visual cortex bilaterally in migraine pts

+light,+ pain
○ Concomitant pain stimulation potentiated visual cortex activation in pt with migraine

44
Q

TRIGEMINOVASCULAR SYSTEM IN MIGRAINE

A
  • peripheral components
  • central components

1) sensitisation/ hyperexcitability

45
Q

periphery TGM

A

Relays TGM nociceptor input from meningeal vessels and dura mater –> CNS

46
Q

central TGM component

A

(inside the BBB)

○ TGM ganglion receives peripheral nociceptive pain signal —> TGM complex (brain stem) –> thalamus –> cortex
- Experience of pain

○ Activation of other central regions (project TO/ FROM the TGM system) contributes to non-pain sx

47
Q

TGM thus leads to hyperexcitability

A

Repeated activation of the trigeminovascular system over time results in a state of nervous system hypersensitivity and sustained pain

Feedback from a sensitized brain may:
1) Potentiate pain signaling
2) Contribute to common migraine symptoms
- Photophobia, phonophobia, and cutaneous/mechanical allodynia

48
Q

CGRP is a ___?

A

Calcitonin gene-related peptide
37 aa neuropeptide (calcitonin family of peptides)

roles: nociception, sensory modulation, vasodilation

49
Q

CGRP receptor found on cell mem of:

A

migraine patho:
- TGM ganglion
- cerebral and meningeal vasculature
- brainstem
- brain (thalamus eg)

other cell types
- vascular smooth muscle cells
-neurons
- glial cells
- mast cells

50
Q

CGRP- receptor comprises of

A

CLR (calcitonin receptor-like receptor) + RAMP1 (receptor activity modifying protein) = heterodimer

translocates from ER –> cell mem

51
Q

activation of GPCR – heterodimer

A

1) ligand binding leads to transient receptor activation
2) induce cellular resp (2nd messenger signalling)
3) receptors inactivated and internalised – ENDOCYTOSIS

  • recycled/ degraded
52
Q

CGRP–CGRP-R signaling in migraine pathophysiology

A

1) activate CGRP-R in TGM
2) CGRP released from storage vesicle by Ca2+ dependent exocytosis

3) peripheral release of CGRP from TGM nerve ending, triggers multiple responses induced by CGRP-R binding ==> sensitise nociceptor TGM neurons

4) peripheral TGM neurons relay migraine pain signals (brainstem –> brain) exp pain

5) central CGRP effect: pain transmission through sensitisation and activation of central processes
- feedback

53
Q

CGRP results in migraine effects of

A

vasodilation
peripheral nociceptor activation

neurogenic inflammation
CSD

central TGM sensory activation
central sensitisation

hypothalamic dysfunction and descending control of brainstem, structures

54
Q

CGRP has high affinity for what else?

A

AMY1-R (has RAMP1 subunit in common)

expressed in vasculature, pancreas and TGM ganglion

physiologic roles: regulate pp glucose, glycemic control, satiation

55
Q

acute management of migraine

A

Mild-mod:
NSAID, non-opioid analgesic, combination

Mod-severe/ mild-mod, respond poorly: migraine-specific agents =
triptans > ergotamine

others: opioids (abusable)
Ditans (5HT1F receptor)
Gepants (Block CGRP receptor)

56
Q

adjunct for aucte tx

A

metoclopramide

Anti-emetics: Relief of migraine-related NV when combined with analgesic medication

57
Q

considerations for acute tx

A

efficacy, safety, comorbidities, concomitant medications

Rapid pain relief & associated sx
Restore ability to function

58
Q

risk and benefits of acute tx

A

Benefits:
* Sx relief

Limitations:
* Potential ADR
- PUD, dependency, tolerance, risk of med overuse headache
* Pt specific CI to use of particular med
* DDI

59
Q

Preventive treatment for which migraine pt?

A

AHS: based on HDM and degree of disability caused by attacks

EHF: any pt with migraine, not well-controlled w/ acute + willingness

60
Q

AHS criteria

A

offered:
=/>6 HDM, no diasbility
=/>4 HDM, some disability
=/> 3 HDM, severe disability

considered:
4-5 HDM, no disability
3 HDM + some
2 HDM + moderate

  • attacks sig interfere with pt daily routines despite acute tx
  • freq attacks (=/>4MHD)
  • CI/ failure/ overuse of acute tx
  • ADR to acute tx
  • pt preference
61
Q

EHF criteria

A

IMPAIRS QOL +

1) attacks cause =/> 2days DISABILITY per mnth & optimised acute tx does not prevent attack

or

2) risk of overuse of acute tx + pt willing to take daily meds

normal is 4-72hrs

62
Q

risk and benefits of preventive tx

A

Potential benefits:
- Avoid escalation in use of acute medications
- May reduce overall cost associated with migraine tx
- MOH

Limitations
- Often associated with pt adherence (ROA)
- SE: dep, cognitive dysfunction, somnolence, constipation, weight gain
- cost of drugs (CGRP ~$2000/ mnth)

63
Q

preventive tx

A

antiseizure meds
bb (propanolol, metoprolol)
ARB

CGRP
- gepants (CGRP-R)
- MABS (anti-CGRP antibody// anti-CGRP receptor Ab)

Neuromodulation device
Neurotoxins

64
Q

initiation of CGRP tx

A

age =/> 18yo and 1

1) 4-7 MMD + inability to tolerate SE/ inadequate 8wk trial of 2 tx clasess + mod disability MIDAS =/>11, HIT >50

or

2) 8-14 MMD + inability to tolerate SE/ inadequate 8wk trial of 2 tx clasess

or

3) chronic migraine +
inability to tolerate SE/ inadequate 8wk trial of 2 tx clasess //
inability to tolerate/ inadequate resp to min. 2 injs (6mnths) onabotulinumtoxinA

65
Q

MIDAS scoring disability asssessment

A

Grade 1 (0 to 5): little or no disability.

Grade 2 (6 to 10): mild disability.

Grade 3 (11 to 20): moderate disability **

Grade 4 (>21): severe disability.

  • how many days in last 3mnths, miss work/ shool
  • how many days in last 3mnths productivity reduced by 50%
  • how many days in last 3mnths, not do HH work
  • how many days in last 3mnths productivity in HH work reduced by 50%
  • how many days in last 3mnths did you miss regular activities (family, social, leisure)
66
Q

HIT (headache impact test) criteria

A

little or no impact (49 or less)
some impact (50–55) **
substantial impact (56–59)
severe impact (60–78).

-how often is pain severe
-how often limit daily activities
- how often wish to lie down
- past 4 wks, how often too tired to work/ daily activities
- past 4 wks, how often felt fed up over HD
- past 4 wks, how often is conc limited

67
Q

assessing tx efficacy (acute, chronic)

A
  1. headache diary
  2. MIDAS (disability assessment)
  3. ADR of medications (affect compliance)
68
Q

continuation of CGRP

A
  • reduction in MHD =/> 50%
  • improvement in any of the migraine-specific pt reported outcome measures
  • MIDAS (=/>5 pt: base 11-20) (reduce >30%: base >20)
  • HIT-6 (=/>5 pt)
  • MPFID (=/>5 pt)

3153 (8 decks)

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