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
chronic migraine
>3 mnths =/>15 MHDs (mnthly headache day) and =/> 8MMDs (mnthly migraine day)
26
MHDS monthly headache day
a day with migraine-type or TTH
27
MMDs monthly migraine day (accompanying characteristics)
=/>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
28
migraine w/ aura at least 2 attacks fulfilling:
=/> 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
migraine pathophysiology
prodrome +/- aura ictal postdrome
30
prodrome caused by
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
neuropeptides like...
leptin, neuropeptide Y and Orexin A/B
32
hypothalamus responsible for
* Nociceptive processing * Control sleep-wake cycle * Feeding * Thirst * Arousal * Autonomic and endocrine regulation
33
prodrome duration and sx
Few hrs - days * Fatigue * Cognitive difficulties * Mood changes * Food cravings * Neck pain * Yawning
34
aura caused by
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
aura duration and sx
5-60mins * Visual aura * Sensory disturbances * Speech disturbances * Motor sx
36
ictal (headache) causes
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
CGRP involvement in migraine pain
- 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
sensitisation and sx (allodynia) in ictal phase
- 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
photophobia in migraine
- 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
headache duration and sx
4-72hrs * Headache * N, V * Photophobia * Phonophobia
41
postdrome caused by
* Region of brain remain activated after headache cessation, olfactory regions, midbrain, hypothalamus
42
postdrome duration and sx
* 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
interictal
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
TRIGEMINOVASCULAR SYSTEM IN MIGRAINE
- peripheral components - central components 1) sensitisation/ hyperexcitability
45
periphery TGM
Relays TGM nociceptor input from meningeal vessels and dura mater --> CNS
46
central TGM component
(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
TGM thus leads to hyperexcitability
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
CGRP is a ___?
Calcitonin gene-related peptide 37 aa neuropeptide (calcitonin family of peptides) roles: nociception, sensory modulation, vasodilation
49
CGRP receptor found on cell mem of:
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
CGRP- receptor comprises of
CLR (calcitonin receptor-like receptor) + RAMP1 (receptor activity modifying protein) = heterodimer translocates from ER --> cell mem
51
activation of GPCR -- heterodimer
1) ligand binding leads to transient receptor activation 2) induce cellular resp (2nd messenger signalling) 3) receptors inactivated and internalised -- ENDOCYTOSIS - recycled/ degraded
52
CGRP–CGRP-R signaling in migraine pathophysiology
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
CGRP results in migraine effects of
vasodilation peripheral nociceptor activation neurogenic inflammation CSD central TGM sensory activation central sensitisation hypothalamic dysfunction and descending control of brainstem, structures
54
CGRP has high affinity for what else?
AMY1-R (has RAMP1 subunit in common) expressed in vasculature, pancreas and TGM ganglion physiologic roles: regulate pp glucose, glycemic control, satiation
55
acute management of migraine
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
adjunct for aucte tx
metoclopramide Anti-emetics: Relief of migraine-related NV when combined with analgesic medication
57
considerations for acute tx
efficacy, safety, comorbidities, concomitant medications Rapid pain relief & associated sx Restore ability to function
58
risk and benefits of acute tx
Benefits: * Sx relief Limitations: * Potential ADR - PUD, dependency, tolerance, risk of med overuse headache * Pt specific CI to use of particular med * DDI
59
Preventive treatment for which migraine pt?
AHS: based on HDM and degree of disability caused by attacks EHF: any pt with migraine, not well-controlled w/ acute + willingness
60
AHS criteria
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
EHF criteria
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
risk and benefits of preventive tx
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
preventive tx
antiseizure meds bb (propanolol, metoprolol) ARB CGRP - gepants (CGRP-R) - MABS (anti-CGRP antibody// anti-CGRP receptor Ab) Neuromodulation device Neurotoxins
64
initiation of CGRP tx
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
MIDAS scoring disability asssessment
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
HIT (headache impact test) criteria
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
assessing tx efficacy (acute, chronic)
1. headache diary 2. MIDAS (disability assessment) 3. ADR of medications (affect compliance)
68
continuation of CGRP
- 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)