Headache and Migraine Flashcards

1
Q

What are the classifications of the types of headaches?

A

Primary: Tension Type Headache, Migraine, Trigeminal Autonomic cephalagias (TACs), Other primary HA disorders

Secondary: Trauma or injury to head and/or neck, cranial or cervical vascular disorder, non-vascular intracranial disorder, infections, homeostasis disorder, psychiatric disorder, HA/facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial/cervical structures

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2
Q

What are the impt triage criteria?

A

SNNOOP10
Systemic symptoms incl fever
Neoplasm in Hx
Neurologic defecit of dysfn
Onset of headache sudden or abrupt
Older age (>50y.o.)
Pattern change or recent onset of headache
Positional headache
Precipitated by sneezing, coughing, exercise
Papilledema
Progressive headache w atypical presentation
Pregnancy or puerperium = 6 weeks post childbirth
Painful eye w autonomic features
Post traumatic onset of headache
Pathology of immune sys as HIV/immunocompromised
Painkiller overuse or new drug at onset of headache

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3
Q

What is SNNOOP10 for?

A

To rule out secondary headache or escalate for medical attention when it satisfies criteria for secondary criteria

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4
Q

Describe the pathophysiology of headache and migraine.

A

Pain sensing nerves of the muscles and blood vessels that surround the head face and neck are set off by stress, muscle tension, enlarged blood vessels etc.
Nerves sense messages to brain –> pain

Myofascial mechanisms esp cervical muscles involves, vascular mechanisms involved in peripheral sensitisation

Central mechanisms involved in central sensitisation, dysfn in descending pain modulation

Genetic disposition plays a role in pathophysiology

Vasodilation of intrcranial extracerebral blood vessels results in activation of perivascular trigeminal nerves

The activation of TGN releases vasoactive neuropeptides to promote neurogenic inflamm

Central pain transmission may activate other brainstem nuclei, resulting in assoc symptoms (NV, photophobia, phonophobia)
Agonists of vascular and neuronal 5HT1 rece subtypes known to result in vasoconstriction of meningreal blood vessels and inhib vasoactive peptide release & pain signal transmission (reversal of migraine)

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5
Q

What are the risk factors for TTH?

A

Fam Hx of polymorphism
Female
Depression and anxiety
Insomnia
Temporomandibular joint disorder
Vit B12, D def
Physical/emotional stress
Activities that cause the head to be held in one position for a long time
Alc
Caffeine
Cold/flu or sinus infections
Dehydration
Hunger

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6
Q

Describe the epidemiology of TTH.

A

Most common type of primary headache - est 1y prevalence 38-86%
Peaks in 4th decade
Female>Male

Infrequent episodic TTH 64%
Frequent episodic TTH 22%
Chronic TTH 0.9-2.2%

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7
Q

What are the specific classification criteria for episodic TTH?

A

Infrequent ETTH
Freq: min 10 headache episodes, average <1d/month (<12 d/year)
Duration: 30min-7d

Frequent ETTH
Freq: min 10 headache episodes, ave 1-14d/month for >3mo BUT <180days/year
Duration: 30min-7d

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8
Q

What are the specific classification criteria for CTTH?

A

Freq: >= 15d/month on ave for >3mo (>=180d/year)
Duration: h-d, unremitting

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9
Q

What are the shared classification criteria for ETTH and CTTH?

A

At least two of the four following:
- Bilateral
- Pressing or tightening (non-pulsating) quality
- Mild or moderate intensity
- Not aggravated by routine physical activity at walking or climbing stairs

Both of the following:
For ETTH
1. No N/V
2. No more than one of photophobia or phonophobia

For CTTH
1. No more than one or photophobia, phonophobia or mild nausea
2. Neither moderate or severe nausea nor vomiting

Not better accounted by another ICHD-3 diagnosis

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10
Q

What are the principles for TTH management?

A

Acute TTH:
Pharmacological
- Paracetamol (along or w caffeine), aspirin
- NSAIDs: Ibuprofen, Diclofenac, Ketoprofen

Chronic TTH:
Pharmacological Prophylaxis
- TCA e.g. amitriptyline
- Mirtazapine, Venlafaxine

Non-pharmacological
- Cognitive behaviour therapy (CBT), biofeedback relaxation
- PT and/or OT
- Lifestyle modif (incl sleep hygiene)

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11
Q

What are the goals of management for TTH?

A

Pain relief, prevent progression to chronic TTH

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12
Q

What are the signs and symptoms of TTH?

A

Pain location: Bilateral
Pain quality: Tightening, pressing, band-like, constant
Pain intensity: Mild to moderate intensity
Effect on activities: Not aggravated by routine activities of daily living
Onset:
Time: 30min-7d, may be better in morning, worse in evening
Others:
- Pericranial or cervical muscle tenderness
- Stiffness in neck
- Decreased appetite

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13
Q

Describe the pathophysiology of migriane.

A

Vasodilation of intrcranial extracerebral blood vessels results in activation of perivascular trigeminal nerves

The activation of TGN releases vasoactive neuropeptides to promote neurogenic inflamm
- CGRP, PACAP
- Released in mayy anatomical regions, incl trigeminal vasculature and cranial parasympathetic sys

Central pain transmission may activate other brainstem nuclei, resulting in assoc symptoms (NV, photophobia, phonophobia)

Agonists of vascular and neuronal 5HT1 rece subtypes are known to result in vasoconstriction of meningeal blood vessels and inhibition of vasoactive neuropeptide release and pain signal transmission (reversal of migraine)

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14
Q

What is the pathophysiology of migraine wrt migraine phases?

A
  1. Prodrome phase
    - Hypothalamus and neuropeptide release implicated
    - Hypothalamus is the target for hypothalamic peptides and modulators
  2. Aura
    - Cotex triggers pain centres –> central sensitisation via cortical spreading depolarisation (large wave of slow spreading depolarisation within grey matter)
    - Cortex also involved w cognitive symptoms
  3. Headache
    - Sensitisation of central and peripheral trigeminal vascular sys
    - Release of neuropeptides
  4. Postdrome
    - Cervical vessels, midbrain & hypothalamus implicated
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15
Q

What are the signs and symptoms of migraine?

A

Pain location: Unilateral or bilateral
Pain quality: Throbbing, pulsating
Pain intensity: Moderate to severe
Effect on activities: Aggravated by or causes avoidance of routine activities of daily living
Time: 4-72h
Other: NV, photophobia, phonophobia, aura (visual[“light show”], sensory, speech disturbance)

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16
Q

Describe the epidemiology of migraine.

A

2nd most burdensome disease worldwide in terms of years lived w disability
Lifetime prevalence of migraine in SG = 9.3%
7.7% of ppl w migraine hv chronic migraine

17
Q

What are the signs & symptoms of migraine wrt the migraine phases?

A
  1. Prodrome
    - Fatugue
    - Food cravings
    - Nausea
    - Cognitive symptoms
    - Neck discomfort
    - Photo, phono, osmophobia
  2. Aura
    - xp by 20-30% of pts w migraine
    - Visual aura = “light display”
    - Sensory disturbance
    - Speech disturbance
    - Motor symptoms
  3. Headache (Ictal)
    - Mod-severe head pain
    - NV
    - Photo,phonophobia
    - Allodynia - scalp sensitivity, no cap, ponytail, glasses on nose bridge
    - Cranial autonomic symptoms
    - Cognitive symptoms
  4. Prodrome
    - NV
    - Photo, phonophobia
    - Fatigue
    - Cognitive symptoms
    - Neck discomfort
  5. Interictal
    - Cont to xp migraine symptoms in absence of headache
    - Cognitive symptoms
    - Fatigue
18
Q

What are the 5 phases of migraine?

A
  1. Prodrome (h-d before)
  2. Aura (5-60min)
  3. Headache [Ictal] (4-72h)
  4. Postdrome (<=12-24h)
  5. Interictal
19
Q

What are the ways we classify migraines?

A

W vs without aura
Episodic vs chronic

20
Q

What is the criteria to classify migraine without aura?

A

At least 5 attacks fulfilling below
- Headache lasting 4-72h (when untreated or unsuccessfully treated)
- Headache has at least two of the following charac:
a. Unilateral
b. Pulsating quality
c. Mod-severe intensity
d. Aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs)
- During headache at least one of the following
1. N and/or V
2. Photo AND phonophobia

Not better accounted for by another ICHD-3 diagnosis

21
Q

What is the criteria to classify migraine with aura?

A

At least 2 attacks fulfilling below
- At least one of the following fully reversible aura:
a. Visual
b. Sensory
c. Speech and/or lang
d. Motor
e. Brainstem
f. Retinal
- At least three of the following six:
1. Min 1 aura symptom that speads gradually over >=5min
2. 2 or more aura symptoms occur in succession
3. Each indi aura symptom lasts 5-60min
4. At least 1 aura symptom is unilateral
5. At least 1 aura symptom is positive
6. The aura is accompanied or followed within 60min by headache

Not better acc by another ICHD-3 diagnosis

22
Q

What is the classification criteria for epidsodic migraine?

A

In lifetime, >=5 migraine attacks lasting 4-72h

23
Q

What is the classification criteria for chronic migraine?

A

Over >3mo
1. >=15MHD = a day w migraine type OR TTH
AND
2. >=8MMD
- >=2 migriane characteristics (symptoms)
- If no aura, >=1 of the following migraine symptoms
a. Photo/phonophobia
b. N/V

24
Q

What are the non-pharmacological management strategies for migraine?

A

Neuromodulation
- FDA approved 4 devices that make use of feedback mech to tries to interface pain transmission process and stop it

Behavioural cognitive therapy
Biofeedback
Relaxation therapies

25
Q

What are the goals of treatment of acute migraine management?

A
  • Rapid & consistent freedom from pain & assoc symptoms, esp most bothersome symptom without recurrence
  • Restored ability to fn
  • Minimal need for repeat dosing or rescue medications
  • Optimal self-care and decrease subseq use of resources
  • Minimal or no ADR
  • Cost effective treatment
26
Q

What are the principles of pharmacological management in acute migraine?

A

Take acute treatment asap
- Assoc w sig beneficial resp within 2h from time of admin, confers sustained pain-free resp over 24h and decreased disability quickly during attacks

Stratified approach (guided by pain severity) is reco over step approach

Consider antiemetics for pts w severe NV

Choose appropriate formulations & dosage form
E.g. Nausea exacerbated w drinking water –> PO disintegrating tab
Severe NV, fullblown symptoms at start –> parenteral

27
Q

Describe the pharmacological management in acute migraines.

A

Migraine specific
- Established efficacy: Triptans, Ergotamine deriv, Gepants, Lasmiditan
- Probably effective: Ergotamine, other forms of dihydroergotamine

Non-migraine specific
- Established efficacy: NSAIDs (aspirin, ibuprofen, diclofenac, naproxen, celecoxib), combi analgesics (acetaminophen, aspirin, caffeine)
- Probably effective: NSAIDs (flurbiprofen, ketoprofen, IV & IM ketoprolac), IV Mg isometheptene-containg cmpds, antiemetics (chlorpromazine, prochlorperazine, promethazine, metoclopramide, droperidol)

28
Q

What are the criteria for preventative migraine treatment?

A

Varies bet AHS & EHF

AHS based on MHD & xtent of disability
Offer when MHD >=3 and severe
Consider when MHD >=2 and moderate

EHF more reco on offering prventative migraine treatment for any pt w migraine who is not well controlled w acute thera alone

29
Q

What are the goals of chronic migraine therapy?

A
  • Reduce attack freq, seveerity, duration and disability
  • Improve responsiveness to and avoid escalation in use of acute treatment
  • Improve fn & reduce disability
  • Reduce reliance on poorly tolerated, ineffective or unwanted acute treatment (also if acute is CI)
  • Reduce overall cost assoc w migraine treatment
  • Enable pts to manage their own disease to enhance a sense of personal control
  • Improve health related QoL
  • Reduce headache related distress and psychological symptoms
30
Q

What are the principles of pharmacological management in migriane prophylaxis?

A

Start low and titrate
- When partial but suboptimal resp/dose limiting ADR, combining preventative drugs from diff classes useful

Set initial target dose. Advise to stop titration if max dose is reached, when efficacy is optimal or when ADR intolerable

Give adequate trial (MIN 8 WEEKS) at target therapeutic dose before determining lack of effectiveness
- If no resp after at least 8 weeks, switch reco
- Injectable CGRP mAbs req at least 3mo treatment for those admi monthly, at least 6mo for quarterly treatments

Partial resp: cumulative benefits may occur over 6-12mo of continued use

Est realistic expectations
- Freq of MMH, MHD, attack duration, attack severity, migraine related disability, psuchological distress due to migraine

31
Q

Describe the pharmacological management in migraine prophylaxis.

A

Established efficacy:
PO
- Candesartan
- Divallroex Na (not avail in SG)
- Frovatriptan (also for menstrual migraine prophylaxis)
- BB: metoprolol, propranolol, timolol
- ASMs: Valproate Na, Topiaramate

Parenteral
- CGRP modulating mabs (e.g. erenumab)

Probably effective
PO
- TCA (e.g. amitriptyline) - routinely used in practice
- BB: Atenolol, Nadolol
- Lisinopril
- Memantine
- Venlafaxine

Pareneteral
- OnavotulinumtoxinA + CGRP mab

32
Q

What are the criteria for initiating CGRP modulating mabs in migraine prophylaxis?

A

Not meant to be first line
- Inabillity to tolerate due to S/E or inadequate resp to 8 week trial of dose established to be potentially effective of two or more of the other efficacious prophylaxis therapy
- Moderate disability (MIDAS >=11 or HIT >50)

33
Q

What are the criteria for continuing CGRP modulating mabs?

A

Reduction in mean MHDs or headach days of at least moderate severity of >=50% relative to pretreatment

Clinically meaningful improvement in any of the following migraine specific pt reported outcome measures
- MIDAS
When baseline 11-20 - Reduction of >=5 pts
When baseline >20 - Reduction of >=30%
- HIT-6
Reduction of >=5 pts

34
Q

Discuss the role of opioids in headache or migraine management.

A

Opioids incl codeine & tramadol, are not reco for routine use in migraine due to lack of evi of superiority to std drugs.

Risk of dependence/abuse

Unless tried everything else, in terror state (hospital couple of doses to get pt out of acute state, send home without)

35
Q

Describe the diagnostic criteria for medication overuse headache?

A

Headache on >/15d/mo in a pt w pre-existing headache disorder and dev as a conseq of
- Regular overuse of acute and/or symptomatic headache drugs for >3mo of
i. Ergotamines, >= 1 opioids, triptans or combi of analgesics on >=10d/mo
ii. Simple analgesics (paracetamol, acetylsalicylic acid, and >=1 NSAID) on >15d/mo for
iii. Any combi of above mentioned drugs or one or more med other than those mentioned avoce, taken for acute or symptomatic treatment of headache on >=10d/mo

Headache cannot be better accounted for by another ICHD-3 diagnosis

35
Q

What are the principles of management of medication overuse headache?

A

Detox phase
Add prophylactic treatment if needed