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stupid brain CA > headache/migraine > Flashcards

headache/migraine Flashcards

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1
Q

pathophysiology of headache

A
  • vasodilation of intracranial cerebrovascular blood vessel -> activation of perivascular trigeminal nerves -> release vasoactive neuropeptides -> promote neurogenic inflammation
  • central pain transmission activate other brainstem nuclei -> associated symptoms
  • hyperresponsiveness of brain
    ** inherited abnormality in Ca or Na channel & Na/K pumps that regulate cortical excitability through release of serotonin and other neurotransmitters
    ** increased levels of excitatory amino acids (glutamate), alteration in level of extracellular K affect migraine threshold
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2
Q

action of serotonin in terms of headache pathophysiology

A
  • agonist of vascular and neuronal 5-HT1 receptor subtype
  • cause vasoconstriction of meningeal blood vessels and inhibition of vasoactive neuropeptide release and pain signal transmission
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3
Q

ICHD-3 classifications of headaches

A

1) primary

  • migraine
  • tension type headache (TTH)
  • other primary HA disorders

2) Secondary

  • trauma/injury to head and/or neck
  • cranial/cervical vascular disorder
  • non-vascular intracranial disorder
  • infection
  • homeostasis disorder
  • HA/facial pain attributed to disorder of cranium, neck, eyes, ears, sinus, teeth, mouth, other facial/cervical structures
  • psychiatric disorder

3) neuropathies, facial pain, other headache

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4
Q

red flags for secondary headache (SNNOOP10)

A

1) systemic symptoms including fever
2) neoplasm in history
3) neurologic deficit/dysfunction
4) onset of headache sudden/abrupt
5) older age (>50)
6) pattern change/recent onset of headache
7) positional headache
8) precipitated by sneezing, coughing, exercise
9) papilledema
10) progressive headache with atypical presentation
11) pregnancy or puerperium
12) painful eye with autonomic features
13) post-traumatic onset of headache
14) pathology of immune system (HIV/immunocompromised)
15) painkiller overuse/new drug at onset of headache

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5
Q

primary headache - cluster headache

A
  • unilateral (around eye or along face)
  • variable pain quality
  • severe - very severe pain intensity
  • restlessness, agitation
  • cranial autonomic symptoms in same side of headache
    ** red, water, or swollen eye
    ** nasal congestion/runny nose, sweating
  • 15 - 180 mins
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6
Q

epidemiology of TTH

A
  • peak in 4th decade
  • female > male
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7
Q

classifications of TTH

A
  • infrequent: < 1 ep per month
  • frequent: 1 - 14 days per month
  • chronic: ≥ 15 days per month
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8
Q

TTH triggers

A

1) physical/emotional stress
2) activities that cause head to be held in one position for long time
3) alcohol, caffeine
4) cold/flu or sinus infection
5) dehydration, hunger

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9
Q

goal of TTH management

A

relief pain, prevent progression to chronic

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10
Q

TTH pharmacological

A

1) acute

  • paracetamol (+/- caffeine), aspirin
  • NSAID: ibuprofen, naproxen, diclofenac, ketoprofen

2) prophylactic

  • 1st line: amitriptyline
  • mirtazapine, venlafaxine
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11
Q

TTH nonpharmacological

A

1) chronic: cognitive behaviour therapy (CBT)
2) biofeedback, relaxation
3) physical +/- occupational therapy
4) lifestyle modification

  • sleep hygiene
  • stress management
  • mindful posture (prevent neck strain)
  • headache diary
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12
Q

tldr clinical phases of migraine

A

1) prodrome
2) aura
3) headache (ictal)
4) postdrome
5) interictal

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13
Q

prodrome of migraine

A

1) duration: ≤ 48 hrs
2) location

  • activation of hypothalamus & neuropeptides in homeostatic function

3) symptoms

  • fatigue, food craving, nausea, cognitive symptoms, neck discomfort, photophobia & phonophobia, mood change
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14
Q

aura of migraine

A

1) duration: 5 - 60 mins
2) pathophysiology

  • cortical spreading depression (CSD)
    ** initial wave of neuronal depolarisation within grey matter -> inhibit cortical activity -> change in synaptic activity, extracellular ion concentration, blood flow, metabolism
    ** activate trigeminovascular system -> aura symptoms

3) aura symptoms

  • visual aura: Scotoma, fortification spectrum
  • sensory disturbance
  • speech disturbance
  • motor symptoms
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15
Q

headache (ictal) of migraine - duration

A

4 -72hrs

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16
Q

headache (ictal) of migraine - pathophysiology

A

1) neuropeptides (CGRP)

  • implicated in head pain & other symptoms
  • neurogenic inflammation, peripheral and central sensitisation of trigeminovascular and other systems

2) sensitisation of central trigeminovascular system

  • primary nociceptors + central trigeminovascular neurons
  • altered sensory processing and brainstem structure -> severity of allodynia and hypersensitivity to pain in migraine

3) photophobia

  • retinal and trigeminal nociceptive input converge in thalamus and project to nociceptive areas of cortex -> exacerbate migraine headache by light
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17
Q

headache (ictal) of migraine - symptoms

A

1) head pain

  • unilateral or bilateral
  • moderate to severe
  • pulsating or throbbing
  • aggravated or causes avoidance of routine activities of daily living

2) photophobia, phonophobia, N/V, allodynia, neck discomfort, cranial autonomic symptoms, cognitive symptoms, fatigue

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18
Q

postdrome of migraine

A

1) duration: ≤ 48 hrs
2) symptoms: photophobia, phonophobia, nausea, fatigue, cognitive symptoms, neck discomfort, difficulty concentrating

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19
Q

interictal of migraine

A

1) pathophysiology

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

2) symptoms: photophobia, phonophobia, cognitive symptoms, fatigue

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20
Q

pathophysiology vs location of brain

A

1) cortex

  • CSD, altered connectivity
  • migraine aura and cognitive symptoms
  • target: neuromodulation

2) release of CGRP and PACAP

  • multiple potential sources/site of action
  • headache or other symptoms
  • target: small molecule antagonist & antibodies

3) thalamus

  • sensitisation and alteration of thalamo-cortical circuit
  • sensory sensitivity & allodynia
  • target: neuromodulation

4) hypothalamus

  • activation in premonitory phase
  • premonitory symptoms
  • target: hypothalamus peptides and modulators

5) upper cervical nerves

  • pain transmission/sensitisation
  • neck pain, head pain
  • target: local injection, neural modulation

6) trigemino-cervical complex

  • pain transmission or sensitisation
  • headache and neck pain
  • target: medication, neuromodulation
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21
Q

trigeminovascular system function

A

1) relay head pain signals to brain

  • periphery component
    ** trigeminal ganglion relay trigeminovascular nociceptive input from meningeal vessel and dura matter to CNS
  • CNS
    ** trigeminocervical complex receive peripheral trigeminovascular nociceptive pain signal from trigeminal ganglion -> relay to cortex via thalamus -> pain
    ** activate other central region -> non pain symptoms

2) repeated activation of trigeminovascular system over time = state of hypersensitivity and sustained pain

3) feedback from sensitised brain may

  • potentiate pain signalling
  • contribute to common migraine symptoms (photophobia, phonophobia, cutaneous/mechanical allodynia)
22
Q

ICHD-3 diagnostic criteria for episodic migraine without aura

A
  • at least 5 attacks fulfilling

1) headache attack last 4 - 72 hrs when untreated or unsuccessfully treated

2) headache has at least 2 of
** unilateral location
** pulsating quality
** moderate/severe pain
**aggravation by/causing avoidance of routine physical activity

3) at least one of: N/V, photophobia and phonophobia

4) not accounted for by another ICHD-3 diagnosis

23
Q

ICHD-3 diagnostic criteria for episodic migraine with aura

A
  • at least 2 attacks fulfilling

1) at least 1 fully reversible aura symptom
** visual, sensory, speech+/- language, motor, brainstem, retinal

2) at least 3 of
** at least 1 aura symptom spread gradually over ≥ 5 mins
** ≥ 2 aura symptoms occur in succession
** each symptoms last 5 - 60 mins
** at least 1 aura symptom unilateral
** at least 1 aura symptom positive
** aura accompanied/followed by headache within 60 mins

3) not accounted for by another ICHD-3 diagnosis

24
Q

ICHD-3 diagnosis for chronic migraine

A

1) > 3 months
2) ≥ 15MHD & ≥ 8 MMD

  • MHD: monthly headache day (migraine/TTH)
  • MMD: monthly migraine day
    ** aura: ≥ 2 migraine characteristics
    ** X aura: ≥ 1 migraine symptoms
25
Q

acute treatment for not severe migraine

A

analgesics

26
Q

type of analgesics used for not severe migraine

A

1) NSAID

  • indication: mild - moderate migraine attack
  • MOA: inhibit pg synthesis -> prevent neurogenically mediated inflammation in trigeminovascular system
  • AE: hypersensitivity, GI, CNS (somnolence, dizzy)
  • caution: previous ulcer disease, renal disease, severe CVS

2) paracetamol
3) aspirin

27
Q

type of migraine specific agents for severe migraine

A

1) sumatriptans
2) cafegort

28
Q

sumatriptan for severe migraine - indication

A

take early in course of attack when mild pain intensity

29
Q

sumatriptan for severe migraine - MOA

A

selective agonist at 5-HT1B and 5-HT1D receptor

  • vasoconstriction of intracranial extracerebral blood vessel
  • inhibit vasoactive peptide released by trigeminal neurons
  • inhibit nociception neurotranmission within triegeminocervical complex
30
Q

sumatriptan for severe migraine - PK

A
  • rapidly absorbed, low plasma protein binding
  • eliminated by oxidative metabolism mediated by MAO
31
Q

sumatriptan for severe migraine - caution

A

some pt experience recurrent migraine within 48 hrs after first triptan dose, require additional dose

32
Q

sumatriptan for severe migraine - SE

A
  • sensation of pressure in chest, nausea, distal paraesthesia, fatigue, dysgeusia, transient BP increase, flushing, sensation of cold/pressure/tightness
  • minor LFT disturbances
33
Q

sumatriptan for severe migraine - CI

A
  • pre-existing conditions

1) stroke/TIA
2) ischaemic coronary artery disease
3) coronary artery vasospasm
4) uncontrolled HTN
5) peripheral artery disease
6) gastrointestinal ischaemia
7) history of hemiplegic or basilar migraine

  • drugs

1) concomitant ergot derivatives within 24h
2) concomitant MAOi or within 2 wks of discontinuation

34
Q

cafergot - MOA

A

1) ergotamine

  • induce vasoconstriction through 5-HT1B or 5HT-1D on intracranial vessels
  • inhibit norepinephrine uptake and alpha-adrenoreceptor -> prolonged vasoconstriction

2) Caffeine

  • vasoconstrict cerebral vasculature through adenosine A2, A2A, A2B receptor agonist
  • may enhance GI absorption of ergotamine by increasing solubility of ergotamine and decrease gastric pH
35
Q

cafergot PK

A
  • rapidly absorbed, high plasma protein binding, low F
  • CYP3A4 metabolism, liver elimination
36
Q

cafergot AE

A

N/V, cramp, insomnia, transient lower limb muscle pain, ergotism (vascular ischaemia)

37
Q

cafergot CI

A
  • pre-existing condition

1) stroke/TIA
2) ischaemic coronary artery disease
3) coronary artery vasospasm
4) peripheral artery disease
5) GI ischaemia
6) history of hemiplegtic or basilar migraine

  • drugs

1) concomitant use of triptans within 24h
2) potent CYP3A4 inhibitor to prevent elevated exposure to ergot toxicity (vasospasm, tissue ischaemia)
3) vasoconstrictor agent

38
Q

indication for geptans/ditans

A

1) CI to or inability to tolerate triptans
2) adequate response to 2/> oral triptans due to either

  • validated acute treatment pt-reported outcome questionnaire
  • clinician attestation
39
Q

indication for preventive treatment of migraine

A

any of the AHS criteria

1) attack significantly interfere with daily life despite acute treatment
2) frequent attack (≥ 4 MHD)
3) CI to liver failure or overuse of acute treatment
4) AE w acute treatment
5) pt preference

40
Q

goal of preventive treatment for migraine

A

1) improve pt condition and QoL
2) reduce cost associated with migraine treatment
3) improve responsiveness to and avoid escalation of acute therapy

41
Q

general principles for preventive treatment of migraine

A

1) start low and titrate

  • until target response/max target dose/tolerability issue
  • if not enough then combine therapy

2) adequate trial

  • oral: min 8 wks at therapeutic dose
    ** if X response then switch
    ** if partial response then check cumulative benefit over 6 - 12 months
  • injectable
    ** inject monthly at least 3 months
    ** inject quarterly at least 6 months

3) realistic expecations

42
Q

choice of therapy for preventive treatment of migraine

A

erenumab (CGRP)

43
Q

pharmacological targets for erenumab

A

1) pain transmission
2) blood flow in cerebral blood vessels
3) neurogenic inflammation

44
Q

requirements for erenumab

A

≥ 18 yo + any of:

1) 4 - 7 migraine days and

  • inability to tolerate response to 8 wk trial of 2 prior treatment options
  • at least moderate disability

2) 8 - 14 MMD + inability to tolerate/inadequate response to 8 wk trial of 2 prior treatment class

3) chronic migraine + either
- inability to tolerate/inadequate response to 8 wk trial of oral of 2 prior treatment class
- inability to tolerate/inadequate response to min 2 quarterly injection of onabotulinumtoxin A

45
Q

criteria for continuation of erenumab

A

either

1) reduction in mean MHD/headache days of at least moderate severity by 50% relative to pre-treatment baseline
2) clinically meaningful improvement in

  • MIDAS
    ** baseline score 11 - 20 = reduction of ≥ 5 points
    ** baseline score > 20: reduction by ≥ 30%
  • MPFID or HIT-6
    ** reduction of ≥ 5 points
46
Q

MOA of erenumab

A

monoclonal antibody calcitonin gene-related peptide (CGRP) inhibitor

  • block CGRP receptor on smooth muscle cells = inhibit vasodilation of cerebral blood vessels, neuronal inflammation and pain transmission
47
Q

erenumab PK

A
  • subcu injection monthly
  • clinical benefit after 3 months
  • linear kinetics: receptor binding saturated
48
Q

AE for erenumab

A

1) GI: constipation, nausea
2) raynaud disease: affect blood flow to fingers and toes -> colour change
3) HTN, joint pain
4) maybe nasopharyngitis

49
Q

successful treatment parameters for migraine

A

1) 50% reduction in freq of days with headache/migraine
2) significant decrease in attack duration/severity (defined by pt)
3) improved response to acute treatment
4) reduction in migraine-related disability & improvement in functioning in impt areas of life
5) improvement in HRQoL & reduction in psychological distress due to migraine

50
Q

assessing treatment effectiveness of migraine

A
  • when to assess
    1) 3 months after initiating monthly treatment
    2) 6 months after starting quarterly treatment
  • how to assess
    ** headache diary to capture changes in attack freq/severity and meds use
51
Q

causes of medication overuse headache (MOH)

A

1) narcotics, barbiturate
2) short term pain relief -> rebound headache -> higher med dose -> repeat

52
Q

ICHD-3 criteria for MOH

A

1) headache occurring on ≥ 15 days per month on pt w pre-existing headache disorder
2) regular overuse for > 3 months of ≥ 1 drug that can be taken for acute +/- symptomatic treatment of headache w medication overused defined as

  • ≥ 10 days per month for ergot derivatives, triptan, opioid, combination analgesic, combination of drugs from different classes that are not individually overused
  • ≥ 15 days/month for nonopioid analgesics, acetaminophen, NSAID

3) not accounted for by another ICHD-3 diagnosis

stupid brain CA (5 decks)

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