Migraine Headache and Variants Flashcards

1
Q

Why should a general dentist care
about headaches?
Because:
(2)

A
  1. The same nerve pathway (Trigeminal) is
    involved and may show up as a toothache,
    gingival pain or facial pain in your patient.
  2. Being able to diagnose referred pain from
    headaches will allow you to refer your patient
    to the proper specialist AND AVOID
    UNNECCESARY DENTAL TX (i.e. RCTs,
    extractions, restorative)
    Migraine pathways
    Headaches occur Most
    frequently on arising in
    the morning therefore the
    DDS must differentiate if
    the head/facial pain is
    from migraine, bruxism or
    obstructive sleep apnea.
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2
Q

Dental Causes of Headache
(2)

A

 Dr. Graff-Radford was the first dentist to become a board member
for the American Headache Society. He became world-renowned in
the headache community, and he helped to change the perception
of dentistry in the medical community as it relates TMD.
 Steven was a trailblazer for dentists, expanding dental pain
management to treat the full spectrum of headaches, and
personally training many residents and dentists

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3
Q

Headaches can mimic acute dental disease
 If located in the
 (three) can mimic dental
disease and cause tooth pain

A

lower half of the face (V2-3)
Migraine, cluster headache, or paroxysmal hemicrania

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4
Q

Dental Pain vs Headache?
1. Acute dental pain may spread unilaterally but (unlike headache)
rarely crosses the midline of the face.
2. Dental pain clinical characteristics:
(3)

A

 Intense, throbbing
 Poorly localized
 Generally provoked by stimulation of the offending tooth (i.e. pressure,
hot/cold)

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5
Q

Headache attributed to
temporomandibular disorder (TMD)
Diagnostic Criteria:
(3)

A

A.Any headache fulfilling criterion C
B. Clinical and/or imaging reveals evidence of TMD
C.Evidence of causation demonstrated by ≥2 of:
1.headache has developed in temporal relation to onset of TMD
2.either or both of:
a) headache has significantly worsened in parallel with progression of
TMD;
b) headache has significantly improved or resolved in parallel with
improvement in or resolution of TMD
3. headache produced or exacerbated by active jaw
movements, passive movements through range of motion of
jaw and/or provocative maneuvers such as pressure on TMJ
and surrounding muscles of mastication
4. headache, when unilateral, is ipsilateral to TMD
D. Not better accounted for by another ICHD-3 diagnosis

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6
Q

Primary
Headache
Disorders
(3)

A
  1. Migraine
  2. Tension-type
    headache
  3. Trigeminal-autonomic
    cephalgias (TAC’s)
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7
Q
  1. Trigeminal-autonomic
    cephalgias (TAC’s)
    (4)
A

 Cluster headache
 Paroxysmal hemicrania
 Hemicrania continua
 SUNCT syndrome

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8
Q
  1. Orofacial pains resembling
    presentations of primary headaches
    (3)
A

 5.1 Orofacial migraine:
 5.1.1 Episodic orofacial migraine
 5.1.2 Chronic orofacial migraine

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9
Q

5.1.1 Episodic orofacial migraine
Diagnostic criteria:
A. At least five
attacks fulfilling
criteria B–D
B. Facial and/or oral
pain, without head
pain, lasting
– hours
(untreated or
unsuccessfully
treated)
C. Pain has at least
two of the following
four
characteristics:

D. Pain is
accompanied by one
or both of the
following:

E. Not better
accounted for by
another ICOP or
ICHD-3 diagnosis

A

4–72

  1. unilateral location 2. pulsating quality 3. moderate or
    severe intensity
  2. aggravation by, or
    causing avoidance
    of, routine
    physical activity
    (e.g. walking or
    climbing stairs)
  3. nausea and/or
    vomiting
  4. photophobia (light
    sensitivity)and
    phonophobia (noise
    sensitivity)
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10
Q

5.1.2 Chronic orofacial migraine
Diagnostic Criteria:

A

 A. Facial and/or oral pain, without head pain, on 15
 days/month for >3 months and fulfilling criteria B
 and C below
 B. Occurring in a patient who has had at least five
 attacks fulfilling criteria B–D for 5.1 Episodic orofacial
 migraine
 C. On 8 days/month for >3 months, fulfilling either
 of the following:
 1. criteria C and D for 5.1.1 Episodic orofacial
 migraine
 2. believed by the patient to be orofacial migraine at
 onset and relieved by a triptan or ergot derivative
 D. Not better accounted for by another ICOP or
 ICHD-3 diagnosis.
 Comment: A Pain Diary must be kept to track headache frequency

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11
Q

Pain sensitive
intracranial
structures
 Include:

A

the skin and blood
vessels of the scalp; the
head and neck muscles;
the venous sinuses; the
arteries of the meninges;
the larger cerebral
arteries; the pain-carrying
fibers of the fifth, ninth,
and tenth cranial nerves;
and parts of the dura
mater at the base of the
brain.
 The brain itself is
insensitive to pain

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12
Q

Impact of
Migraines
 American Migraine Foundation is
fundraising for research on
migraines
 – million Americans are estimated
to have severe migraine
headaches.
 Migraine will affect –% of women
over a lifetime.
 Annual lost productivity in the U.S.
due to migraine costs over $ 1
billion per year.

A

36
30

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13
Q

 Severe type of headache that affects
approximately –% of the world
population or 1 Billion
 Gender Prevalence:
 Episodes may occur at any time of the

A

10
2-3:1 W, M
day or night

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14
Q

Onset of migraine occurs in the first — life decades,
then the frequency decreases. — gender
distribution is equal.

A

four
Childhood

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15
Q

Introduction
 Clinical Characteristics
 Scalp tenderness occurs in – of the
patients during or after the headache
 A — factor or familial history
is present in most migraineurs
 More than –% of migraineurs have
less than two attacks per month.

A

2/3
genetic
50

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16
Q

Pathophysiology
 Migraines & trigeminal autonomic cephalgias cause activation of the
— system causing release of inflammatory chemical
mediators in the brain known as —.
 The — receptor (5-HT) gets activated. — acts as a
neurotransmitter in the CNS & is a potent —. It is found in
the brain, platelets & intestine.
— is believed to play a MAJOR role in
migraine pathogenesis

A

Trigeminovascular
neuropeptides
serotonin
vasoconstrictor
Calcitonin gene related peptide (CGRP)

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17
Q

Introduction
 A small group of migraineurs transform into CHRONIC
daily headache which is now classified as …
 (Previous classification was Medication
Overuse or Rebound Headache since use
of analgesics and migraine abortive
medications >2days/week can trigger
daily headaches in some individuals)
 — is effective for treatment
of daily persistent migraines.

A

daily
persistent migraine- Headaches occur ≥ 15 times per
Month
Onabotulinum A

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18
Q

Family History
Familial tendency:
 –% of migraineurs have a parent
with the disorder and up to –% have
at least one first-degree relative with
migraine
 chromosome – is linked to migraines
 – headaches rarely occur within
the same family
 —% of tension-type headaches
sufferers have family members with
similar headaches

A

50-60, 80
19
cluster
40

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19
Q

Comorbidity of Migraine
 Migraine is Comorbid with:
(4)

A
  1. stroke
  2. epilepsy
  3. depression
  4. anxiety disorders
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20
Q

 In patients with migraine, anxiety disorders & major
depression, the onset of — generally precedes
the onset of migraine, whereas the onset of major
— usually follows the onset of migraine

A

anxiety
depression

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21
Q

skipped
Psychiatric Comorbidity of
Migraine
Odds Ratio
 Major depression –
 Manic episode –
 Anxiety disorder –
 Panic disorder –

A

4.5
6.0
3.2
6.6

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22
Q

International Headache Society
(IHS) Classification of Migraine
(4)

A
  1. Migraine with aura (Classic Migraine)
  2. Migraine without aura (Common Migraine)
     Many patients have both forms
     Aura can precede, accompany, or follow the actual
    headache attack.
     Aura prevalence is: Male-female ratio of 1:2
     3. EPISODIC MIGRAINE < 15 migraine days/month
     4. CHRONIC MIGRAINE >15 migraine days/month
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23
Q

1.1 Migraine without aura
Diagnostic Criteria
(A-E)

A

A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hr (untreated or unsuccessfully
treated)
C. Headache has 2 of the following characteristics:
D. During headache 1 of the following:
E. Not better accounted for by another ICHD-3 diagnosis

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24
Q

C. Headache has 2 of the following characteristics:
(4)

A
    1. unilateral location
    1. pulsating quality
    1. moderate or severe pain intensity
    1. aggravation by or causing avoidance of routine physical activity (i.e., walking, climbing
      stairs)
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25
Q

D. During headache 1 of the following:
(2)

A
    1. nausea and/or vomiting
    1. photophobia and phonophobia
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26
Q

Migraine Attack
Phases
(4)

A
  1. Prodrome - occurs hours
    to days before the
    headache.
  2. Aura - immediately
    precedes or
    accompanies the
    headache.
  3. Headache
  4. Headache Resolution-
    may take days
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27
Q

Prodrome
(3)

A

 Change in mood or behavior (i.e. depressed,
hyperactive, euphoric, talkative, drowsy,
restless, or irritable).
 Neurological (i.e. sensitivity to light & noise,
difficulty concentrating, yawning,&
hypersomnia).
 General (i.e. stiff neck, food cravings, cold
feeling, anorexia, sluggish & thirsty)

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28
Q

Aura
 Approximately –% of migraine attacks
are “with aura”.
 Many patients have both forms
 The aura consists of gradually
spreading neurological symptoms that
usually precede the headache by –
minutes
 Most common symptoms are (2)

A

30
5-60
visual
disturbances such as flashing lights
(scotoma) or a zigzag pattern
(fortification spectra)

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29
Q

Sensory Auras
 motor symptoms (i.e. weakness or atonia) - –%
prevalence
 hyperkinetic movement disorders (i.e. chorea)
 speech abnormalities (i.e. aphasia- absence of language
or dysarthria- poorly articulated speech) –%
prevalence

A

18
17-20

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30
Q

1.2.1 Migraine with typical aura
(4)

A

A. At least 2 attacks fulfilling criteria B and C
B. Aura of visual, sensory and/or speech/language
symptoms, each fully reversible, but no motor,
brainstem or retinal symptoms
C. 2 of the following 4 characteristics:
1. 1 aura symptom spreads gradually over ≥5 min,
and/or 2 symptoms occur in succession
2. each individual aura symptom lasts 5-60 min
3. 1 aura symptom is unilateral
4. aura accompanied or followed by headache
in <60 min
D. Not better accounted for by another ICHD-3 diagnosis,
and TIA excluded

31
Q

1.2.1.2 Typical
aura
without headache
(2)

A

A. Fulfils criteria for 1.2.1
Migraine with typical aura
B. No headache accompanies
or follows the aura within
60 min

32
Q

Headache Phase
 Location:
 Pain:
 — is common although food cravings
may occur
 nausea (–%), vomiting (–%)
 — cause patient to seek a
dark, quiet room
 — will typically worsen migraine

A

may be bilateral (40%) or start on
one side and become generalized
intensity varies ,however, average
rating reported is 5/10 on Numeric Rating
Scale (0=no pain, 10=worst pain)
anorexia
90, 33
photo/phonophobia
Exercise

33
Q

Headache Phase
Systemic Symptoms
(11)

A

blurry vision
nasal stuffiness
anorexia
hunger
diarrhea
abdominal cramps
polyuria
pallor
 sensations of hot / cold
 sweating
 scalp tenderness

34
Q

Headache Phase
Affective Alterations Include:
(7)

A

 impairment of concentration (common)
 impairment of memory (less common)
 depression
 fatigue
 anxiety
 nervousness
 irritability

35
Q

Resolution
Phase
 pain —
 … may occur
 some migraine sufferers
report —
following an attack
while others report
— and —

A

diminishes
fatigue, irritability,
listlessness, impairment
of concentration, or
mood change
euphoria
depression and malaise

36
Q

Aggravating or Precipitating
Factors for Headache

A

 Menstruation or pregnancy due to
estrogen level changes
 Stress
 Alcohol (esp. red wine)
 Caffeine
 Smoking
 relaxation after stress
 fatigue
 inadequate or excessive sleep
 missing a meal
 weather change (i.e. high
humidity)
 high altitude
 perfumes or chemical fumes
 food triggers
 physical activity
 coughing
 exposure to glare or flickering
lights
 loud noise

37
Q

Past Headache History
 Ask patient about:
(4)

A

 Previous medications prescribed (dose
& length of time taken)
 Non-pharmacological therapies
(biofeedback, psychotherapy,
acupuncture & chiropractic)
 Current medications
 Withdrawal or rebound headache -
produced by excessive use of NSAIDS,
barbiturates, triptans, narcotics &
ergots. Limit usage to 2 days/week.

38
Q

Social History
(6)

A
  1. Identify source of stress
  2. Recent major life changes
  3. Job satisfaction
  4. Exposure to drugs/toxins in workplace
  5. Habit history (i.e. alcohol, tobacco, caffeine &
    recreational drugs)
  6. Sleep habits (i.e. keep bedtime and awakening
    time the same each day. Depression, anxiety,
    sleep apnea produces morning headaches)
39
Q

Migraine Management
(3)

A

Psychotherapy: Patient education, stress reduction and
trigger avoidance
Non-pharmacologic methods
Pharmacologic methods

40
Q

Pharmacologic methods
(2)

A

Abort the migraine
Prevent the migraine

41
Q

Non-Pharmacologic
Methods (Behavioral
Modifications)
 May Help:
(8)
Less likely to help:
(2)

A

 Regular sleep
 Regular exercise
 Regular meals
 Avoid chocolate
 Avoid tyramine/MSG
in foods
 Limit caffeine
 Eliminate alcohol
 Biofeedback/stress
management

Avoid milk products
Avoid citrus products

42
Q

Non-pharmacologic
Methods
 Encourage good —
 Patients should …
 Same schedule should be
maintained even on the
—.
 Migraine attacks frequently
begin in the — hour of sleep
when sleep has been
lengthened

 Stress management
 Decreases — nervous
system responsiveness

A

sleep hygiene
go to sleep and
arise in the morning at the same
time each day
weekends
last
autonomic

43
Q

Non-pharmacologic Methods
 Psychotherapy:
(4)

A
  1. Relaxation training
  2. Biofeedback
  3. Hypnosis
  4. Cognitive behavior therapy
44
Q

Migraine Medications
1. Abortive medications:
2. Prophylactic medications:

A

treat
Acute phase.

preventive- recommended if
headache frequency is 2 or more
headaches per week.

45
Q

Pharmacologic Methods
 Migraines that occur less than twice a
week are managed with —
medications
 Treatment is provided during the onset
of the attack (within – minutes of
onset for optimal outcome)
 Migraines that occur more frequently
should be managed with — medications

A

abortive
20
both preventive
and abortive

46
Q

skipped
Abortive migraine
medications
(9)

A

 Acetaminophen
 Aspirin
 Butalbital, caffeine & analgesics
 Caffeine adjuvant
 Isometheptene
 Narcotics
 NSAIDs
 Ergotamine
TRIPTANS:

47
Q

skipped
TRIPTANS:
 5-HT 1B/1D Agonists:
(6)

A

 Sumatriptan (Imitrex)
 Zolmitriptan (Zomig)
 Naratriptan (Amerge)
 Rizatriptan (Maxalt)
 Eletriptan (Relpax)

48
Q

skipped
Abortive Medications
 Examples of Ergot derivatives
(5)

A

 Cafergot suppositories / tablets
 Wigraine suppositories / tablets
 Ergostat sublingual tablets
 Dihydroergotamine: DHE-45 SC
and IV
Migranal nasal spray

49
Q

Abortive Medications
All ergotamine preparations
are capable of producing
(6)
Frequent use of
ergotamine tartrate–more
than — days per week–
can result in ergot dependency

A
  • Nausea, vomiting, paresthesias,
    muscle cramps, HTN and angina in
    sensitive individuals

two

50
Q

Abortive
Medications:
Analgesics
 In a small number of
patients analgesic
medications (i.e. aspirin,
acetaminophen, and
NSAIDs) can be useful in
aborting migraine
 When these medications
are helpful they should be
used because of their

A

low
toxicity and side effects
 Generally safe when used
infrequently
 Potential for overuse

51
Q

skipped
Other
treatments
(5)

A

 Rimegepant (PO)
 CGRP Receptor
Antagonist
 Both preventative and
acute pain reilief
 Take 75mg q 2 days
 Lasmotodine

52
Q

Abortive Medications:
Triptans
Sumatriptan (Imitrex)
(3)

A
  • Available in nasal spray, tablet and
    subcutaneous injection
  • Has the shortest half life
  • Response for recurrence of headache pain 12-
    24 hours after administration
53
Q

Naratriptan hydrochloride (Amerge)
5-6 hour half life
(2)

A
  • Slower onset of action
  • Longest half life (5-6 hours)
54
Q

Triptans: Abortive Medications
(3)

A

 Zolmitriptan (Zomig) (more rapid Tmax)
 Rizatriptan (Maxalt) (more rapid Tmax)
 Eletriptan (Relpax)

55
Q

 Zolmitriptan (Zomig) (more rapid Tmax)
(2)

A

 Fast onset of action and early efficacy
 Available in tablet and nasal spray

56
Q

 Rizatriptan (Maxalt) (more rapid Tmax)
(2)

A

 Available in tablet and wafer oral
disintegrating tablet
 Fast onset of action and early efficacy

57
Q

 Eletriptan (Relpax)
(2)

A

 Onset of action is 1 hour
 Half-life is 5 hours

58
Q

Abortive
Medications:
Triptans
Therapeutic effect:
Triptans- come in many different dosage
forms
Have particular beneficial influence in
controlling — as well as —
For patients with early or significant nausea
or vomiting select a non-oral route of
administration

A

nausea
headache

59
Q

Therapeutic effect:
* Restores
* Inhibits
* Restores

A

vascular integrity
neuropeptide release/inflammation
central inhibition of pain pathway

60
Q

Triptans
(5-HT Serotonin Agonists)
 Cause:
(2)
 Contraindications:
(3)

A

 Cranial vasoconstriction
 Coronary vasoconstriction

 Coronary artery disease
 Heart disease & uncontrolled
hypertension
 Stroke

61
Q

skipped
Preventive Migraine
Medications
Beta-blockers: (propranolol,
andosol, atenolol)
Calcium channel blockers:
(verapamil)
Antidepressants:
Tricyclic
SSRI
MAOI
(5)

A
  1. Serotonin antagonists:
    (methergine, methysergide)
  2. Anticonvulsants: (valproic
    acid, gabapentin,
    topiramate))
  3. CGRP Antagonists (Aimovig,
    Emgality) – injected 2x first
    month then monthly
  4. NSAIDs
62
Q

Preventive
Medications
 Frequent migraine attacks are best
managed with medications that, when
taken regularly, decrease the likelihood of
the …
 Provide antagonist activity at the — receptors
 Drugs effective for preventing migraine
attacks include:

A

next attack
5-HT2 and the 5-HT1c

 Beta adrenergic Blockers
 Beta blocker effect on the 5-HT
receptors
 Act centrally to inhibit the
central beta receptors and
decrease the enhancing
adrenergic pathways

63
Q

Calcium channel blockers
* Act on — receptors
* Inhibit
* Inhibit
* Prevent — of cerebral neurons

A

5-HT
contraction of vascular smooth
muscle
prostaglandin formation
hypoxia

64
Q

Serotonin antagonists
* Examples(two)
* * Blocks the development of

A
  • Methysergide (Sansert)
  • Periactin
    neurogenic
    inflammation
65
Q

Divalproex (Depakote)
(2)

A
  • Inhibits firing of 5-HT neurons
  • Enhanced post-synaptic response to
    GABA (gamma-aminobutyric acid)
66
Q

Topiramate (Topamax)
Blocks
* Does not affect
* Causes

A

voltage-dependent sodium and calcium
channels

reuptake or binding of
neurotransmitters
weight loss

67
Q

Gabapentin (Neurontin)
(2)

A
  • Structurally related to GABA but does not interact
    with GABA receptors
  • Identify and function remain to be elucidated
68
Q

Preventive
Migraine
Medications
INDICATIONS :
(4)

A
  • 2 or more attacks per
    month that produce
    disability > 3 days
  • Abortive medications
    not effective
  • Use of abortive
    medications > 2x/week
  • Special circumstances
    i.e. hemiplegic migraine
69
Q

Calcitonin Gene
Related Peptide
(CGRP)Receptor
Inhibitors
 is widely expressed in the
peripheral and central nervous
systems
 αCGRP is highly expressed in
— neurons
 Inhibits — pathways
 These Monclonal Antibodies Used
for cancer treatment do Not cause
—.
 For prevention of — migraine
ONLY (prophylaxis)

A

sensory
inflammatory
immunosuppression
acute

70
Q

Calcitonin Gene Related
Peptide Antagonists
Marketed
Name AIMOVIG® EMGALITY® AJOVY® TBD
Generic
name Erenumab Galcanezum
ab
Fremanezu
mab
Eptinezumb
†† Produced
in yeast.
provide …

A

effective, differentiated therapy for acute migraine
treatment and prevention of frequent episodic and chronic
migraine

71
Q

Onabotulinum toxin type A
 Potent —
 Weakens —
 Inhibits —
 FDA treatment option for Chronic
Migraines >– days/month
 Interrupts pain cycle & may alter
neurotransmitter secretory function in
both afferent & efferent motor nerves
 Therapeutic injections have an average
duration of – weeks before re-injection is
necessary

A

neurotoxin
painful muscles
muscle contractions
15
12

72
Q

Onabotulinum A Toxin
1. Used for — NOT responsive to medications
2. Injected at – sites
3. Repeated every – Months
4. Research has demonstrated effectiveness in treatment of
headaches and muscle pain
5. Advantages:
6. Potential Side Effects:

A

Chronic Migraine Headache
32
3
no drug-drug interactions and no systemic side effects
are risk of weakness at injection site

73
Q
A