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
D. During headache 1 of the following: (2)
* 1. nausea and/or vomiting * 2. photophobia and phonophobia
26
Migraine Attack Phases (4)
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
27
Prodrome (3)
 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)
28
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)
30 5-60 visual disturbances such as flashing lights (scotoma) or a zigzag pattern (fortification spectra)
29
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
18 17-20
30
1.2.1 Migraine with typical aura (4)
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
1.2.1.2 Typical aura without headache (2)
A. Fulfils criteria for 1.2.1 Migraine with typical aura B. No headache accompanies or follows the aura within 60 min
32
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
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
Headache Phase Systemic Symptoms (11)
blurry vision nasal stuffiness anorexia hunger diarrhea abdominal cramps polyuria pallor  sensations of hot / cold  sweating  scalp tenderness
34
Headache Phase Affective Alterations Include: (7)
 impairment of concentration (common)  impairment of memory (less common)  depression  fatigue  anxiety  nervousness  irritability
35
Resolution Phase  pain ---  ... may occur  some migraine sufferers report --- following an attack while others report --- and ---
diminishes fatigue, irritability, listlessness, impairment of concentration, or mood change euphoria depression and malaise
36
Aggravating or Precipitating Factors for Headache
 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
Past Headache History  Ask patient about: (4)
 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
Social History (6)
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
Migraine Management (3)
Psychotherapy: Patient education, stress reduction and trigger avoidance Non-pharmacologic methods Pharmacologic methods
40
Pharmacologic methods (2)
Abort the migraine Prevent the migraine
41
Non-Pharmacologic Methods (Behavioral Modifications)  May Help: (8) Less likely to help: (2)
 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
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
sleep hygiene go to sleep and arise in the morning at the same time each day weekends last autonomic
43
Non-pharmacologic Methods  Psychotherapy: (4)
1. Relaxation training 2. Biofeedback 3. Hypnosis 4. Cognitive behavior therapy
44
Migraine Medications 1. Abortive medications: 2. Prophylactic medications:
treat Acute phase. preventive- recommended if headache frequency is 2 or more headaches per week.
45
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
abortive 20 both preventive and abortive
46
skipped Abortive migraine medications (9)
 Acetaminophen  Aspirin  Butalbital, caffeine & analgesics  Caffeine adjuvant  Isometheptene  Narcotics  NSAIDs  Ergotamine TRIPTANS:
47
skipped TRIPTANS:  5-HT 1B/1D Agonists: (6)
 Sumatriptan (Imitrex)  Zolmitriptan (Zomig)  Naratriptan (Amerge)  Rizatriptan (Maxalt)  Eletriptan (Relpax)
48
skipped Abortive Medications  Examples of Ergot derivatives (5)
 Cafergot suppositories / tablets  Wigraine suppositories / tablets  Ergostat sublingual tablets  Dihydroergotamine: DHE-45 SC and IV Migranal nasal spray
49
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
* Nausea, vomiting, paresthesias, muscle cramps, HTN and angina in sensitive individuals two
50
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
low toxicity and side effects  Generally safe when used infrequently  Potential for overuse
51
skipped Other treatments (5)
 Rimegepant (PO)  CGRP Receptor Antagonist  Both preventative and acute pain reilief  Take 75mg q 2 days  Lasmotodine
52
Abortive Medications: Triptans Sumatriptan (Imitrex) (3)
* 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
Naratriptan hydrochloride (Amerge) 5-6 hour half life (2)
* Slower onset of action * Longest half life (5-6 hours)
54
Triptans: Abortive Medications (3)
 Zolmitriptan (Zomig) (more rapid Tmax)  Rizatriptan (Maxalt) (more rapid Tmax)  Eletriptan (Relpax)
55
 Zolmitriptan (Zomig) (more rapid Tmax) (2)
 Fast onset of action and early efficacy  Available in tablet and nasal spray
56
 Rizatriptan (Maxalt) (more rapid Tmax) (2)
 Available in tablet and wafer oral disintegrating tablet  Fast onset of action and early efficacy
57
 Eletriptan (Relpax) (2)
 Onset of action is 1 hour  Half-life is 5 hours
58
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
nausea headache
59
Therapeutic effect: * Restores * Inhibits * Restores
vascular integrity neuropeptide release/inflammation central inhibition of pain pathway
60
Triptans (5-HT Serotonin Agonists)  Cause: (2)  Contraindications: (3)
 Cranial vasoconstriction  Coronary vasoconstriction  Coronary artery disease  Heart disease & uncontrolled hypertension  Stroke
61
skipped Preventive Migraine Medications Beta-blockers: (propranolol, andosol, atenolol) Calcium channel blockers: (verapamil) Antidepressants: Tricyclic SSRI MAOI (5)
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
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:
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
Calcium channel blockers * Act on --- receptors * Inhibit * Inhibit * Prevent --- of cerebral neurons
5-HT contraction of vascular smooth muscle prostaglandin formation hypoxia
64
Serotonin antagonists * Examples(two) * * Blocks the development of
* Methysergide (Sansert) * Periactin neurogenic inflammation
65
Divalproex (Depakote) (2)
* Inhibits firing of 5-HT neurons * Enhanced post-synaptic response to GABA (gamma-aminobutyric acid)
66
Topiramate (Topamax) Blocks * Does not affect * Causes
voltage-dependent sodium and calcium channels reuptake or binding of neurotransmitters weight loss
67
Gabapentin (Neurontin) (2)
* Structurally related to GABA but does not interact with GABA receptors * Identify and function remain to be elucidated
68
Preventive Migraine Medications INDICATIONS : (4)
* 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
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)
sensory inflammatory immunosuppression acute
70
Calcitonin Gene Related Peptide Antagonists Marketed Name AIMOVIG® EMGALITY® AJOVY® TBD Generic name Erenumab Galcanezum ab Fremanezu mab Eptinezumb †† Produced in yeast. provide ...
effective, differentiated therapy for acute migraine treatment and prevention of frequent episodic and chronic migraine
71
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
neurotoxin painful muscles muscle contractions 15 12
72
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:
Chronic Migraine Headache 32 3 no drug-drug interactions and no systemic side effects are risk of weakness at injection site
73