migraines Flashcards
Why should a general dentist care about headaches?
Because:
1. The same nerve pathway?
2. Being able to diagnose referred pain from
headaches will allow you to?
- The same nerve pathway (Trigeminal) is involved and may show up as a toothache,
gingival pain or facial pain in your patient. - 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)
Why should a general dentist care about headaches?
Because:
Headaches occur Most frequently when during the day?
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
Headaches can mimic acute dental disease
If located in?
what forms can mimic dental disease and cause tooth pain?
If located in the lower half of the face (V2-3)
Migraine, cluster headache, or paroxysmal hemicrania can mimic dental
disease and cause tooth pain
Dental Pain vs Headache?
1. Acute dental pain distribution?
2. Dental pain clinical characteristics:
sensation
location?
Generally provoked by ?
- Acute dental pain may spread unilaterally but (unlike headache) rarely crosses the midline of the face.
- Dental pain clinical characteristics:
Intense, throbbing
Poorly localized
Generally provoked by stimulation of the offending tooth (i.e. pressure, hot/cold)
Headache attributed to temporomandibular disorder (TMD)
Diagnostic Criteria:
A. Any headache fulfilling?
B. Clinical and/or imaging?
C.Evidence of causation demonstrated by ≥2 of:
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
Primary Headache Disorders
- Migraine
- Tension-type headache
- Trigeminal-autonomic cephalgias (TAC’s)
Cluster headache
Paroxysmal hemicrania
Hemicrania continua
SUNCT syndrome
Orofacial pains resembling presentations of primary headaches
5.1 Orofacial migraine:
5.1.1 Episodic orofacial migraine
5.1.2 Chronic orofacial migraine
Episodic orofacial migraine Diagnostic criteria:
A. At least ? attacks fulfilling criteria?
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. At least five attacks fulfilling criteria B–D
B. Facial and/or oral pain, without head pain, lasting 4–72 hours (untreated or
unsuccessfully treated)
C. Pain has at least two of the following four characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe intensity
4. aggravation by, or causing avoidance of, routine physical activity (e.g. walking or climbing stairs)
D. Pain is accompanied by one or both of the following:
1. nausea and/or vomiting
2. photophobia (light sensitivity) and phonophobia (noise sensitivity)
E. Not better accounted for by another ICOP or ICHD-3 diagnosis
Chronic orofacial migraine Diagnostic Criteria:
A. Facial and/or oral pain, without head pain, on ? days/month for >? months and fulfilling criteria?
B. Occurring in a patient who has had at least ? attacks fulfilling criteria ? for ?
C. On ? days/month for >? months, fulfilling either of the following:
1. criteria ? for ?
2. believed by the patient to be ? at onset and relieved by?
D. Not better accounted for by?
Comment: ?
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
are migraine unilateral or bilateral
either
Pain sensitive intracranial
structures
Include: the skin and blood vessels of the scalp; the
head and neck muscles; the venous sinuses; thea rteries 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
Impact of 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?
36 million Americans are estimated to have severe migraine headaches.
Migraine will affect 30% of women over a lifetime.
Annual lost productivity in the U.S. due to migraine costs over $ 1 billion per year
Migraines:
Severe type of headache that affects approximately % of the world
population or?
Gender Prevalence:
Episodes may occur when?
Severe type of headache that affects approximately 10% of the world population or 1 Billion
Gender Prevalence: 2-3F: 1M
Episodes may occur at any time of the day or night
onset of migraine in lifetime
Onset of migraine occurs in the first four life decades, then the frequency decreases. Childhood gender distribution is equal
sharp increase in females may be due to estrogen
migraines
Clinical Characteristics:
what occurs in 2/3 of the patients during or after the headache?
genetics role?
More than 50% of migraineurs have how many attacls per month?
Scalp tenderness occurs in 2/3 of the patients during or after the headache
A genetic factor or familial history is present in most migraineurs
More than 50% of migraineurs have less than two attacks per month
migraine Pathophysiology
Migraines & trigeminal autonomic cephalgias cause activation of? causing release of?
what gets activated? what is released? actions of this? found where?
what is believed to play a MAJOR role in migraine pathogenesis?
Migraines & trigeminal autonomic cephalgias cause activation of the
Trigeminovascular system causing release of inflammatory chemical
mediators in the brain known as neuropeptides.
The serotonin receptor (5-HT) gets activated. Serotonin acts as a
neurotransmitter in the CNS & is a potent vasoconstrictor. It is found in
the brain, platelets & intestine.
Calcitonin gene related peptide (CGRP) is believed to play a MAJOR role in
migraine pathogenesis
A small group of migraineurs transform into?
A small group of migraineurs transform into CHRONIC daily headache which is now classified as daily persistent migraine- Headaches occur ≥ 15 times per Month
previous classification of chronic daily migraines
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)
what can be an effective tx in daily migraines
Onabotulinum A is effective for treatment
of daily persistent migraines.
Family History of migraines>?
% 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
cluster headaches genetics?
% of tension-type headaches sufferers have family members with
similar headaches
50-60% of migraineurs have a parent with the disorder and up to 80% have
at least one first-degree relative with migraine
chromosome 19 is linked to migraines
cluster headaches rarely occur within the same family
40% of tension-type headaches sufferers have family members with
similar headaches
Migraine is Comorbid with:
Comorbidity of Migraine
Migraine is Comorbid with:
1. stroke
2. epilepsy
3. depression
4. anxiety disorders
In patients with migraine, anxiety disorders & major depression, the onset of anxiety generally precedes the onset of migraine, whereas the onset of major depression usually follows the onset of migrain
International Headache Society (IHS) Classification of Migraines
- Migraine with aura (Classic Migraine)
- Migraine without aura (Common Migraine)
* Many patients have both forms - EPISODIC MIGRAINE < 15 migraine days/month
- CHRONIC MIGRAINE >15 migraine days/month
Psychiatric Comorbidity of Migraine odds ratios:
Major depression
Manic episode
Anxiety disorder
Panic disorder
when can aura occur relative to migraine
Aura can precede, accompany, or follow the actual
headache attack
aura sex prevalence
Aura prevalence is: Male-female ratio of 1:2
Migraine without aura Diagnostic Criteria
A. At least 5 attacks fulfilling criteria?
B. Headache attacks lasting?
C. Headache has 2 of the following characteristics:
D. During headache 1 of the following:
E. Not better accounted for by?
Migraine Attack Phases
- Prodrome - occurs hours to days before the headache.
- Aura - immediately precedes or accompanies the headache.
- Headache
- Headache Resolution- may take days
Prodrome
Change in ?
Neurological ?
General ?
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)
Aura
Approximately % of migraine attacks are “with aura”.
Many patients have?
The aura consists of?
Most common symptoms are ?
Approximately 30% 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 5-60 minutes
Most common symptoms are visual disturbances such as flashing lights
(scotoma) or a zigzag pattern (fortification spectra)
Sensory Aura
Sensory Auras
? symptoms) - % prevalence
hyperkinetic?
speech? % prevalence?
motor symptoms (i.e. weakness or atonia) - 18% prevalence
hyperkinetic movement disorders (i.e. chorea)
speech abnormalities (i.e. aphasia- absence of language or dysarthria- poorly articulated speech) 17-20% prevalence
Migraine with typical aura diagnostic criteria
A. At least 2 attacks fulfilling?
B. what is present>?
C. 2 or more of the following 4 characteristics:
D. Not better accounted for by ?
typical aura without headache
A. Fulfils criteria for?
A. Fulfils criteria for 1.2.1 Migraine with typical aura
B. No headache accompanies or follows the aura within 60 min
Headache Phase
Location:
Pain:
what behavior is common?
GI signs?
lights?
Exercise will?
Location: may be bilateral (40%) or start on one side and become generalized
Pain: intensity varies ,however, average rating reported is 5/10 on Numeric Rating
Scale (0=no pain, 10=worst pain)
anorexia is common although food cravings may occur
nausea (90%), vomiting (33%)
photo/phonophobia cause patient to seek a dark, quiet room
Exercise will typically worsen migraine
Headache Phase
Systemic Symptoms
Headache Phase
Affective Alterations Include:
impairment of concentration (common)
impairment of memory (less common)
depression
fatigue
anxiety
nervousness
irritability
Resolution Phase
pain?
what may occur?
some migraine sufferers report what following attacks?
pain diminishes
fatigue, irritability, listlessness, impairment of concentration, or mood change may occur
some migraine sufferers report euphoria following an attack
while others report depression and malaise
Aggravating or Precipitating
Factors for Headache
Food Triggers for Migraines
Past Headache History
Ask patient about:
Previous ?
Non-pharmacological ?
Current?
Withdrawal or rebound?
Ask patient about:
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
Social History for migraines
1. Identify source of ?
2. Recent major ?
3. Job?
4. Exposure to ?
5. Habit ?
6. Sleep ?
- Identify source of stress
- Recent major life changes
- Job satisfaction
- Exposure to drugs/toxins in workplace
- Habit history (i.e. alcohol, tobacco, caffeine & recreational drugs)
- Sleep habits (i.e. keep bedtime and awakening time the same each day. Depression, anxiety, sleep apnea produces morning headaches)
Migraine Management flow chart
Non-Pharmacologic Methods (Behavioral Modifications) for migraine prevention
Non-pharmacologic Methods of migraine prevention: sleep
Non-pharmacologic Methods of migraine prevention: stress
Stress management
Decreases autonomic nervous
system responsiveness
psychotherapy for migraines
- Relaxation training
- Biofeedback
- Hypnosis
- Cognitive behavior therapy
Migraine Medications roles
- Abortive medications: treat Acute phase.
- Prophylactic medications: preventive- recommended if headache frequency is 2 or more headaches per week
Pharmacologic Methods
Migraines that occur less than twice a week are managed with?
Treatment is provided during the?
Migraines that occur more frequently should be managed with?
Migraines that occur less than twice a week are managed with abortive medications
Treatment is provided during the onset of the attack (within 20 minutes of onset for optimal outcome)
Migraines that occur more frequently should be managed with both preventive and abortive medications
Effective Migraine Treatment based on pain levels
Abortive migraine medications
Acetaminophen
Aspirin
Butalbital, caffeine & analgesics
Caffeine adjuvant
Isometheptene
Narcotics
NSAIDs
Ergotamine
TRIPTANS:
5-HT 1B/1D Agonists:
Sumatriptan (Imitrex)
Zolmitriptan (Zomig)
Naratriptan (Amerge)
Rizatriptan (Maxalt)
Eletriptan (Relpax)
Ergot derivatives:
indications?
what can be the action of these rx?
forms?
abortive medication
Abortive Medications
Examples of Ergot derivatives
Cafergot suppositories / tablets
Wigraine suppositories / tablets
Ergostat sublingual tablets
Dihydroergotamine: DHE-45 SC and IV
Migranal nasal spray
All ergotamine preparations
are capable of producing what ADEs
- Nausea, vomiting, paresthesias, muscle cramps, HTN and angina in sensitive individuals
ergot dependency
Frequent use of ergotamine tartrate–more than two days per week–
can result in ergot dependency
Abortive medications: Analgesics
In a small number of patients what can be useful?
When these medications are helpful they should be used because of?
safety?
Potential for ?
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
Other rx treatments for migraines
CGRP antag name? used for?
Rimegepant (PO): CGRP Receptor Antagonist
Both preventative and acute pain reilief
Take 75mg q 2 days
Lasmotodine
Abortive Medications:
Triptans
Zolmitriptan (Zomig)
onset/efficacy?
forms?
Fast onset of action and early efficacy
Available in tablet and nasal spray
Rizatriptan (Maxalt) (more rapid Tmax)
Available in?
onset/efficacy?
Rizatriptan (Maxalt) (more rapid Tmax)
Available in tablet and wafer oral
disintegrating tablet
Fast onset of action and early efficacy
Abortive Medications: Triptans
therapeutic effect?
- Restores vascular integrity
- Inhibits neuropeptide release/inflammation
- Restores central inhibition of pain pathway
triptans forms
many available and doses
triptans can also control what other effect of migraines?
Have particular beneficial influence in
controlling nausea as well as headache
For patients with early or significant nausea
or vomiting what route of admin should be considered
For patients with early or significant nausea
or vomiting select a non-oral route of
administration
Triptans
(5-HT Serotonin Agonists)
Cause what vasculature changes;
Cranial vasoconstriction
Coronary vasoconstrictio
triptans contraindications
Contraindications:
Coronary artery disease
Heart disease & uncontrolled hypertension
Stroke
Preventive Migraine
Medications
Preventive
Medications
Frequent migraine attacks are best
managed with ?
Provide antagonist activity at ?
Frequent migraine attacks are best managed with medications that, when taken regularly, decrease the likelihood of the next attack
Provide antagonist activity at the 5-HT2 and the 5-HT1c receptors
Beta adrenergic Blockers use for prevention
Beta blocker effect on ?
Act to?
Beta blocker effect on the 5-HT receptors
Act centrally to inhibit the central beta receptors and decrease the enhancing adrenergic pathway
Calcium channel blockers for prevention
* Act o?
* Inhibit?
* Inhibit formation of?
* Prevent ?
- Act on 5-HT receptors
- Inhibit contraction of vascular smooth muscle
- Inhibit prostaglandin formation
- Prevent hypoxia of cerebral neurons
Serotonin antagonists
* Examples
* Blocks development of?
- Methysergide (Sansert)
- Periactin
- Blocks the development of neurogenic inflammation
Divalproex (Depakote)
* Inhibits?
* Enhanced post-synaptic response to?
- Inhibits firing of 5-HT neurons
- Enhanced post-synaptic response to GABA
Topiramate (Topamax)
* Blocks>?
* Does not affect?
* Causes what additional effect?
- Blocks voltage-dependent sodium and calcium channels
- Does not affect reuptake or binding of neurotransmitters
- Causes weight loss
Gabapentin
Structurally related to?
* Identify and function?
Structurally related to GABA but does not interact
with GABA receptors
* Identify and function remain to be elucidated
Preventive Migraine Medications INDICATIONS :
- 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
Calcitonin Gene Related Peptide (CGRP)Receptor Inhibitors
CGRP is widely expressed in?
αCGRP is highly expressed in?
Inhibits?
form? do not cause?
use for migraineS?
is widely expressed in the peripheral and central nervous systems
αCGRP is highly expressed in sensory neurons
Inhibits inflammatory pathways
These Monclonal Antibodies Used for cancer treatment do Not cause immunosuppression
For prevention of acute migraine ONLY (prophylaxis)
Calcitonin Gene Related Peptide Antagonists
provide what for migraine tx?
provide effective, differentiated therapy for acute migraine treatment and prevention of frequent episodic and chronic migraine
injected once per month and used as prophylaxis
CGRP antagonist names
Ab’s (mab suffix)
Onabotulinum toxin type A
Potent?
mm effect?
Inhibits?
FDA treatment option for?
moa?
Potent neurotoxin
Weakens painful muscles
Inhibits muscle contractions
FDA treatment option for Chronic
Migraines >15 days/month
Interrupts pain cycle & may alter neurotransmitter secretory function in both afferent & efferent motor nerves
onabotulinum toxin duration
Therapeutic injections have an average
duration of 12 weeks before re-injection is
necessary
Onabotulinum A Toxin
1. Used for?
2. # Injection sites
3. how often?
4. Research has demonstrated effectiveness in?
5. Advantages:
6. Potential Side Effects:
Onabotulinum A Toxin
1. Used for Chronic Migraine Headache NOT responsive to medications
2. Injected at 32 sites
3. Repeated every 3 Months
4. Research has demonstrated effectiveness in treatment of
headaches and muscle pain
5. Advantages: no drug-drug interactions and no systemic side effects
6. Potential Side Effects: are risk of weakness at injection site
