Transcript Your Difficult Patient with Recurrent Spells Has Migraine

YOUR DIFFICULT PATIENT
WITH RECURRENT SPELLS
HAS MIGRAINE
David Lee Gordon, M.D., FAAN, FANA, FAHA
Professor and Chair
Department of Neurology
The University of Oklahoma Health Sciences Center
OU Neurology
DLG DISCLOSURES
FINANCIAL DISCLOSURE
I have nothing to disclose
UNLABELED/UNAPPROVED USES
DISCLOSURE
I have nothing to disclose
OU Neurology
MIGRAINE & RECURRENT SPELLS
LEARNING OBJECTIVES
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Relate a practical definition of migraine
Determine when the following symptoms are due to
migraine:
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Abdominal pain
Chest pain
Vertigo
Syncope
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Confusion
Hemiparesis
Aphasia
Headache
Name the three overarching considerations when
prescribing migraine therapy
Describe the appropriate abortive and prophylactic
therapies for migraine
OU Neurology
CASE 1: PRESENTATION
 58-year-old woman with history of pseudoseizures,
gastroparesis, and anxiety with noncardiac chest pain
 Admitted 18 times to 3 different hospitals in last 6
months with normal EEGs, video EEGs, cardiac
catheterizations, EGD, & colonoscopy
 One year of constant headache and lower abdominal
cramping pain and daily diarrhea for which she takes
daily Reglan & Lortab
 Now transferred from outside hospital for acute stroke
and found to have psychiatric aphasia on exam
OU Neurology
CASE 2: PRESENTATION
 28-year-old tearful woman with “pain all over,” unable to move L side
due to pain and with bilateral blurred vision
 Six weeks ago, had difficulty holding objects in L hand, then noted
“waves of pain” in both shoulders radiating over minutes into both
hands, L > R, followed by a lightning sensation into L thigh, radiating
into L toes
 Lyrica caused intolerable lethargy, Cymbalta ineffective after 1 month
 One month ago, symptoms became constant without relief from daily
Fentanyl patch, Tylenol, ibuprofen, Lortab, and Dilaudid
 Lost nursing job 3 weeks ago when she became bedbound with daily
vertigo and occipital headache radiating to R temple & eye
 For last week, severe R chest pain (R anterior axilla to upper back)
 For last few days, blurred vision in both eyes, initially intermittent,
then constant
 For one day, nausea and vomiting
OU Neurology
CASE 3: PRESENTATION
 80-year-old distraught man with intractable, intermittent,
12-hour episodes of vertigo, diplopia, ataxia, nausea,
and vomiting occurring every 5-6 days that left him
disabled and housebound
 MRI brain normal
 Symptoms became constant several months ago despite
taking daily Voltaren, Protonix, and Zofran
 Famous quaternary referral center #1 – no diagnosis
 Famous quaternary referral center #2 – progressive,
degenerative disease
 On exam, he had gait ataxia
OU Neurology
MIGRAINE: WHAT IT IS NOT
MIGRAINE DOES NOT MEAN HEADACHE
“Headache is never the sole symptom of
migraine, nor indeed is it a necessary
feature of migraine attacks.”
Oliver Sacks, Migraine, Revised & Expanded, 1992
A book intended for laypersons with multiple descriptions of
the varied symptoms (“phenomenology”) of migraine.
Heavy reading, but very informative.
Oliver Sacks also wrote the book Awakenings, later
turned into a movie in which Robin Williams played
the role of Oliver Sacks
OU Neurology
HEADACHE VS. MIGRAINE:
SYMPTOM VS. SYNDROME
Headache
Pain in the head
Migraine
A syndrome of episodic brain dysfunction with
systemic manifestations (that may include
headache)
Migraine is by far the most common cause of
recurrent, episodic headache without sequelae, but…
migraine with NO headache is also very common.
OU Neurology
MIGRAINE: WHAT IT IS
PRACTICAL DEFINITION & DESCRIPTION
Genetic condition in which a person has a
predisposition to suffering recurrent transient
episodes (attacks) of
brain dysfunction with
systemic manifestations that may include:
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headache/neck pain – from mild to severe, variable location
focal neurologic symptoms – mimics stroke/TIA
GI symptoms (upper or lower) – equals IBS, mimics gallstones
chest pain – mimics heart attack, equals atypical noncardiac CP
autonomic dysfunction – BP, pulse, sinus congestion, etc.
“triggered” by hormonal or environmental changes or
other medical conditions, and consisting of
4 possible phases (prodrome, aura, pain, postdrome).
OU Neurology
MIGRAINE TRIGGERS
 Hormonal changes
 Stress (esp. stress “letdown”), exercise, thyroid
 Estrogen (menarche, pregnancy, hormonal contraceptives, menopause)
 Environmental changes or exposures
 Weather (barometric pressure), motion
 Scents, smoke, fumes
 Sleep changes
 Deficiency or excess, change in shift
 Diet changes
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Hunger
Alcohol (all types, but esp. red wine)
Artificial foods (nitrates, MSG, sulfites, aspartame, sucralose)
Dehydration
 Medical conditions
 Head trauma, fever
 Cerebral blood flow changes (AVM, endarterectomy/angioplasty)
OU Neurology
MIGRAINE PHASES:
PRODROME/PREMONITORY*
1.
2.
3.
4.
Prodrome
Aura
Pain
Postdrome
 Mood changes
 Irritability, depression, euphoria/hyperactivity
 Difficulty concentrating
 Stiff neck
 Fatigue, malaise, yawning
 Autonomic/GI symptoms
*ICHD-3 suggests
elimination of the term
“prodrome” & substituting
“premonitory” instead
 constipation, diarrhea, urinary frequency
 Anorexia or food cravings
 esp. foods that increase serum serotonin and/or
magnesium, e.g., chocolate, bananas, nuts, peanut
butter, sweets, fatty foods
May begin hours to days before attack, persist through all 4 phases—
likely related to serotonin, magnesium, hypothalamic changes
OU Neurology
1.
2.
3.
4.
MIGRAINE PHASES:
AURA (1 of 2)
Prodrome
Aura
Pain
Postdrome
 Transient neurologic symptoms
 Due to cortical spreading excitation/depression
 Symptoms referable to location of transient chemical
changes in cerebral cortex
 Pattern of symptoms
 Recurrent & stereotypical (previous similar spells)
 Gradual onset
 Migratory (1 part of body to another) over mins to hrs
 Progressive (1 type of symptom to another)
 Duration minutes to hours
Chemical chain reaction in the brain leads to
focal symptoms that change during an attack
OU Neurology
MIGRAINE PHASES:
AURA (2 of 2)
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2.
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Prodrome
Aura
Pain
Postdrome
 Types of symptoms
 Visual—Usually “positive” (scintillation) followed by negative (scotoma)
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Shimmering, scintillating, flashing lights
Spots, dots, bubbles, lines (zigzag, wavy, heat off pavement)
Any color, but often silver, gray, or clear
Usually associated w/ motion, e.g., moving, vibrating, coalescing
Sensory—Usually “positive” (tingling) followed by negative (numbness)
Motor—Hemiparesis
Cognitive—Aphasia, confusion, amnesia, olfactory hallucinations
Brainstem—Vertigo, ataxia, diplopia, tinnitus, dysarthria,  LOC
Autonomic
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N/V, anorexia, dyspepsia, abdominal cramping, flatulence, diarrhea
Horner, sinus congestion/epistaxis, facial/scalp flushing (e.g., red ear)
Hypothermia, mild fever
Hypertension, hypotension, syncope, palpitations, arrhythmias
*Migraine causes HA & HTN, but HA, per se, does not cause HTN
OU Neurology
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MIGRAINE PHASES:
PAIN
Prodrome
Aura
Pain
Postdrome
 Headache characteristics—No specific pattern
 Location variable
 Unilateral, bilateral
 Anterior (frontal, periorbital, etc.), posterior (occipital, neck)
 Diffuse, focal (e.g., nummular = coin-shaped)
 Throbbing, pulsating, pounding, pressure, squeezing, dull, aching
 Severe, moderate, mild, absent
 Onset usually gradual; duration hours, days, weeks
 Associated symptoms
 Sensory phobias – photo, phono, kinesio, thermo, osmo
 Allodynia – pain due to light touch, breeze, hair moving, etc.
 “Lightheadedness” – vibratory or buzzing paresthesia in head
Trigeminal nerve (CN5) & cervical nerve root sensitization in the meninges
results in headache, sensory phobias, neuropathic symptoms
OU Neurology
MIGRAINE PHASES:
POSTDROME
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Prodrome
Aura
Pain
Postdrome
Fatigue, malaise
Difficulty concentrating
Mood changes
Muscle aches
Scalp tenderness
Food cravings or anorexia
The migraine hangover
OU Neurology
MIGRAINE PATHOPHYSIOLOGY
A JIGSAW PUZZLE WITH MISSING PIECES
Trigger
Hypothalamic dysfunction &
hyperexcitable cortex (esp. occiput)
Prodrome
Cortical spreading depression
(excitation/depression w/
hyperemia/oligemia esp. occiput)
Aura
Spreading depression in insula
or brainstem serotonergic &
noradrenergic dysfunction
Dysautonomia
CN V/cervical root sensitization with
pain receptor stimulation & release of
neuropeptides (e.g., CGRP)
Headache/
Arterial changes/
Sensory phobias
Platelet & serum serotonin levels decrease during attacks of
migraine, tension headache, IBS, & PMS.
Cerebral serotonin & magnesium decrease during a migraine attack.
OU Neurology
MIGRAINE WITH AURA:
MRI BRAIN FINDINGS
 Deep-white matter “UBOs”
common in migraine w/ aura
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White on T2 & FLAIR
Located at gray-white junction
Small, round, indistinct borders
Often confused with:
 Multiple sclerosis plaques
 Strokes (“small-vessel disease,”
“arteritis,” “vasculitis”)
 Significance & cause unknown
 Further evaluation not necessary
 Reassure patient
Kruit MC et al. JAMA 2004;291:427
“Unidentified Bright Objects”
(UBOs) of migraine seen
on FLAIR MRI
OU Neurology
MIGRAINE WITHOUT AURA
“OFFICIAL” DEFINITION PER ICHD-3
 Frequency
 > 5 episodes
 Duration
 4-72 h untreated
 HA quality (> 2)
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Unilateral
Pulsating
Moderate or severe
 w/ physical activity
 Associated features (> 1)
 Nausea &/or vomiting
 Photo- & phonophobia
 No other cause of sxs
“The diagnostic difficulty most often
encountered among primary headache
disorders is to discriminate between
tension-type headache and mild
migraine without aura.”
Cephalalgia 2013;33(9):629-808
The ICHD-3 migraine criteria are useful for scientific studies, but are
too restrictive & impractical for daily use & were written from
perspective of physicians with focus on headache.
ICHD-3 = International Classification of Headache Disorders, 3rd ed.
OU Neurology
MIGRAINE WITH AURA
“OFFICIAL” DEFINITION PER ICHD-3
“Recurrent attacks, usually lasting minutes, of unilateral fully
reversible visual, sensory, or other central nervous system symptoms
that usually develop gradually and are usually followed by headache
and associated migraine symptoms.”
 Frequency: > 2 attacks
 Aura: > 1 of the following
fully reversible aura sxs
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visual
sensory
speech &/or language
motor
brainstem
retinal
 Characteristics: > 2 of 4 following
 > 1 aura sx spreads gradually over > 5
min &/or > 2 sxs occur in succession
 each individual aura sx lasts 5-60 min
(though motor sxs may last 72 h &
“persistent aura without infarction” may
last > 1 wk)
 > 1 aura sx is unilateral (incl. aphasia)
 aura accompanied, or followed w/in 60
min, by HA
 No other cause of sxs
Cephalalgia 2013;33(9):629-808
OU Neurology
MIGRAINE WITH AURA
TYPES PER ICHD-3
 Migraine w/ typical aura
 Visual
 Sensory
 Migraine w/ brainstem aura
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Dysarthria
Vertigo
Tinnitus
Hypacusis
Diplopia
Ataxia
 level of consciousness
 Hemiplegic migraine (HM)
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Familial HM type 1 (CACNA1A)
Familial HM type 2 (ATP1A2)
Familial HM type 3 (SCN1A)
Familial HM other loci
Sporadic hemiplegic migraine
 Retinal migraine (monocular)
OU Neurology
MIGRAINE WITH “TYPICAL” AURA
DESCRIPTIONS PER ICHD-3
 Migraine w/ visual aura
 Most common (> 90%) aura
 Fortification spectrum –
zigzag figure that may
gradually spread & assume
laterally convex shape w/
angulated scintillating edge,
leaving absolute or relative
scotoma in its wake
 Scotoma without positive
phenomenon may occur
 Migraine w/ sensory aura
 2nd most frequent aura
 Pins & needles moving
slowly from point of origin
affecting 1 side of body,
face, &/or tongue
 Numbness may occur in its
wake
 Numbness may also be the
only symptom
OU Neurology
MIGRAINE GLASSES MAKE THE
DIAGNOSIS MORE CLEAR
Symptoms that seemed vague and psychiatric are clearly
due to migraine when seen through the proper lenses
MIGRAINE
Diagnosis without
migraine understanding—
things don’t make sense,
therefore patient is “crazy”
MIGRAINE
Diagnosis with
migraine understanding—
a pattern emerges
OU Neurology
MIGRAINE IS A DISTINCT SYNDROME OF
BOTHERSOME, BUT “BENIGN” SPELLS
 Lifelong (childhood through adulthood) history of
multiple different types of similar “spells”
 Main symptom headache, GI upset, chest pain, visual
symptoms, tingling, vertigo, confusion, etc.
 Associated with mood changes, food cravings, sensory
phobias
 Triggered by stress letdown, weather changes, estrogen
changes, dehydration, hunger, etc.
 Normal tests
 Complete resolution between spells—though taking daily
analgesic, triptan, decongestant, or muscle relaxant makes
symptoms constant
 Family history of spells similar to those suffered by pt
But obtaining accurate past & family histories is challenging
OU Neurology
WHY MIGRAINE IS REALLY, REALLY
COMMON, BUT NOBODY KNOWS IT
 “Regular” / “ordinary” headaches are migraines
 Tension headaches are migraines
 Frequent co-occurrence in patients and similar epidemiology,
clinical features, & treatment responses
 Actually migraines triggered by stress letdown
 Sinus headaches are migraines
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Respond to migraine prophylactic agents
Respond acutely to triptans (migraine abortive agents)
Do not respond to antibiotics
Sinus artery dilatation occurs in migraine
 Not all migraine attacks include headache
 Aura without headache (visual, sensory, vertigo, etc.)
 Abdominal migraine (= irritable bowel syndrome)
 Precordial migraine (= noncardiac atypical chest pain)
OU Neurology
CONDITIONS LIKELY DUE TO
(OR RELATED TO) MIGRAINE
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Tension-type headache
Sinus headache
Regular/ordinary headache
Cervicogenic headache
Premenstrual syndrome
Irritable bowel syndrome
Functional dyspepsia
Infantile colic
Motion sickness
Chronic pelvic pain
Recurrent vertigo/Meniere
 Panic attacks
 Atypical noncardiac chest pain
 Intermittent headache w/
transient hypertension
 Transient global amnesia
 Episodic confusion
 POTS (postural orthostatic
tachycardia syndrome)
 Syncope of unknown cause
 Postconcussion/posttraumatic
headache
 Stroke-like spells (TIA mimic)
These conditions cause temporary symptoms that are said to be
of unknown cause, but which may be explained by migraine
OU Neurology
NOT DIAGNOSING MIGRAINE LEADS TO
WASTED DOLLARS & LIVES
 Imaging studies (CT, MRI, endoscopy, colonoscopy, etc.)
 Medications
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Antibiotics (bacterial resistance)
Decongestants (chronic nasal congestion, HTN, chronic symptoms)
Anxiolytics, antidepressants (social consequences of false diagnosis)
Antithrombotic agents (hemorrhage)
Narcotics (chronic symptoms, drug-seeking behavior caused by docs)
 Surgeries
 Gallbladder
 Uterus and ovaries
 Sinus and ear
 Disability, retirement, divorce
OU Neurology
WHY DON’T MORE DOCTORS KNOW
ABOUT MIGRAINE?
 Migraine training is often inadequate
 Physicians have limited time to spend with patients
 Diagnosis is based on history; with limited time, history is cursory and
important details are missed
 Exam & tests are normal, leading to assumption of psychiatric illness
 Physicians have limited confidence beyond their specialty
 Neurologists deal with headaches
 GI doctors deal with stomach and intestine symptoms
 Ob-Gyn doctors deal with woman issues
 ORL / ENT doctors deal with ear, nose, sinus symptoms
 Cardiologists deal with cardiac causes of chest pain
 Pain specialists deal with peripheral (not CNS) pain
OU Neurology
MIGRAINE THERAPY:
THE TWO KINDS
Prophylactic and Abortive Agents
 Prophylactic agents (preventers)
 If a patient takes certain medications every day, s/he
is likely to have less frequent and less severe
migraines
 Abortive agents (stoppers)
 If a patient takes certain medications as soon as
possible at the start of a migraine attack, s/he may
either stop the attack or make it less severe
OU Neurology
MIGRAINE THERAPY: THE 3
OVERARCHING CONSIDERATIONS
 Avoid medication-overuse syndrome
 Limit use of all combined abortive agents to < 2 d/wk
(except prescription naproxen)
 Use prophylactic therapy to enable patient to use
abortive therapy < 2 d/wk
 Kill 2 birds with 1 stone
 Choose prophylactic agent(s) that treat other
conditions pertinent to the patient
 Aim to prevent ALL migraine symptoms—not
just headache
OU Neurology
MEDICATION-OVERUSE SYNDROME/
ANALGESIC REBOUND HEADACHE
Near-daily use of certain drugs—esp. migraine abortive
agents—causes migraine symptoms to be constant
 Caused by:
 Analgesic, triptan, decongestant, muscle relaxant use > 2
days/week
 Any analgesic (over-the-counter to narcotic) other than
prescription naproxen
Note: ondansetron & PPIs may also trigger migraine
 Relationship to migraine:
 More common in migraineurs
 Changes migraine symptoms from intermittent to chronic (incl.
headache, GI, chest pain, tingling, vertigo, etc.)
 Common cause of chronic migraine & status migrainosus
 Renders all migraine therapies ineffective
OU Neurology
MIGRAINE PROPHYLACTIC THERAPY:
GENERAL PRINCIPLES
 Kill 2 birds with 1 stone
 No agent initially developed for migraine; when choosing
an agent, address concurrent conditions (e.g.,
hypertension, depression, anxiety, patient weight,
seizures, osteoarthritis, insomnia, stool consistency)
 Different patients respond differently to different drugs
 Each agent/dose change takes > 4 wk to take full effect
 Start low, go slow
 Start one med, low-dose
  q2-4 wks to maximize efficacy vs. toxicity, but do NOT
make automatic increases
 May eventually need more than one med
OU Neurology
MIGRAINE PROPHYLACTIC THERAPY:
TOP CHOICES BY MECHANISM
There is no “class effect”—a patient may respond well to a drug
after not responding to a different drug in the same category
 Antihypertensive agents
 candesartan (Atacand)
 lisinopril (Prinivil, Zestril)
 nadolol (Corgard)
 propranolol (Inderal)
 Antiepileptic drugs
 topiramate (Topamax)
 divalproex (Depakote)
 Tricyclic antidepressants
 nortriptyline (Pamelor)
 amitriptyline (Elavil)
 Serotonin-norepinephrine
reuptake inhibitor (SNRI)
 venlafaxine ER
 Over the counter
 magnesium oxide
 vitamin B2 (riboflavin)
 melatonin
 NSAID
 naproxen (Naprosyn)*
OU Neurology
MIGRAINE PROPHYLACTIC THERAPY:
SIDE EFFECTS
Side effects that may influence agent choice
All antihypertensives
hypotension
Beta blockers
depression, sedation, asthma
Tricyclic antidepressants
weight gain, sedation, constipation
Divalproex
weight gain, hair loss, polycystic ovaries
Topiramate
weight loss, abnl cognition, nephrolithiasis
Naproxen
ulcers, renal disease
Magnesium
loose stools
OU Neurology
MIGRAINE PROPHYLACTIC THERAPY:
TOP CHOICES BY AGE
 Children & Young Adults
 topiramate
 nortriptyline / amitriptyline
 nadolol / propranolol
 Older Adults
 candesartan (Atacand) / lisinopril
 nortriptyline / amitriptyline
 divalproex (Depakote)
 venlafaxine (Effexor)
 All Ages—primary or adjunct
 naproxen  peri-predictable triggers / other pain
 magnesium oxide  constipation
 melatonin  insomnia
OU Neurology
MIGRAINE ABORTIVE THERAPY:
GENERAL PRINCIPLES
 Triptans—migraine-specific serotonin agonists—are most effective
(bind to subsets of serotonin 1 receptor—1D & 1B)
 Triptans may cause vasospasm; safety uncertain if:
 Migraine associated w/ aphasia, hemiplegia, or vertigo
 Vascular disease or risk factors (including hypercoagulability)
 Patient < 12 or > 65 years of age
 Analgesics may also be effective as abortive therapy
 Narcotics are generally NOT indicated for headache—limit their use to
pregnant women and those with vascular disease, esp. the elderly
 Take all abortive therapy early, e.g., triptan efficacy 2/3 when HA mild,
1/3 when HA moderate
 Take analgesics and triptans < 2 d/wk to avoid medication-overuse
headaches
OU Neurology
MIGRAINE ABORTIVE THERAPY:
SEROTONIN (5-HT) AGONISTS
TRIPTANS
ERGOTS
Selective 5-HT1D/1B agonists
Nonselective 5-HT1D agonists
Fast onset/Short half-life
 eletriptan (Relpax)
 rizatriptan (Maxalt & Maxalt MLT)
 zolmitriptan (Zomig & Zomig ZMT)
 almotriptan (Axert)
 sumatriptan (Imitrex PO, PN ,SC)
 Cafergot (PO, PR)
 DHE
Slow onset/Long half-life
 frovatriptan (Frova)
 naratriptan (Amerge)
 sumatriptan/naproxen sodium
(Treximet)
 DHE-45 IV, IM
 Migranal PN
TRIPTAN + NSAID
In most cases, start with the highest recommended triptan dose,
e.g., sumatriptan 100 mg, eletriptan 40 mg, rizatriptan 10 mg.
Take as early as possible at onset; may repeat x 1 after 2 h;
do not exceed 2 tabs / 24 h; do not exceed 2 d / week.
OU Neurology
MIGRAINE ABORTIVE THERAPY:
NON-NARCOTIC ANALGESICS
While all these agents can be effective when used as early as
possible at migraine onset, they all cause medication-overuse
syndrome if used > 2 days per week
 Nonspecific single-agent analgesics
 Aspirin, acetaminophen (Tylenol), NSAIDs
 Nonspecific combination analgesics
 Excedrin Migraine (acetaminophen, aspirin, caffeine)
 BC Powder (acetaminophen, aspirin, caffeine)
 Goody’s Headache Powder (aspirin, salicylamide, caffeine)
 Midrin, Amidrine, Duradrin, Epidrin (acetaminophen,
dichloralphenazone, isometheptene)
 Fiorinal (aspirin, butalbital, caffeine)
 Fioricet, Esgic (acetaminophen, butalbital, caffeine)
OU Neurology
MIGRAINE ABORTIVE THERAPY:
PARENTERAL AGENTS IN HOSPITAL/ED
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These IV agents
Normal saline – 1 L IV bolus
are preferable to
Magnesium sulfate – 1 g IV
oral, IV, or
transdermal
Valproic acid (Depacon) – 500 mg IV
analgesics for ED
Prochlorperazine (Compazine) – 10 mg IV & hospitalized
patients with
Metoclopramide (Reglan) – 10 mg IV
headache
Chlorpromazine (Thorazine) – 25 mg IV
Dihydroergotamine (DHE) – 0.5-1.0 mg IV or IM
These agents may be repeated q8h PRN.
Note there are many options for migraine abortive therapy in the ED or
inpatient setting that are not analgesics—and narcotics, per se, are
RARELY necessary
Avoid reflexively giving PRN Tylenol or narcotics!
OU Neurology
CASE 1: PRESENTATION
 58-year-old woman with history of pseudoseizures,
gastroparesis, and anxiety with noncardiac chest pain
 Admitted 18 times to 3 different hospitals in last 6
months with normal EEGs, video EEGs, cardiac
catheterizations, EGD, & colonoscopy
 One year of constant headache and lower abdominal
cramping pain and daily diarrhea for which she takes
daily Reglan & Lortab
 Now transferred from outside hospital for acute stroke
and found to have psychiatric aphasia on exam
OU Neurology
CASE 1: CLARIFICATION & OUTCOME
 Clarification of “pseudoseizure” episodes:
 First lightheadedness, then loss of consciousness and tone
 Rapid awakening with vertigo, nausea, vomiting, headache, confusion
 Final diagnoses:
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Syncopal migraine
Migraine with vertigo aura
Abdominal migraine
Precordial migraine
Medication overuse syndrome
Functional overlay (aphasia)
The patient does
NOT have
pseudoseizures,
gastroparesis, or
anxiety-induced
chest pain.
 Outcome:
 On topiramate, all symptoms markedly improved & the patient went to
the ED only four times in the next four years
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CASE 2: PRESENTATION
 28-year-old tearful woman with “pain all over,” unable to move L side
due to pain and with bilateral blurred vision
 Six weeks ago, had difficulty holding objects in L hand, then noted
“waves of pain” in both shoulders radiating over minutes into both
hands, L > R, followed by a lightning sensation into L thigh, radiating
into L toes
 Lyrica caused intolerable lethargy, Cymbalta ineffective after 1 month
 One month ago, symptoms became constant without relief from daily
Fentanyl patch, Tylenol, ibuprofen, Lortab, and Dilaudid
 Lost nursing job 3 weeks ago when she became bedbound with daily
vertigo and occipital headache radiating to R temple & eye
 For last week, severe R chest pain (R anterior axilla to upper back)
 For last few days, blurred vision in both eyes, initially intermittent, then
constant
 For one day, nausea and vomiting
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CASE 2: CLARIFICATION & OUTCOME
 Blurred vision = whitish-tan wavy lines or “heat-off-the-pavement”
throughout her vision in both eyes
 Since early childhood
 Intermittent headaches, bioccipital, radiating to right temple and eye with
nausea, vomiting, sensory phobias, photopsia (star bursts), tingling (head,
neck, both hands), & vertigo (saw multiple doctors for vertigo)
 For the last few years, episodes of intermittent severe R abdominal pain
with bloating, nausea, vomiting, and diarrhea occurring daily for a week,
followed by constipation for a few days, then recurrent abdominal pain;
no gallstones; cholecystectomy did not help
 Diagnoses: Status migrainosus due to medication overuse syndrome,
migraine with aura (visual, sensory, vertigo), abdominal migraine,
precordial migraine, depression with anxiety
 Management: All analgesics discontinued except prescription naproxen;
topiramate & venlafaxine begun; 3 weeks later, patient markedly
improved, started new RN job, &, after 3 days promoted to manager
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CASE 3: PRESENTATION
 80-year-old distraught man with intractable, intermittent,
12-hour episodes of vertigo, diplopia, ataxia, nausea,
and vomiting occurring every 5-6 days that left him
disabled and housebound
 MRI brain normal
 Symptoms became constant several months ago despite
taking daily Voltaren, Protonix, and Zofran
 Famous quaternary referral center #1 – no diagnosis
 Famous quaternary referral center #2 – progressive,
degenerative disease
 On exam, he had gait ataxia
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CASE 3: FAMILY HX & OUTCOME
 His sister has similar episodes
 With candesartan and magnesium oxide,
symptoms markedly improved—over next 6
months, patient had no vertigo, diplopia, nausea,
or vomiting; he had persistent, mild, 1-hour
episodes of gait ataxia upon awakening two
days a week that resolved by late morning and
did not interfere with his activities of daily living
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OTHER CASES
 The 2 women (ages 60 & 20) with intractable nausea,
vomiting, abdominal pain, & diarrhea on TPN, Fentanyl
patch, & oral narcotics
 The 65 yo woman with daily HA x 50 years
 The 50 yo woman with retinal infarction & daily diarrhea
 The 4 yo boy with post-social debilitating GI pain
 The 63 yo tearful woman with schizophrenia, diabetes
mellitus type II, hypertension, obesity, & past history of
TIAs; now with acute aphasia & left hemiparesis for
which she received IV tPA
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MIGRAINE & RECURRENT SPELLS
LEARNING OBJECTIVES


Relate a practical definition of migraine
Determine when the following symptoms are due to
migraine:
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Abdominal pain
Chest pain
Vertigo
Syncope

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Confusion
Hemiparesis
Aphasia
Headache
Name the three overarching considerations when
prescribing migraine therapy
Describe the appropriate abortive and prophylactic
therapies for migraine
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THE END
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