HEADACHE:

A PRACTICAL APPROACH
 OBJECTIVE
S
Be able to identify common types of Primary headache syndromes seen in primary
care:

Migraine

Cluster Headache

Muscle TensionHeadache

Avoid triggers contributing to medication overuse headache

Differentiate between treatment options for migraines, both acutely and as a preventative

Be aware of emerging therapies for migraines

PRIMARY HEADACHE SYNDROMES
 Migraine with or without aura

 Trigeminal neuralgia (autonomic cephalagia)

 Tension type headache

 Primary stabbing/coughing/exertional/sex related headache

 Thunderclap headache

 New daily persistent headache syndrome

 COMMON SECONDARY
HEADACHES
Medication Overuse Headache

Intracranial Bleeding (Subdural hematoma, Subarachnoid or intra

cerebral hge)

Low Pressure Syndromes (CSF leak)

High Pressure Syndromes (venous occlusion, mass, edema)

Infection (Meningitis, Encephalitis, Brain abcess)

Inflammatory (Temporal arteritis, other vasculitis, arthritis)

Acute Stroke or Blood & Nocturnal Hypoxia

Referred pain from other structure (orbit, temporomandibular joint, neck)

INTRODUCTION

NO pain receptors in the parenchyma [the brain tissue itself]

Pain receptors ARE present in:
Blood vessels
Meninges
Scalp
Skull
MEDICATION OVERUSE
HEADACHE
 MEDICATION OVERUSE
HEADACHE
Also known as Rebound Headache

Defined as:

Headache present on >15 days/month.

Regular overuse for >3 months of one or more drugs that can be taken for acute and/or symptomatic

treatment of headache.

Headache has developed or markedly worsened during medication overuse.

Ther Adv Drug Saf. 2014 Apr; 5(2): 87–99.

MEDICATION OVERUSE
HEADACHE

Can be precipitated by many agents:

NSAIDs
Acetaminophen
Aspirin
Caffeine
Triptans
Opioids
Butalbital
Ergotamines
 PATHOPHYSIOLOGY
Etiology is uncertain given multiple medication triggers

Present in patients predisposed to headache

Consideration given to chronic low serotonin, elevated CGRP and central sensitization

Ther Adv Drug Saf. 2014 Apr; 5(2): 87–99.

 MEDICATION OVERUSE
HEADACHE
Goal: withdrawal of offending agent

Baseline headache pattern can therefore be established

Achieved by one of three methods:

Abrupt withdrawal

Gradual wean

Steroid taper – data does not prove superiority

After successful wean, relapse is 20-40%

Limit future abortive use to no more than twice weekly in susceptible patients
MIGRAINE
 INTRODUCTION
Prevalence:
Women 25% (lifetime)
Men 8% (lifetime)
Highest from 25-50 years of age

Genetics
About 70% of migraineurs have a positive family history in a first-
degree relative
Unknown mode of transmission
STRANGE (SCARY) FACTS
Increased prevalence of:
MVP (Mitral Valve prolapse)
PFO (Patent foramen ovale)
HTN
Stroke
Epilepsy
Atopic allergies
Asthma
IBS
Depression
Bipolar disease
Anxiety disorders
Panic attacks
 MIGRAINE
The International Classification of Headache Disorders, 3rd edition

A. At least five attacks fulfilling criteria B–D

B. Headache attacks lasting 4–72 hours (when untreated or unsuccessfully treated)
C. Headache has at least two of the following four characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs)

D. During headache at least one of the following:

1. nausea and/or vomiting
2. photophobia and phonophobia

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

Cephalalgia 2018, Vol. 38(1) 1–211
MIGRAINE

Migraine without aura [common migraine]

Migraine with aura [classic migraine]
Pathophysiology

The neurovascular theory:

Pathophysiology

The neurovascular theory:

 STAGES OF MIGRAINE

Phases of a Migraine Attack

Pre-HA Headache Post-HA

Intensity

Premonitory/ Aura Mild Moderate to Postdrome

Severe HA
Prodrome

Time

Adapted from Cady RK. Clin Cornerstone. 1999;1(6):21-32.

PRODROME
Mood Changes
Irritability, depression, sleepy, apathy
Neurologic symptoms
Yawning, photo/phonophobia, vision
changes
Constitutional symptoms
Fatigue, pallor, fluid retention, myalgia
Alimentary symptoms
Hunger, anorexia, nausea, diarrhea
AURA

15% of patients
Episode of focal
neurologic changes
Develop over 5 to 15
minutes & last up to
60 minutes
Visual, weakness,
numbness, confusion
HEADACHE

Headache lasts hours to days

Migraine head pain unilateral in 56 – 68% of patients
90% of patients have coexisting nausea
Constitutional symptoms common
POSTDROME

Depression
Drowsiness
Cognitive changes
Memory loss
Difficulty with concentration
 TREATMENT PHILOSOPHY

If the pain can be stopped early, the cascade of pain

responses can be controlled
Headache needs to be caught before central sensitization
occurs
Patients may receive the greatest benefit from their migraine
medication if they:
Practice early intervention
Use a fast-acting migraine medication
 GENERAL TREATMENT
Avoid triggers!
Maintain regular sleep schedule
Maintain regular meal schedule
Low tyramine
Limit caffeine
Avoid nitrates/nitrites/MSG
Limit chocolate
Reduce stress
Adequate water intake
 TREATMENT OPTIONS
Two Treatment Approaches
• Acute therapy
Work quickly to relieve migraine pain and other symptoms
Are taken only at migraine onset
• Preventative therapy
Prevent or reduce the number of migraine attacks
Are taken on a daily basis
MIGRAINE ABORTIVES

NSAIDs
Triptans
Acetaminophen/Butalbital/Caffeine
OTC migraine preparations “Excedrin Migraine”
DHE
ACUTE TREATMENT

NSAIDS
Inhibit prostaglandin formation, thus reducing
inflammation
Naproxen
Ibuprofen
ASA
COX2 inhibitors
ACUTE TREATMENT
Triptans
Selective 5-HT1B/1D agonists
Block actions of 5-HT such as dilation of cranial arteries/AV anastomoses,
neurogenic dural plasma extravasation
Use early!
More effective in mild/moderate pain
Caution about rebound
ACUTE
TREATMENT
Triptans:
Almotriptan (Axert)
Eletriptan(Relpax)
Frovatriptan (Frova)
Naratriptan (Amerge)
Rizatriptan(Maxalt)
Sumatriptan(Imitrex)
Zolmitriptan(Zomig)
ACUTE
TREATMENT
Triptans side effects:
Chestpressure/heaviness
Jaw tightness
Dizziness
Somnolence
Fatigue
Nausea
Paresthesias
ACUTE
TREATMENT
Triptans
Relative contraindication:
Complicated migraine
CAD, CVD, PVD
Smoker + oral contraception
Severe HTN
ACUTE
TREATMENT
Ergotamine tartrate
Available for over 50 years
Vasoconstrictors
Oral, SL, IV, PR
Caution about rebound, dependence
Contraindicated:
CVD
CAD
PVD
Severe HTN
Sepsis
CKD
Hepatic disease
Pregnancy
ACUTE
TREATMENT
OTC agents
Cautious of rebound!

Opioids are NOT considered appropriate abortive agents except in cases

of last resort.
STATUS
MIGRAINOSUS
Migraine lasting greater than 72 hours in duration
Refractory to conventional treatment
Steroid burst – oral methylprednisolone, prednisone
“Headache cocktail”:
Ketorolac 60mg IM
Diphenhydramine 50mg IM
Prochlorperazine 10mgIM
Patient must have adriver
 PROPHYLACTIC
TREATMENT
Indicated in patients with:
>2 migraines permonth
Attacks lasting for several days per week
Severity/frequency that critically impacts patient’s daily life
Abortive therapies are contraindicated, ineffective, overused, not tolerated
Uncommon migraine type (hemiplegic, basilar, prolonged aura, migrainous infarction)
PROPHYLACTIC
TREATMENT
Start low and go slow!
Adequate trial with adequate dose
Consider comorbid conditions when choosing a medication
May add a second medication
REDUCE FREQUENCY

Seizure Medications
Topiramate, valproate, gabapentin, zonisamide
Blood Pressure Medications
Beta Blockers: propranalol, nadolol
Ca+ Channel Blockers: verapamil
Antidepressants
Tricyclics: amitriptyline, nortriptyline
Combos: venlafaxine
BOTULINUM
TOXIN
FDA approved for chronic migraine
Defined as headache present for 15 days per month or more
Administered every 12 weeks
OTHER TREATMENT
OPTIONS

Magnesium glycinate 400mg bid

Riboflavin 400mg daily
Melatonin
CoQ10
Butterbur/Feverfew/Skullcap
Acupuncture
Biofeedback/Yoga/Meditation
OTHER TREATMENT
OPTIONS
Vagus Nerve Stimulation
Spring TMS
Transcranial magneticstimulation
Cefaly
Tens-likeunit
EMERGING MIGRAINE
THERAPY
Primary Most
Sponsoring INN or Code Molecular Advanced
Company Name Format Target Phase Indications
Alder
ALD403/ Humanized Migraine
Biopharmace CGRP Phase 3
eptinezumab IgG1 prevention
uticals
Migraine and
Eli Lilly and LY2951742/ Humanized cluster
CGRP Phase 3
Company galcanezumab IgG4 headache
prevention
Teva
TEV‐48125/ Humanized Migraine
Pharmaceuti CGRP Phase 3
frestanezumab IgG2 prevention
cals

Amgen/Nova AMG334/ Human CGRP Migraine

Phase 3
rtis erenumab IgG2 receptor prevention

Clin Pharmacol Drug Dev. 2017 Nov-Dec; 6(6): 534–547.

TENSION-TYPE HEADACHE
 TENSION-TYPE HEADACHE:
DIAGNOSTIC
CRITERIA
At Least 10 Episodes Fulfilling the Criteria Below
Headache Description of Headache Associated Symptoms
lasting
30 minutes Two of the following: AND Both of the following:
to 7 days Pressing/tightening quality No nausea or vomiting
(nonpulsating)
Photophobia and
Mild or moderate intensity phonophobia are
(may inhibit, does not prohibit absent, or one but
activities) not the other
is present
Bilateral location

No aggravation by walking up
stairs or similar routine physical
activity

Olesen J. Cephalalgia. 1988;8(Suppl 7):1-96.

TREATMENT

Acute
NSAIDs
Acetaminophen
Muscle relaxers ?
Chronic
TCA
Physical Therapy
Occipital NerveBlock
CLUSTER
HEADACHE
CLUSTER HEADACHE: DIAGNOSTIC
CRITERIA
At Least 5 Attacks Fulfilling the Criteria Below
Frequency Description of Headache Associated Symptoms
of attacks: All of the Following:
1 every AND One of the Following
other day Severe Present on the Pain Side:
to 8 per
day Unilateral orbital, Conjunctival Miosis
supraorbital, and/or injection
Ptosis
temporal location Lacrimation
Eyelid edema
Lasts 15 to Rhinorrhea
180 minutes
(untreated) Nasal congestion

Forehead and facial sweating

Olesen J. Cephalalgia. 1988;8(Suppl 7):1-96.

CLUSTER
HEADACHE
Location: strictly unilateral, often periorbital or temporal

Pain characteristics: constant, severe, burning, or boring

Frequency: 1-6(+) per day

Demographics: Males : Females  6 : 1

Duration: 15-180 minutes

Associated symptoms: autonomic symptoms – (ipsilateral to pain)
tearing, rhinorrhea, conjunctival injection, eyelid edema, ptosis,
pupillary miosis, restlessness
CLUSTER HEADACHE

Triggers: ETOH, REM sleep, diurnal or annual cycles

Treatment:
Abortive: high-flow oxygen, DHE, triptans
Bridge therapy: steroids
Prophylactic: Verapamil, Divalproex Sodium, Topirimate, Lithium
 RED FLAGS OF SECONDARY
HEADACHE
Arousal from sleep or precipitated by valsalva

Fever, neck stiffness with limited ROM

Significant postural component

New focal deficit or seizure

Hx of head injury

New thunderclap headache (peak intensity w/in 5 minutes)

New headache in HIV, cancer, elderly, or pregnant patient

Papilledema

Temple tenderness, jaw claudication, or fever >50 yr

WHEN TO IMAGE A
HEADACHE?
If hx of migraine & no red flags, imaging is NOT warranted

If no hx of migraine but diagnostic criteria met & no red flags, imaging is NOT warranted

IF atypical headache, consider imaging case by case

If red flags, Consensus opinion:

MRI brain w/o gadolinium is more sensitive

CT head w/o contrast is more sensitive for acute blood

WORK UP IN SETTING OF RED FLAGS
“EVERY HEADACHE DOES NOT NEED EVERY
EVALUATION”
 Exertional headaches CTA or MRA

New deficit not consistent with aura MRI without contrast

Focal Tenderness in elderly +/- jaw claudication ESR or CRP

Obese w/ visual complaints dilated eye exam

Thunderclap headache CT

Fever, meningismus CT and lumbar puncture

High pressure features MRV or CTV

WHAT IF PATIENT DEMANDS
IMAGING?

CT imaging is very low yield in routine headache

cases
Counsel patients on risk of imaging and chance
of a distracting incidental finding
1 in 8100 risk of cancer for routine head CT in
women and 1 in 11,080 in men

Evans RW. Diagnostic testing for the evaluation of headaches. Neurol Clin.
1996;14;1-26.
 CASE REVIEW
28 yr obese female presents with 1 month of increasing headaches that
are frontal in nature with phonophobia and light sensitivity, often worse in
the morning.
She also reports vague transient visual obscurations throughout the day
with position change.
Upon questioning, she also has some pulsatile tinnitus. Your exam
reveals an obese female with a nonfocal exam.
Your aren’t confident in your funduscopic exam but you cannot see
spontaneous visual pulsations.
 WHAT FEATURES SUGGEST THIS IS NOT
MIGRAINE?

1. Visual obscurations with position change

40%

2. Exclusively Frontal Nature

9%

3. Absence of Spontaneous Venous Pulsations

9%
4. All of the Above
43%
 Answer: D All of the above

Diagnosis: Idiopathic Intracranial

Hypertension
IDIOPATHIC INTRACRANIAL
HYPERTENSION: INITIAL WORK
UP
Send for dilated eye exam if you cannot be
certain of papilledema
Urgent (within 48 hours) MRI/MRV of brain to
exclude mass or sinus thrombosis
Referral for LP for opening pressure and neuro
consult for definitive treatment
TRIGEMINAL AUTONOMIC
CEPHALGIAS: NOT YOUR MOTHER’S
MIGRAINE
Primary headaches w/ brief episodes of SEVERE unilateral
headaches w/ ipsilateral AUTONOMIC features
Within the group of TACs, difficult to distinguish
Distinction from MIGRAINE is important because
-TAC Headaches are disabling
-Treatment Strategies are different
-Misdiagnosis can be costly
 WHAT ARE THE TRIGEMINAL
AUTONOMIC CEPHALGIAS?
Highest Attack Lowest Attack
Frequency Freqency

Short lasting Paroxysmal Cluster Hemicrania

Neuralgiform Hemicrania Headaches Continua
Headache
(SUNCT/SUNA)
Shortest Duration Longest Duratio
CLINICAL FEATURES OF
TACS
Pain is knife like, boring, or stabbing
SEVERE to VERY SEVERE pain
Site is often temple or orbit
Duration of attacks are shorter than migraine on the
order of minutes (except HC)
Autonomic features are always present with attacks
Often episodic or clustering
AUTONOMIC FEATURES OF
TAC: REQUIRES > 1
IPSILATERAL
Conjunctival injection
Lacrimation
Nasal congestion or discharge
Miosis
Ptosis
HORNER’S
SYNDROME

http://www.reviewofophthalmology.com/content/d/oculoplastics/c/32801/
DO YOU NEED TO IMAGE THE
TACS?

YES!!! Non-urgent MRI brain w/o contrast. Lesions

in or around the pituitary can mimic TACs

Persistent INTER-ATTACK autonomic features

require CTA brain and neck emergently

TACs can mimic carotid dissection

ROLE OF PRIMARY
CARE

Recognize TAC
Order appropriate imaging (MRI for all, CTA for
persistent autonomic exam findings)
Initiate abortive and bridge therapies
Consult electronically or formally with neurology
 CASE
PRESENTATION:
A 44 yo man presents with right sided, knifelike, periorbital attacks waking him
from sleep.
He reports nasal congestion and watering of the right eye with the attacks. The
attacks peak quickly, are intolerable making him restless, and seem to relent
within 20-30 minutes.

He has had 5 attacks mostly nocturnally in 2 weeks but none prior. His
neurologic and general medical exam are normal, but on medication review you
can see he has a new prescription for Tadalafil in the last month.
 WHAT IS THE LIKELY
DIAGNOSIS?

1. Spontaneous Carotid Dissection

2. Hypothalamic Mass
3. Cluster Headache
4. Paroxysmal Hemicrania
ANSWER? CLUSTER
HEADACHE
Nocturnal attack predominance
Short duration (15-180 mins)
Autonomic features during attack
Male predominance 1:3
Alcohol, NTG, or PDE-5 inhibitors can triggers
WORK-UP: NEW CLUSTER
HEADACHE
Non-urgent MRI brain w/o gadolinium
EKG to screen for heart block for utilization of CCB
Consider consult electronically or formally with neurology
TREATMENT: CLUSTER
HEADACHE
Abortive: 1st Line: Trial of high flow 02 (10-15 L
via nonrebreather) prn onset of attack
2nd Line: Sumatriptan 4-6 mg SQ or
20 mg nasal spray up to bid
Bridge Therapy: Prednisone, 60-80 mg/day taper over 2-
4 weeks.
Preventive: Verapamil 240-480 mg/d divided in 3 doses,
short acting preferred, titrate slowly
 CASE PRESENTATION:
A 56 yr female presents with 4 months of steady, 3/10 side-locked headaches with
superimposed attacks of severe, stabbing temple pain 3- 4x week lasting 2-4 hours
without nausea,photophobia, phonophobia

During the severe attacks, she has a perception of a foreign body in her left eye and left
eyelid appears “droopy”.
She has tried rizatriptan and sumatriptan with minimal response and takes amitriptyline
50 mg qhs with no reduction in frequency after 8 weeks.

She does not use additional analgesics.

 WHAT IS THE LIKELY
DIAGNOSIS?

1. Giant cell Arteritis

2. Chronic Migraine
3. Hemicrania Continua
4. Medication overuse Headache
ANSWER? HEMICRANIA
CONTINUA
Often misdiagnosed as migraine
Side locked steady headache with
superimposed severe unilateral attacks
Autonomic features during severe attacks which
can last hours to days
Female predominance 2:1
Uniquely responsive to indomethacin
WORK-UP: NEW HEMICRANIA
CONTINUA

Non-urgent MRI brain w/o gadolinium

Serum creatinine for planned indomethacin use
Consider formal or electronic consult with
neurology
TREATMENT: OF HEMICRANIA
CONTINUA

Abortive: Indomethacin up to 300 mg daily

(often requires higher than FDA approved
maximum daily dose of 150 mg).

Preventives: topirimate, melatonin, occipital

nerve blocks and occipital nerve stimulators
 CASE
PRESENTATION

• 34yrfemale with pmhx of anxiety, insomnia and migraine

w/oaura presents with a 5 day history of her typical migraine to your
clinic.

• She is tearful and overwhelmed after trying home strategies of rizatriptan plus

ibuprofen for 3 doses over 2 days.

• She appears uncomfortable but has a nonfocal exam.
DIAGNOSIS? STATUS
MIGRAINOSUS
Description:
A debilitating migraine attack lasting for more than 72
hours.
Diagnostic criteria:
Features of Migraine without aura typical of previous
attacks except duration
Headache has both:
unremitting for >72 hours and severe intensity
Not attributed to another disorder
STATUS MIGRAINOSUS TREATMENT
PEARLS
In future, treat typical migraine attack quickly & early to
avoid central sensitization
Recurrence w/in 24 hours = effective therapy with TOO SHORT of
HALF LIFE! Change to LONG-ACTING triptan (frovatriptan) or repeat
second dose of initial medication (table 1-1)

Failed Response to Initial Appropriate therapy = Novel or

combination RESCUE Strategy needed
Consider using combination of lower risk therapies which
can be synergistic
IN-OFFICE RESCUE THERAPIES: INITIAL
STEPS
Step 1: Start an IV and hydrate
Step 2: Provide a dopamine receptor antagonist, IM or IV (risks of
akathisia, dystonia, and hypotension):
metoclopramide 10 mg IV
promethazine 12.5-25 mg IM or IV
prochlorperazine 10 mg IV
Step 3: Consider a repeat trial of DHE or triptan unless cardiac risks or
max dose already received
Sumatriptan 6 mg SQ or 20 mg intranasal
Dihydroergotamine 0.5-1 mg IV
 IN-OFFICE RESCUE TREATMENTS: STEP
4
Abortive Agent Dosing and route Risks/comments

Magnesium Sulfate 500-1000 mg IV Hypotension

30-60 mg IM or IV Gastritis
Ketorolac
400-1200 mg IV Risk of acute
Sodium Valproate hyperammonemia if on TPX

Risk of avascular necrosis, data

Methylprednisolone 100-200 mg IV mixed

4-16 mg IV Risk of avascular necrosis,

Dexamethasone evidence in HA >72 hours
 CASE
PRESENTATION
32 yr F with migraine since 16 yr, frequency 2-4x/month until 1 year ago
with now nearly 25 days of headache a month,15 of which are severe.

Often awakening her in the morning with her typical migraine features
(unilateral, nausea, photophobia) and other days having more mild diffuse
headache with allodynia.

She has used abortive combination of , aspirin, caffeine for 7 years and
currently uses 4-6 pills on bad days and 2 pills on good days with
intermittent use of ibuprofen 600 mg.
She is inconsistently taking propranolol 20 mg bid.

Her neurologic and general exam including fundi are entirely normal.
WHAT FACTORS HAVE INCREASED THE FREQUENCY OF HER
HEADACHE?

1. Type of Abortive compound used

2%

2. Frequency of use of abortive

15%

3. Pre-existing headache type

0%
4. All of the above
84
%
15
ANSWER?
ALL OF THE
ABOVE
DIAGNOSIS: MEDICATION
OVERUSE HEADACHE (MOH)
Headache > 15 days a month
Regular overuse of abortive treatments for > 3 months
Pattern has worsened during medication overuse
Headache improves within 2 months of removing
overuse
Preventives FAIL to reduce headaches
MOH APPROACH AND
TREATMENT
Withdraw Abortive (wean barbiturates and opioids, stop
triptans, NSAIDS, DHE, OTCs abruptly)
Treat Withdrawal Headache (steroid taper)

Amplify Preventive (use evidence base migraine

preventives)
Re-Introduce selective, infrequent (<2x/week) and
appropriate abortive
Encourage complimentary therapies and overall
reduction in triggers
A CHILD WITH PULSATILE HEADACHE AND
VOMITING
A 6 years and 10 months child, was admitted to vomiting and nonfebrile unilateral headache.
Neurologic examination had normal results. The episodes were preceded by a sensation of
sickness, and lasted about 5–10 minutes each. Pallor, poorly defined abnormal ocular
movements, and transitory unresponsiveness were also reported by his parents.
After the episode, the child asked to sleep.
Acetaminophen and ibuprofen were prescribed to Control symptoms. BUT NOT RESPONDE

Al episode observed during clinical examination: the child reported a sudden

feeling of sickness and a severe unilateral pulsatile headache, followed by nausea.
Left eyelid myoclonus followed, and the child described a short-lasting sensation of blindness.
Then his head turned toward the right and he became unresponsive for about 20 seconds.
Soon after, he vomited and became bradycardic (sinus rhythm, 35– 40 bpm).
Questions for consideration:

1. What is the differential diagnosis?

2. What features of the history help make certain entities more or less likely?

3. What testing would you obtain at this point to confirm the diagnosis?

4. What is the prognosis for this patient?

5. Would you prescribe a treatment, and, if yes, which one?

 D/D: INTRACRANIAL MASS (TUMOR, BLEED,
INFECTION) AND ENCEPHALITIS
Migraine (mainly basilar migraine), gastroenteritis, vagal syncope, cyclic vomiting

syndrome, intoxication, and partial seizures (occipital or temporal lobe epilepsy).

Vascular syndromes (Klippel-Trenaunay-Weber, arteriovenous malformations of the

brain), familial dysautonomia (e.g., Riley-Day syndrome), breath-holding spells of early

infancy progressing to isolated syncope, postural orthostatic tachycardia syndrome

(POTS), and metabolic diseases.

The diagnosis of autonomic seizures is suggested by the episodic

recurrence of unexplained vomiting or abdominal pain, migraine, or other

autonomic symptoms, with EEG showing focal OCCIPITAL seizure activity.

A 33-YEAR-OLD WOMAN WITH SEVERE POSTPARTUM
OCCIPITAL HEADACHES
A 33-year-old woman with history of occasional “migraines” complained of severe occipital headache,
following an uncomplicated full-term vaginal delivery under epidural anesthesia.

This headache was qualitatively and quantitatively different from her usual headaches.

The diagnosis of low intracranial pressure headache related to inadvertent dural puncture was considered
and 2 epidural autologous blood patches were performed with no relief.

One week postpartum she presented to US with complaints of poor concentration, difficulty in finding
words, getting dressed, and feeding herself, and left arm numbness.

Examination showed a blood pressure of 179/119 mm Hg, poor attention span, apraxia, and decreased
sensation in the left hand. General physical examination was unrevealing.
HEAD MRI (DAY 0) SHOWED FLUID-ATTENUATED
INVERSION RECOVERY (FLAIR)
hyperintensities and diffusion restriction with positive apparent diffusion coefficient
(ADC) map in the right parietal lobe and in the splenium of the corpus callosum.

The diagnosis of posterior reversible encephalopathy syndrome (PRES)

ON the third hospital day, she became cortically blind and mute, and had motor
perseverations and left-sided weakness.

Repeat head MRI showed marked worsening with lesions involving the cortex and
subcortical white matter of the parietal, posterior frontal, and occipital lobes, bilaterally.

Question for consideration:

1. What is the differential diagnosis?

The differential diagnosis of multifocal infarcts in the
distribution of many

vascular territories is wide.

Emboli from heart and aorta, disseminated intravascular coagulopathy,

thrombotic thrombocytopenic purpura, moyamoya disease, vasculitis, or

viral/bacterial/fungal infections and primary CNS angiitis.

Question for consideration:

1. What studies/tests should be performed??

RCVS
SUMMARY

Identify headache type

Implement acute vs chronic therapies
Avoid medication overuse