Transcript MANAGAMENT OF MIGRAINE

Headaches
Dr. Mohammad Reza Najafi
Professor of Neurology
‫دکترمحمدرضانجفی‬
‫استاد مغزواعصاب‬
Introduction
Nearly everyone is subject to headache from time to time;
moreover, 40% of all people have severe headaches annually
The brain mechanism that generates headaches is
activated by many factors.
Genetic factors probably augment
the system, so that some people are susceptible to
more frequent or more severe head pain.
Headache is usually a benign symptom and only occasionally
is a manifestation of a serious illness, such as
brain tumor, aneurysmal rupture or giant cell arteritis.
The first issue to resolve in the care of a patient with
headache is to differentiate benign and more ominous
causes.
Painful state characteristics
1- Quality
2- Severity
3- Location
4- Duration
5- Time course
6- Intensity
7- Mode of onset
8- Time - intensity curve
9- Conditions that produce ,
exacerebation, relieve
10- personality of patients
IHS Classification of
Headache
Part I: The Primary Headaches
1. Migraine
 2. Tension-type headache
 3. Cluster headache and other trigeminal
autonomic cephalalgias
 4. Other primary headaches

Part II: The Secondary Headaches
5. Headache attributed to head and/or
neck trauma
 6. Headache attributed to cranial or
cervical vascular disorder
 7. Headache attributed to non-vascular
intracranial disorder
 8. Headache attributed to a substance or
its withdrawal
 9. Headache attributed to infection

10. Headache attributed to disorder of
homoeostasis
 11. Headache or facial pain attributed to
disorder of cranium, neck, eyes, ears,
nose, sinuses, teeth, mouth or other facial
or cranial structures
 12. Headache attributed to psychiatric
disorder

Part III: Cranial Neuralgias Central and
Primary Facial Pain and Other Headaches
13. Cranial neuralgias and central causes
of facial pain
 14. Other headache, cranial neuralgia,
central or primary facial pain

Tension-type headache (TTH)

Tension-type headache (TTH) represents one of the
most costly diseases because of its very high
prevalence.

TTH is the most common type of headache, and it
is classified as episodic (ETTH) or chronic (CTTH).

It had various ill-defined names in the past
including tension headache, stress headache, muscle
contraction headache, psychomyogenic headache,
ordinary headache, and psychogenic headache.
Episodic tension-type headache

At least 10 previous headaches fulfilling
the following criteria; number of days
with such headache fewer than 15 per
month

Headaches lasting from 30 minutes to 7
days
Characteristics of tension type
headache
At least 2 of the following pain characteristics:
Pressing/tightening (nonpulsating) quality
Mild or moderate intensity (may inhibit but does not prohibit activities)
Bilateral location
No aggravation from climbing stairs or similar routine physical activity
Both of the following: No nausea or vomiting
Photophobia and phonophobia absent or only one present
Secondary headache types not suggested or confirmed
Chronic tension-type headache
Average headache frequency of more than 15 days per month
for more than 6 months fulfilling the following criteria
At least 2 of the following pain characteristics:
Pressing/tightening (nonpulsating) quality
Mild or moderate intensity (may inhibit but does not prohibit
activities)
Bilateral location
No aggravation from climbing stairs or similar routine
physical activity
Both of the following: No vomiting
No more than one of the following: nausea, photophobia, or
phonophobia
Secondary headache types not suggested or confirmed
Pathophysiology of TTH



Pathogenesis of TTH is complex and
multifactorial, with contributions from both
central and peripheral factors.
In the past, various mechanisms including
vascular, muscular (ie, constant overcontraction
of scalp muscles), and psychogenic factors were
suggested.
The more likely cause of these headaches is
believed now to be abnormal neuronal
sensitivity and pain facilitation, not abnormal
muscle contraction.

Various evidence suggests that, like
migraine, TTH is associated with
exteroceptive suppression (ES2),
abnormal platelet serotonin, and
decreased cerebrospinal fluid betaendorphin.
Epidemiology
Frequency
Rasmussen et al reported a lifetime
prevalence of TTH of 69% in men and
88% in women in the Danish
population.[2] The patient may experience
more than one primary headache
syndrome.
Tension headache
Sex
Women are slightly more likely to be affected than
men.
The female-to-male ratio for TTH is approximately
1.4:1.
In CTTH, female preponderance is 1.9:1.
Age
TTH can occur at any age, but onset during
adolescence or young adulthood is common. It
can begin in childhood.
History
Tension-type headaches (TTHs) are
characterized by pain that is usually mild
or moderate in severity and bilateral in
distribution.
Unilateral pain may be experienced by 1020% of patients. Headache is a constant,
tight, pressing, or bandlike sensation in
the frontal, temporal, occipital, or parietal
area (with frontal and temporal regions
most common).
Physical
Patients with TTH have normal findings on
general and neurologic examinations.
Some patients may have tender spots or
taut bands in the pericranial or cervical
muscles (trigger points).
Causes
Various precipitating factors may cause TTH in
susceptible individuals. One half of patients with TTH
identify stress or hunger as a precipitating factor.
 Stress - Usually occurs in the afternoon after long
stressful work hours
 Sleep deprivation
 Uncomfortable stressful position and/or bad posture
 Irregular meal time (hunger)
 Eyestrain
Differential Diagnoses
Aseptic Meningitis
Lyme Disease
Migraine Headache
Migraine Variants
Pseudotumor Cerebri
Laboratory Studies
The diagnosis of tension-type headache
(TTH) is clinical.
As with the other primary headaches, no
specific diagnostic test is available for
TTH.
Occasionally, studies may be required to
exclude secondary headache disorders.
Imaging Studies
Neuroimaging studies are important to rule out
secondary causes of headache, including neoplasms
and cerebral hemorrhage.
MRI imaging shows the greatest detail of cerebral
structures and is especially useful in evaluating the
posterior fossa.
CT scan with contrast is a viable alternative but is
inferior to MRI for viewing structures in the
posterior fossa.
Neuroimaging is indicated if the headaches are
atypical in any way or if they are associated with
abnormalities in the neurologic examination.
Migraine Headache
Practice Essentials
Migraine is a complex disorder
characterized by recurrent episodes of
headache, most often unilateral and in
some cases associated with visual or
sensory symptoms—collectively known
as an aura—that arise most often before
the head pain but that may occur during
or afterward.
 Migraine is most common in women and
has a strong genetic component.

Signs and symptoms
Typical symptoms of migraine include the following:
 Throbbing or pulsatile headache, with moderate to severe
pain that intensifies with movement or physical activity
 Unilateral and localized pain in the frontotemporal and
ocular area, but the pain may be felt anywhere around the
head or neck
 Pain builds up over a period of 1-2 hours, progressing
posteriorly and becoming diffuse
 Headache lasts 4-72 hours
 Nausea (80%) and vomiting (50%), including anorexia and
food intolerance, and light-headedness
 Sensitivity to light and sound
Features of migraine aura are as
follows:
May precede or accompany the headache phase or
may occur in isolation
Usually develops over 5-20 minutes and lasts less
than 60 minutes
Most commonly visual but can be sensory, motor,
or any combination of these
Visual symptoms may be positive or negative
The most common positive visual phenomenon is
the scintillating scotoma, an arc or band of
absent vision with a shimmering or glittering
zigzag border
Physical findings during a migraine
headache may include the following:
Cranial/cervical muscle tenderness
Horner syndrome (ie, relative miosis with 1-2 mm
of ptosis on the same side as the headache)
Conjunctival injection
Tachycardia or bradycardia
Hypertension or hypotension
Hemisensory or hemiparetic neurologic deficits
(ie, complicated migraine)
Adie-type pupil (ie, poor light reactivity, with near
dissociation from light)
Diagnosis
The diagnosis of migraine is based on patient history.
 IHS diagnostic criteria are that patients must have
had at least 5 headache attacks that lasted 4-72
hours (untreated or unsuccessfully treated) and that
the headache must have had at least 2 of the
following characteristics :
Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by or causing avoidance of routine
physical activity (eg, walking or climbing stairs)
In addition, during the headache the
patient must have had at least 1 of the
following:
 Nausea and/or vomiting
 Photophobia and phonophobia
 Finally, these features must not have
been attributable to another disorder.

Classification of migraine









Migraine without aura (formerly, common migraine)
Probable migraine without aura
Migraine with aura (formerly, classic migraine)
Probable migraine with aura
Chronic migraine
Chronic migraine associated with analgesic overuse
Childhood periodic syndromes that may not be
precursors to or associated with migraine
Complications of migraine
Migrainous disorder not fulfilling above criteria
Migraine variants include the
following:
Childhood periodic syndromes
Late-life migrainous accompaniments
Basilar-type migraine
Hemiplegic migraine
Status migrainosus
Ophthalmoplegic migraine
Retinal migraine
migraine variant
A migraine variant may be suggested by focal
neurologic findings, such as the following, that
occur with the headache and persist temporarily
after the pain resolves:
Unilateral paralysis or weakness - Hemiplegic
migraine
Aphasia, syncope, and balance problems - Basilartype migraine
Third nerve palsy with ocular muscle paralysis and
ptosis, including or sparing the pupillary
response - Ophthalmoplegic migraine
Testing and imaging studies


Selection of laboratory and/or imaging studies to
rule out conditions other than migraine headache
is determined by the individual presentation (eg,
erythrocyte sedimentation rate and C-reactive
protein levels may be appropriate to exclude
temporal/giant cell arteritis).
Neuroimaging is not necessary in patients with a
history of recurrent migraine headaches and a
normal neurologic examination.
What is a Migraine Aura?
Migraine Triggers

Food

Disturbed sleep pattern

Hormonal changes

Drugs

Physical exertion

Visual stimuli

Auditory stimuli

Olfactory stimuli

Weather changes

Hunger

Psychological factors
Triggers: Changes in Daily Cycles
Triggers: Environment or Diet
Triggers: Mental
Migraine
Major Forms:
 Migraine without aura (common) 70%
 Migraine with aura (classical) 25%
 Migraine variants and complicated
migraine 5%
Phases of Acute Migraine

Prodrome

Aura

Headache

Postdrome
The Stages of a Migraine Attack
PRODROME


Vague premonitory symptoms that begin from
12 to 36 hours before the aura and headache
Symptoms include
 Yawning
 Excitation
 Depression
 Lethargy
 Craving or distaste for various foods
Duration – 15 to 20 min
AURA
Aura is a warning or signal before
onset of headache
Symptoms

Flashing of lights

Zig-zag lines

Difficulty in focussing
Duration : 15-30 min
HEADACHE


Headache is generally unilateral and is
associated with symptoms like:
 Anorexia
 Nausea
 Vomiting
 Photophobia
 Phonophobia
 Tinnitus
Duration is 4-72 hrs
POSTDROME (RESOLUTION PHASE)
Following headache, patient complains of

Fatigue

Depression

Severe exhaustion

Some patients feel unusually fresh
Duration: Few hours or up to 2 days
MIGRAINE: CLINICAL FEATURES
Migraine Without Aura
No aura or Prodrome
Migraine With Aura
Aura or prodrome is present
Unilateral throbbing headache Unilateral throbbing headache
may be accompanied by nausea and later becomes generalised
and vomiting
During headache, patient
complains of phonophobia and
photophobia
Patient complains of visual
disturbances and may have
mood variations
MIGRAINE - PATHOPHYSIOLOGY
VASCULAR THEORY
Intracerebral
blood vessel vasoconstriction – aura
Intracranial/Extracranial blood vessel vasodilation –
headache

SEROTONIN THEORY
Decreased

serotonin levels linked to migraine
Specific serotonin receptors found in blood vessels of brain
PRESENT UNDERSTANDING
Neurovascular process, in which neural events result in
activation of blood vessels, which in turn results in pain
and further nerve activation
NEUROVASCULAR PROCESS
Arterial
Activation
Release of
Neurotransmitter
Worsening of Pain
Cascade of events underlying
migraine
Pain / headache
Triggers
Brain excitability
Trigeminovascular
activation
Cascade of
neurochemical
events
NO
glutamate
5-HT
Lumen
Afferent firing via
trigeminal nerve
How Migraine Works
3
4
Changes in nerve cell
activity and blood flow
may result in visual
disturbance,
numbness or tingling,
and dizziness.
Chemicals in the brain
cause blood vessel
dilation and inflammation
of the surrounding tissue
5
2
The inflammation
irritates the trigeminal
nerve, resulting in
severe or throbbing pain
Electrical impulses
spread to other
regions of the brain.
1
Migraine originates deep
within the brain
Prognosis

Migraine is a chronic condition, but
prolonged remissions are common. One
study showed that among persons who
had migraine during childhood, 62%
were migraine free for more than 2 years
during puberty and as young adults but
that only 40% were still migraine free at
age 30 years.

The severity and frequency of migraine
attacks tend to diminish with increasing
age. After 15 years of suffering migraines,
approximately 30% of men and 40% of
women no longer have migraine attacks.
Cluster Headache



Cluster headache (CH), also known as histamine
headache, is a primary neurovascular primary
headache disorder, the pathophysiology and
etiology of which are not well understood.[1]
As the name suggests, CH involves a grouping of
headaches, usually over a period of several
weeks.
According to the diagnostic criteria developed by
the International Headache Society (IHS), CH has
the following characteristics

The patient experiences attacks of severe
or very severe, strictly unilateral pain
(orbital, supraorbital, or temporal pain)
that last 15-180 minutes and occur from
once every other day to 8 times a day

The attacks are associated with 1 or more
of the following (all ipsilateral):
conjunctival injection, lacrimation, nasal
congestion, rhinorrhea, forehead and
facial sweating, miosis, ptosis, or eyelid
edema
Cluster Headache Classification
CH may be usefully classified into 2 main
forms as follows:
Episodic CH, in which at least 2 cluster
phases lasting 7 days to 1 year are
separated by a cluster-free interval of 1
month or longer
Chronic CH, in which the clusters occur
more than once a year without remission
or the cluster-free interval is shorter than
1 month
Medication overuse headaches
Affects 1 in 50 adults
 Females:males 5:1
 First noted with phenacetin/ergotamine
 More common with aspirin/
NSAIDs/paracetamol/codeine/DF118
 Can take several weeks to resolve after
medication withdrawl
 Key feature-pre-emptive use of analgesia

Medication overuse headachescont.
Low doses daily carry larger risk than
higher doses weekly
 Esp common if using simple analgesia
more days than not per month
 Using triptans, codeine >10days per
month
 Worse on awakening in the morning
 Worse after physical exertion
