Migraine and other headaches

BY:- Lulu Abebe

 Topic Learning outcome
At the end of this topic students will able to :-
1. Discuss the pathomechanisms of headache
2. Identify RED FLAGS of secondary head aches/Organic
headache – headaches associated with medical conditions
 Hypertension
 Brain tumor
 Systemic illnesses
3. Diagnose, differentiate and treat major type of
primary/functional headaches
Migraine head ache
Cluster headache
Tension type headache
Psychogenic headache
 Outline of this topic
 Overview of head aches
 Classification
1. Secondary headaches
2. Primary headaches
Approach
 History taking
• Onset
• Characteristics of the pain
• Location& duration of pain
• Pattern & duration
• Time prediction
• Aura symptoms
• Associated symptoms
• Precipitating factors
• Current medication
 Introduction
Definition
 Headache refers to pain in any part of the head, the scalp, face
and the interior of the head.
Overview /Epidimiology
 One of the most common complaints encountered by physicians in
day to day practice.
 Overall prevalence of migraine is estimated to be 12-16% .
 Severe, disabling headache is reported annually by 40% of
individuals worldwide.
 HA affects 95% of people in their lifetime.
 Headache affects 75% of people in any one year.
 One in 10 people have migraine.
 Headache is among the most common reasons patients seek
medical attention.
 Pathomechanisms of headache

Pain occurs
1. When peripheral nociceptors are stimulated in response to
tissue injury
visceral distension
2. When pain-producing pathways of the peripheral or CNS
are damaged or activated inappropriately
3. When Intracranial masses causes deform, displace, or
exert traction on
 Vessels
 Dural structures or
 Cranial nerves at the base of the brain
 these changes - long before intracranial pressure rises
 Pathomechanisms of headache…
Summary
what the cause of that pain ?
 The most particular areas involved
 Dara mater –stimulation
 CN-5 irritation( trigeminal nerve)
 neck and head muscles – agitation
 stimulation , irritation and agitation of these structure/
region will causes head ace
 Major -Head ache classification

 A classification system developed by the International

Headache Society characterizes headache as
1. primary headaches
2. secondary headaches
 Head ache classification –differences

1.Secondary headaches 2. Primary headaches

 are those caused by  are those in which headache
exogenous disorders and its associated features are
 often manifestations of an the disorder in itself
 not life-threatening, may create
underlying serious,
sometimes life-threatening, sever pain, incapacitate
patients, and, with frequent
illness
attacks, reduce their quality of
 diagnosis - typically rests on
life.
their clinical context,  diagnose -not by physical
physical findings, or findings or laboratory tests, but
laboratory abnormalities. by their distinctive symptoms.
 no identifiable underlying cause
 RED FLAG of secondary headaches
1. S- systemic symptoms- e.g. fever, myalgia ,
2. weight loss
3. - secondary risk factors –HIV, malignancies and
4. immunosuppression
5. N- Neurological deficit – e,g, weakness of one side
6. O-Old => 50 years age
7. O- On set of the head ache – if abrupt (acute)
8. P-Papilla edema – swelling of the upper disk
9. P-Positional-if worse when lying down & better when sitting up
10. P-Pattern change( intensity ) – e,g. sever sudden stabbing pain
11. P-Precipitated by valsalva maneuvers -decrease venous drainage
increases ICP –worse head ache
valsava maneuver - es venous drainage increase ICP- lead to head
ache
Major cause Categories of secondary head ache
 There are three different major categories of secondary head ache
These are
1) Head ache due to -A mass occupying lesion
A. Accumulation/increased in blood
B. Accumulation/increased in CSF
C. Accumulation/ increased in brain tissue
2) Other CNS Pathology
A. meningitis
B. encephalitis
C. Cerebral venous sinus thrombosis (CVST)
D. History of Trauma on neck and head region carotid or vertebral
artery dissection
HORNER syndrome
neck pain ,tinnitis(pulsating)
E. Idiopathic intracranial hypertension (pseudo tumor cereberi)
3-External CNS Pathology or disorders
A. Sinusitis
B. Acute Angle Closure Glaucoma
C. Giant cell arteritis /temporal arteritis
D. Trigeminal neuralgia
 1. Head aches-due to a mass occupying lesion
A. A- Accumulation/increased in blood b/c of hx of trauma
Epidural hematoma
 subdural hematoma,

 patient present with HA, seizure , ICP intrapanchemal

hematoma – hypertension
PT. Thunderclap head ache -the worst head ache – this may be due
to subarachnoid hemorrhage– do they have meningitis sign ?
like N/V, photophobia, phonophobia, neck stiffness
neuro-deficits – weakness
suspect arachnoid hemorrhage
 B. Increased in brain tissue
 Increased in brain tissue – normal or abnormal
eg. Pituitary tumor – pituitary adenoma is one of the most common
pituitary tumor
 this tumor may compress brain tissue / vessels
bitemporal hemianopia- it indicate pituitary adenoma
– increased PRL(prolactinoma) -
& this is potential signs of
 Galactorrhea

 gynecomactia

 menstrual abnormality and decreased libido

 Brain abscess
Because of different factors –
 bacterial
 viral
 patient present with - classic type of head
ache ,fever , neuro-deficit –depend on
abscess site compression –
 visual abnormality if abscess compression is
on occipital
 contralateral motor abnormality if abscess
compression is on motor cortex
 Brain tumor
 Glioblastoma (G.B.M.)- glial cell tumor

 meningioma – meninges membrane tumor

 Metastases type-the spread to brain from other site

 in this case head ache is positional have high risk of seizures

and has systemic symptoms-like low grade fever and do they

have wt. loss

Increase in CSF
hydrocephalus
 Hydrocephalus is the buildup of fluid in the
cavities (ventricles) deep within the brain. The
excess fluid increases the size of the ventricles

Due to hydrocephalus increases CSF ICP

 Pt. present with -head ache ,decreased level of
consciousness and others sign and symptoms
seizure
 3-Other CNS pathology
 An irritation of the meninges
 meningitis – inflammation of meninges
 encephalitis- inflammation of brain tissues

 Patient present with head ache , fever, meningitis sign ,

neurodeficits-depending on location of inflammation
 If viral encephalitis pt. present with Behavioral change – or
altered mental status
 Altered mental status—drowsiness, inattention, disorientation,
memory loss, frontal release signs (grasp, suck, snout),
perseveration
 Cerebral venous sinus thrombosis (CVST)

 Usually due to blockage/ clots within venous sinus in the

brain
 Is female pt. – suspect hypercoagulable abnormality , on
contraceptive drug, pregnant, eclamsia
 Usually to some types of blockage within the venous
( clot or blockage)
 patient clinical presentation - increases – ICP- n/v ,
papilla edema , loss of consciousness –head ache etc
seisure
 carotid or vertebral dissection
 usually secondary to some types of trauma –Horner
syndrome
clinical presentation
Neck pain
Tinnitus –pulsating head ache
Idiopathic intracranial hypertension – pseudo tumor
 head ache
 increased ICP-N/V, papilla edema, DLC
 compressed CN-V which lead to diplopia - double
vision
 carotid or vertebral dissection ..
 Precipitated by valsava maneuver
 This is common in female who are obsess & who are on
contraceptive
 MRI -imaging is normal
 Dx- lumbar puncture- increases
 External CNS pathology
• Sinusitis – A condition in which the tissue lining the sinuses (small
hollow spaces in the bones around the nose) becomes swollen or
inflamed.

patient clinical presentation -

 head ache , low grade fever , rhinorrhea which is purulent , tenderness

ACUTE ANGE CLOSURE

 Increased pressure in the front chamber (anterior chamber) of the
eye due to sudden (acute) blockage of the normal circulation of fluid
within the eye.
pt – present with –head ache on orbit area

occularhypremia , decreased vision + ICP S/S

 GIANT CELL ARTERITIS

 Temporal (giant cell) arteritis is an inflammatory disorder

of arteries that frequently involves the extra cranial
carotid circulation
 Pt – present with head ache usually over temporal , jaw
claudication , visual change can lead to blindness,
 commonly associated with -Polymyalgia rheumatica-
stiffness & pain in the muscle
 Dx –ESR , temporal artery biopsy
 Trigeminal head ache
 Particular distribution to v2, v3

 Usually described as unilateral stabbing head ache ,

electric, lightening and lancinating type of pain
 no neurodeficits

 This pain exacerbated by touch/even by chewing and

wind blow
 Happen some times 10-100 time/day – high risk for
suicide
 Trigeminal head ache
 Dx – MRI / MRA – which shows compression on
trigeminal nerve CN-V by the superior cerebellar artery
 Primary/functional /Idiopathic headache) - ~85%

 its prevalence ~85% of headache cases

Major Classification
 Migraine
 Tension-type headache(TTH)
 Cluster headache
 Approach to a patient with headache
1. Onset
 ACUTE HEADACHES
 Headaches that are new in onset are commonly a symptom of
serious illness and therefore demand prompt evaluation

 SUBACUTE HEADACHES
 Sub-acute headaches occur over a period of weeks to months

 CHRONIC HEADACHES
 Headaches that have occurred for years
 Approach to a patient with headache …
2. Characteristics of the pain
 Throbbing
 stabbing
 Burning
 Dull aching
 Cold sensation
 Crawling sensation
 Itching sensation
 Tightness
 Heaviness
 Approach to a patient with headache history taking …
3. Localization and radiation
 Generalized
 Unilateral
 bitemporal
 Occipital
 Frontal
 over the vertex
 periorbital
 Approach to a patient with headache history taking
…
4. Pattern and duration
 Intermittent- periodic
 Continuous
 In clusters

5. Time predilection
 Nocturnal
 On awakening
 Afternoons
6. Aura symptoms
 Presence or absence of aura
 Characteristics of aura
 Visual
 Paresthesia
 Olfactory
Approach to a patient with headache history taking …

7 . Associated symptoms
 Nausea and vomiting
 Photophobia
 Noise intolerance
8. Precipitating factors
 Dietary – alcohol, chocolate, caffiene, cheese, nuts, yoghurt
 Sleep deprivation
 Particular odors
 Psychological stress,
 Hunger
 Weather changes
Approach to a patient with headache history taking
…
9. Current medication
 Prescription drugs -contribute/cause headache (oral
contraceptive, etc.)
 Overusing analgesia

 Using recreational drugs

 MIGRAINE HEADACHE
 Migraine is Greek word hemikranios which means “half
head,”
 It is usually an episodic headache associated with certain
features such as
 sensitivity to light
 sound, or movement;
 Nausea and vomiting often accompany the headache
 A migraine attack has three phases: premonitory
(prodrome), headache phase, and postdrome; each has
distinct and sometimes disabling symptom
 General features - migraine
 Familial in 80% of cases(classical type)
 Usually begins in childhood or adolescence
 3 times as many females as males.
 Magraine pts are particularly sensitive to environmental
and sensory stimuli; migraine-prone patients do not
habituate easily to sensory stimuli.
 Headache can be initiated or amplified by various
triggers,
 Pathogenesis/ Pathomechanisms
1- Vascular theory
 Extracranial vessels become distended and pulsatile during a
migraine attack
 Vasoconstrictors (eg, ergots) improve the headache
 vasodilators (eg, nitroglycerin) provoke an attack
 It activates trigeminal fibers causing the headache
phase
2.Neurotransmitters
Serotonin receptors

 Dorsal raphe -highest concentration of serotonin receptors

-generator of migraine and the main site of drug action
 Clinical feature
 Throbbing or pulsatile(pain quality)
 Unilateral and localized in front, temporal and ocular but
can be felt anywhere (site)
 Builds over 1-2 hrs(time to maximum intensity) and
typically lasts 4-72 hrs(duration).
 Nausea (80%) and vomiting (50%)
 2/3 is migraine without aura
Triggers
 Migraine phases
Divided into four phases:
1. the premonitory phase, which occurs hours or days
before the headache
2. the aura, which comes immediately before the headache
3. the headache itself
4. the postdrome
 Prodromal phase
 The first phase of a migraine attack for most
patients is the premonitory (prodromal) phase
consisting of some or all of the following:
Yawning
 tiredness
 cognitive dysfunction
 mood change
 neck discomfort
 polyuria, and
food cravings; this can last from a few hours to days .
In approximately 10-60% of migraineurs
 Aura phase
Visual Auras
 Colorless glittering Scotomata

 Black-and-white zigzag patterns (Fortification lines)

 Photopsias - regular angular patterns

 may evolve into scotoma or temporary homonymous hemianopia/loss

of vision in half visual felid.

Sensory auras
 Paresthesias (pins and needles) that typically begin in the hand, move
up the arm
 3. The headache phase
 Throbbing headache/pulsating
 Unilateral mainly - frontal, temporal, periorbital
 Onset is usually gradual
 Usually lasts 4 to 72 hours in adults (2-48 hors in children)
 Is aggravated by head movement or physical activity.
 Associated features
 Nausea, vomiting
 sensory hyperexcitability,
 Photophobia
 Phonophobia,
 4. Postdrome or postictal phase
 May feel tired, washed out, irritable and listless
 May have impaired concentration
 Feel scalp tenderness
 Some feel
 Unusually refreshed or euphoric, OR
 Have depression and malaise.
 Migraine headache-major classification

1. Migraine without aura

2. Migraine with aura
3. Chronic migraine
4. Status migranine
 1. Migraine without aura-diagnostic criteria
A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 h (untreated or unsuccessfully
treated)
C. Headache has ≥ 2 of the following characteristics:
1.unilateral location
2.pulsating quality
3.moderate or severe pain intensity
4.aggravation by routine physical activity (eg, walking, climbing stairs)
D. During headache ≥1 of the following:
1.nausea and/or vomiting
2.photophobia and phonophobia
E. Not better accounted for by another ICHD-3 diagnosis
 2. Diagnostic criteria for migraine with typical
aura
A. At least 2 attacks fulfilling criteria B and C
B. Aura of visual, sensory and/or speech/language
symptoms, each fully reversible
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. Aura symptom is unilateral
4. Aura accompanied or followed in <60 min by headache
D. Not better accounted for by another ICHD-3
diagnosis, and TIA excluded
 Most common aura symptoms
• The most common aura -Visual
Fortification spectrum
Scintillating/shining brightly
Scotoma/partially diminished visual acuity
 Difference & similarity
Migraine with Aura Migraine without Aura
 Previously labeled classic • Previously- common migraine
migraine • Affect about 70% of pt with
 Affects only about 20-30% migraine
of migraine patients • Arising without warning
 Aura represent cortex or • Throbbing headache
brain dysfunction & qualities , located temporal ,
typically precedes or or pereorbital, usually
accompanies headache unilateral
 Common aura-visual • Episode lasting 4-72hrs
hallucinations
 Women & Migraine headache
 often first onset at menarche, recurs premenstrually, and is
aggravated by some oral contraceptives.
 Most women with migraine report attacks occur immediately before
or at the beginning of their menses
 about 10% of them suffer migraines exclusively at this time.
 During pregnancy, about 70% of women experience dramatic relief,
but usually only during their second or third trimesters.
 pregnancy can also have adverse effects. About 10% -experience
their first attack during pregnancy.
 About 10–20% of pregnant women - have more frequent or more
severe attacks than usual
 No miscarriage, eclampsia, or fetal malformations.
 Status migrainosus
• Attacks that persist for more than 3 days are known
as Status Migraine
• RX: Admission may be required
• Fluid replacement
• Correction of electrolyte imbalance
• Suppression of vomiting
• DHE IV combined with antiemetic
• Corticosteroids(dexamethasone or prednisone)
• Best to avoid narcotic and benzodiazepine
 Chronic migraine
• Headache for >15 days per month for at least
3 months
 Psychiatric disorders and Migraine

• Migraine is associated with

• MDD,
• bipolar disorder,
• panic disorder, and
• social phobia,
• all occurring twice as often in those with migraine
compared with those without it.

• Health-related outcomes are poorer in those with both

migraines and a psychiatric disorder than in those with
either condition alone
 TREATMENT of MIGRAINE
 1. Treating the acute migraine headache(Abortive
treatment)
 2. Prophylactic treatment
 3. Avoiding precipitating factors
1. Treating the acute migraine
headache(Abortive treatment)
 When migraine frequency is less than 2 times
per month
 Pts take medications on an acute basis to abort
an incipient migraine or reverse a full-blown
one.
 They are rapidly effective for moderate to
severe migraine and some are available as
injections, sublingual wafers, and nasal sprays.
 Treatment of Acute Migraine
DRUG DOSAGE

1. Simple Analgesics:- Acetaminophen, Two tablets or caplets q6h (max 8 per day)
aspirin, caffeine ASA-900-1300 mg
2. NSAIDs
 Naproxen________________________ 220–550 mg po bid
 Ibuprofen _______________________ 400 mg po q3–4h
 Tolfenamic acid __________________ 200 mg po; may repeat ×1 after 1–2 h
 Diclofenac K ____________________ 50 mg po with water
3. 5-HT1B/1D Receptor Agonists—Triptans
ORAL 1 or 2 tablets at onset, then 1 tablet q½h
 Ergotamine 1 mg, caffeine 100 mg___ (max 6 per day, 10 per week)
 Naratriptan______________________ 2.5-mg tablet at onset
 Rizatriptan_______________________ 5–10-mg tablet at onset
 Sumatriptan_____________________ 50–100-mg tablet at onse
 Frovatriptan_____________________ 2.5-mg tablet at onset
 Almotriptan______________________ 12.5-mg tablet at onset
 Eletriptan_______________________ 40 or 80 mg at onset
 Zolmitriptan___________________ 2.5-mg tablet at onset
 Treatment of Acute Migraine
DRUD DOSAGE
 Nasal 1 spray (0.5 mg) is administered, followed
 Dihydroergotamine______ in 15 min by a second spray
 Sumatriptan___________ 5–20 mg intranasal spray as 4 sprays of 5
mg or a single 20 mg spray
 Zolmitriptan___________ 5 mg intranasal spray as one spray
 Parenteral
 Dihydroergotamine______ 1 mg IV, IM, or SC at onset and q1h (max 3
mg/d, 6 mg per week)
 Sumatriptan____________ 6 mg SC at onset (may repeat once after 1
h for max of 2 doses in 24 h)
4. Dopamine Receptor Antagonists-ORAL
 Metoclopramide______
 Prochlorperazine______ 5–10 mg/d
Parenteral 1–25 mg/d
 Chlorpromazine ____
 Metoclopramide_____ 0.1 mg/kg IV at 2 mg/min; max 35 mg/d
 Prochlorperazine______ 10 mg IV
10 mg IV
 Ergotamine and DHE, which are primarily vasoconstrictors, are also
rapidly effective
 Excessive use of the vasoconstrictors may lead to persistent,
excessive vasoconstriction (ergotism) in the coronary arteries, digits,
and elsewhere.
 vasoconstrictors might precipitate a miscarriage or cause fetal
malformations, ergotamine and DHE, unlike triptans, are
unequivocally contraindicated in pregnant women.
 Finally, administration of either a triptan or vasoconstrictor to
patients already under treatment with an SSRI or SNRI risks causing
the serotonin syndrome.
 parenterally - antiemetic, such as metoclopramide (Reglan). Cause
dystonic reactions identical to those induced by dopamine-blocking
antipsychotics-prophylactically administer diphenhydramine
 Migraine attacks lasting more than 3 days (status migrainosus)
usually lead to prostration, prolonged painful distress, and
dehydration.
 Patients suffering from such prolonged, refractory illness
benefit substantially from parenteral medication, intravenous
fluids, antiemetics, and a quiet, dark refuge.
 must often hospitalize patients in status migrainosus.
 Medically supervised withdrawal from over-the-counter
medications, opioids, or even excessive conventional
antimigraine medicines may also require hospitalization
 2. Prophylactic treatment
Suggestion for preventive treatment
1. Headache attack > 4 /month
2. Duration of a single attack > 24 hrs
3. Major disruptions in the patients lifestyle with significant
disability that lasts 3 or more days
4. Abortive therapy fails or overused (2/wk)
5. Symptomatic medications are contraindicated or ineffective
6. Hemiplegic migraine or rare headache attacks with risk of
permanent neurologic injury.
Most preventive medicines fall into three categories:
 Antidepressants -TCA
 Antihypertensive, and
 Antiepileptic's. –VALPROATE &
 TCA
 amitriptyline & nortriptyline, reduce the severity, frequency,
and duration of migraine.
 They have mood elevating effect
 may ameliorate migraine because they suppress REM sleep,
which is the phase when migraine attacks tend to develop.
 enhance serotonin, they have analgesic effect
 most patients are young and require only small doses of
TCAs compared to those used to treat depression, the side
effects of TCAs in this situation are rarely a problem.
 for preventing migraine, SSRIs are ineffective compared to
TCAs.
• Dosage-Amitryptyline – 10-50mg(150) mg /day
 Antihypertensive-β-blockers
• Prophylaxis treatment for migraine, as well as for
treatment of essential tremor
• avoid prescribing β-blockers to migraine patients with
comorbid depression because of their tendency to
precipitate or exacerbate mood disorders.
• AEDs, such as topiramate and valproate, offer preventive
treatment for migraine, as well as for neuropathic pain
and epilepsy.
• Dosage-Propranolol 40–240 mg/day, should be avoided
in asthma
• Others (eg, metoprolol,atenolol, timolol, nadolol) -
probably as effective as propranolol
 Valproate
 suppress migraine by reducing 5-HT neurons firing in the
dorsal raphe nucleus or by altering trigeminal GABA A
receptors in the meningeal blood vessels.
 its side effects, especially weight gain, often preclude its
use.
chronic migraine
 Botulinum toxin injections reduce the frequency or
severity of migraines that both last 4 hours or longer and
occur at least 15 times a month.
 botulinum toxin injections reduce the impact of migraines
and improve a patient’s quality of life.
 Chronic daily headache
 Is defined as - headaches attack , each lasting 4 hours or
longer, for at least 15 days each month for at least 3
months
 Patients with chronic daily headache typically describe
generalized, waxing and waning, dull, pressing, and
nonpulsatile pain, which is usually only mild to
moderate in severity.