Headache Headache

Headache

Headache
Headache Headache
Headache
HeadacheHeadache Headache
APPROACH TO HEADACHEHEADACHE
DISORDERS
Headache
Headache
Dr. Mahendra Thakre
01-07-2021 Headache Headache
Headache
Headache
Headache Headache

Headache
Questions to be answered while evaluating a headache patient

• What type of headache is it ?

• Can I classify this headache, and if so how?

• What are the differential diagnosis?

• Do I need to investigate? brain scan?

• What to offer—reassurance, treatment, something else?

• What is the most sensible management approach?

WHAT IS THE HEADACHE……?
WHERE DOES IT COMES FROM……?
 Pain-sensitive Structures

• Intracranial pain-sensitive structures • Extracranial pain-sensitive structures

• The arteries of the Circle of Willis and • The external carotid artery and its
their medium-sized branches, branches,
• Meningeal (Dural) arteries, • Scalp and neck muscles,
• Large veins and Dural venous sinuses, • Skin and cutaneous nerves,
and portions of the dura near blood • Cervical and cranial nerves V, VII, IX,
vessels, and X
• Mucosa of sinuses, teeth, eyes, nose

Brain Parenchyma , Pia, Arachnoide, Scull and Ventricules are not pain sensitive
 Epidemiology

• Lifetime prevalence of headache is 96%, with a female predominance

Headache Has
• At least 90% of headache is primary headache Been
• The global active prevalence of
Underestimated,
– Tension-type headache: 40%
– Migraine: 10%. Underrecognized
• Trigeminal autonomic cephalgia's are rare. Under-treated
• The most common TAC is cluster headache, with 0.1% prevalence.
• Sinister causes of headache are rare, 0.1% of all headaches Throughout The
World.

WHO ranks migraine as

the third most prevalent medical condition
the second most disabling neurological disorder.
 Classification : General Principles

• A classification system developed by the International Headache Society

characterizes headache as

• Primary headaches are those in which headache and its associated features are the
disorder in itself,
• Secondary headaches are those in which head pain is a symptom of an underlying
disease affecting pain-sensitive structures
• Painful Cranial Neuropathies, other facial pain and other headaches
International Classification of Headache Disorders (ICHD)

ICHD-1 1988

ICHD-2 in 2004

ICHD-3rd edition (beta

version) Cephalalgia 2013

ICHD-3 in 2016
 From Headache
Classification
Committee of the
International
Headache Society
(IHS). 2018. The
International
Classification of
Headache
Disorders, third ed.
Cephalalgia 38 (1),
1–211. https://doi.
org/10.1177/0333
102417738202.
 1:Migraine classification

• 1.1 Migraine without aura

• 1.2 Migraine with aura
(typical aura, brainstem aura, retinal, hemiplagic)
• 1.3 Chronic migraine
• 1.4 Complications of migraine
(status, infarction, aura trigered seizure)
• 1.5 Probable migraine
• 1.6 Episodic syndromes that may be
associated with migraine
(abdominal, Vertigo, torticollis)

©International Headache Society 2018

 2:Tension-type headache (TTH)

2.1 Infrequent episodic tension-type headache

2.2 Frequent episodic tension-type headache
2.3 Chronic tension-type headache
2.4 Probable tension-type headache
 3:Trigeminal autonomic cephalalgias (TACs)

3.1 Cluster headache

3.2 Paroxysmal hemicrania
3.3 Short-lasting unilateral neuralgiform
headache attacks
(SUNCT: with conjunctival ingestion and tearing ,
SUNA: with cranial autonomic symptoms)
3.4 Hemicrania continua
3.5 Probable trigeminal autonomic cephalalgia
Trigeminal neuralgia
 4:Other primary headache disorders

4.1 Primary cough headache

4.2 Primary exercise headache
4.3 Primary headache associated with sexual activity
4.4 Primary thunderclap headache
4.5 Cold-stimulus headache
4.6 External pressure headache
4.7 Primary stabbing headache
4.8 Nummular headache
4.9 Hypnic headache
4.10 New daily persistent headache (NDPH)
 Clinical history: Pattern-recognition

• 1. How many different headache types does • 4. Cause questions

the patient experience? – Predisposing factors?
– Separate histories are necessary for each.. – Aggravating/relieving factors?
– Family history of similar headache?
• 2. Time questions
• 5. Response to headache questions
– Why consulting now? – What does pt do during attack ?
– How recent in onset? – How much is activity limited?
– How frequent? – What medication used?
– How long lasting? • 6. State of health between attacks
– Completely well, or residual or persisting
• 3. Character questions symptoms?
– Intensity of pain? – Concerns, anxieties, fears about recurrent
– Nature and quality of pain? attacks?
– Site and spread of pain?
– Associated symptoms?
 Types of Headaches

• Many individuals have more than one type of headache.

• Migraine headaches and tension-type headaches often occur in the same individual.
• Change in an established headache pattern can indicate a new condition
 Onset of Headaches

• “A stable headache” : almost always of benign origin.

• “Recent onset headache” : from 1 to 12 months : the greater risk of a secondary

cause.

• The “worst ever” headache: suggest an intracranial lesion.

• “thunderclap headache” : Headaches of rapid (over seconds to minutes) onset : an

intracranial hemorrhage, usually SAH,CVST, SIH, RCVS, acute hypertensive crisis.

• If no underlying cause : Primary Thunderclap Headache

 Onset of Headaches

• Migraine headaches often begin in childhood, adolescence, or early adulthood.

• Onset of a new headache in patients older than 50 years : intracranial lesion (e.g.,
subdural hematoma) or giant cell (temporal or cranial) arteritis (GCA)

• A history of antecedent head or neck injury: SDH and dissection of the carotid or
vertebral arteries

• Posttraumatic headaches can occur following head injury

 Frequency and Periodicity of Episodic Headaches

• Monitoring headache frequency, duration, intensity, headache triggers, and

medication use in a diary is helpful
• Chronic migraine : headache occurring on > 15 days per month for > 3 months that
has the features of migraine on > 8 days per month.

• Episodic cluster headaches : occur daily for several weeks or months and are
followed by a lengthy headache-free interval.

• Chronic cluster headaches: occur at least every other day for > 1 year or with
remissions lasting < 3 months
 Frequency and Periodicity of Episodic Headaches

• Tension-type headaches can be

– Episodic (<12 days/year) or
– Frequent (≥12 and <180 days/year) or
– Chronic (≥15 days/month on average for >3 months).
 Temporal Profile

• Untreated migraine : peaks within 1–2 hours of onset and lasts 4–72 hours.

• Tension-type headaches: build up over hours and last hours to days to years.

• Cluster headache: peaks within minutes and last from 15 to 180 minutes (usually
45–120 minutes). It is more common in men and are infrequently inherited.

• Paroxysmal hemicrania: Headaches similar to cluster but lasting only 2–30 minutes
and occurring several or many times a day, more common in women and are
prevented by indomethacin
 Temporal Profile

• Hemicrania Continua : a chronic, continuous, unilateral headache of moderate

severity with superimposed attacks of more intense pain associated with autonomic
features

• SUNCT and SUNA : paroxysms of V1 trigeminal nerve pain lasting 5–240 seconds
but occurring 3–200 times per day.

• Occipital neuralgia and trigeminal neuralgia manifest as brief shock-like pains,

often triggered by stimulation
 Time of Day and Precipitating Factors

• Migraine headaches: often begin in the morning.

• Tension-type headaches : present during much of the day and are often more
severe later in the day.

• A headache that disturbs sleep or is worse on waking may be caused by increased

intracranial pressure.

• Headache that awaken patients from sleep

– Cluster headaches
– Hypnic headaches
– Obstructive sleep apnea
 Triggers

• Migraine headaches : bright light, menstruation, weather changes, caffeine

withdrawal, fasting, alcohol, sleeping more or less than usual, stress and release
from stress, certain foods and food additives, perfume and smoke, and others.

• A cluster headache : Alcohol within minutes of ingestion.

• Intracranial Lesion: bending, lifting, coughing, or Valsalva maneuver

• Exertional headache and or sexual activity : subarachnoid hemorrhage, arterial

dissection, and RCVS.
 Triggers

• Positional headache: Intermittent headaches that are worsened by sitting or

standing and improved by lying down are characteristic of a cerebrospinal fluid
(CSF) leak.

• Lancinating face pain triggered by facial or intraoral stimuli occurs with trigeminal
neuralgia.

• Glossopharyngeal neuralgia typically causes throat or ear pain that is triggered by

chewing, swallowing, or talking.
Location
 Quality and Severity

• Migraine pain : pulsating quality, throbbing

• Cluster headache: severe, boring, and steady and

often described as a “hot poker.”

• SUNCT : moderately severe pain , sharp and stabbing.

• Tension-type headaches : a steady feeling of fullness, tightness, or pressure or like a

band.

• Trigeminal neuralgia: pain is severe, brief, sharp, electric shock–like.

 Accompanying Symptoms

• Nausea, vomiting, photophobia, phonophobia,

and osmophobia characteristically accompany
migraine attacks.

• Ipsilateral miosis, ptosis, lacrimation, conjunctival

injection, and nasal stuffiness commonly
accompany cluster headache, paroxysmal
hemicrania and hemicrania continua.

• ipsilateral conjunctival injection and tearing

suggest SUNCT.
 Accompanying Symptoms

• Horner syndrome : carotid artery dissection.

• Acute transient or persistent monocular visual loss: GCA and carotid dissection
and stenosis
• A jaw claudication, or tenderness of the scalp arteries in an older person : GCA.
• Jaw pain and reduced range of jaw movement, joint clicking :Temporomandibular
joint dysfunction
• Persistent or progressive diffuse or focal CNS symptoms, seizures: structural SOL.
• A red eye : Acute Glaucoma.
• Transient visual obscurations upon standing, pulsatile tinnitus, diplopia and
papilledema : increased intracranial pressure, IIH
Horner syndrome
 Aggravating and Mitigating Factors

• Worsening on coughing : Intracranial etiology.

• Worsening in the upright position and/or relief with recumbency suggests
Intracranial Hypotension.
• Cluster Headache : Pts tend to in an agitated state, pacing and moving
• Migraine patients typically prefer to lie still.
• Rest, sleep, and avoidance of light and noise tend to benefit the migraineur.
• Local application of pressure or heat or cold, and brief intense physical activity may
alleviate the pain of cluster headache.
 Other clinical history

• Family History of Headaches

• Prior Treatment
• Disability: The Migraine Disability Assessment Scale (MIDAS) is a useful and
validated clinical tool
• Other Medical or Neurological Problems
• Patient Concerns and Reasons for Seeking Help
Red flag signs of secondary headache
 Examination
• Neurological examination
• Funduscopic examination
• Blood pressure measurement is recommended:
• Examine the head and neck for
– muscle tenderness (generalized or with tender ‘nodules’), stiffness,
– limitation in range of movement and crepitation.
• In children, some paediatricians recommend that head circumference is measured
at the diagnostic visit and plotted on a centile chart.
 Investigations
• Full blood count and erythrocyte sedimentation
• Plain radiography of the skull and Cervical spine x-rays
• Lumbar puncture
• Electro-encephalography (EEG)
• Computed tomography (CT)
• Magnetic resonance imaging (MRI)
• Cerebral angiography
• Isotope scanning and Doppler flow studies
 Imaging Modality of Choice to
Investigate Causes of Headache
 Migraine: Introduction

• Migraine is a chronic paroxysmal neurological disorder characterized by

multiphase attacks of head pain and a myriad of neurological symptoms.
• Migraine is the second most prevalent neurologic disorder (after tension-type
headache),
• with a female-to-male ratio of 3:1 and
• An estimated 1-year prevalence of approximately 15% in the general population
• A family history of migraine is common, with the heritability estimated to be
approximately 42%
• The risk of migraine is polygenic
Migraine: the clinical attack
 Migraine Prodrome/premonitory phase

• Prodrome occurs hours or even days • Physical symptoms,

before the headache begins.
✓ Muscle stiffness, especially in the neck
• It often acts as a warning sign that a ✓ Altered perception of heat and cold
migraine is imminent. ✓ Increased thirst, Increased urination
✓ Food cravings, Loss of appetite
• About 60% of people with migraine
experience prodromal symptoms. ✓ Yawning
✓ Constipation, Diarrhoea
• Physical symptoms ✓ Fluid retention
• Psychological symptoms ✓ Sensitivity to light and/or sound
 Migraine Aura

• One or more fully reversible focal ✓ Scintillation scotomas

neurological symptoms. ✓ Bright rim around an area of visual loss
• 20% of migraine sufferers (fortification spectra)
• develops over five to twenty minutes and ✓ Flashing lights
lasts for up to one hour. ✓ Jagged lines
• Most commonly visual, sensory or, more ✓ Visual resizing or reshaping of objects
rarely, motor. ✓ Blurred vision
✓ Unilateral sensory parasthesia Muscular
weakness
✓ Partial paralysis on one side of the body
✓ Temporary dysphasia
fortification spectra / Scotoma
Hemianopic loss of vision
Unilateral sensory paresthesia
 Headache Phase

✓ Headache lasts from 4-72 hours • Frequently is present on awakening in

✓ Moderate or severe pain the morning.
✓ Usually gradual in onset • Nausea accompanies the headache in
✓ Throbbing, pounding or pulsating in 70-90% and leads to vomiting in 20-
character, 50%.
✓ Exacerbated by routine physical activity • Photophobia, Phonophobia and
✓ Extends from the periorbital and frontal Osmophobia.
areas backwards to the temporo-parietal • Stiffness or tenderness of the neck.
and occipital regions and can sometimes
extend to the shoulder area. • Other possible symptoms
 Migraine Postdrome

• The postdromal or resolution phase ✓ Fatigue

follows the headache and may last for up ✓ Sore muscles
to 48 hours. ✓ Food intolerance
• Many of the symptoms of this phase ✓ Malaise
appear initially during the prodrome or
with the headache phase. ✓ Alteration in mood
• A minority of sufferers immediately after ✓ Impaired concentration
an attack feel energized, euphoric and can ✓ Scalp tenderness
return to normal activities at once. ✓ Decreased energy requiring a period of
rest.
 Migraine: Patho-Physiology

• Headache may originate from

– Normal physiologic response or
– Pain- pathways of the peripheral or central nervous system (CNS) are damaged or
activated inappropriately.
• Pain-producing cranial structures are : include the scalp, middle meningeal artery,
dural sinuses, falx cerebri, and proximal segments of the large pial arteries.
• Non pain-producing are: The ventricular ependyma, choroid plexus, pial veins, and
much of the brain parenchyma are.
 Key Structure: Trigeminocervical Complex

• The key structures involved in primary

headache appear to be
– The large intracranial vessels and
dura mater
– The peripheral terminals of the
trigeminal nerve
– The trigeminocervical complex
– The pain modulatory systems in the
brain that receive input from
trigeminal nociceptors
Brainstem pathways
The key pathway for pain in
migraine is the trigeminovascular
input from the meningeal vessels,
which passes through the
trigeminal ganglion and synapses
on second-order neurons in the
trigeminocervical complex.
These neurons in turn project in
the quintothalamic tract and,
after decussating in the
brainstem, synapse on neurons in
the thalamus.
Important modulation of the
trigeminovascular nociceptive
input comes from the dorsal
raphe nucleus, locus coeruleus,
and nucleus raphe magnus.
 Diagnostic criteria Migraine
WITHOUT AURA WITH AURA
A. At least 5 attacks fulfilling criteria B–D A. At least 2 attacks fulfilling criteria B–C
B. Headache attacks lasting 4–72 hours (untreated B. One or more of the following fully reversible aura
or unsuccessfully treated) symptoms:
C. Headache has at least two of the following 1) Visual 2) Sensory 3) Speech/Language/both
characteristics: 4) Motor 5) Brainstem 6) Retinal
1. unilateral location C. At least three of the following six characteristics:
2. pulsating quality 1. at least one aura spreads over >5 minutes
3. moderate or severe pain intensity 2. Two or more aura symptoms occur in succession
4. aggravation by or limitation of routine 3. each aura symptom lasts 5–60 minutes
physical activity 4. at least one unilateral aura symptom
D. During headache at least one of the following: 5. at least one positive aura symptom
1. nausea and/or vomiting 6. the aura is accompanied, or followed within 60
2. photophobia and phonophobia minutes, by headache
E. Not attributed to another disorder ICHD-3 D. Not better accounted for by another ICHD-3
diagnosis diagnosis
 Chronic migraine
• Headaches (suggestive of migraine or tension headaches) on ≥15 days/month for >3
months that fulfill the following criteria:
• Occurring in a patient who has had at least five attacks meeting the criteria for
migraine without aura or the criteria for migraine with aura or both
• On ≥8 days/month for >3 months, features of migraine without aura or of migraine
with aura or believed by the patient to be migraine at onset that is relieved by a
triptan or ergot derivative
• Not better accounted for by another ICHD-3 diagnosis
Migraine aura Transient ischaemic attack
First attack usually in teens/20s First attack usually in older population

Slow evolution over several minutes Sudden (seconds)

<1 hour (typically 20–30 mins Variable – 2 minutes–24 hours
Precedes and resolves before onset of typical Occurs with or without headache, with no temporal
migraine headache relationship
Present in 99% of auras Monocular, negative (black) scotoma
Homonymous positive (bright) scotoma gradually (amaurosis fugax)
enlarging across visual field into a scintillating
crescent

Present in one-third of auras – usually in association with May occur without visual symptoms
visual symptoms May include legs
Rarely affects legs Negative (loss of power)
Positive (‘pins and needles’)

Aura resolves before onset of headache and Up to 25% associated with concurrent
associated symptoms headache
 Occipital epilepsy

Occipital epilepsy vs Migraine with aura

Occipital epilepsy Migraine with aura Basilar migraine

Visual hallucination
Duration Seconds to 1min 5 to 30 minutes 5 to 30 minutes
1to 3min
Daily frequency As a rule Rare None
characteristics Colored circular patterns Achromatic or black and Evolving blindness
Usually moving to opposite white linear patterns Other feature are rare
side of visual field Usually expanding from the /exceptional
center to periphery of
visual hemifield
Evolving to blindness Rare Rare As a rule
Tonic deviation of eyes Exclusive None None
Impairment of Frequent exceptional Frequent but whiteout
consciousness With convulsion convulsions
Post ictal vomiting
 Initial management

• Reassurance
• Symptomatic treatment
• Discussion of potential predisposing and triggering factors
• Develop management strategy
• Diary cards to confirm diagnosis, assess frequency and duration of attacks, and
response to symptomatic treatment
• Regular follow-up
 Headache diaries

• Patients should be asked to keep a daily record of

– all their symptoms and
– all treatments taken for headache, including dose and time(s) taken.
• The pattern of attacks is a very helpful pointer
– to the right diagnosis, particularly if the diagnosis is unclear or more than one
type of headache is present.
 Proposed Treatment Algorithm for the Clinical Management of
Migraine.
• NSAIDs considered as a first-line medications for migraine attacks.
• If NSAIDs provide no pain relief, offer an oral triptan.
• If an oral triptan provides no pain relief, other triptans should be offered.
• Combination therapy with naproxen sodium should be offered to patients who
have inadequate pain relief with triptan.
• Offer subcutaneous sumatriptan when a patient has had inadequate pain relief with
all oral triptans.
• Ditans and gepants may be considered as third line
• Antiemetic agents may be offered as adjunctive therapy.
• Initiation of preventive treatment should be considered for patients who have at
least 2 migraine days per month and are adversely affected despite therapy.
N engl j med 383;19 nejm.org November 5, 2020
 Triptan Contraindications

• Triptans are contraindicated in individuals with

• a history of stroke,
• heart attack, coronary artery disease,
• hemiplegic migraine,
• uncontrolled hypertension,
• migraine with brainstem aura, and
• peripheral vascular disease.
• Rizatriptan, zolmitriptan, and sumatriptan should be avoided within 14 days of using
a monoamine oxidase inhibitor
 Preventive medications—general principles

• Begin with the lowest possible dose;

• Stop dose escalation when adverse events occur, or when efficacy or target dose
achieved
• Consider comorbid and coexistent illnesses when selecting drug,
• A 2–3 month trial is necessary to determine efficacy; a 6-month trial might be
necessary before the maximal response is evident
• Target goals: reduction in frequency, severity, or duration of acute attacks, or a
combination of these
• Discuss family planning and potential adverse fetal effects
• Discuss potential adverse drug-related events with patients
Migraine preventive therapy should be considered when one or
more of the following are present:
• Three or more moderate or severe headache days per month causing functional
impairment and that are not consistently responsive to acute treatments
• At least 6 to 8 headache days per month even if acute medications are effective
• Contraindications to acute migraine treatments
• Particularly bothersome symptoms even if infrequent attacks (eg, migraine with
brainstem aura, hemiplegic migraine)
• Migraine has a significant impact on patient’s life despite lifestyle modifications,
trigger avoidance, and use of acute treatment
• Patient is at risk of developing medication-overuse headache
The American Academy of Neurology’s ratings for level of evidence that each medication is
effective for migraine prevention include the following:
A = medication with established efficacy (at least two Class 1 trials);
B = medication probably effective (one Class 1 or two Class 2 studies);
C = medication possibly effective (one Class 2 study);
U = inadequate or conflicting data to support or refute medication efficacy

“medieval aspirin”
 MIGRAINE DURING PREGNANCY

Pharmacological treatment of migraine during pregnancy and breastfeeding, Amundsen, S. et. al. Nat. Reviews Neurol. advance
online publication 17 March 2015; corrected online 19 March 2015;
Pharmacological treatment of migraine during pregnancy and breastfeeding, Amundsen, S. et. al. Nat. Reviews Neurol. advance
online publication 17 March 2015; corrected online 19 March 2015;
 Emerging treatments

• Lasmiditan is a highly selective 5HT1F receptor agonist that has been shown in
randomised, doubleblind, placebocontrolled studies to be effective for the acute
treatment of migraine

• CGRP receptor antagonists (gepants) have been developed and shown to be

effective for the acute treatment of migraine. ubrogepant and rimegepant

• CGRP receptor monoclonal ab:

– Erenumab,
– Fremanezumab,
– Galcanezumab, and
– Eptinezumab.
 Botox for Migraine:

• Botox for Migraine: for chronic migraine sufferers.

• Half the injection sites should be on the left side of the head and half on the right.
• If there is a predominant pain location, further injections may be given (up to the
maximum dosage).
• The recommended re-treatment schedule is every twelve-24 weeks.
• Contraindications: In the presence of infection at the proposed injection site(s) and
an individuals with a known hypersensitivity’
• It is not advised: During pregnancy, unless clearly necessary
 Summary
• Red flags signs should be used to determine the need for investigation to exclude
serious secondary headache disorders.

• We should be familiar with the IHS classification

• Ideal headache management needs correct diagnosis, right choice of medications, a

sound rapport with the patient

• Headache Medicine is a new emerging area that is on the way to becoming a

credible subspeciality

• Treatment is evolving with emerge of ditans, geptans and mabs.

• Reference
– Headache Classification Committee of the International Headache
Society (IHS) The International Classification of Headache Disorders, 3rd
edition, Cephalalgia 2018, Vol. 38(1) 1–211
– Pathophysiology of Migraine, Daniela Pietrobon and Michael A. Annu.
Rev. Physiol. 2013. 75:365–91
– Migraine David W Dodick the lancet March 6, 2018
http://dx.doi.org/10.1016/ S0140-6736(18)30478-1
– Neurological disorders: a public health approach, WHO
– Headache and Other Craniofacial Pain Ivan Garza, Todd J. Schwedt, Carrie
E. Robertson, Jonathan H. Smith 103 chapter bradley
Thank you………..
An 1819 caricature by George
Cruikshank depicting a headache.
 Tension-Type Headache
• Symptomatic treatment

Amitriptyline is the treatment of choice for frequent episodic and chronic tension-type
headache
• Prophylaxis treatment
 Recommendations for
Trigeminal Autonomic Cephalalgias/ Cluster Headache
Preventive treatment recommendations for
trigeminal autonomic cephalalgias
 Menstrual Headaches
• Fifty per cent of women with
migraine report an association
with menstruation
• Menstrual migraine is more
severe and difficult to treat

Prevalence of migraine: age and sex

Source: from the American Migraine
Study II. Headache 2001; 41: 646–57.
 Two types
• Pure menstrual migraine without aura
• Diagnostic criteria
A. Attacks in a menstruating woman,
fulfilling criteria for migraine without
aura
B. Attacks occur exclusively on day 1 ± 2 of
menstruation in at least two out of
three menstrual cycles and at no other
times of the cycle
• Menstrually-related migraine without
aura
• Diagnostic criteria
A. Attacks in a menstruating woman, fulfi
lling criteria for migraine without aura
B. Attacks occur on day 1 ± 2 of
menstruation in at least two out of
three menstrual cycles and additionally
at other times of the cycle
 Treatment
• There is no difference in symptomatic treatments for
menstrual and non-menstrual migraine attacks.
• All the triptans available are effective for treating menstrual
attacks.
• Encouraged to eliminate non-hormonal triggers. by avoiding
dehydration and long periods without eating.
• Hysterectomy has no role.
 Perimenstrual prophylactic strategies
for menstrual migraine
Strategy Who Regimen
Mefenamic acid Menstrual attacks on 2–3 days before
500 mg 3–4 times daily days 1–3 of bleeding expected
Naproxen Migraine associated onset of menstruation
550 mg 1–2 times daily with until first 2–3 days of
menorrhagia and/or bleeding
dysmenorrhoea
Perimenstrual estradiol Regular and predictable Three days before
1.5 mg in 2.5 g gel/ menses expected onset of
100 μg patch Must be ovulating menstruation for seven
(check progesterone days total
level)
Sumatriptan Regular and predictable Two to three days
25 mg three times daily menses before expected onset
of menstrual migraine
for five days total
Perimenstrual oestrogen supplements
• Only consider for women
with regular and predictable
menstruation.
• If other strategies fail,
oestrogen supplementation
when oestrogen is naturally
declining before the onset of
menses
• No additional progestogens
are necessary for endo-
metrial protection provided a
Incidence of migraine, urinary estrone-3-glucuronide (E1G)
woman is producing her own and pregnanediol-3-glucuronide (PdG) levels on each day of
natural progesterone. the menstrual cycle
 Childhood Periodic Syndromes
✓Abdominal migraine,
✓cyclical vomiting syndrome,
✓benign paroxysmal vertigo and
✓benign paroxysmal torticollis of infancy
• are closely related to migraine
• The diagnosis of each disorder is based on well-defined clinical
criteria and the absence of abnormalities on clinical
examination
 Childhood Periodic Syndromes
• Minimum investigations of a child with recurrent episodic
vomiting or abdominal pain
– Urine culture
– Blood count and biochemical screen, including acute phase reactants
– Abdominal ultrasound during an attack, for renal enlargement
– Urine examination for amino acids, short chain organic acids and
porphyrins during an attack;
– Acid–base balance, lactate/pyruvate ratio and ammonia during an
attack
 Diagnostic criteria
Benign Paroxysmal Torticollis Of Benign Paroxysmal Vertigo Of
Infancy Childhood
A. Episodic attacks, in a young child, A. At least five attacks fulfilling criterion B
with all of the following B. Multiple episodes of severe vertigo,occurring
characteristics and fulfilling without warning and resolving spontaneously
criterion B: after minutes to hours
1. tilt of the head to one side, with or C. Normal neurological examination, audiometric
without slight rotation
2. lasting minutes to days
and vestibular functions between attacks
3. remitting spontaneously and D. Normal electroencephalogram
tending to recur monthly
B. During attacks, symptoms and/or
signs of one or more of the
following:
1. pallor, irritability, malaise
2. vomiting, ataxia
C. Normal neurological examination
between attacks
D. Not attributed to another disorder
 Abdominal Migraine Cyclical Vomiting
A. At least 5 attacks fulfilling A. At least five attacks fulfilling
criteria B–D criteria B and C
B. Attacks of abdominal pain B. Episodic attacks, stereotypical in
lasting 1–72 hours the individual patient, of intense
C. Abdominal pain has all of the nausea and vomiting lasting
following characteristics: from one hour to fi ve days
1. midline location, periumbilical/
poorly localized C. Vomiting during attacks occurs
2. dull or ‘just sore’ quality at least four times an hour for at
3. moderate or severe intensity least one hour
D. During abdominal pain at least D. Symptom-free between attacks
two of the following:
E. Not attributed to any other
1. anorexia, nausea
2. vomiting, pallor
disorder
E. Not attributed to another
disorder
 Treatment
Childhood Periodic Syndromes
• Management of BPTI
– reassured about the benign course of the condition and of the complete
recovery over a period of 2–3 years.
– No specific treatment is required
• Management of abdominal migraine
– a full assessment of the child, exclude other treatable organic causes
– search for avoidable trigger factors, such as stress, travel, prolonged
fasting, irregular sleep
– simple oral analgesics with or without metoclopramide or domperidone
can be tried.
– explanation and reassurance
• Management of CVS
– should be started as early as possible after the onset of symptoms and
before the start of vomiting.
– rest, given small and frequent amounts of fluids
– Oral ondansetron has proved effective
– Prevention of dehydration ORT
– Preventive treatment, including pizotifen, amitriptyline or erythromycin,
may be necessary in children with frequent episodes requiring hospital
admissions
– Encouraging a healthy lifestyle
 Summary
• Primary headache disorders are diagnosed according to
duration and frequency of attacks, and thus depend on
accurate history taking, with headache diaries if necessary.
• Migraine (not TTH) is the most common episodic headache
disorder that prompts consultation to a physician in secondary
care, and is often misdiagnosed.
• Chronic daily headache is not a diagnosis and a cause must be
identified. Associated analgesic medication overuse must
always be considered before attributing it to chronic TTH.
 Summary
• Red flags signs should be used to determine the need for
investigation to exclude serious secondary headache disorders.
• We should be familiar with the IHS classification
• Ideal headache management needs correct diagnosis, right
choice of medications, a sound rapport with the patient
• Headache Medicine is a new emerging area that is on the way
to becoming a credible subspeciality
• Need of headache clinics
• Reference
– Harrisons, 17th edition
– Cecil's medicine 23rd edition
– Davidson's Principles Of Medicine 20th edition
– ABC of headache by Anne MacGregor, Alison Frith. 2009
– Neurological disorders: a public health approach, WHO
– How do I diagnose headache?
J R Coll Physicians Edinb 2006; 36:336–342
– Optimising Primary Headache Management
K Ravishankar japi vol. 54 december 2006
– L J Stovner et al The global burden of headache : a documentation of
headache Prevalence and disability worldwide
Cephalalgia,2007, 27,193–210
Thank you………..
Diagnostic criteria tension-type headache
EPISODIC CHRONIC
A. At least 10 episodes occurring on A. Headache occurring on ≥15 days per
<15 days per month on average for month on average for three months
three months (<180 days a year) (≥180 days a year) and fulfilling
and fulfilling criteria B–D criteria B–D
B. Headache lasting from 30 minutes B. Headache lasts hours or may be
to 7 days continuous
C. Headache has at least two of the C. Headache has at least two of the
following characteristics: following characteristics:
1. bilateral location 1. bilateral location
2. pressing/tightening (non-pulsating) 2. pressing/tightening (non-pulsating)
quality quality
3. mild or moderate intensity 3. mild or moderate intensity
4. not aggravated by routine physical 4. not aggravated by routine physical
activity such as walking or climbing activity such as walking or climbing
stairs stairs
D. Both of the following: D. Both of the following:
1. no nausea or vomiting 1. No more than one of photophobia,
2. no more than one of photophobia phonophobia or mild nausea
or phonophobia 2. No moderate/severe nausea/vomiting
E. Not attributed to another disorder E. Not attributed to another disorder
 Diagnostic criteria
CLUSTER HEADACHE PAROXYSMAL HEMICRANIA
A. At least 5 attacks fulfilling criteria B– A. At least 20 attacks fulfilling criteria B–
D D
B. Severe or very severe unilateral B. Attacks of severe unilateral orbital,
orbital, supraorbital and/or supraorbital or temporal pain lasting
temporal pain lasting 15–180 2–30 minutes
minutes if untreated C. Headache is accompanied by at least
C. Headache is accompanied by at one of the following:
least one of the following: 1. ipsilateral conjunctival
1. ipsilateral conjunctival injection injection/lacrimation
and/or lacrimation 2. ipsilateral nasal congestion/
2. ipsilateral nasal congestion and/or rhinorrhoea
rhinorrhoea 3. ipsilateral eyelid oedema
3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial sweating
4. ipsilateral forehead and facial 5. ipsilateral miosis/ ptosis
sweating D. Attacks have a frequency above 5 per
5. ipsilateral miosis and/or ptosis day for more than half of the time,
6. a sense of restlessness or agitation although lower frequency may occur
D. Attacks have a frequency from one E. Attacks are prevented completely by
every other day to eight per day therapeutic doses of indometacin
E. Not attributed to another disorder F. Not attributed to another disorder
“A Migraine Generator”
Activation of meningeal nociceptors by increased
parasympathetic tone
The triggering of pain via the trigeminovascular pathway
Cortical spreading depression