Headache

Introduction
• Headache refers to pain in any part of the
head, the scalp, face and the interior of
the head.
• One of the most common complaints
encountered by physicians in day to day
practice.
• Overall prevalence of migraine is
estimated to be 12%to 16 % .
• Severe, disabling headache is reported
annually by 40% of individuals worldwide.
 .

 Headache affects 95% of people

in their lifetime.
 Headache affects 75% of people
in any one year.
 One in 10 people have migraine.
 One in 30 people have headache
more often than not, for 6
months or more.
 .

Pathomechanism
Pain occurs
1.When peripheral nociceptors are stimulated
in response to
a.tissue injury
b.visceral distension
2.When pain-producing pathways of the
peripheral or central nervous system (CNS)
are damaged or activated inappropriately
 .

3- Intracranial masses cause headache

– when they 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
4- Impaired central inhibition as a result of
perturbation of intracerebral serotonergic
projections - possible mechanism of headaches
from
– cerebral ischemia,
– benign intracranial hypertension after
reduction of the pressure,
– febrile illnesses.
 Classification of Headache
1. Primary headaches –Idiopathic
(Functional headache) - ~85%
with no identifiable underlying cause
 Migraine
 Tension-type headache
 Cluster headache
 psychogenic
 Classification of Headache cont’d
2. Secondary headaches –
Symptomatic (organic) - ~15%
 Underlying condition such as trauma or a
mass lesion.
 Intracranial diseases
 Cranial trauma
 Extra cranial causes – eye, ear problems
 Toxic or systemic illnesses – febrile
illnesses
 Post lumbar puncture
History taking

.
 History taking
1. Characteristics  Crawling sensation
of the pain  Itching sensation
Throbbing  Tightness
stabbing  Heaviness
Burning
Dull aching
Cold sensation
 History taking cont’d

2. Localization and radiation

Generalized
Unilateral
bitemporal
Occipital
Frontal
over the vertex
periorbital
 History taking cont’d

3. Pattern and duration

Intermittent- periodic
Continuous
In clusters
4. Time predilection
Nocturnal
On awakening
Afternoons
 History taking cont’d
5. Aura symptoms
Presence or absence of aura
Characteristics of aura
Visual
Paresthesia
Olfactory
6. Associated symptoms
Nausea and vomiting
Photophobia
Noise intolerance
 History taking cont’d

7. Precipitating factors
Dietary – alcohol, chocolate,
Sleep deprivation
Particular odors
Psychological stress
Weather changes
 History taking cont’d

8. Current medication
 Prescription drugs -contribute/cause
headache (oral contraceptive, etc.)
 Overusing analgesia
 Using recreational drugs
 MIGRAINE

• .
 .

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
2- Neurovascular theory
 migraine is primarily a neurogenic process with
secondary changes in cerebral perfusion
3-Cortical spreading depression
 the primary cortical phenomenon or aura phase
 it activates trigeminal fibers causing the
headache phase
 .

Neurotransmitters

1.Serotonin receptors

• Dorsal raphe -highest concentration of

serotonin receptors -generator of migraine
and the main site of drug action

2. Involvement of NMDA receptors- glutamate

General features - migraine
 Familial in 80% of cases(classical type)
 Usually begins in childhood or
adolescence
 Precipitating factors
Stress
Diets –cheese, wine,
Sleep deprivation
Menses
Specific odor etc.
 Classification of migraine(IHS)
1. Migraine without aura
2. Migraine with aura
 Typical aura with migraine headache
 Typical aura without headache
 Familial hemiplegic migraine (FHM)
 Sporadic hemiplegic migraine
 Basilar-type migraine
3. Childhood periodic syndromes
4. Complications of migraine
Chronic migraine
Status migrainosus , +++
AND ++
Migraine without aura (common migraine) - IHS

1. Five attacks lasting from 4 to 72 hours are

required.
2. Two of the following four pain characteristics:
unilateral location
pulsating quality
moderate to severe intensity
aggravation by routine physical activity
3. Associated symptoms
Nausea or vomiting
Photophobia and phonophobia
Migraine with aura (classic migraine)
 At least two attacks that are not
attributable to another disorder
 Fewer attacks are required to make a
diagnosis of migraine with aura
 May be less severe, of shorter duration, or
both
 Aura - Visual Auras , Sensory auras
usually lasts 20–30 minutes
typically precedes the headache
occasionally it occurs only during the
headache.
 Migraine Phases
Divided into four phases:
the premonitory phase, which occurs
hours or days before the headache
the aura, which comes immediately
before the headache
the headache itself
the postdrome
 Migraine Phases
1. The premonitory phase
 In approximately 10-60% of migraineurs
 Hours to days before the onset of
headache
Autonomic symptoms
Psychological
 Depression, euphoria
 Irritability, Restlessness,
 Mental slowness,or Hyperactivity,
 Fatigue, Drowsiness
Neurologic - photophobia, phonophobia,
hyperosmia
 Migraine Phases cont’d
2. Aura
• Visual Auras
Colorless glittering Scotomata
Black-and-white zigzag patterns
(Fortification lines)
The phenomenon of a geometric pattern
with expansion from the center to the
periphery of the visual field
Photopsias - regular angular patterns
may evolve into scotoma or temporary
homonymous hemianopia
 Migraine Phases cont’d

….2. Aura
• Sensory auras
Paresthesias (pins and needles) that
typically begin in the hand, move up the
arm
Move into the face and tongue over a
period of 10 to 15 minutes
Often associated with a visual aura
 Migraine Phases cont’d
3. The headache itself
 Throbbing headache
 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,
 Migraine Phases cont’d

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.
 Status migrainosus
• Attacks that persist for more than 3
days are known as Status Migraine
 Other migraine variants
 Hemiplegic migraine
• Weakness which may last longer than
60 minutes(ie, much longer than a
typical aura).
• It may be sporadic, or familial with an
autosomal dominant inheritance.
 Vertebrobasillar migraine
 dysarthria, vertigo, tinnitus, deafness,
diplopia, ataxia, decreased level of
consciousness, and bilateral sensory
symptoms.
 .

Ophthalmoplegic ‘‘migraine’’:
 reclassified as a cranial neuralgia
(secondary headache syndrome),
rather than a form of migraine.
 Typical migraine headache is
associated with an external
ophthalmoplegia (most commonly 3rd
nerve palsy
 The headache often lasts a week or
more, with a latency between
headache onset and ophthalmic
symptoms of up to four days.
 ..

Childhood periodic syndromes (migraine

precursors)
 cyclical vomiting,
 abdominal ‘‘migraine’’
 benign paroxysmal vertigo
 ..

Chronic migraine
A. Headache (tension-type and/or migraine)
on >15 days per month for at least 3
months
B. Occurring in a patient who has had at
least 5 attacks fulfilling criteria for
migraine without aura
C. Fulfill -criteria for migraine without aura
D. No medication overuse and not
attributed to another causative disorder
 Course and outcome of
Migraine
Commonly life long • Temporary relief
Frequency and during pregnancy
severity varies • Increased
• ½ will have less susceptibility
frequent migraine during menses
• 1/3 will have no • Improvement
migraine during menopause
• 1/6 will have • Changing pattern
unchanged course of the headache
 .

Psychiatric disorders and Migrain

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
 Analgesics – ASA, paracetamol,
ibuprofen, sumatriptan
 Ergotamine - 1-2 mg during the aura
phase or at the onset of headache
 Antiemetics – e.g.promethazine 25 mg
stat
 For migraine status – corticosteroid
 .

2. Prophylactic treatment
 The drugs must be taken daily

 Can stabilize migraine and prevent

attacks

 Depends on the frequency of attacks and

how effective the acute treatment is
Frequency of migraine attacks is
greater than 2x per month
 .

– Duration of individual attacks is longer

than 24 hours
– Significant disability that lasts 3 or more
days
– Abortive therapy fails or is overused
– Use of abortive medications more than
twice a week

**Treatment duration: after 6 months of stable

state trial of drug withdrawal
 .

Prophylactic medications include the

following:
– Tricyclic antidepressants
– Beta blockers
– Antiepileptic drugs
– Calcium channel blockers
– Selective serotonin reuptake inhibitors
(SSRIs)
– NSAIDs
– Serotonin antagonists
– Botulinum toxin
a- Anti-depressant drugs
Tricyclics/venlafaxine appear effective, but
SSRIs –not useful
Amitryptyline – 10-50mg(150) mg /day
dothiepin 25 mg/day
b- Beta-blockers
Propranolol 40–240 mg/day, should be
avoided in asthma
Others (eg, metoprolol,atenolol, timolol,
nadolol) - probably as effective as
propranolol
c- Anticonvulsant
Sodium valproate (500–2000 mg/day)
 Teratogenicity and weight gain limit
usefulness in women
Topiramate (100 mg/day)
Gabapentin (up to 1800 mg/day)
 Evidence less robust than for
valproate/topiramate
d- Methysergide (up to 12 mg/day) -
Effective, but rare serious fibrotic adverse
effects: should not be used for longer than
6 months
 .

The major drugs and their daily dose are

 Propranolol (40 to 240 mg)
 Amitriptyline (30 to 150 mg)
 Valproate (500 to 2,000 mg)
 Verapamil (120 to 480 mg)
 Phenelzine (45 to 90 mg)
 Methysergide (4 to 12 mg)

Injection of botulinum toxin (Botox) into

sensitive temporalis and other cranial
muscles
 .

3. Avoiding precipitating factors

Specific for each individual
Give awareness so that they recognize the
precipitant and avoid it
Dietary
Specific odors
Emotional
Weather,. Etc
 Excess caffeine intake or withdrawal of
caffeine
 Birth control pills has been associated with
an increased frequency and severity of
migraine
 Comorbidity–Epilepsy/Migraine
The mechanisms of the association between
migraine and epilepsy are complex and
may be multifactorial.
Migraine may cause epilepsy by inducing
brain ischemia and injury.
Epilepsy may cause migraine by
activating the trigeminovascular system.
Shared environmental risk factors may
contribute to comorbidity
 head injury.
 genetic risk factors
An altered brain state (increased
excitability) might increase the risk of
both migraine and epilepsy
 Women and Migraine
• 3X more after menarche.
• ~ 25% of women have migraine
during their reproductive years.
• Changing hormonal environment like
menarche, menstruation, OCP,
pregnancy, menopause, can have a
profound effect on the course of
migraine.
 Menstrual migraine

• ~70 % of female migraineurs report

menstrual association.
1,True/pure menstrual migraine (TMM)
occur exclusively during menstruation
( -2 to +3);prevalance 7-21%
2. Menstrual associated migraine; 35-
56%
3,premenstrual migraine −7 and −3
before menstruation
 pathogenesis of menstrual
migraine
• estrogen withdrawal before menstruation
is a trigger for migraine.
• Estrogen withdrawal may modulate
hypothalamic β-endorphin, dopamine, β-
adrenergic, and serotonin receptors.
• This complex relationship causes
significant downstream effects such as a
reduction in central opioid tone, dopamine
receptor hypersensitivity.
 Management of Menstrual Migraine

 Acute Menstrual Migraine Therapy

• does not differ from the treatment of migrain
unassociated with menstruation.
 Prophylactic Menstrual Migraine Therapy
• Cyclic (Perimenstrual) Days −3 Though +3
NSAIDs
Triptans and Ergots
• Noncyclic (Throughout Cycle)
Tricyclic antidepressants,BB, CCB Anticonvulsants
 Oral Contraception in Female
Migraineurs

• Oral contraceptives have a variable effect on

migraine.
• Migraine may begin after starts taking oral
• Preexisting migraine may worsen in severity or
frequency, or change in character
• Migraine attacks may lessen after an OCP
• Majority of women no change in pattern
• The risk for ischemic stroke increased in women
with migraine who were using OCP
• Recommendations to use low-dose Combine OC
 Migraine and Pregnancy
• 70% experience improvement or remission.
• Attacks can either remain unchanged or
worsen.
• If remission occurs during pregnancy,
migraine often recurs in them postpartum
period.
• Drug treatment should be limited
acetaminophen (650 to 1000 mg) and
metoclopramide
 Cluster Headache
(Previously called migrainous
neuralgia)
.

Clinical features
 Acute, non-throbbing, unilateral
headache- (excruciating in intensity
and is deep, nonfluctuating, and
explosive in quality)
 No aura
 Periorbital localization
 Radiates to forehead, temple and
cheek
 Occurs in clusters
 Lasts 30 minutes to 2 hours
 .

Associated symptoms
Blocked nostrils
Rhinorrhea
Conjunctivitis
Flush and edema of cheeks
In 20%, family history of similar
headache
 .

• Men are affected more often than women -

8:1.
• Most patients begin experiencing headache
between the ages of 20 and 50 years
• Alcohol provokes attacks in about 70% of
patients but has no effect when the bout is
over
• Rarely do foods or emotional factors activate
the mechanism, in contradistinction to
migraine
• Periodicity of attacks is evident in at least
85% of patients.
• Nocturnal hours in about 50% of patients
 .

Pathomechanism
Paroxysmal vasodilatation
Abnormal serotonergic
neurotransmission at different sites
Differential diagnosis
Migraine
Trigeminus neuralgia
Sinusitis
Brain tumor
 .

Treatment - for the period of the attack

• Ergotamine 3 mg PO or 1mg IM
• Sumatriptan 6 mg subcutaneous.
• Start prednisolone (50-75mg/day) and
verapamil (up to 240 mg/day, sometimes
higher) at the beginning of a cluster, tailing
the steroids after 2–3 weeks, but continuing
verapamil until the cluster has resolved.
• NSAID :Indometacin (up to225 mg/day)
– Start at 25 mg three times daily for first
week, then 50 mg three times daily for
second week, and 75 mg three times daily in
third week
 Headaches of
psychiatric disorders

• .
 Clinical features
1. Odd cephalic pain
Burning sensation
Feeling of tightness
Crawling sensations
Wound-like pain
Numbness
heaviness,
Cold/heat sensations, etc.
 Clinical features cont’d
2. Variable localization
 Unilateral
 Generalized
 Over the vertex
 Changing locations
 Occurring at different sites at the
same time
3. Variable time predilection and precipitant
for the head pain
4. Intractable to different analgesics
 Clinical features cont’d
5. Additional symptoms of common
psychiatric disorders leading to or
accompanied by such head pain
Depressive disorders
Anxiety disorders
Somatoform disorders
 Treatment
Treat the primary psychiatric disorder
Antidepressants
Anxiolytic drugs
Counseling - psychotherapy
 Headaches of brain
tumor

• .
 Clinical features
 Deep seated, non-throbbing, aching
or bursting
 Localization
o Initially at the site of the tumor
o Later generalized
 Pattern
o Initially – paroxysmal
o Later persistent
 Clinical features cont’d

 Time predilection
o Worse on awakening, or early morning
hours
 Associated symptoms
o Focalizing neurologic signs –paralysis,
aphasia, etc.
o Sign of increased intracranial pressure –
projectile vomiting, blurring of vision,
etc.
 Treatment
 Primary tumor treatment
o Chemotherapy
o Radiation
o Surgery
 Reduce the increased intracranial
pressure
o Dexamethsone 4 mg QID
 Analgesics
o Including opoid analgesics e.g. morphine
 Trigeminus neuralgia
( tic douloureux)

• .
 Clinical features
Idiopathic
 Unilateral
 Intense, stabbing pain over the lower face
(Maxillary and mandibular branch of the
5th cranial nerve)
 Paroxysmal
 Intermittent, recur frequently, day and
night
 Duration
o Few seconds up to 1-2 minutes
 Clinical features cont’d
 Precipitated by
 Any stimulus applied to face, lips,
or gums
Shaving
Talking
Yawning
chewing
 .

Differential diagnosis
Idiopathic –
o compression of the trigeminal roots
by a tortuous blood vessel
Multiple sclerosis
Aneurysm of the basillary artery
Tumor of cerebellopontine angle
 Treatment
 Drug treatment
 Carbamazepine 200 - 1000 mg/day
 Clonazepam 2 – 8 mg/day
 Phenytoin 200 – 800 mg/day
 Surgical treatment – if drugs fail
 Alcohol injection into the affected nerve
 Sectioning of the trigeminus root
 Stereo tactic – thermocoagulation of the
trigeminus root
Tension-type headache

.
 ..

TENSION-TYPE HEADACHE
 Tension headache - chronic headaches of unapparent
cause that lack features characteristic of migraine or
cluster headache
 Underlying pathophysiologic mechanism is unknown
 Tension is unlikely to be primarily responsible.
 Contraction of neck and scalp muscles- probably a
secondary phenomenon
 Is a chronic disorder that begins after age 20.
 Characterized by frequent (often daily) attacks of
nonthrobbing, bilateral occipital head pain
 Not associated with nausea, vomiting, or prodromal
visual disturbance
 Likened to a tight band around the head.
 Women are more commonly affected than men.
 Epidemiology

• True incidence is not known.

• Average age at onset 30-39 years
• Male: female = 4:5 (esp white women)
• Lifetime prevalence in the general
population ranging b/n 30% and 78%
• Prevalence of chronic TTH is 2-3%
 Clinical features
• Mild to moderate intensity.
• Bilateral
• Non throbbing
• Without other associated features.
Pain described as
• Dull, pressure, head fullness, head feels large,
like a tight cap, band like, heavy weight on
my head.
Precipitating factors
• Stress
 TTH classification
1, Infrequent episodic tension-type headache
2, Frequent episodic tension-type headache
3, Chronic tension-type headache

 Pathogenesis: unknown
Psychological & environmental factors can
initiate the pain cycle
 .

Treatment
• Simple analgesics, such as aspirin or
acetaminophen or other NSAIDs,
• Drugs that relieve anxiety or depression,
• Preventive: Amitriptyline for chronic TTH
• Ancillary measures
– Massage,
– Meditation,
– biofeedback techniques
– Relaxation techniques