Headache

Classification
Classification system by the
International Headache Society
I.

Primary headaches
those in which headache is not associated with
demonstrable organic disease or structural neurologic
abnormality.

II. Secondary headaches

those attributed to the causative disorder.

Primary Headache
90%
1. Tension-type
2. Migraine
3. Cluster
4. Exertional

Secondary Headache
10%
1. Infection
2. Head injury
3. Vascular disorders
4. Brain tumor
5. Drugs
6. Ophtalmological
7. ENT cause
8. Dental
9. Others

Anatomy & Physiology of Headache

Headache may originate from either or both
mechanisms
1. Stimulation of nociceptors(pain)
2. Damage or inappropriate activation of pain
-producing pathways of the peripheral(PNS)
or central nervous system (CNS)

Pain-sensitive
cranial structures
1. Scalp
Pain insensitive
2. middle meningeal structures
artery
1. ventricular
3. Dural sinuses
ependyma
4. falx cerebri
2. choroid plexus
5. proximal
3. pial veins
segments of the
4. brain parenchyma
large pial arteries

key structures involved in primary

headache
1.Trigeminovascular system - peripheral
terminals of the trigeminal nerve that
innervate large intracranial vessels and dura
mater .
2.Trigeminocervical complex - Lower portion
of trigeminal nucleus, which receives input
from the 1 st and 2nd cervical nerve roots.
3.Pain-processing regions - such as the
thalamus and the cortex
4.Pain-modulatory systems that modulate
input from trigeminal nociceptors

High risk features

1. "Worst" headache ever
2. Worsening over days or weeks
3. Abnormal neurologic examination
4. Fever or unexplained systemic signs
5. Vomiting that precedes headache
6. Pain induced by bending, lifting, cough
7. Pain that disturbs sleep or presents immediately
upon awakening
8. Known systemic illness - hiv
9. Onset after age 55
10.Pain associated with local tenderness, e.g.,
region of temporal artery

Clinical Evaluation of Acute,

New-Onset Headache
I. History
II. Clinical examination
III. Investigation

HISTORY
1. O/D/P/ location/character/pattern of
2.
3.
4.
5.
6.
7.
8.

radiation/frequency/severity
Precipitating factors
Aggravating/ Relieving factors
Systemic symp. like fever, vomiting
Neurologic symp.
Eye/ENT/ Dental symp.
Drugs drug abuse,
Others - family history,

1. Detailed neurologic examtn (first step)

2. ENT / EYE/ Dental examination
3. CVS exam including BP
4. Cranial arteries by palpation
5. Cervical spine
6. Brain imaging MRI, CT
. In patients with abnormal examination
. history of fever, recent-onset severe

headache
7. LP in meningitis

Tension-Type Headache (TTH)

chronic headache characterized by bilateral tight,

bandlike discomfort.
Pain typically builds slowly, fluctuates in severity, and

may persist more or less continuously for many days.

Headache may be episodic or chronic (present >15 days

per month).
TTH are completely without accompanying features such

as nausea, vomiting, photophobia, phonophobia,

osmophobia, throbbing, and aggravation with movement.

Pathophysiology
Exact not known.
likely that TTH is due to disorder of CNS pain

modulation alone, unlike migraine, which

involves a more generalized disturbance of
sensory modulation.
Genetic contribution.
No clear evidence for tension as an etiology.
Muscle contraction has been considered to be
a feature that distinguishes TTH from
migraine.

Treatment
1. Simple analgesics such as acetaminophen,

aspirin, or NSAIDs.
2. Behavioral approaches including relaxation
.
3. Triptans - effective in TTH when the patient
also has migraine.
4. For chronic TTH - amitriptyline (only proven
treatment )

MIGRAINE
Primary headache recurrent & benign
2nd most common cause of headache
F > M
Various triggers
Glare bright lights
Sounds
Hunger
excess stress
physical exertion
stormy weather
menses
Sleep disturbances
alcohol or other chemical stimulation

Triggers

Strong
smells

Weather

Strenous
Activity

Foods

Addictions

Sleep
disturbances

Hunger
hunger

Diagnostic Criteria for Migraine

Repeated attacks of headache lasting 472 h in

patients with a normal physical examination, no other
reasonable cause for the headache, and:
At Least 2 of the
Following Features:

Plus at Least 1 of the

Following Features:

Unilateral pain

Nausea/vomiting

Throbbing pain

Photophobia and
phonophobia

Aggravation by movement
Moderate or severe
intensity

Pathogenesis
Exact not known
Probably due to dysfunction of

monoaminergic sensory control systems

located in the brainstem and thalamus
Involvement of the 5-HT; (also known as
serotonin) in migraine.
Data also support a role for dopamine.
Migraine genes - familial hemiplegic migraine
(FHM) reveal involvement of ion channels. Eg
FHM 1, FHM 2, FHM 3.

Symptoms Accompanying Severe

Migraine Attacks
Common
Nausea , Vomiting, Photophobia, Scalp
tenderness, Visual disturbances, Paresthesias
Less common
Vertigo, Photopsia, Diarrhea, Fortification
spectra
Rarely
Syncope, Seizure, Confusional state

Variants of migraine
Acephalgic migraine
Patients experience recurrent neurologic
symptoms, often with nausea or vomiting, but
with little or no headache.

Diagnosis
1. Mainly based on history
2. Rule out secondary causes & other primary

headaches
3. headache diary
.helpful in making the diagnosis
.helpful in assessing disability and the
frequency of treatment for acute attacks
4. Migraine Disability Assessment Score (MIDAS)
.assess the extent of a patient's disease and
disability

Management
1. Non pharmacological
2. Pharmacological
i. Acute attack
ii. prophylaxis

Non pharmacological
1. Avoidance of triggers
2. Regulated lifestyle - healthy diet, regular

exercise, regular sleep patterns, avoidance

of excess caffeine , smoking , alcohol.
3. Stress reduction techniques - include yoga,
meditation, hypnosis, and conditioning
techniques such as biofeedback.

Pharmacological Acute attack

I. Simple Analgesics
. Acetaminophen, aspirin
II. NSAIDs
. Naproxen, Ibuprofen
III. 5-HT1 Agonists
A. Oral

Ergot alkaloids - Ergotamine,

Triptans - Sumatriptan, Zolmitriptan, Naratriptan
B. Nasal
Dihydroergotamine, Sumatriptan, Zolmitriptan
C. Parenteral
Dihydroergotamine, Sumatriptan

Cont..
IV. Dopamine Antagonists [ adjunct

therapy ]
A. Oral- Metoclopramide, Prochlorperazine
B. Parenteral- Metoclopramide,
Prochlorperazine , Chlorpromazine
V. Others [ as last resort ]
Butorphanol
Narcotics

1st line Rx

Analgesics/NSAIDS/Metoclopramide
2nd line Rx Triptans/ Ergot alkaloids
Drugs are most effective when taken early in
the migraine attack.

5-HT1 Receptor Agonists

Acts on 5-HT1B/1D receptors.
Ergotamine and dihydroergotamine are
nonselective receptor agonists
Triptans are selective 5-HT 1B/1D receptor agonists.
Rizatriptan and eletriptan are the most efficacious
triptans.
Triptans are not effective in migraine with aura
unless given after the aura is completed and the
headache initiated.
5-HT1B/1D agonists contraindicated in CVS and
cerebrovascular disease.

Dopamine Antagonists
Drug absorption is impaired during migraine
because of reduced GIT motility so dopamine
antagonist decrease nausea/vomiting and
restore normal gastric motility.

Pharmacological Prophylaxis
In subset of patients with five or more attacks a

month.
The mechanism of action of these drugs is unclear;
brain sensitivity is modified.
Patients are usually started on a low dose of a
chosen treatment; the dose is then gradually
increased, up to a reasonable maximum to achieve
clinical benefit.
Drugs must be taken daily, and there is usually a lag
of at least 212 weeks before an effect is seen.
Once disease is stabilization, the drug is continued
for ~6 months and then slowly tapered to assess the
continued need.

1. Flunarizine
2. Beta blocker - Propranolol
3. Anticonvulsants Topiramate, Valproate,

Gabapentin
4. Tricyclics Amitriptyline, Dothiepin,
Nortriptyline
5. Others Methysergide, Pizotifen

Trigeminal Autonomic Cephalalgias

[TAC]
Group of primary headaches that includes
1. Cluster headache
2. Paroxysmal hemicrania
3. SUNCT (short-lasting unilateral neuralgiform headache attacks

with conjunctival injection and tearing)

4. SUNA (short-lasting unilateral neuralgiform headache attacks
with cranial autonomic symptoms).
.TACs are characterized by relatively short-lasting head pain
associated with cranial autonomic symptoms, such as
lacrimation, conjunctival injection, or nasal congestion
.Pain is usually severe and may occur more than once a day.
.Patients with TACs should undergo pituitary imaging and
pituitary function tests as there is an excess of TAC
presentations in patients with pituitary tumorrelated headache.

Clinical Features of the Trigeminal Autonomic Cephalalgias

Cluster Headache
Gender Pain
Type
Severity
Site
Attack frequency

Duration of attack
Autonomic
features

M>F
Stabbing, boring
Excruciating
Orbit, temple
1/alternate day8/d

15180 min
Yes

Migrainous
Yes
featuresb
Alcohol trigger
Yes
Cutaneous triggers
No
Indomethacin

effect
Abortive treatment Sumatriptan injection
or nasal spray

Oxygen

Paroxysmal
Hemicrania
F=M
Throbbing, boring,
stabbing
Excruciating
Orbit, temple
140/d (>5/d for
more than half the
time)
230 min
Yes

SUNCT
FM
Burning, stabbing,
sharp
Severe to
excruciating
Periorbital
3200/d

Yes

5240 s
Yes (prominent
conjunctival injection
and lacrimation)a
Yes

No
No
Yesc

No
Yes

No effective
treatment

Lidocaine (IV)