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neck pain, autonomic reactions (sweating, flushing,

OUTLINE tachycardia)
• Alleviating: rest or sleep, history of medications and
I. HEADACHE response
A. History Taking • Activities of daily living (can be a marker of severity and
II. INTERNATIONAL CLASSIFICATION OF depression)
HEADACHE DISORDERS 3RD ED (ICHD-3)
A. Pain-sensitive Structures in the Brain II. INTERNATIONAL CLASSIFICATION OF
III. PRIMARY HEADACHE HEADACHE DISORDERS 3RD ED (ICHD-3)
A. Migraine
1. Aura I. Primary headache
2. Pathogenesis A. Migraine
3. Neuroimaging B. Tension-type Headache
4. Treatment C. Trigeminal autonomic cephalalgias (TAC)
B. Tension-type Headache D. Other primary headache disorders
II. Secondary Headache
1. Pathogenesis
A. Attributed to trauma or injury to head and/or neck
2. Treatment
B. Attributed to cranial or cervical vascular disorder
C. Trigeminal Autonomic Cephalalgias C. Attributed to non-vascular intracranial disorder
(TAC) D. Attributed to a substance or its withdrawal
1. Cluster Headache E. Attributed to infection
2. Paroxysmal Hemicrania F. Attributed to disorder of homeostasis
3. Short-lasting Unilateral Neuralgiform G. Attributed to disorder of the cranium, neck, eyes, nose,
Headache Attack sinuses, teeth, mouth or other facial or cervical
4. Hemicrania Continua structure
IV. NOTES FROM MEET/ Q & A H. Attributed to psychiatric disorder
V. TEST YOUR KNOWLEDGE III. Neuropathies, Facial Pains and other headaches
A. Painful lesions of the cranial nerves and other facial
VI. REFERENCES
pain
VII. APPENDIX B. Other headache disorder

I. HEADACHE A. PAIN-SENSITIVE STRUCTURES IN THE BRAIN

• One of the most common neurologic complaints • The brain parenchyma itself cannot feel pain
• Can be the disease itself (primary headache) or a • Skin, subcutaneous tissue, muscles, extracranial arteries,
manifestation of another underlying disease (secondary external periosteum of the skull
headache) • Delicate structures of the eye, ear, nasal cavities and
• Episodic (<15 days per month) paranasal sinuses (sinus headache)
• Chronic (>15 days per month) • Intracranial venous sinuses and their large tributaries
• Parts of the dura at the base of the brain and arteries within
<4 hours >4 hours the dura
• Cluster headache • Migraine • Middle meningeal and superficial temporal arteries
• SUNCT/SUNA • Tension type • First 3 cervical nerves and cranial nerves as they pass
• Paroxysmal hemicrania headache through the dura
• Hemicrania
Table 1. Based on duration
III. PRIMARY HEADACHE
A. HISTORY TAKING
• Location: where does the pain starts A. MIGRAINE
• Quality: tight, dull, pressure, throbbing, stabbing, burning, • Periodic commonly unilateral, usually pulsatile headaches
bursting
• Often begins in childhood, adolescence or early adult life
• Radiation: where does it spread from the point of origin (80% before age 30)
• Severity: ask for the pain scale/numerical value of the pain • Usually familial (60-80%)
• Timing/Time: onset, frequency, catamenial, duration • Frequency diminishes during advancing years
• Associated symptoms: nausea, vomiting, photophobia • Usually hemicranial, throbbing/pulsating
(sensitivity to extreme light), phonophobia (sensitivity to
• Severe pain
extreme sounds), unintentional weight loss, focal deficits,
• Third most prevalent disorder in the world

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• May be accompanied by nausea, vomiting, sensitivity to light 1.6 Episodic syndromes that may be associated with
(photophobia), noise (phonophobia/sonophobia), smells migraine
(osmophobia) 1.6.1 Recurrent gastrointestinal disturbance
• Commonly intensified by head movement 1.6.1.1 Cyclical vomiting syndrome
• Relieved by lying down, rest and sleep, dark and quite room 1.6.1.2 Abdominal migraine
• Cease during the second and third trimester of pregnancy 1.6.1.3 Benign paroxysmal vertigo
• Use of birth control pills is associated with increased 1.6.1.4 Benign paroxysmal torticollis
frequency of migraine
2. Pathogenesis
• Some patients link dietary items: chocolate, cheese, fatty
food, oranges, tomatoes, onions, excess caffeine or caffeine • Vascular Theory
withdrawal o Distention and excessive pulsation of the
external carotid artery
• During the preceding day, the patient may have mild changes
o Aura: reduction in blood flow resulting to
in mood, hunger, or anorexia, drowsiness or frequency
cortical depression
yawning
• Trigeminal Involvement
• Temporal scalp vessels may be tender
o Extra cranial and intracranial vessels are
• Worsened by strain or jarring of the body and head
innervated by CN V
• Catamenial migraine/menstrual migraine
o Subserves both pain and autonomic functions
- Seen in younger women during their premenstrual
o Release of substance P, calcitonin gene-
period
related peptide (CGRP)
- Presumed to be due to drop in estradiol levels but it
• Serotonin
could be more complex process according to studies
o Serotonin is discharged from platelets at the
onset of headache
1. Aura
o Serotonin acts as a humoral mediator in the
• Ushered in by Disturbance of nervous function
neural and vascular components of migraine.
• Usually last for 30 minutes
• Most often visual: 3. Neuroimaging
- Unformed flashes of white or silver light, rarely
multicolored (Photophasia)
- Enlarging blind spot with a shimmering edge
(scintillating scotoma)
- Dazzling zigzag lines (teichopsia)
- Blurred, shimmering or cloudy vision
• Others: numbness and tingling of the lips, face, and hand;
slight confusion of thinking, weakness of an arm or leg,
mild aphasia, dysarthria, uncertainty of gait and
drowsiness
Figure 1. White matter abnormalities (esp. in migraine with aura)
• Certain patients will have the same aura for every
migraine attack 4. Treatment
It all starts with history taking – is it chronic or episodic?
1. Migraine If the patient has chronic migraine, it is better to start with
1. 1 Migraine without aura preventive therapy.
1. 2 Migraine with aura • Preventive
1.2.1 Migraine with typical aura - Reduce attack frequency, severity, duration and
1.2.1.1 Typical aura with headache disability
1.2.1.2 Typical aura without headache - Improve responsiveness to abortive treatment
1.2.2 Migraine with brainstem aura and avoid its escalation
1.2.3 Hemiplegic migraine - Reduce overall cost associated with migraine
1.2.3.1 Familial hemiplegic migraine treatment
1.2.3.2 Sporadic hemiplegic migraine - Pharmacologic, interventional, biobehavioral,
1.2.4 Retinal migraine neurostimulation, nutraceuticals, and lifestyle
1.3 Chronic Migraine modification
1.4 Complications of Migraine o Candesartan, Propranolol, Metoprolol
1.4.1 Status migrainosus o Divalproex sodium/ Valproate sodium,
1.4.2 Persistent aura without infarction Topiramate
1.4.3 Migrainous infarction
o Erenumab
1.4.4 Migraine- aura triggered seizure
o Botolinum toxin A
1.5 Probable migraine
1.5.1 Probable migraine without aura
1.5.2 Probable migraine with aura
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• Abortive/ Acute Migraine (given as needed)
- Rapid freedom from Pain and associated
symptoms
- Restore Function
- Minimal need for repeat dosing or rescue
medication
o Triptans: sumatriptan
o NSAIDs: aspirin, celecoxib, diclofenac,
ibuprofen, naproxen, paracetamol
o Antiemetics: chlorpromazine,
metoclopramide
B. TENSION-TYPE HEADACHE
• Usually bilateral, with occipitonuchal, temporal or frontal
predominance, or diffuse extension over the top of the top of
the cranium.
• Dull, aching, fullness, tightness, pressure by a band, feeling
that the head is swollen and may burst
• Absence of aura, photo/phonophobia, lateralization.
Interference with ADL
• Gradual onset, may persist for days, weeks or months
• Arise in middle age and coincide with anxiety, fatigue,
depression
• Severe
• Although sleep is usually undisturbed, the headache is
present when the patient awakens, or it develops soon
afterward, and the common analgesic remedies have little or
no beneficial effect if the pain is of more than mild to
moderate severity
1. Pathogenesis
• Tense pericranial and trapezius
• Recently, nitric oxide has been implicated in the genesis
of tension-type headaches, specifically by creating a
central sensitization to sensory stimulation from cranial
structures
• Unclear
2. Treatment
• Brief periods: NSAIDS
• Chronic: anxiolytics and antidepressants (amitriptyline)
• Massage, meditation, relaxation techniques
C. TRIGEMINAL AUTONOMIC CEPHALALGIAS
(TAC)
1. Cluster headache
2. Paroxysmal hemicrania
3. Short lasting unilateral neuralgiform headache attacks
o Short-lasting unilateral neuralgiform headache with
conjunctival injection and tearing (SUNCT)
o Short-lasting neuralgiform headache attacks with cranial
autonomic symptoms (SUNA)
4. Hemicrania continua
Pathogenesis
• Hypothalamus---> trigeminal nerve
o (The signals come to your hypothalamus and this pain
signals are transmitted to your trigeminal nerve and will
PREPARED BY: CMED 2B
be transmitted mainly through V1 and V2. Because of
the involvement of the trigeminal nerve, there will be
accompaniment of sympathetic and parasympathetic
symptoms)
• With sympathetic and parasympathetic symptoms
• Similar in clinical characteristics
• Differ in duration and treatment of choice
• Other distinct characteristics
1. Cluster Headache
• Temporal, cluster pattern
• Severe unilateral orbital location (pain, back in their eye)
• Very intense, throbbing, radiates to the forehead,
temple, and cheeks
• Nightly occurrence, between 1-2 hours after the onset of
sleep
• Same time every day ---> “Alarm clock headaches”
• Can happen several times during the night for several
consecutive days---> “cluster”
• Rapid onset: 5-10 minutes
• Duration: 30-90 minutes
• Severe
• Adult men (age range: 20-50 years, male-to-female ratio
5:1)
• Associated with vasomotor phenomena lasting 15-
180 minutes: blocked nostril, rhinorrhea, injected
conjunctivum, lacrimation, miosis, flush and edema of
the cheek
• During the attack the patient becomes restless very
striking characteristic
• Patients arise from bed during the attack, sit in a chair
and rock or pace the floor
• Possible triggers:
o cigarette smoke, alcohol, strong odors, change to a
high altitude, bright light, exercise or exertion, heat,
food that contain nitrates like bacon or luncheon
meat
• Acute attack:
o Triptans, lidocaine nasal spray, oxygen
• Preventive: corticosteroids like prednisone, divalproex
sodium, gabapentin, lithium, topiramate, verapamil
2. Paroxysmal Hemicrania
• Severe unilateral orbital, supraorbital and/or temporal
pain lasting for 2-30 minutes
• Associated with vasomotor phenomena lasting for 15-
180 minutes: blocked nostril, rhinorrhea, injected
conjunctivum, lacrimation, miosis, flush edema of the
cheek
• Unlike cluster headache:
- Shorter duration
- Occur many times each day, no preponderance of
night attacks
- More frequent attacks
- More predominant in women (3:1)
- Completely respond to indomethacin 25-50 mg
TID
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3. Short-lasting Unilateral Neuralgiform Headache Attacks
• Short-lasting Unilateral Neuralgiform Headache with
Conjunctival Injection and Tearing (SUNCT)
- Severe unilateral orbital, supraorbital and/or
temporal pain lasting 5-240 seconds
- Associated with vasomotor phenomena: injected
conjunctivum, lacrimation
- Treatment: IV lidocaine (acute), Lamotrigine 10-300
mg/day (initial: 25 mg/day, topiramate 50-200
mg/day, gabapentin 90-2700 mg/day)
• Short-lasting Unilateral Neuralgiform Headache
Attacks with Cranial Autonomic Symptoms
- Severe unilateral orbital, supraorbital and/or
temporal pain lasting 5-240 seconds
- Associated with vasomotor phenomena: blocked
nostril, rhinorrhea, miosis, flush and edema of the
cheek
- Treatment: IV lidocaine (acute), Lamotrigine 10-300
mg/day (initial: 25 mg/day, topiramate 50-200
mg/day, gabapentin 90-2700 mg/day)
Figure 2. Patterns of pain in SUNCT/SUNA
Lidocaine Indomethacin Triptans
Lamotrigine Lidocaine
Gabapentin Prednisone
Topiramate Divalproex sodium
Gabapentin
Lithium
Topiramate
Verapamil
Figure 3. Duration and Treatments of Trigeminal Autonomic
Cephalalgias
4. Hemicrania Continua
• Continuous nature (> 3 months) because of a mild,
background pain
• Can be exacerbated to produce moderate or greater
intensity of pain
• Responds absolutely to Indomethacin 25 mg TID
• May also use celecoxib, aspirin, short term prednisone,
some reports of topiramate
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(003) HEADACHE
IV. NOTES FROM THE MEET
• Normally, a patient with migraine will present a duration of at
least 4 hours (can last between 4-72 hours)
• Migraine can have no episodes of aura
• MRI is really better for patients with migraine because if you
order CT-Scan, more often than not you will not see anything.
(MRI is more sensitive than your CT-scan)
• In primary headaches and you have already ruled out any
other possible causes of headache, no need to order MRI/CT-
scan. Migraine is largely a clinical diagnosis
• In prescribing medications for migraine, the 1st thing that you
have to establish is the frequency. When you have more than
14 days of attacks per month, it is very advisable to give a
preventive medication. In a case of 2-3x per week or 12
attacks per month, it is not exactly falling into chronic migraine
where it is not greater than 14 days in a month. In that case,
you can just give anti-pain medications like your NSAIDs. But
TRIPTANS (Sumatriptan) is the best drug for migraine. It is an
OTC drug however it is somewhat expensive. It provides
immediate, lasting and complete relief of the headache
• If it is a woman that is complaining of migraine, you will have
to ask if it’s related to her monthly menses. Because
sometimes we can give prophylactic treatment few days (3 to
5 days) before the expected day one of menses. That being
said, premise is that the patient must have a regular menstrual
cycle.
• In the case of migraine, try to rule out first any other causes
of primary headache disorders that can mimic migraine such
as cluster headaches. As the name itself, it happens in
clusters and usually these are alarm clock headaches, they
happen every day and usually just after the onset of sleep.
That’s why it is important to ask for the pattern. Also try to ask
for paroxysmal hemicrania because it happens between 2-30
minutes but what rules that out is the location of the headache.
Because for paroxysmal hemicrania, it’s orbital or temporal
and radiates to the whole half of the cranium.
• Chronic migraine is very disabling especially for patients with
a pain scale of 8 to 9. They can fall into depression
• Photophobia vs. migraine. Photophobia happens during the
migraine. It actually worsens it. Photophobia is a part of the
cascade. It’s not an aura, but it is an associated symptom of
migraine. Not all migraines start with severe pain immediately
during the attack. Sometimes they can start from 3/10
evolving to 8/10. However, the pathologic process is
happening already that’s why someone can experience
associated symptoms such as photophobia. Photophobia is
just an associated symptoms not really an organic problem of
the brain
• It’s OK to take tramadol even if the migraine or headache is
already more than a day. It’s still an analgesic
• Treatment of migraine is the same regardless if with or without
aura
• It is possible in migraine to have both different visual
symptoms such as photopsia and scotoma at the same time.
More often than not, same aura happens for every patient
• Classic migraine can transform into a migraine with aura.
Remember in vascular theory, aura is associated with
decreased blood flow in some of your blood vessels.
• Aura and epilepsy are better proven with an EEG because the
origin of the seizure focus will be consistent with the aura
whereas when you do it in patients with migraine, it is normal.
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V. TEST YOUR KNOWLEDGE

MODIFIED TRUE OR FALSE. Write T if the statement is TRUE.
Write the correct answer if the statement is FALSE.

1. A migraine is said to be episodic if the headache usually

comes for an average of 10 days per month
2. Catamenial migraine is usually seen in postmenopausal
women
3. Women typically experience cluster headaches
4. SUNCT is associated with vasomotor phenomena: injected
conjunctivum and lacrimation
5. The best pharmacologic management for paroxysmal
hemicrania is an NSAID

MULTIPLE CHOICE. Select the best answer

6. For many years, migraine with aura was referred to as:

a. Classic Migraine
b. Common Migraine
c. Psychologic Migraine
d. BahalaKa Migraine
7. Pathogenesis of migraine where there is a release of
substance P, calcitonin gene-related peptide (CGRP)
a. Vascular
b. Trigeminal
c. Serotonin
d. Dopamine
8. Has been described in the past under a variety of names,
including paroxysmal nocturnal cephalalgia, migrainous
neuralgia, histamine cephalalgia (Horton's headache)
a. SUNCT
b. SUNA
c. Cluster Headache
d. Paroxysmal Hemicrania
9. Said to be the most common variety of headache, is usually
bilateral, with occipitonuchal, temporal, or frontal
predominance, or diffuse extension over the top of the
cranium.
a. Migraine
b. SUNCT
c. Tension Headache
d. SUNA
10. Trigeminal Autonomic Cephalalgias, except
a. Paroxysmal Hemicrania
b. SUNCT
c. Histamine Cephalalgia
d. None of the Above

10D
ANSWER KEY: 1T 2Premenstrual 3Men 4T 5T 6A 7B 8C 9C

VI. REFERENCES

• Andal, V.M (February, 2022). Headache. Youtube.

https://www.youtube.com/watch?v=Yu2cYiHaCPE
• Ropper, A., Samuels, M., & Klein, J. (2014). Adams and
Victor’s Principles of Neurology 10th Edition (10th ed.).
McGraw-Hill Education / Medical.

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VII. APPENDIX

COMMON TYPES OF HEADACHES

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