NNC CMU

Chiang Mai University

Headache Essential 2024

Surat Tanprawate, MD, MSc(Lond.), FRCP(T)

President of Thai Headache Society
Head of Headache Unit, Chiang Mai University
 Neurology CMU

Topics

• Headache Classi cation

• Secondary headache you should know

• Primary headache and its management you should know

• Cranial neuralgia you should know

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Ventricles, aqueduct of Sylvius,
Choroid plexuses
--24 observations, 4 subjects
--a balloon placed through a small
opening into anterior horn and body
of lateral ventricle

Scalp, galea (epicranial aponeurosis), fascia, muscles:

--150 observations, 30 subjects
--thermal,chemical, mechanical, electrical stimulation

Harold G Wolff and Bronson

Ray (1940)
Dural artery (middle meningeal artery):
--96 observations, 11 subjects
--stimuli: faradizing, distending, stroking,
stretching, crushing
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Pain sensitive intracranial structures
Meningeal
Dura
blood vessel

Pain matrix
Thalamus

Trigeminal ganglia

Trigeminocervical
complex

upper cervical
nerve roots
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Secondary headache NNC CMU

Primary headache

Migraine
Neuralgias
TTH

TACs

Other
primary
headache
 Prof. Jes Olesen, Denmark

http://ihs-classi cation.org
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 Neurology CMU

• Part One: The Primary Headache

• Migraine, Tension-type headache, Trigeminal autonomic
cephalalgias, Other primary headache disorders

• Part Two: The Secondary Headache

• Headache attributed to …
• Part Three: Painful Cranial Neuropathies, other Facial
Pain and Other Headaches

• Painful lesions of the cranial nerves

• other facial pain and Other headache disorders
• Appendix
ICHD-III
 History taking and PE (possible localisation, cause)
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Clinical Headache Syndrome NNC CMU

Criteria Character
- Red flag sign
- Symptoms -> cause
- Atypical feature for
primary headache

Primary headache Cranial neuralgia

Migraine, TTH, TACs, other Secondary and other facial
primary headache disorder headache pain

International classi cation of headache disorder-III (ICHD) beta

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S/S suggestive serious cause of secondary headache
 Neurology CMU

Age > 50 ( rst onset) Healthy young age Side locked headache

Headache after trauma/neck Temporal pro les: chronic, Morning headache

injury episodic, complete wax and
wane

Abnormal neurological exam; Character: non- xed/ Headache non-response to

including papilledema, alternated site or mild bilateral medication
sti ness of neck
Temporal pro les: sudden Speci c triggers: internal Headache with TACs
severe, worsening headache (sleep, anxiety, menstruation), characters
external (environment)

Concurrent events: pregnancy,

immunocompromise, systemic Headache response to
symptome migraine speci c medication

Provoking activity: exercise,

cough, wake up from sleep,
postural headache etc.
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Basic data Female 75 y.o.

Occiput, temporal,
Headache characters
bilateral
Localization - diffuse, IIP
Cause - vascular
Associated features Photophobia, nausea

Clinical headache syndrome - “Thunderclap headache”

Triggers Lying down, neck ex

DDx… First onset, peak at

Duration, progression the onset with
constant pain, 5 day

PE Normal

Ix CT brain, LP
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 Neurology CMU

Possible causes of
Thunderclap
headache
 Diagnostic approach in TCH

CT

Positive Negative

Subarachnoid hemorrhage Lumbar puncture

Stroke
CVST
Positive Negative
Pituitary apoplexy
Retrochival hematoma
Subarachnoid
PRES MRI
hemorrhage

Positive Negative

Stroke MR angiography or
SIH magnetic resonance
Pituitary apoplexy venography
Retrochival hematoma
PRES Positive Negative

Aneurysm Primary
CVST TCH
Dissection
Schwedt TS et al. Thunderclap headache. Lancet Neurol 2006;5: 621-31 RCVS
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Causes and Clues
• Subarachnoid haemorrhage (SAH)

• clues: stiffness of neck, abnormal CSF

• Cerebral venous sinus thrombosis (CVST) (10% of CVST)

• clues: sign of IICP, seizure, focal neurological de cit ->

MRI, CTV brain

• Pituitary apoplexy

• clues: acute headache, ophthalmoplegia, diminished visual

acuity, alter mental status, MRI brain (may miss by CT)
DW Dodick. J. Neurol. Neurosurg. Psychiatry 2002;72;6-11
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Causes and Clues
• Cervicocephalic arterial dissection

• clues: ipsilateral forehead headache, ipsilateral horner’s

syndrome, delay focal neurological de cit

• Acute hypertensive crisis

• clues: bilateral dull aching severe headache, evidence of end

organ damage, severe high BP

• Spontaneous intracranial hypotension (14% of SIH))

• clues: headache on changing position, low ICP, Imaging

shows tonsillar descent, meningeal thickening
DW Dodick. J. Neurol. Neurosurg. Psychiatry 2002;72;6-11
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Reversible Cerebral Vascoconstriction Syndrome (RCVS)

• headache, with or without focal de cits and/or

seizures, has led to angiography (with “string of
beads” appearance) and diagnosis of RCVS

• thunderclap onset and headache has resolved

within 3 months of onset
Ducros A, et al. Practical Neurology 2009 9(5)
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 Neurology CMU

Pituitary apoplexy and Thunderclap Headache

Pituitary apoplexy is an uncommon clinical syndrome characterized
by acute headache, ophthalmoplegia, diminished visual acuity, and
altered mental status caused by the sudden hemorrhage or
infarction of a pituitary gland that invariably harbors an adenoma
Pascual J. J Headache Pain 2008
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Cough headache with posterior occupying lesion

Arachnoid cyst Dermoid tumor Meningioma

Pascual J. J Headache Pain (2008) 9:259–266
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Headache triggered by changing posture

Triggers
Cervicogenic headache, posterior
fossa lesion, tension-type
Changing posture
headache, myofascial pain

Increase intracranial pressure (of

Postural change (related to
any causes), intraventricular lesion,
gravitational)
intracranial hypotension (CSF leak)

Migraine, primary exertional

headache, intracranial lesions,
Activities
extracranial/vascular lesion with
in ammation
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Headache attributed to CSF pressure
(increased/low)

• Increase CSF pressure • Low CSF pressure (<6

(>25 cm) cm)

• idiopathic intracranial • spontaneous

hypertension (IIH) intracranial
hypotension
• secondary to
metabolic, toxic, • post-dural puncture
hormonal causes headache

• secondary to • CSF stula headache

hydrocephalus
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the MRI brain of 45 years-old patient with headache while changing position
showing thickening of pachymeninges and low CSF pressure
 Neurology CMU

Sponteneous Intracranial Hypotension (IIH)

Orthostatic headache with low ICP due to CSF leak
Headache related with position
Associated imaging signs of “brain sag”
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Giant Cell Arteritis (GCA)

• Headache (esp. temporal headache) is the most common
symptoms of GCA, and it present as the rst symptoms around
33-48%

• Prevalence of headache in GCA : 71-85%

• Headache usually predominates in temporal and occipital areas

(with an acute or subacute onset), usually continuous headache
described as ‘throbbing’ with hyperesthesia of the scalp and
partially relieved by analgesics
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• New onset headache (throbbing, dull,
constant) 60-90%
GCA symptoms
• Scalp tenderness (temper or occiput)
40-70%

• Polymyalgia rheumatica 50%

• Jaw/tongue claudication 30-50%

• Limb claudication 5-15%

• Systemic symptoms (weight loss, fatigue,

anorexia) 20-50%

• Visual loss (permanent 15%, transient 20%)

• Diplopia 10%
Headache attributed to Giant Cell Arteritis Neurology CMU
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GCA signs
• ESR > 50 in 90%

• ESR > 100 in 60%

• Non-cardiac CRP > 2x normal in 90%

• Anemia 30%, Elevate WBC 30%

• Absent temporal artery pulse 40%

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GCA: Suggested tapering regime by BSR

• 40-60 mg prednisolone until symptoms and lab result are normal

(2-4 weeks)

• Reduce dose by 10 mg every 2 weeks to 20 mg

• Reduce dose by 2.5 mg every 2-4 weeks to 10 mg

• Reduce dose by 1 mg every 1-2 months if there is no relapse

Dasgupta B, et al. Rheumatology. 2010; 49:1594–7.

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Potential new treatment for GCA

• Tocilizumab is approved for RA and block IL-6

• MTx and Azathiopirine

• Etanerccept TNF alpha inhibitor

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Common primary headache

Migraine
Component

Migraine
without aura

ICHD-III
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Primary headache disorders

Migraine Tension-type Trigeminal Other primary
headache Autonomic headache
(TTH) Cephalalgias disorder
(TACs)
Migraine without aura Chronic migraine
Migraine with aura Complication of migraine
- Migraine with typical aura - Status migranosus
- Migraine with brainstem aura - Persistent aura without infarction
- Hemiplegic migraine - Migrainous infarction
- Retinal migraine - Migraine aura-triggered seizure

Episodic syndromes that may be associated with migraine

- Recurrent gastrointestinal disturbance (Cyclical vomiting syndrome, Abdominal
migraine )
- Benign paroxysmal vertigo
- Benign paroxysmal torticollis
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Migraine Pathophysiology
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Migraine phases and pathophysiology

craving
headache
yawning/tired
aura nausea/vomiting Resolution
uid retention
photo-/phonophobia
perception

Prodrome Aura Headache Resolution Postdrome

phase phase phase phase phase

CSD: cortical spreading depression; TVS: trigeminovascular system

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 Acute
Intensity Rx Preventive Rx

Allostatic load/Risk factor for progression

Trigger
Trigger Trigger

Frequency

Depression/Anxiety
Insomnia
Office syndrome
Co-morbidity/Complication Medication Overused
AEs from Med
Etc.
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Typical aura:
99% 31% -Visual
-Sensory
-Speech
6%

18%

n=163
Michael B. R. et al. Brain 1996: 119, 355-361
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Feature Migraine TIA

onset progressive sudden

progressive rate slow non

different symptoms in succession simultaneous

type of visual symptoms negative or positive negative

territory cortical vascular

duration long (30-60 min) short (10-15 min)

Jean Schoenen and Peter S Sándor. Lancet Neurol 2004; 3: 237–45

 Migraine treatment

• Give the information of migraine

• Life style modi cation

• Acute medication

• Preventive medication
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 Pharmacotherapy of
acute migraine attack
Non-speci c Speci c
• Acetaminophen, • Dihydroergotamine

• NSAIDs • Ergotamine

• ca eine • Triptan

• opioids

• neuroleptic
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Possible Sites of Action of Triptans in the
Trigeminovascular System
 Acute treatment
• E ective acute migraine
treatment could eliminate
central sensitization and
prevent migraine progression

• On the other hand, overused

acute medication leads to
MOH

• Acute and preventive

treatment need to be adjust
simultaneously
Ailani J et al. Headache 2021;61:1021–1039.
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4.3 days per month at baseline tend to be CM

4.3 days/month

“Once you have more attacks,

you get more attacks”
Bigal ME et al. Headache 2006;46:1334-1343
 Migraine evolution

Dorsolateral pontine activity in EM Dorsolateral pontine activity in CM even in resting state

Pain threshold

CGRP level

“Magic Number”

0 2 4 8 15 30
LFEM MFEM HFEM CM
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Anti-epileptic drug Anti-Depressant

Topiramate
Amitryptylline
Valproic acid
Nortriptylline
Lamotrigine
Venlafaxine
Gabapentin

Botulinum toxin
Beta-blocker injection 155-195 U
for Chronic migraine
Propranolol
Atenolol
Timolol Calcium
Metoprolol mAb CGRP
channel blocker
Erenumab
Flunarizine
Fremanezumab
Cinnarizine
Galcanezumab
Verapamil
Eptinezumab
4-6 month duration
Sacco et al. The Journal of Headache and Pain (2020) 21:76
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Tension-Type Headache
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Tension-type headache A. At least 10 episode of headache
Episodic B. Lasting from 30 minutes to 7 days
infrequent vs frequent
Chronic C. At least two of the following four
characteristics
Pericranial tenderness 1. bilateral location
with/without
2. pressing or tightening (non-pulsating) quality
3. mild or moderate intensity
4. not aggravated by routing physical activity
such as walking or climbing stairs
D. Both of the following:
1. no nausea or vomiting
2. no more than one of photophobia or
photophobia
E. Not better accounted for by another ICHD-3
diagnosis
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Abortive therapy-analgesic drugs

Substance Dose Level of recommendation

Ibuprofen 200 - 800 mg A

Ketoprofen 25 mg A

ASA 500 -1000 mg A

Naproxen 375 - 550 mg A

Diclofenac 12.5 - 100 mg A

Paracetamol 1000 mg A

Caffeine comb. 65 - 200 mg B

Bendtsen L. et al. Eur J of Neurol 2010;17:1318-1325
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Prophylactic therapy

Drugs Dose Level of

recommendation
Amitrtyptyline 30-75 mg A

Mirtazapine 30 mg B

Venlafaxine 150 mg B

Clomipramine 75-150 mg B

Maprotiline 75 mg B

Mianserin 30-60 mg B
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AMT on TTH
• Trials

• between 6 weeks to 6 months

• from episodic (high frequency) to CTTH
• 30% headache reduction found from 6 weeks of treatment
• Highdose > 75mg/d did not provide headache relieve, but
had signi cant side effects
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Prophylactic therapy - Non-pharmacologic therapy

Treatment Level of recommendation

Psycho-behavioral treatment

- EMG biofeedback A

- Cognitive-behavioral therapy C

Physical therapy C

Acupuncture C
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Trigeminal Neuralgia /
Trigeminal Neuropathy
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Pain attributed to lesion or disease of
trigeminal nerve (ICHD-III)

Present Microvascular Trigeminal Painful trigeminal

compression neuralgia neuropathy

Secondary Idiopathic
Classic trigeminal
trigeminal trigeminal
neuralgia
neuralgia neuralgia
• Herpes zoster
• Post-herpetic neuralgia
• Post-traumatic
• Purely, attributed to… • Purely, • Other disorder
paroxysmal • Multiple sclerosis paroxysmal • Idiopathic
• concomitant • Space occupying • concomitant
continuous lesion continuous
pain • Other cause pain
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Lambru G, et al. Pract Neurol 2021;21:392–402.

Thank you for your
kind attention