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HEADACHE
CLASSIFICATION
Put forward by the INTERNATIONAL HEADACHE SOCIETY
ANATOMICAL LOCALISATION
The key structures involved in primary headache appear to be
as follows –
a. The trigeminovascular system (the trigeminal nerve innervating the
large cranial vessels and dura mater).
b. The trigeminocervical complex(caudal part of trigeminal nucleus
extending into the dorsal horns of upper cervical spinal cord. It
receives input from C1 and C2 nerve roots )
c. Rostral pain processing regions such as ventroposteromedial
thalamus and the cortex.
d. The pain- modulatory systems that modulate input from trigeminal
nociceptors and influence the vegetative functions, such as
hypothalamus and brainstem structures.
RED FLAG SIGNS OF HEADACHE
CLINICAL EVALUATION
 For acute headache –
severe and reach maximal intensity within seconds to minutes.
Also called “thunderclap headaches. It is a medical emergency. Probable
causes could be –
Subarachnoid hemorrhage
Intracranial infections
Cervical artery dissection(younger age, involves cervical internal carotid and
vertebral arteries, presence or absence of neck trauma. associated with Horner
syndrome, Diplopia, Amaurosis fugax, Dysgeusia)
Acute hypertensive crisis (paroxysmal rise in SBP>160mmHg) and/or DBP
>120mmHg. classically manifests as headache, seizures, and neurologic signs
usually visual change. Headache resolves within 1 hour after normalization of
blood pressure)
CLINICAL EVALUATION(CONTD.)
 Ischemic stroke (Up to 50% have headaches prior to neurologic deficits)
 Pituitary apoplexy(due to rapid enlargement of a pituitary adenoma from hemorrhage or
infarction , Presents with sudden-onset headache, visual impairment , vomiting , and altered
cognition, more frequent in males[ M:F 2:1], mean age in the 5th decade.)
Colloid cyst of the third ventricle(benign tumors most commonly located in the third ventricle
near the foramen of Monro. Hydrocephalus may develop if a cyst blocks cerebrospinal fluid
flow.)
Primary thunderclap headache (severe headache with sudden onset that reaches maximum
intensity in less than 1 minute, a diagnosis of exclusion)
APPROACH TO A CASE OF
SUSPECTED SAH
APPROACH TO A CASE OF CNS
INFECTION
Headache, fever +/- nuchal rigidity
Altered mental status
Meningoencephalitis,
ADEM,
encephalopathy, mass
lesion
meningitis
ye
s
n
o
Obtain blood culture and
start empirical
antimicrobial therapy
syes
APPROACH TO A CASE OF CNS
INFECTION(CONTD)Imaging : CT or MRI (PREFERRED)
Mass lesion No mass lesion
Abcess or tumour
Appropriate
medical and/ or
surgical
interventions
White
matter
abnormaliti
es
Focal or
generalised
grey matter
abnormalitie
s or normal
Encephalitis
ADEM
no
Immediate blood culture
and L.P
Pleocytosis with
PMNs,
protein, glucose,
Gram stain or AFB
stain positive
Pleocytosis with
MNCs, normal
protein & glucose,
negative gram
stain or AFB stain
APPROACH TO A CASE OF CNS
INFECTION(CONTD)
Bacterial process
including tubercular
infection
Go for viral panel, fungal
culture, VDRL
CLINICAL EVALUATION(CONTD.)
For episopdic headache –
The most common pattern of headache in the general population
is episodic or intermittent headaches. The primary episodic headache
disorders with the absence of red flag signs are –
 Migraine (without and with aura) and Migraine variants – hemiplegic
migraine and basilar-type migraine
 Episodic tension-type headache
 Trigeminal autonomic cephalalgias (Cluster headache, Paroxysmal
hemicrania, SUNCT syndrome
 Other primary headache syndromes(Hypnic headache, Primary
stabbing headache, Primary cough headache, Primary sexual
headache)
CLINICAL EVALUATION(CONTD.)
The most common
secondary causes of episodic headache include:
 Headaches induced by acute substance use (i.e., due to use of
certain medications such as sildenafil) or substance withdrawal
(i.e., alcohol hangover headache)
Headaches attributable to eyestrain (i.e., refractive errors)
Headaches attributable to sinus infections (although this is rarely
a cause of frequent (>1/month) headaches)
1.2 MIGRAINE WITH AURA
DESCRIPTION:
Recurrent unilateral fully reversible visual, sensory or other CNS symptoms that
usually develop gradually and are usually followed by headache and associated
migraine symptoms.
DIAGNOSTIC CRITERIA:A. At least two attacks fulfilling criteria B and C
B. One or more of the following fully reversible aura symptoms:
1. visual
2. sensory
3. speech and/or language
4. motor
5. brainstem
6. retinal
C. At least two of the following four characteristics:
1. at least one aura symptom spreads gradually over ≥5 minutes, and/or two or
more symptoms occur in succession
2. each individual aura symptom lasts 5-60 minutes1
3. at least one aura symptom is unilateral.
4. the aura is accompanied, or followed within 60 minutes, by headache
MIGRAINE VARIANTS
 migraine with brain stem aura - Migraine with aura symptoms clearly
originating from the brainstem (e.g –dysarthria, vertigo, tinnitus,
hyperacusis, diplopia, ataxia.)
hemiplegic migraine - Migraine with aura including motor
weakness(fully reversible)
Retinal migraine - Repeated attacks of monocular visual disturbance,
including scintillations, scotomata or blindness, associated with
migraine headache.(other causes of amaurosis fugax have to be
excluded)
TREATMENT MODALITIES
Acute attack –
triptans(5HT-1B/1D agonists,Inhibit release of CGRP & substance
P, Inhibit activation of the trigeminal nerve, Inhibit vasodilation in the
meninges)
 ergots(Bind to 5HT, NE, DA, alpha and beta receptors, Constrict peripheral and
cranial blood vessels)
 Antiemetics
 NSAIDs(diclofenac, naproxen, aspirin)
Prevention –
beta blockers (propranolol, timolol, nadolol)
CCBs(verapamil, flunnarizine)
TREATMENT MODALITIES(CONTD)
Antidepressants
Antiepileptics (divalproex sodium, topiramate)
Botulinum toxin – FDA approved usage in chronic migrane, 155-195
units injected into muscles of face, neck and head
TENSION TYPE HEADACHE
Occurs in up to 80% of the population
Pathophysiology unclear
 Theory of increased muscle tension is unproven
 Icreased pain sensitivity.
Pain characteristics
 Bandlike, bilateral
 Extends from forehead to sides of temples
 Involves posterior neck muscles in cape-like distribution
Treatment First line: analgesics (Aspirin, acetaminohen
NSAIDs), High risk of rebound headaches.
 PAROXYSMAL HEMICRANIA - severe, strictly unilateral pain which is
orbital, supraorbital, temporal or in any combination , lasting 2–30
minutes, many times a day, associated with ipsilateral conjunctival
injection, lacrimation, nasal
congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis
and/or eyelid oedema. They respond absolutely to indomethacin.
Short-lasting unilateral neuralgiform headache attacks - moderate or
severe, unilateral headache lasting seconds to minutes, occurring at
least once
a day and usually associated with lacrimation and redness of the
ipsilateral eye.
HEMICRANIA CONTINUA - Persistent, unilateral headache, associated
with ipsilateral conjunctival injection, lacrimation, nasal congestion,
rhinorrhoea, forehead and facial sweating, miosis, ptosis and/or
eyelid oedema, and/or with restlessness or agitation.
The headache is absolutely sensitive to indomethacin.
HYPNIC HEADACHE - Frequently recurring headache attacks
developing only during sleep, causing wakening and lasting for up to
4 hours, without characteristic associated symptoms and not
CHRONIC DAILY HEADACHE
Chronic daily headache (CDH) is a symptom rather than a
diagnosis. CDH refers to the presence of headache on ≥15 days
per month for ≥3 months. Worldwide, 3%–5% of the general
population has CDH. clinicians need to be vigilant for secondary
causes of chronic headaches in their patients.
 Causes of chronic daily headache - Chronic migraine, Chronic
tension-type headache, Chronic cluster, Hemicrania continua,
Medication-related, Post-traumatic, cervical spine disorders,
temporomandibular joint (TMJ)/dental pathology, Metabolic
(Obstructive sleep apnea, hypoxia, hypercarbia, carbon monoxide,
Thyroid disease).
THANK YOU

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Headache

  • 2. CLASSIFICATION Put forward by the INTERNATIONAL HEADACHE SOCIETY
  • 3. ANATOMICAL LOCALISATION The key structures involved in primary headache appear to be as follows – a. The trigeminovascular system (the trigeminal nerve innervating the large cranial vessels and dura mater). b. The trigeminocervical complex(caudal part of trigeminal nucleus extending into the dorsal horns of upper cervical spinal cord. It receives input from C1 and C2 nerve roots ) c. Rostral pain processing regions such as ventroposteromedial thalamus and the cortex. d. The pain- modulatory systems that modulate input from trigeminal nociceptors and influence the vegetative functions, such as hypothalamus and brainstem structures.
  • 4. RED FLAG SIGNS OF HEADACHE
  • 5. CLINICAL EVALUATION  For acute headache – severe and reach maximal intensity within seconds to minutes. Also called “thunderclap headaches. It is a medical emergency. Probable causes could be – Subarachnoid hemorrhage Intracranial infections Cervical artery dissection(younger age, involves cervical internal carotid and vertebral arteries, presence or absence of neck trauma. associated with Horner syndrome, Diplopia, Amaurosis fugax, Dysgeusia) Acute hypertensive crisis (paroxysmal rise in SBP>160mmHg) and/or DBP >120mmHg. classically manifests as headache, seizures, and neurologic signs usually visual change. Headache resolves within 1 hour after normalization of blood pressure)
  • 6. CLINICAL EVALUATION(CONTD.)  Ischemic stroke (Up to 50% have headaches prior to neurologic deficits)  Pituitary apoplexy(due to rapid enlargement of a pituitary adenoma from hemorrhage or infarction , Presents with sudden-onset headache, visual impairment , vomiting , and altered cognition, more frequent in males[ M:F 2:1], mean age in the 5th decade.) Colloid cyst of the third ventricle(benign tumors most commonly located in the third ventricle near the foramen of Monro. Hydrocephalus may develop if a cyst blocks cerebrospinal fluid flow.) Primary thunderclap headache (severe headache with sudden onset that reaches maximum intensity in less than 1 minute, a diagnosis of exclusion)
  • 7. APPROACH TO A CASE OF SUSPECTED SAH
  • 8. APPROACH TO A CASE OF CNS INFECTION Headache, fever +/- nuchal rigidity Altered mental status Meningoencephalitis, ADEM, encephalopathy, mass lesion meningitis ye s n o Obtain blood culture and start empirical antimicrobial therapy syes
  • 9. APPROACH TO A CASE OF CNS INFECTION(CONTD)Imaging : CT or MRI (PREFERRED) Mass lesion No mass lesion Abcess or tumour Appropriate medical and/ or surgical interventions White matter abnormaliti es Focal or generalised grey matter abnormalitie s or normal Encephalitis ADEM no Immediate blood culture and L.P Pleocytosis with PMNs, protein, glucose, Gram stain or AFB stain positive Pleocytosis with MNCs, normal protein & glucose, negative gram stain or AFB stain
  • 10. APPROACH TO A CASE OF CNS INFECTION(CONTD) Bacterial process including tubercular infection Go for viral panel, fungal culture, VDRL
  • 11. CLINICAL EVALUATION(CONTD.) For episopdic headache – The most common pattern of headache in the general population is episodic or intermittent headaches. The primary episodic headache disorders with the absence of red flag signs are –  Migraine (without and with aura) and Migraine variants – hemiplegic migraine and basilar-type migraine  Episodic tension-type headache  Trigeminal autonomic cephalalgias (Cluster headache, Paroxysmal hemicrania, SUNCT syndrome  Other primary headache syndromes(Hypnic headache, Primary stabbing headache, Primary cough headache, Primary sexual headache)
  • 12. CLINICAL EVALUATION(CONTD.) The most common secondary causes of episodic headache include:  Headaches induced by acute substance use (i.e., due to use of certain medications such as sildenafil) or substance withdrawal (i.e., alcohol hangover headache) Headaches attributable to eyestrain (i.e., refractive errors) Headaches attributable to sinus infections (although this is rarely a cause of frequent (>1/month) headaches)
  • 13. 1.2 MIGRAINE WITH AURA DESCRIPTION: Recurrent unilateral fully reversible visual, sensory or other CNS symptoms that usually develop gradually and are usually followed by headache and associated migraine symptoms. DIAGNOSTIC CRITERIA:A. At least two attacks fulfilling criteria B and C B. One or more of the following fully reversible aura symptoms: 1. visual 2. sensory 3. speech and/or language 4. motor 5. brainstem 6. retinal C. At least two of the following four characteristics: 1. at least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession 2. each individual aura symptom lasts 5-60 minutes1 3. at least one aura symptom is unilateral. 4. the aura is accompanied, or followed within 60 minutes, by headache
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  • 15. MIGRAINE VARIANTS  migraine with brain stem aura - Migraine with aura symptoms clearly originating from the brainstem (e.g –dysarthria, vertigo, tinnitus, hyperacusis, diplopia, ataxia.) hemiplegic migraine - Migraine with aura including motor weakness(fully reversible) Retinal migraine - Repeated attacks of monocular visual disturbance, including scintillations, scotomata or blindness, associated with migraine headache.(other causes of amaurosis fugax have to be excluded)
  • 16. TREATMENT MODALITIES Acute attack – triptans(5HT-1B/1D agonists,Inhibit release of CGRP & substance P, Inhibit activation of the trigeminal nerve, Inhibit vasodilation in the meninges)  ergots(Bind to 5HT, NE, DA, alpha and beta receptors, Constrict peripheral and cranial blood vessels)  Antiemetics  NSAIDs(diclofenac, naproxen, aspirin) Prevention – beta blockers (propranolol, timolol, nadolol) CCBs(verapamil, flunnarizine)
  • 17. TREATMENT MODALITIES(CONTD) Antidepressants Antiepileptics (divalproex sodium, topiramate) Botulinum toxin – FDA approved usage in chronic migrane, 155-195 units injected into muscles of face, neck and head
  • 18. TENSION TYPE HEADACHE Occurs in up to 80% of the population Pathophysiology unclear  Theory of increased muscle tension is unproven  Icreased pain sensitivity. Pain characteristics  Bandlike, bilateral  Extends from forehead to sides of temples  Involves posterior neck muscles in cape-like distribution Treatment First line: analgesics (Aspirin, acetaminohen NSAIDs), High risk of rebound headaches.
  • 19.  PAROXYSMAL HEMICRANIA - severe, strictly unilateral pain which is orbital, supraorbital, temporal or in any combination , lasting 2–30 minutes, many times a day, associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis and/or eyelid oedema. They respond absolutely to indomethacin. Short-lasting unilateral neuralgiform headache attacks - moderate or severe, unilateral headache lasting seconds to minutes, occurring at least once a day and usually associated with lacrimation and redness of the ipsilateral eye. HEMICRANIA CONTINUA - Persistent, unilateral headache, associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis and/or eyelid oedema, and/or with restlessness or agitation. The headache is absolutely sensitive to indomethacin. HYPNIC HEADACHE - Frequently recurring headache attacks developing only during sleep, causing wakening and lasting for up to 4 hours, without characteristic associated symptoms and not
  • 20. CHRONIC DAILY HEADACHE Chronic daily headache (CDH) is a symptom rather than a diagnosis. CDH refers to the presence of headache on ≥15 days per month for ≥3 months. Worldwide, 3%–5% of the general population has CDH. clinicians need to be vigilant for secondary causes of chronic headaches in their patients.  Causes of chronic daily headache - Chronic migraine, Chronic tension-type headache, Chronic cluster, Hemicrania continua, Medication-related, Post-traumatic, cervical spine disorders, temporomandibular joint (TMJ)/dental pathology, Metabolic (Obstructive sleep apnea, hypoxia, hypercarbia, carbon monoxide, Thyroid disease).
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Editor's Notes

  1. Pain sensitive cranial structures – scalp, meningeal arteries, dural sinuses, falx cerebri, proximal segments of large pial arteries.