This document summarizes several primary headache syndromes: Tension type headache is the most common and involves gradual onset of bilateral dull pain that increases throughout the day. Migraine is the second most common and involves severe unilateral throbbing pain along with nausea, vomiting, and sensitivity to light and sound. Trigeminal neuralgia causes brief, severe facial pain triggered by activities like eating or shaving. Cluster headache is characterized by severe unilateral pain around the eye accompanied by redness, tearing and nasal congestion. These primary headache syndromes are differentiated based on their symptoms and pathophysiology.

1. HEADACHE

2. PRIMARY HEADACHE SYNDROMES
• Tension type headache
• Migraine
• Trigeminal Neuralgia
• Atypical facial pain
• Cluster headache
• Benign paroxysmal
headaches

3. TENSION TYPE
• Most common-69%
• Episodic or chronic
• Gradual onset , radiate forward from occiput
• Bilateral, dull, tight, band like pain
• Less in morning, pain increase as day goes on
• No accompanying N,V, throbbing, sensitivity to
light, sound or movement

4. Pathophysiology
• Primary disorder of CNS pain modulation
• Precipitating factors
Stress: usually occurs in the afternoon after long
stressful work hours or after an exam
Sleep deprivation
Uncomfortable stressful position and/or bad
posture
Irregular meal time (hunger)
Eyestrain
Caffeine withdrawal
Dehydration

5. 2 Theories
Muscle tension around head and neck
Malfunctioning pain filter located in brain stem,
brain misinterprets information and interprets
this signal as pain. One of the main
neurotransmitters which is probably involved is
serotonin

6. Management
• Paracetamol,Aspirin,NSAIDs
• Behavioral approach-relaxation
• Chronic-amitriptyline

7. MIGRAINE
• 2nd most common-16%
• 15% women and 6% men
• Severe, episodic, unilateral,throbbing pain
• Nausea,Vomiting
• Sensitivity to light ,sound, movement
• Genetic predisposition

8. Classical Migraine or Migraine
with AURA
 Symptom Triad
Paroxysmal headache
nausea &/or vomiting
aura of focal neurological events(visual)
20-25%

9. AURA
• flashing lights, silvery zigzag lines moving across
visual field over a period of 20 minutes
sometimes leaving a trail of temporary visual
field loss
• Sometimes-Auditory ,Olfactory, gustatory
hallucinations
• Sensory aura-spreading front of tingling and
numbness, from one body part to another

11. Rare aura:
• Vertigo
• Aphasia
• Hemiparesis
• Delirium
Migraine with limb weakness-Hemiplegic
migraine
Symptoms of aura do not resolve leaving
permanent neurological damage-Complicated
migraine

12. Common Migraine or Migraine
without AURA
• Paroxysmal headache
• Vomiting +/-
• NO AURA

13. Simplified Diagnostic Criteria for
MIGRAINE
At least 2 of the + At least 1 of the
following: following:
• Unilateral pain
• Throbbing pain • Nausea/vomitting
• Aggravation by • Photophobia and
movement phonophobia
• Moderate or severe
intensity

14. Clinical phases of a migraine
attack
Vulnerability
Attack Initiation
Prodrome
Aura
Pain
Postdrome

15. Triggers
• Flashing lights • Menstruation
• Loud sounds • Pregnancy
• Strong odors • Menopause
• Stress • Oral Contraceptives
• Hunger • Sleep changes
• Fatigue • Caffeine
• Alcohol • Chocolate
• Smoking • Tyramine
• MSG

16. Pathophysiology of Migraine
• Cortical spreading
depression
• Vascular
• Low Serotonin
• Melanopsin receptor

17. Cortical spreading depression of
LEAO
• Dysfunction of ion channels-Quick
depolarization(activation) followed by long-
lasting depression over an area of cortex
• Release of inflammatory mediators
• Irritation of cranial nerve roots-trigeminal

18. Vascular
Vasoconstriction of blood vessels in brain-Aura
(begins in occipital lobe)
Vasodilatation of scalp blood vessels
Inflammation
Pain

19. Migraine Pain-Trigeminovascular
• Key pathway for pain is trigeminovascular input
from meningeal vessels
• Modulation of trigeminovascular input comes
from dorsal raphe nucleus, locus coeruleus and
nucleus raphe magnus

21. Management
• Acute attack-
aspirin/paracetamol+metoclopromide/
domperidone
• Severe attack-Sumatriptan
• Frequent attacks-
Propranolol,Amitriptyline,Sodium valproate or
Topiramate

22. Trigeminal Neuralgia
• Lancinating pain in 2nd
and 3rd divisions of
trigeminal nerve
• >50yrs
• Severe, brief ,repetitive
pain causing patient to
flinch
• Precipitated by touching
trigger zones—washing,
shaving, eating, cold wind

23. Pathophysiology
• Compression of trigeminal N by aberrant loop of
cerebellar arteries as nerve enters brainstem
• Other benign compressive lesions
• Multiple sclerosis- TN occurs due to plaque of
demyelination in trigeminal root entry zone

24. Management
• Carbamazepine-DOC
• Intolerant-Gabapentin/Pregabalin
• Injection of alcohol into peripheral branch of
nerve
• Posterior craniotomy to relieve vascular
compression of trigeminal nerve

25. Atypical facial pain
• Persistent idiopathic facial pain
• Continuous, burning/crushing,unremittent,
centred over maxilla usually left side
• Middle aged women
• Early form of trigeminal neuralgia
• Rx-Amitriptyline, Gabapentin

26. Other causes of facial pain
Sinusitis
• Frontal-pain more in morning, decreases as day
progresses, stooping and blowing nose increase
pain
• Ethmoid and Sphenoid-pain over vertex, less in
morning and increase gradually

28. Post herpetic
neuralgia-continuous,
burning pain
sensitive to light
touch, shingles

29. THANK YOU