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
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
10.
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
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
20.
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
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