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HEADACHE
PRIMARY HEADACHE SYNDROMES


•   Tension type headache
•   Migraine
•   Trigeminal Neuralgia
•   Atypical facial pain
•   Cluster headache
•   Benign paroxysmal
    headaches
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
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
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
Management

• Paracetamol,Aspirin,NSAIDs
• Behavioral approach-relaxation
• Chronic-amitriptyline
MIGRAINE

•   2nd most common-16%
•   15% women and 6% men
•   Severe, episodic, unilateral,throbbing pain
•   Nausea,Vomiting
•   Sensitivity to light ,sound, movement
•   Genetic predisposition
Classical Migraine or Migraine
with AURA

 Symptom Triad
Paroxysmal headache
nausea &/or vomiting
aura of focal neurological events(visual)
  20-25%
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
Rare aura:
• Vertigo
• Aphasia
• Hemiparesis
• Delirium
Migraine with limb weakness-Hemiplegic
  migraine
Symptoms of aura do not resolve leaving
  permanent neurological damage-Complicated
  migraine
Common Migraine or Migraine
without AURA

• Paroxysmal headache
• Vomiting +/-
• NO AURA
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
Clinical phases of a migraine
attack
           Vulnerability
                           Attack Initiation


           Prodrome



             Aura



             Pain


           Postdrome
Triggers

•   Flashing lights •   Menstruation
•   Loud sounds •       Pregnancy
•   Strong odors •      Menopause
•   Stress          •   Oral Contraceptives
•   Hunger          •   Sleep changes
•   Fatigue         •   Caffeine
•   Alcohol         •   Chocolate
•   Smoking         •   Tyramine
                    •   MSG
Pathophysiology of Migraine

                  • Cortical spreading
                    depression
                  • Vascular
                  • Low Serotonin
                  • Melanopsin receptor
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
Vascular

 Vasoconstriction of blood vessels in brain-Aura
   (begins in occipital lobe)

  Vasodilatation of scalp blood vessels

               Inflammation

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

• Carbamazepine-DOC
• Intolerant-Gabapentin/Pregabalin
• Injection of alcohol into peripheral branch of
  nerve
• Posterior craniotomy to relieve vascular
  compression of trigeminal nerve
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
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
Post herpetic
 neuralgia-continuous,
 burning pain
 sensitive to light
 touch, shingles
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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
  • 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
  • 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
  • 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
  • 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
  • 27.
  • 28. Post herpetic neuralgia-continuous, burning pain sensitive to light touch, shingles