Headache migraine

1. NUR AINA BINTI AB KADIR

2. GENERAL PRINCIPLES
•Associated features
are the disorders
itself
PRIMARY
•Exogenous
disordersSECONDARY

3. COMMON CAUSES OF HEADACHE

4. ANATOMY&PHYSIOLOGY
• Peripheral nociceptors are stimulated tissue
injury,visceral distension
• Pain producing pathways of the peripheral/ CNS
are damaged/activated inappropiately
• Cranial structures(pain producing): scalp, middle
meningeal artery, dural sinuses, falx cerebri,
proximal segments of the large pial arteries

5. CLINICAL EVALUATION OF ACUTE, NEW
ONSET HEADACHE
• New& severe VS recurrent over many years
• Probability of finding a potentially serious cause &
need prompt evaluation, proper treatment
• 1st step: complete neurologic examination
• Abnormal examination/history of recent-onset
headache CT/MRI study
• General evaluation of acute headache might include
the investigation of CVS & renal status by BP
monitoring & urine examination

6. Cont..
• Psychological state : relationship exist
between head pain and depression
• Underlying recurrent headache disorders may
be activated by pain follows otologic/
endodontic surgical procedures.

7. HEADACHE SYMPTOMS THAT SUGGEST
A SERIOUS UNDERLYING DISORDER
• “WORST” headache ever
• 1st severe headache
• Subacute worsenig over days/weeks
• Abnormal neurologic examination
• Fever/unexplained systemic signs
• Vomiting that precedes headache
• Pain induced by bending,lifting,cough
• Pains that disturbs sleep/presents immediately upon awakening
• Known systemic illness
• Onset after age 55
• Pain associated with local tenderness eg.: region of temporal artery

8. MIGRAINE
• Second most common cause of headache
• Episodic headache with certain features such as sensitivity
to light, sound, and movement
• Headache often accompanied by nausea and vomiting
• A benign and recurring syndrome of headache associated
with other symptoms of neurologic dysfunction in varying
admixtures.
• Sensitive to environmental and sensory stimuli

9. PATHOPHYSIOLOGY
1) Vascular theory

10. 2) Cortical spreading depression
• Activation of cells in the trigeminal  vasoactive neuropeptides,
calcitonin gene–related peptide (CGRP), at vascular terminations of
the trigeminal nerve and within the trigeminal nucleus.
• Centrally, the second-order trigeminal neurons cross the midline
and project to ventrobasal and posterior nuclei of the thalamus for
further processing.
• Other brainstem region : nucleus locus coeruleus in the pons and
the rostroventromedial medulla.

12. PATHOPHYSIOLOGY
3) Involvement of neurotransmitter 5-
hydroxytryptamine
- methysergide : first drug capable of
preventing migraine attacks
- triptans : potent agonists of 5-HT1B, 5-HT1D,
5-HT1F

14. PATHOPHYSIOLOGY
4) Role of dopamine
- migraine symptoms can be induced by
dopaminergic stimulation
- dopamine receptor antagonists are effective
especially when given parenterally or
concurrently with other antimigraine agents

15. PATHOPHYSIOLOGY
• Migraine has a strong genetic component
5) Familial hemiplegic disorders
- rare type of migraine with aura
FHM MUTATIONS
FHM1 CAY2.1 (P/Q)-type voltage-gated calcium
channel CACNA1A gene
FHM2 Na+-K+ATPase ATP1A2 gene
FHM3 Neuronal voltage gated sodium channel
SCN1A

16. • Hormonal influences – usually occur during
menstruation
• Contraceptive pill - exacerbate migraine in many
patients
• Dietary precipitants - cheese, chocolate, red wine
• Psychological stress - pt tend to have attacks at
weekends/beginning of a holiday (may be associated
with vasodilatation of extracranial vessels, but may be
due to disturbed neuronal activity in the hypothalamus

17. DIAGNOSIS & CLINICAL FEATURES
Repeated attacks of headache lasting 4-72 hours in
patients with a normal physical examination, no other
reasonable cause for the headache and:
At least 2 of the following
features
Plus at least 1 of the following
features
Unilateral pain Nausea/vomiting
Throbbing pain Photophobia and phonophobia
Aggravation by movement
Moderate or severe intensity

18. TREATMENT
• NON PHARMACOLOGIC MANAGEMENT
– Identify and avoid of specific headache triggers
– Change of lifestyles
– Reduce stress

19. TREATMENT
• ACUTE ATTACK THERAPIES FOR MIGRAINE
– Mild migraine : oral agents
– Severe attacks : parenteral therapy
– Drugs :
• 5-HT1B/1D receptor agonists
• Ergot alkaloids
• NSAIDs
• Dopamine receptor antagonists

20. •Simple Analgesics
•Acetaminophen, aspirin, caffeine : Two tablets or caplets q6h (max 8
per day)
•NSAIDs
•Naproxen :220–550 mg PO bid
•5-HT1 Agonists
•Oral
•Ergotamine One 2 mg sublingual tablet at onset
•Nasal
•Dihydroergotamine
•Prior to nasal spray, the pump must be primed 4 times; 1 spray (0.5
mg) is administered, followed in 15 min by a second spray

21. Cont..
• Parenteral
• Dihydroergotamine : 1 mg IV, IM, or SC at onset
and q1h
• Sumatriptan:6 mg SC at onset
• Dopamine Antagonists
• Oral
• Metoclopramide :5–10 mg/d
• Parenteral
• Chlorpromazine 0.1 mg/kg IV at 2 mg/min; max
35 mg/d

22. OTHER
• Other
• Oral
• Acetaminophen, 325 mg, plus dichloralphenazone, 100
mg, plus isometheptene, 65 mg
• Two capsules at onset followed by 1 capsule q1h (max
5 capsules)
• Nasal
• Butorphanol 1 mg (1 spray in 1 nostril), may repeat if
necessary in 1–2 h
• Parenteral
• Narcotics

23. TREATMENT
• PREVENTIVE TREATMENT
– Frequency of attacks is >2 per month
– Duration of attacks is >24 hours
– Disturb patient's lifestyle, with significant disability
that lasts 3 or more days
– Acute attack therapies fails or is overused

24. DRUGS DOSES
Antiepileptic drugs : valproate 400-600 mg bid
Beta blockers : propranolol 40-120mg bid
Tricyclic antidepressants :
amitriptyline
10-75 mg at night
Serotonergic drugs:
methysergide
1-4 mg qd
Pizotifen 0.5-2 mg qid

25. SECONDARY HEADACHE
MENINGITIS
INTRACRANIAL
HEMORRHAGE
BRAIN TUMOR
TEMPORAL
ARTERITIS
GLAUCOMA

26. • MENINGITIS
• Acute,severe headache
with neck stiff, fever
• Lumbar puncture is
mandatory
• Striking accentuation of
pain with eye
movement
• INTRACRANIAL
HEMORRHAGE
• Acute,severe headache
with stiff neck,no fever
suggest subarachnoid
hemorrhage

27. • BRAIN TUMOR
• Chief complaints of headache-
30%
• Pain: intermittent deep, dull
aching of moderate intensity
• Disturb sleep:10%
• Vomitingheadcahe by
weeks: posterior fossa brain
tumors
• h/o amenorrhea&
galactorrhea prolactin-
secreting pituitary
adenoma/PCOS
• Head pain appear abruptly
after bending,
lifting,coughing posterior
fossa mass, a Chiari
malformation, low CSF volume
• GLAUCOMA
• Prostrating headache with
nausea& vomiting
• Starts with severe eye pain
• On P/E: eye is often red with a
fixed,moderately dilated pupil

28. TEMPORAL ARTERITIS
• Inflammatory disorder of arteries(extracranial carotid circulation)
• Common disorder of elderly
• Half of the patient with untreated TA blindness
• Symptoms: headache, polymyalgia rheumatica, jaw claudication,
fever and weight loss
• Pain usually appears gradually over a few hours before peak
intensity is reached; occasionally, it is explosive in onset.
• The quality of pain:throbbing; it is almost invariably described as
dull and boring, with superimposed episodic stabbing pains

29. REFERENCE
• Harrison’s Principle of Internal Medicine, 18th
Edition, Volume 1
• Davidson’s Principles and Practice of
Medicine, 22nd Edition
• http://emedicine.medscape.com/article/1142
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