headache neurological sight of question.ppt

Headache etiology pathogenesis clinic diagnostics and treatment

1. Headaches
Alan Chan, MD

2. •12-16 % prevalence
•Tension most common
•Cluster HA men > women
•All other types women > men
•International Headache Society (IHS)
classification updated in 2004
• HA, cranial neuralgia, facial pain
syndromes.

3. HA
•Migraine – 2/3 unilat, 1/3 bilat or global;
crescendo pattern, pulsating; 4-72 hr; +/-
aura
•Tension – bilat, pressure/tightness
variable; indeterminate length
•Cluster – unilat, quick and explosive;
patient active; < 3 hr; ipsilat facial
symptoms – tearing, nasal congestion,
Horner’s, rarely focal neuro symptoms

4. Ddx – less common
•Paroxysmal hemicrania
•Idiopathic stabbing headache
•Cold-stimulus headache
•Benign cough headache
•Benign exertional headache
•Headache associated with sexual activity

5. Other HA
•Secondary HA – associated with trauma,
vascular disorder, nonvascular intracranial
disorder, substance use or withdrawal,
infection, metabolic disorder, other facial
or cranial structures

6. Get some hx
•Triggers
–Diet, stress, hormones, sensory stimuli,
change in habit or environment
•Important questions in history
–frequency of severe headache (difficult to
function)
–frequency of milder HA
–frequency of taking analgesics
–change in HA

7. Image if…
•recent significant change in pattern,
frequency, or severity
•worsening despite therapy
•focal neurological signs/symptoms
•HA with exertion, cough, or sexual activity
•Orbital bruit
•Onset after age 40

8. Migraine
•episodes of severe HA typically with
nausea +/- photo/phonophobia

9. Pathophysiology - NOT vascular
dilatation of blood vessels
•Primary neuro dysfunction leading to
premonitory symptoms, aura, HA, and
postdrome
•Central process either brainstem or
cortical spreading depression
–causes aura, activates trigeminal nerve
afferent fibers, alter blood brain barrier (BBB)
permeability

10. •trigeminovascular system – activity leading to
stimulation releases vasoactive neuropeptides of
substance P, calcitonin gene-related protein
(CGRP, which is a profound endogenous
vasodilator), neurokinin A, activation of
arachadonic acid cascade
•sensitization – neurons get progressive more
sensitive to nociceptive and non-nociceptive
stimulation

11. More…
•Genetics – approx 3x risk in patients with relatives who
had migraines. Non-Mendelian pattern of inheritance
•Prodrome – 60% of people with migraine; can occur 1-2
days prior to HA onset. Includes depression, irritability,
constipation, euphoria, food craving, increased yawning.
•Aura – 25%; typically visual like scotoma, but can be
sensory, verbal, or motor
•Headache – typically unilateral and throb/pulse
•Postdrome – exhausted, sudden head mvt causes pain

12. Diagnosis – without aura
•Headache attacks last 4 to 72 hours
•Headache has at least two of the following
characteristics: unilateral location; pulsating quality;
moderate or severe intensity; aggravation by routine
physical activity
•During headache at least one of the following occurs:
nausea and/or vomiting; photophobia and phonophobia
•At least five attacks occur fulfilling the above criteria
•History, physical examination, and neurologic
examination do not suggest any underlying organic
disease

13. Aura
•At least one of the following characteristics without motor weakness:
–Fully reversible visual symptoms including positive features (eg,
flickering lights, spots, or lines) and/or negative features (eg, loss of
vision)
–Fully reversible sensory symptoms including positive features (eg, pins
and needles) and/or negative features (eg, numbness)
–Fully reversible dysphasic speech disturbance
•Aura has at least two of the following characteristics:
–Homonymous visual symptoms and/or unilateral sensory symptoms
–At least one aura symptom develops gradually over ≥5 minutes and/or
different aura symptoms occur in succession over ≥5 minutes
–Each symptom lasts ≥5 and ≤60 minutes

14. Complications
•Chronic (>15 days a month for > 3 months
in absence of drug overuse)
•Status migrainosus - > 72 hr and
debilitating
•Persistent aura without infarction – aura >
1 wk
•Migrainous infarction – deficit > 1 hr and
positive imaging
•Migraine triggered seizure

15. Acute therapy
•NSAIDs, combo Tylenol/ASA/caffeine,
triptans, ergots like dihydroergotamine
(DHE), opioids (but weak evidence only for
butorphanol nasal and worry about abuse
and transformation into chronic daily HA),
IV metoclopramide.

16. Preventive Tx – can take as long as
2-3 months to see benefit.
•Treat if >2 a month that last > 3 days of disability,
contraindication to acute tx, > 2 times a week use of
acute tx, presence of uncommon conditions
•Nonselective beta blockers – propranolol studied the
most
•TCA (better for mixed migraine and tension HA) like
amitriptylline as others not studies as much; limited
evidence for fluoxetine
•Anticonvulsants - divalproex sodium and sodium
valproate, limited evidence for gabapentin
•NSAIDs – only naproxen with modest effect, but overuse
syndrome
•Serotonergic agent – ergot like DHE

17. •Keep a headache diary of related activities
and triggers!

18. Cluster Headache
•trigeminal autonomic cephalalgias, which
are short, unilat, severe with autonomic
symptoms (ptosis, miosis, lacrimation,
conjunctival injection, rhinorrhea, nasal
congestion)

19. •Prevalence - <1 %
•Dx – very typical. < 3 hrs
•Tx – Acute –
•O2, triptans, octreotide, lidocaine
(intranasal), ergot
•Preventive – CCB like verapamil,
glucocorticoids, lithium (limited evidence),
topiramate
• Others less used – pizotifen (anti
serotonergic), valproic acid, capsaicin,
ergot, melatonin, indomethacin, triptans

20. Tension type headache (TTH)
•Most common
•Types – infrequent episodic (< 1 /month),
freq episodic (1-14/month), and chronic (>
15 days a month)
•PP – multifactorial. Normally innocuous
stimuli are interpreted as pain in the dorsal
horn neurons. Some genetic role.
Women slightly more than men. Blacks
less than whites.

21. Dx – usually non descript!
•TTH is characterized by having at least two of
the following four features:
•The location of the pain is bilateral in either the
head or neck
•The quality of the pain is steady (eg, pressing or
tightening) and nonthrobbing
•The intensity of the pain is mild to moderate
•There is no aggravation of the headache by
normal physical activity

22. •In addition to these criteria, there must be
at least 10 headache episodes fulfilling all
other ICHD-2 criteria, which include the
following:
•The duration of pain is between 30
minutes to 7 days
•The headache is not attributable to
another disorder

23. Tx
•Acute – early tx, some may require a higher
dose, avoid overuse, consider preventive.
Tylenol, NSAIDs, ASA. Add some caffeine, but
may get side effects. Butalbital and opioids
generally not recommended.
•Preventive – TCAs, Serotonin-NE reuptake
inhibitors like venlafaxine, behavioral like CBT,
relaxation, biofeedback

24. References
•Uptodate.com
•Snow V, Weiss K, Wall EM, et al.
Pharmacologic Management of Acute Attacks of
Migraine and Prevention of Migraine Headache.
Ann Int Med. 2002. 137(10): 840-849.
•Clinch CR. Evaluation of Acute Headaches in
Adults. Am Fam Physician. 2001. 63(4): 685-
693.
•Tepper SJ, Spears RC. Acute Treatment of
Migraine. Neuro Clinics 2009. 27(2): 417-427