Headaches
Differentiating the benign from the serious
By Dr. Cuong Ngo-Minh
Back to Basics
April 16th 2009
Objectives LMCC
• Differentiate benign vs serious headache via symptoms
and signs, investigation
• Pathophysiology of migraine and pain sensation of other
cause of headache
• Identify patients requiring brain imaging
• Conduct effective plan of management on acute vs
chronic setting, appropriate use of medication
• Appreciate impact of misdiagnosis and mistreatment
(CLEO)
Etiology of headache disorders 1
Primary
•
Migraine (pulsatile, 2-72 hours, incapaciating photo-phono-phobia,):
- Migraine without aura (common migraine)
- Migraine with aura (classic migraine)
•
Cluster Headache (recurrent severe periorbital attacks)
•
Tension-type headache (eg posterior neck muscle contraction)
The Medical Council of Canada
(2005)
Etiology of headache disorders 2
Secondary
• H/a assoc. with vascular disorders:
–
–
–
–
–
Subarachnoid hemorrhage (Emergency!)
Temporal arteritis (risk of blindness)
Venous thrombosis
Intracranial hematoma (including epidural, subdural)
Severe arterial hypertension
• H/a assoc. with nonvascular intracranial disorders:
– Infection (meningitis, abscess, sinusitis)
– ↑ CSF pressure (intracranial mass lesion or hydrocephalus)
• Miscellaneous:
– Medication: side effect nitroglycerin or withdrawal (analgesics)
– Psychological disorders
The Medical Council of Canada
(2005)
History for headache :
• Onset (Acute vs slowly progressive) , frequency, duration
(hours,days?) , quality, intensity (worse ever?) , location,
triggers (worse with exertion?, food? menstruation?) and
ameliorating factors, assoc sx (pulsatility, photo-phonophobia)
Functional impairment (work, IADLs)
• Red flags (neuro symptoms, severity of disability) for serious disease
to differentiate between the causes of h/a.
• Select patients in need of immediate management based on red
flags on history and physical signs
Clinical,diagnostic imaging, laboratory findings 1
• Vitals, Level of conscioussness, Head and neck, Neurological exam,
(especially visual, motor, reflex, sensory, speech or cognitive),
if + finding investigation is warranted.
• Identify patients that require referral/brain imaging
1) new/explosive onset, 2) change in pattern, 3) jaw claudication,
4) limb girdle pain, 5) worse with stooping over, straining, coughing;
6) neurological signs on exam 7) temporal artery tenderness.
• X-rays and other tests may also be used if sinusitis is suspected
Gray J, Therapeutic Choices
(2007)
Red flags for serious headache
Age of onset
Middle-aged to elderly pt
Type of onset
Severe and abrupt
Temporal sequence
Progressive severity or increased
frequency
Pattern
Significant change in h/a
pattern.
Neuro signs
Stiff neck, focal signs,
Reduced consciousness
Systemic signs
Fever, appears sick, abnormal
examination
Gray J, Therapeutic Choices
(2007)
Migraine headache
• Unilateral in more than 50 % pts, Pulsating or throbbing in 50 %
• Bilateral more common than previously thought.
• Migraine can begin on one side then switch to other side.
• Headache phase usually lasts between 2 and 72 hrs.
• Invariably associated w~ other sx: nausea, vomiting, and diarrhea.
• Heightened sensory perceptions such as photophobia,
phonophobia, & increased sensitivity to smell occur during attacks.
• More common in individuals w/ family hx. More in women
(women w/ mother w/ migraine)
Prevalence: 19% of women in gen. pop
• Common triggers: certain foods (aged cheese, chocolate), alcohol
menstruation, stress, worry, lack of sleep, fatigue.
Migraine without aura (common migraine)
• Typically episodic
• Prodromal phase: Sx of excitation or inhibition of CNS,
i.e., elation, irritability, excitability, increased appetite or
craving for certain foods, especially sweets; depression,
sleepiness, and fatigue. Occurs in 30% of pts.
• Prodrome sx may precede migraine attack by up to 24
hrs.
• Aura:
Migraine with aura 1
– Definition: focal neurological phenomena that precede or
accompany the attack.
– Appear over 5 to 20 minutes. Last ≤ than 60 minutes.
– 20–30% of clients suffering from migraine
Chronology of headache phase from end of aura (3 patterns):
a) within 60 minutes
b) delayed up to several hours
c) No headache
Young, William B. and Silberstein, Stephen D., Migraine and Other Headaches. St. Paul,
Minn: AAN Press, 2004.;
Evans, Randolph W., MD, and Matthew, Ninan T., MD. Handbook of Headache, Second
Edition. Philadelphia: Lippincott Williams & Wilkins. 2005
; Silberstein, Stephen D.; Lipton, Richard B.; Goadsby, Peter J. Headache in Clinical
Practice Second Edition. Andover: Thomson Publishing Services. 2002.
• Aura:
Migraine with aura 2
– Visual, sensory, or motor in nature.
– Visual aura is the most common. Subtypes
– a) photopsia: unformed FLASHES of white and/or black or rarely
of multicolored lights
– b) scintillating scotoma: dazzling zigzag lines (if arranged like a
castle = "fortification spectra" or "teichopsia"). Some patients
complain, tunnel vision and hemianopsia.
– Auditory or olfactory hallucinations,
– SomatoSENSORY: paresthesias, eg. pins-and-needles can
migrate up the arm → face, lips and tongue (ipsilateral).
Or temporary dysphasia, vertigo and hypersensitivity to touch.
Ddx TIA
Clinical,diagnostic imaging, laboratory findings 2
• Lumbar puncture if subarachnoid hemorrhage, encephalitis, high- or
low-pressure headache symptoms or meningitis is suspected.
• Laboratory tests (on an individual basis)
– ESR for suspected temporal arteritis
– Endocrine, biochemical, infection work-up
– Search for malignancy if indicated
• Facial pain may need a thorough assessment by a dental specialist
familiar with headaches and facial pain and/or an ENT specialist if
sinus or other ENT disorders are suspected.
Gray J, Therapeutic Choices
(2007)
Key elements in Hx and PE for h/a
Diagnosis
Question/Maneuver
Assist in narrowing differential dx,
comparing previous presentations
Previous hx of h/a, types, freq, tx
Serious underlying pathology
Look for red flags
Migraine
Hx of throbbing, photophobia, assoc
nausea, unilateral pattern, pos family hx,
hx of aura
Analgesic rebound h/a
Hx of med use (types, freq, qty)
Assist in planning tx and screen for
depression, chronicity of hx, likelihood of
compliance, and motivation for recovery
Psychosocial hx: previous hx of
anxiety/depression; substance abuse;
current life stresses; activity/exercise
level; patient’s worries about the h/a
Serious underlying pathology
Screening neuro exam
TMJ, sinusitis, cervical arthritis, or
temporal arteritis
Palpate head, neck, and scalp
Sloane, PD et al. -The Essentials
of Family Medicine (2002)
Diagnosis & Initial Assessment of Headache
Headache
Abrupt
Recurrent
Severe or new onset
Typical pattern with mild to moderate pain
Immediate assessment
Elective assessment
Rule out SAH and meningitis
Usually benign primary h/a disorder
Migraine
Symptomatic or prophylactic tx.
Tension-type
Symptomatic or prophylactic tx.
Gray J, Therapeutic Choices
(2007)
Progressive
Accompanied by neurologic
symptoms and signs
Assess as soon as possible
Possible mass lesion
Other
Symptomatic or prophylactic tx.
Treatments for benign headache syndrome 1
• Symptomatic tx
– Analgesics
• Ibuprophen, naproxen, and ASA or acetaminophen
with or without codeine and/or butalbital, are used for
mild to moderate h/a pain.
• Non-opioid meds should be used less than 15 days per
month (re: prevent REBOUND h/a)
• Butalbital compounds, Tylenol #3 and other opioids have
limited use, should be used less than 10 days per month, in
benign h/a disorders b/o the potential for addiction.
• Medication over-use h/a can result from overuse of
analgesics/ rebound/ dependency, which limits their longterm potential.
Gray J, Therapeutic Choices
(2007)
Treatments for benign headache syndrome 2
• Symptomatic tx.
– Ergot derivatives
• Ergotamine acts on serotonin receptors and is classically
used for migraines and cluster h/a but use is limited by side
effects. They may cause rebound h/a if used 10 days per
month or more.
– Triptans
• They act on the serotonin (HT-5) subclass 1B and 1D
receptor, on extracerebral blood vessels and neurons, and
the mechanism of action is prevention of neurologically
sterile inflammatory responses around vessels and
vasoconstriction.
• They are contraindicated in patients with cardiac disorders,
sustained hypertension, basilar and hemiplegic migraine.
Gray J, Therapeutic Choices
(2007)
Treatments for benign headache syndrome 3
• Symptomatic tx.
– Other classes of drugs
• Corticosteroids can be useful in many h/a disorders, including
status migraine, cluster h/a, and cerebral neoplasms with
edema (especially metastatic lesions, temporal arteritis).
• Other drugs include metoclopramide (maxeran)
phenothiazines, Ketorolac, meperidine, indomethacin,
dimenhydrinate and domperidone.
Gray J, Therapeutic Choices
(2007)
Treatments for benign headache syndrome 4
• Symptomatic tx.
Prophylactic tx. Is indicated if the migraine attacks are
severe enough to interfere with the patient’s quality of
life, or if the patient has three or more severe per month
that fail to respond adequately to symptomatic tx.
–
–
–
–
–
Beta-blockers
Calcium channel blockers
Tricyclic antidepressants
Anti-epileptic drugs (Valproic acid, topirimate, gabapentin)
Serotonin agonists (methysergide)
Gray J, Therapeutic Choices
(2007)
Patient education and counseling for management
of benign headache syndrome
• A calendar or diary of h/a is useful f/u assessment
• A record of medications (usefulness, dosage, side effects) should be
kept.
• Reassurance and explanation are most important to the patient in
the long term.
• Always offer hope to the patient with chronic h/a even if no cure is
available; most primary h/a can be controlled
• For tension ha, attempt to modify or eliminate the stressor with
behaviour modification, biofeedback, relaxation therapy, yoga,
exercise, and so on.
Gray J, Therapeutic Choices
(2007)
Physicians’ legal liability for negligence (CLEO 5.4)
• Physicians are legally liable to their patients for causing harm
through a failure to meet the standard of care that is applicable
under the particular circumstances under consideration.
• In a patient with headache, the primary care physician may miss a
serious headache, such as subarachnoid hemorrhage. The diagnosis
is missed most often because of incomplete clinical assessment.
Although serious causes for headache are not frequent, failure to
diagnose has potentially disastrous consequences. Legal liability
may result.
Applied scientific principles 1
• Intracranial structures that are pain-sensitive:
– Dura, tributary veins, venous sinuses, meningeal vessels, tentorium
– carotid, vertebrobasilar, cerebellar, and cerebral arteries
• Pathophysiology of migraine
– Platelet aggregation occurs in CNS
– Release of serotonin from the synapses
– Increase & decrease in the levels of blood-brain catecholamines,
norepinephrine and epinephrine
– Origin of aura
• ↓blood flow changes → ↓ brain activity of cerebral cortex
(referred to as spreading depression) →
• ↑ inflammation of trigeminal nerves →
• ↑ pain in the meninges.
Applied scientific principles 2
– Trigeminoneurovascular system
• Afferent trigeminal neurons transmit pain sensation →
• back to the central nervous system →
↑ efferent parasympathic pathway (via facial nerve also
pterygopalatine and otic ganglia) →
↑ Release vasoactive peptides (eg.VIP vasoactive intestinal
peptide)
↑ vasodilation pericranial vasculature
Moskowitz MA. The neurobiology of vascular head pain. AnnNeurol
1985;16:157-68.
Source of information
• Guidelines for the diagnosis and management of migraine in clinical
practice CMAJ 1997;156(9): 1273-87
• Merck manual
• Therapeutic choices 5th edition 169-187