HeadachesHeadaches

Differentiating the benign from the Differentiating the benign from the seriousserious

By Dr. Cuong Ngo-MinhBy Dr. Cuong Ngo-Minh

Back to Basics Back to Basics April 16th 2009 April 16th 2009

Objectives LMCCObjectives LMCC• Differentiate benign vs serious headache via Differentiate benign vs serious headache via

symptoms and signs, investigationsymptoms and signs, investigation

• Pathophysiology of migraine and pain sensation Pathophysiology of migraine and pain sensation of other cause of headacheof other cause of headache

• Identify patients requiring brain imagingIdentify patients requiring brain imaging

• Conduct effective plan of management on acute Conduct effective plan of management on acute vs vs

chronic setting, appropriate use of medicationchronic setting, appropriate use of medication

• Appreciate impact of misdiagnosis and Appreciate impact of misdiagnosis and mistreatmentmistreatment (CLEO)(CLEO)

The Medical Council of Canada (200The Medical Council of Canada (2005)5)

Etiology of headache disorders 1Etiology of headache disorders 1

• Migraine (pulsatile, 2-72 hours, incapaciating photo-phono-Migraine (pulsatile, 2-72 hours, incapaciating photo-phono-phobia,):phobia,):

- Migraine without aura (common migraine)- Migraine without aura (common migraine)

- Migraine with aura (classic migraine)Migraine with aura (classic migraine)

• Cluster Headache (recurrent severe periorbital attacks)Cluster Headache (recurrent severe periorbital attacks)

• Tension-type headache (eg posterior neck muscle contraction)Tension-type headache (eg posterior neck muscle contraction)

Primary

The Medical Council of Canada (200The Medical Council of Canada (2005)5)

Etiology of headache disordersEtiology of headache disorders 22

• H/a assoc. with vascular disorders:H/a assoc. with vascular disorders:– Subarachnoid hemorrhage (Emergency!)Subarachnoid hemorrhage (Emergency!)– Temporal arteritis (risk of blindness)Temporal arteritis (risk of blindness)– Venous thrombosisVenous thrombosis– Intracranial hematoma (including epidural, subdural)Intracranial hematoma (including epidural, subdural)– Severe arterial hypertensionSevere arterial hypertension

• H/a assoc. with nonvascular intracranial disorders:H/a assoc. with nonvascular intracranial disorders:– Infection (meningitis, abscess, sinusitis)Infection (meningitis, abscess, sinusitis)– ↑ ↑ CSF pressure (intracranial mass lesion or hydrocephalus)CSF pressure (intracranial mass lesion or hydrocephalus)

• MiscellaneousMiscellaneous::– Medication: side effect nitroglycerin or withdrawal (analgesics)Medication: side effect nitroglycerin or withdrawal (analgesics)– Psychological disordersPsychological disorders

Secondary

History for headache :History for headache :

• Onset (Acute vs slowly progressive) , frequency, duration Onset (Acute vs slowly progressive) , frequency, duration (hours,days?) , quality, intensity (worse ever?) , location, (hours,days?) , quality, intensity (worse ever?) , location,

triggers (worse with exertion?, food? menstruation?) and triggers (worse with exertion?, food? menstruation?) and ameliorating factors, assoc sx (pulsatility, photo-ameliorating factors, assoc sx (pulsatility, photo-phonophobia) phonophobia)

Functional impairment (work, IADLs)Functional impairment (work, IADLs)

• Red flags (neuro symptoms, severity of disability) for Red flags (neuro symptoms, severity of disability) for serious disease to differentiate between the causes of h/a.serious disease to differentiate between the causes of h/a.

• Select patients in need of immediate management based Select patients in need of immediate management based on red flags on history and physical signson red flags on history and physical signs

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Clinical,diagnostic imaging, laboratory Clinical,diagnostic imaging, laboratory findings 1findings 1

• Vitals, Level of conscioussness, Head and neck, Neurological Vitals, Level of conscioussness, Head and neck, Neurological exam, (especially visual, motor, reflex, sensory, speech or exam, (especially visual, motor, reflex, sensory, speech or cognitive), cognitive),

if + finding investigation is warranted.if + finding investigation is warranted.

• Identify patients that require referral/brain imagingIdentify patients that require referral/brain imaging 1) new/explosive onset, 2) change in pattern, 3) jaw 1) new/explosive onset, 2) change in pattern, 3) jaw

claudication, claudication, 4) limb girdle pain, 5) worse with stooping over, straining, 4) limb girdle pain, 5) worse with stooping over, straining,

coughing;coughing; 6) neurological signs on exam 7) temporal artery tenderness.6) neurological signs on exam 7) temporal artery tenderness.

• X-rays and other tests may also be used if sinusitis is X-rays and other tests may also be used if sinusitis is

suspectedsuspected

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Red flags for serious headacheRed flags for serious headache

Age of onsetAge of onset Middle-aged to elderly ptMiddle-aged to elderly pt

Type of onsetType of onset Severe and abruptSevere and abrupt

Temporal sequenceTemporal sequence Progressive severity or Progressive severity or increased frequencyincreased frequency

PatternPattern Significant change in h/a Significant change in h/a pattern.pattern.

Neuro signsNeuro signs Stiff neck, focal signs,Stiff neck, focal signs,

Reduced consciousnessReduced consciousness

Systemic signsSystemic signs Fever, appears sick, Fever, appears sick, abnormal examinationabnormal examination

Migraine headacheMigraine headache

• Unilateral in more than 50 % pts, Pulsating or throbbing in 50 Unilateral in more than 50 % pts, Pulsating or throbbing in 50 %%

• Bilateral more common than previously thought.Bilateral more common than previously thought.• Migraine can begin on one side then switch to other side.Migraine can begin on one side then switch to other side.

• Headache phase usually lasts between 2 and 72 hrs.Headache phase usually lasts between 2 and 72 hrs.• Invariably associated w~ other sx: nausea, vomiting, and Invariably associated w~ other sx: nausea, vomiting, and

diarrhea.diarrhea.• Heightened sensory perceptions such as photophobia, Heightened sensory perceptions such as photophobia,

phonophobia, & increased sensitivity to smell occur during phonophobia, & increased sensitivity to smell occur during attacks.attacks.

• More common in individuals w/ family hx. More in women More common in individuals w/ family hx. More in women (women w/ mother w/ migraine)(women w/ mother w/ migraine)

Prevalence: 19% of women in gen. popPrevalence: 19% of women in gen. pop

• Common triggers: certain foods (aged cheese, chocolate), Common triggers: certain foods (aged cheese, chocolate), alcohol menstruation, stress, worry, lack of sleep, fatigue.alcohol menstruation, stress, worry, lack of sleep, fatigue.

Migraine without aura (common migraine)Migraine without aura (common migraine)

• Typically episodicTypically episodic

• Prodromal phase: Sx of excitation or inhibition of Prodromal phase: Sx of excitation or inhibition of CNS, i.e., elation, irritability, excitability, CNS, i.e., elation, irritability, excitability, increased appetite or craving for certain foods, increased appetite or craving for certain foods, especially sweets; depression, sleepiness, and especially sweets; depression, sleepiness, and fatigue. Occurs in 30% of pts.fatigue. Occurs in 30% of pts.

• Prodrome sx may precede migraine attack by up Prodrome sx may precede migraine attack by up to 24 hrs.to 24 hrs.

Migraine with aura 1Migraine with aura 1• Aura:Aura:

– Definition: focal neurological phenomena that Definition: focal neurological phenomena that precede precede or or accompanyaccompany the attack. the attack.

– Appear over 5 to 20 minutes. Last Appear over 5 to 20 minutes. Last ≤≤ than 60 minutes. than 60 minutes.– 20–30% of clients suffering from migraine20–30% of clients suffering from migraine

Chronology of headache phase from end of aura (3 Chronology of headache phase from end of aura (3 patterns):patterns):

a)a) within 60 minutes within 60 minutes

b)b) delayed up to several hoursdelayed up to several hours

c) No headachec) No headacheYoung, 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.

Migraine with aura 2Migraine with aura 2• Aura:Aura:

– Visual, sensory, or motor in nature.Visual, sensory, or motor in nature.– Visual Visual auraaura is the most common. Subtypes is the most common. Subtypes– a) a) photopsiaphotopsia: unformed FLASHES of white and/or black : unformed FLASHES of white and/or black

or rarely of multicolored lights or rarely of multicolored lights – b) b) scintillating scintillating scotomascotoma: dazzling zigzag lines (if : dazzling zigzag lines (if

arranged like a castle = "fortification spectra" or arranged like a castle = "fortification spectra" or "teichopsia"). Some patients complain, "teichopsia"). Some patients complain, tunnel visiontunnel vision and and hemianopsiahemianopsia. .

– Auditory or olfactory hallucinations,Auditory or olfactory hallucinations,

– SomatoSENSORY: SomatoSENSORY: paresthesiasparesthesias, eg. pins-and-needles , eg. pins-and-needles can migrate up the arm can migrate up the arm →→ face, lips and tongue face, lips and tongue (ipsilateral).(ipsilateral).

Or temporary Or temporary dysphasiadysphasia, , vertigovertigo and hypersensitivity to and hypersensitivity to touch. Ddx TIAtouch. Ddx TIA

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Clinical,diagnostic imaging, laboratory Clinical,diagnostic imaging, laboratory findings 2findings 2

• Lumbar puncture if subarachnoid hemorrhage, encephalitis, Lumbar puncture if subarachnoid hemorrhage, encephalitis, high- or low-pressure headache symptoms or meningitis is high- or low-pressure headache symptoms or meningitis is suspected.suspected.

• Laboratory tests (on an individual basis)Laboratory tests (on an individual basis)– ESR for suspected temporal arteritisESR for suspected temporal arteritis– Endocrine, biochemical, infection work-upEndocrine, biochemical, infection work-up– Search for malignancy if indicatedSearch for malignancy if indicated

• Facial pain may need a thorough assessment by a dental Facial pain may need a thorough assessment by a dental specialist familiar with headaches and facial pain and/or an specialist familiar with headaches and facial pain and/or an ENT specialist if sinus or other ENT disorders are suspected.ENT specialist if sinus or other ENT disorders are suspected.

Sloane, PD et al. -The Essentials of FSloane, PD et al. -The Essentials of Family Medicine (2002)amily Medicine (2002)

Key elements in Hx and PE for h/aKey elements in Hx and PE for h/aDiagnosisDiagnosis Question/ManeuverQuestion/Maneuver

Assist in narrowing differential dx, Assist in narrowing differential dx, comparing previous presentationscomparing previous presentations

Previous hx of h/a, types, freq, tx Previous hx of h/a, types, freq, tx

Serious underlying pathologySerious underlying pathology Look for red flags Look for red flags

Migraine Migraine Hx of throbbing, photophobia, assoc Hx of throbbing, photophobia, assoc nausea, unilateral pattern, pos family nausea, unilateral pattern, pos family hx, hx of aura hx, hx of aura

Analgesic rebound h/a Analgesic rebound h/a Hx of med use (types, freq, qty)Hx of med use (types, freq, qty)

Assist in planning tx and screen for Assist in planning tx and screen for depression, chronicity of hx, depression, chronicity of hx, likelihood of compliance, and likelihood of compliance, and motivation for recovery motivation for recovery

Psychosocial hx: previous hx of Psychosocial hx: previous hx of anxiety/depression; substance abuse; anxiety/depression; substance abuse; current life stresses; activity/exercise current life stresses; activity/exercise level; patient’s worries about the h/a level; patient’s worries about the h/a

Serious underlying pathology Serious underlying pathology Screening neuro exam Screening neuro exam

TMJ, sinusitis, cervical arthritis, or TMJ, sinusitis, cervical arthritis, or temporal arteritis temporal arteritis

Palpate head, neck, and scalp Palpate head, neck, and scalp

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Diagnosis & Initial Assessment of HeadacheDiagnosis & Initial Assessment of Headache

Headache

AbruptSevere or new onset

RecurrentTypical pattern with mild to moderate pain

ProgressiveAccompanied by neurologic

symptoms and signs

Immediate assessmentRule out SAH and meningitis

Elective assessmentUsually benign primary h/a disorder

Assess as soon as possiblePossible mass lesion

MigraineSymptomatic or prophylactic tx.

Tension-typeSymptomatic or prophylactic tx.

OtherSymptomatic or prophylactic tx.

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Treatments for benign headache syndrome Treatments for benign headache syndrome 11

• Symptomatic txSymptomatic tx– AnalgesicsAnalgesics

• Ibuprophen, naproxenIbuprophen, naproxen, and , and ASAASA or or acetaminophenacetaminophen with or without with or without codeinecodeine and/or and/or butalbitalbutalbital, are used for , are used for mild to moderate h/a pain.mild to moderate h/a pain.

• Non-opioid meds should be used less than 15 days per Non-opioid meds should be used less than 15 days per month (re: prevent REBOUND h/a)month (re: prevent REBOUND h/a)

• ButalbitalButalbital compounds, Tylenol compounds, Tylenol #3#3 and other opioids and other opioids have limited use, should be used less than 10 days per have limited use, should be used less than 10 days per month, in benign h/a disorders b/o the potential for month, in benign h/a disorders b/o the potential for addiction.addiction.

• Medication over-use h/a can result from overuse of Medication over-use h/a can result from overuse of analgesics/ rebound/ dependency, which limits their analgesics/ rebound/ dependency, which limits their long-term potential.long-term potential.

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Treatments for benign headache syndrome Treatments for benign headache syndrome 22

• Symptomatic tx.Symptomatic tx.– Ergot derivativesErgot derivatives

• ErgotamineErgotamine acts on serotonin receptors and is acts on serotonin receptors and is classically used for migraines and cluster h/a but use classically used for migraines and cluster h/a but use is limited by side effects. They may cause rebound is limited by side effects. They may cause rebound h/a if used 10 days per month or more.h/a if used 10 days per month or more.

– TriptansTriptans

• They act on the serotonin (HT-5) subclass 1B and 1D They act on the serotonin (HT-5) subclass 1B and 1D receptor, on extracerebral blood vessels and receptor, on extracerebral blood vessels and neurons, and the mechanism of action is prevention neurons, and the mechanism of action is prevention of neurologically sterile inflammatory responses of neurologically sterile inflammatory responses around vessels and vasoconstriction.around vessels and vasoconstriction.

• They are contraindicated in patients with cardiac They are contraindicated in patients with cardiac disorders, sustained hypertension, basilar and disorders, sustained hypertension, basilar and hemiplegic migraine.hemiplegic migraine.

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Treatments for benign headache syndrome Treatments for benign headache syndrome 33

• Symptomatic tx.Symptomatic tx.– Other classes of drugsOther classes of drugs

• Corticosteroids can be useful in many h/a disorders, Corticosteroids can be useful in many h/a disorders, including status migraine, cluster h/a, and cerebral including status migraine, cluster h/a, and cerebral neoplasms with edema (especially metastatic lesions, neoplasms with edema (especially metastatic lesions, temporal arteritis).temporal arteritis).

• Other drugs include metoclopramide (maxeran) Other drugs include metoclopramide (maxeran) phenothiazines, Ketorolac, meperidine, indomethacin, phenothiazines, Ketorolac, meperidine, indomethacin, dimenhydrinate and domperidone.dimenhydrinate and domperidone.

Gray J, Therapeutic Choices (2007)Gray J, Therapeutic Choices (2007)

Treatments for benign headache syndrome Treatments for benign headache syndrome 44

• Symptomatic tx.Symptomatic tx.ProphylacticProphylactic tx. Is indicated if the migraine attacks tx. Is indicated if the migraine attacks

are severe enough to interfere with the patient’s are severe enough to interfere with the patient’s quality of life, or if the patient has quality of life, or if the patient has three or more three or more severe per month that fail to respond adequately severe per month that fail to respond adequately to symptomatic txto symptomatic tx..

– Beta-blockersBeta-blockers– Calcium channel blockersCalcium channel blockers– Tricyclic antidepressantsTricyclic antidepressants– Anti-epileptic drugs (Valproic acid, topirimate, Anti-epileptic drugs (Valproic acid, topirimate,

gabapentin)gabapentin)– Serotonin agonists (methysergide)Serotonin agonists (methysergide)

Gray J, Therapeutic Choices (2007) Gray J, Therapeutic Choices (2007)

Patient education and counseling for Patient education and counseling for management of benign headache syndromemanagement of benign headache syndrome• A calendar or diary of h/a is useful f/u assessmentA calendar or diary of h/a is useful f/u assessment

• A record of medications (usefulness, dosage, side effects) A record of medications (usefulness, dosage, side effects) should be kept.should be kept.

• Reassurance and explanation are most important to the Reassurance and explanation are most important to the patient in the long term.patient in the long term.

• Always offer hope to the patient with chronic h/a even if no Always offer hope to the patient with chronic h/a even if no cure is available; most primary h/a can be controlledcure is available; most primary h/a can be controlled

• For tension ha, attempt to modify or eliminate the stressor For tension ha, attempt to modify or eliminate the stressor with behaviour modification, biofeedback, relaxation with behaviour modification, biofeedback, relaxation therapy, yoga, exercise, and so on.therapy, yoga, exercise, and so on.

Physicians’ legal liability for negligence Physicians’ legal liability for negligence (CLEO 5.4)(CLEO 5.4)

• Physicians are legally liable to their patients for causing Physicians are legally liable to their patients for causing harm through a failure to meet the standard of care that is harm through a failure to meet the standard of care that is applicable under the particular circumstances under applicable under the particular circumstances under consideration.consideration.

• In a patient with headache, the primary care physician may In a patient with headache, the primary care physician may miss a serious headache, such as subarachnoid miss a serious headache, such as subarachnoid hemorrhage. The diagnosis is missed most often because of hemorrhage. The diagnosis is missed most often because of incomplete clinical assessment. Although serious causes for incomplete clinical assessment. Although serious causes for headache are not frequent, failure to diagnose has headache are not frequent, failure to diagnose has potentially disastrous consequences. Legal liability may potentially disastrous consequences. Legal liability may result.result.

Applied scientific principles 1Applied scientific principles 1• Intracranial structures that are pain-sensitive:Intracranial structures that are pain-sensitive:

– Dura, tributary veins, venous sinuses, meningeal vessels, Dura, tributary veins, venous sinuses, meningeal vessels, tentoriumtentorium

– carotid, vertebrobasilar, cerebellar, and cerebral arteriescarotid, vertebrobasilar, cerebellar, and cerebral arteries

• Pathophysiology of migrainePathophysiology of migraine– Platelet aggregation occurs in CNSPlatelet aggregation occurs in CNS– Release of serotonin from the synapsesRelease of serotonin from the synapses– Increase & decrease in the levels of blood-brain Increase & decrease in the levels of blood-brain

catecholamines, norepinephrine and epinephrinecatecholamines, norepinephrine and epinephrine– Origin of auraOrigin of aura

• ↓↓blood flow changes blood flow changes → ↓→ ↓ brain activity of cerebral cortex brain activity of cerebral cortex (referred to as spreading depression) (referred to as spreading depression) → →

• ↑ ↑ inflammation of inflammation of trigeminal nerves trigeminal nerves →→• ↑↑ pain in the meninges. pain in the meninges.

Applied scientific principles 2Applied scientific principles 2

– Trigeminoneurovascular systemTrigeminoneurovascular system

• Afferent trigeminal neurons transmit pain sensation Afferent trigeminal neurons transmit pain sensation →→

• back to the central nervous system back to the central nervous system → →

↑ ↑ efferent pefferent parasympathic pathway (via facial nerve also arasympathic pathway (via facial nerve also pterygopalatine and otic ganglia) pterygopalatine and otic ganglia) → →

↑ ↑ Release Release vasoactive peptides (eg.VIP vasoactive vasoactive peptides (eg.VIP vasoactive intestinal peptide)intestinal peptide)

↑↑ vasodilation vasodilation pericranial vasculaturepericranial vasculature

Moskowitz MA. The neurobiology of vascular head pain. AnnNeurol 1985;16:157-68.

Source of informationSource of information

• Guidelines for the diagnosis and management of migraine Guidelines for the diagnosis and management of migraine in clinical practice CMAJ 1997;156(9): 1273-87in clinical practice CMAJ 1997;156(9): 1273-87

• Merck manualMerck manual

• Therapeutic choices 5th edition 169-187Therapeutic choices 5th edition 169-187