Approach to Headache

DR MELODY ASUKILE
BSC, MBCHB, MMED
A D A P T E D F R O M P R O F D E A N N A S AY L O R
Headache
Caused by irritation/trauma/ischemia to pain-sensitive structures in the head
◦ Meninges, blood vessels, nerves and muscles

Primary goal when seeing a patient with headache is to differentiate primary

from secondary headaches
◦ Primary: idiopathic disorders without an underlying identifiable cause
◦ Migraine, tension-type, cluster headache, etc
◦ Secondary: identifiable disorder causing headache
◦ Subarachnoid hemorrhage, vasculitis, tumor, etc.
Headache History
Characteristics of pain Mnemonic
◦ Character (dull, throbbing, tightness, lancinating) S – site
◦ Does not distinguish well between headache etiologies O – onset
◦ Location C – character
◦ Associated symptoms R – radiation
◦ Constitutional symptoms A - association
◦ Visual disturbance T – timing
◦ Photophobia, phonophobia E – exacerbating/relieving
◦ Nausea, vomiting
S – severity
◦ Rhinorrhea, lacrimation
◦ Loss of consciousness
Headache History
Define acuity of headaches
◦ Acute, subacute are almost always secondary headaches
◦ Chronic are usually primary headache disorders

Precipitating factors
◦ Tension, stress, fatigue
◦ Systemic infection (sinusitis, viral, malaria)
◦ Particular foods
◦ Bright lights
◦ Chewing, coughing, lying down, etc

Auras
Headache History
Temporal pattern of headache
◦ Time of day when they typically occur and resolve
◦ Typical severity of headache
◦ Typical duration of headache
◦ Change in frequency or severity over time
Relieving factors
◦ Positional (improved with lying down, standing up)
◦ Sleep
◦ Darkness
Headache History
Exacerbating factors
◦ Positional
◦ Worsened with coughing, sneezing, Valsalva, bending forward
◦ Exertional activities
◦ Emotion, stress, etc

Prior headache history

◦ Characteristics, frequency and severity of headaches in the past

Medication history
◦ Types of medications tried and their effects on headaches
◦ Frequency of medications
Headache History
PMHx
◦ Immunocompetent vs immunocompromised
◦ Cancer history
◦ Autoimmune/inflammatory conditions
FHx
◦ Others with similar headaches
SHx
◦ Substances
Headache Physical Examination
Vital signs
Scalp tenderness
Neck – meningism, paraspinal tenderness/spasm
Mental status
Fundoscopic examination
◦ Papilledema

Extraocular movements
◦ 6th nerve palsies

Focal neurologic deficits

Management
If red flag symptoms or abnormal examination findings, must rule out secondary cause of
headache
◦ Brain imaging
◦ Lumbar puncture
◦ Other targeted investigations

If no red flag symptoms, normal neurological examination, and history consistent with a primary
headache disorder, patient usually does not need imaging or further investigations
Primary Headache
Disorders
 HEADACHES: GBD and Epidemiology
Most of the world’s population lives in regions without accurate epidemiologic data
Global prevalence in adults 18-65 years old
◦ Migraine: 15%
◦ Tension-type headache: 21%
◦ Chronic headaches, including MOH: 3%

GBD 2013: combined, 3rd leading cause of years of healthy life lost to disability (YLD)
◦ Migraine: 7th most common chronic condition (850 million people); 6th cause of YLD
◦ TTH: 2nd most common chronic condition (1.6 billion people)
◦ MOH: 18th cause of YLD
Migraine
Headache 80% common migraines
◦ Unilateral ◦ Without aura
◦ Pulsatile 20% classic migraines
◦ Moderate to severe intensity ◦ With aura
◦ Associated symptoms M:F 1:3
◦ Photophobia
◦ Phonophobia Onset is early in life
◦ Nausea ◦ 25% during 1st decade
◦ Vomiting ◦ 55% by 20 years of age
◦ Worsened by routine physical activity ◦ >90% by 40 years of age

FHx of migraine is common

Migraine
Examination normal
No further workup is needed if history is supportive, examination is normal, and it’s presenting
at a typical age
Treatment
◦ Lifestyle factors
◦ Prophylactic therapy
◦ Abortive therapy
Migraine
Lifestyle factors
◦ Avoid triggers
◦ Adequate hydration
◦ Adequate rest
◦ Avoid hunger

Prophylactic treatment – indicated when headaches occur more > 2 times/week

◦ Tricyclic antidepressants (amitriptyline, nortriptyline, etc)
◦ Beta-blockers (propranolol)
◦ Antiepileptic drugs (valproic acid, topiramate, gabapentin, lamotritigine)
◦ Calcium channel blockers (verapamil)
◦ Vitamins (magnesium, riboflavin)
Migraine
Abortive therapies
◦ Aspirin
◦ NSAIDs
◦ Paracetamol
◦ Triptans
◦ Ergots
◦ Anti-emetics
◦ Caffeine
Severe headache/ status migrainosus
◦ “Migraine cocktails” – metoclopramide, diphenhydramine and ketorolac given in combination
◦ IV steroids or prednisolone taper
◦ IV magnesium
◦ IV valproic acid
◦ IV/IM thorazine
Tension Type Headache
Chronic recurrent headaches without an identifiable cause that lack features of migraine
headaches
◦ Usually squeezing or band-like
◦ Bilateral
◦ Often occipital
◦ No associated aura
◦ Attacks often less frequent but longer duration

Many patients have mixed headache types with some similar to migraine
Treatment is similar to migraine
Medication Overuse Headache
Aka Transformed headache
Chronic daily headache that develops after frequent use of abortive therapy for headaches
◦ Use on more than 2-3 days/week
◦ Can be triggered by any abortive therapy, including caffeine

Treatment
◦ Withdrawal of all abortive therapies for two weeks
◦ Prednisolone taper during this time
◦ Begin prophylactic medication
◦ After two weeks, can begin using abortive therapy again but not more than 2-3 days per week
Cluster Headache
M >> F
Mean age of onset – 25 years
Usually no family history
Clusters of brief, very severe headaches
◦ Unilateral, constant, non-throbbing
◦ Last 15 minutes to 2 hours
◦ Commonly occur at night
◦ Recur daily, often at same time of day, for cluster of weeks or months
◦ Can be headache free between clusters for months or years
◦ Associated with unilateral conjunctival injection, lacrimation, rhinorrhea, Horner syndrome
◦ Often precipitated by alcohol
Cluster Headache
Treatment
◦ Abortive therapy
◦ High flow oxygen by facemask is most effective
◦ Triptans, dihydroergotamine can also be used
◦ Prophylactic therapy used during cluster of headaches
◦ Verapamil
◦ Ergotamine rectal suppositories at bedtime
◦ Prednisolone 60 mg/daily x 1 week then taper over 1 week
◦ Lithium
◦ Indomethacin
Secondary Headaches
Subarachnoid Hemorrhage
Spontaneous vs traumatic
◦ 75% due to rupture of aneurysm
◦ Also rupture of arteriovenous malformation (AVM), other vascular anomalies
6 per 100,000 population annually
◦ M:F 1:1
◦ Most commonly during 40s or 50s
Thunderclap headache / worst headache of life
◦ 50% present with loss of consciousness
◦ Vomiting, neck stiffness common
◦ Can also have fever
◦ Focal findings more common with ruptured AVM
Subarachnoid Hemorrhage
CT scan
◦ 90% sensitive within first 24 hours
LP
◦ Indicated if CT does not reveal SAH
◦ Elevated opening pressure
◦ RBC >100,000
◦ Does not decrease
◦ Xanthochromia > 12 hours after headache
◦ WBC can be elevated
◦ Glucose can be low
Vessel imaging
◦ CTA vs cerebral angiogram
Subarachnoid Hemorrhage
Complications
◦ Recurrent hemorrhage (20% of patients within 2 weeks)
◦ Doubles mortality rate
◦ Intraparenchymal extension causing focal deficits
◦ Vasospasm
◦ Delayed arterial narrowing in blood vessels surrounded by subarachnoid blood
◦ Leads to ishcemis stroke in > 1/3 of cases
◦ Can begin 4 days after hemorrhage, peaks at 10-14 days, then resolves
◦ Risk increases proportionally to amount of subarachnoid blood
◦ Hydrocephalus
◦ Seizures
◦ Diabetes insipidus
Subarachnoid Hemorrhage
Treatment
◦ SBP < 160
◦ Bedrest with elevation of head of bed to 30 degrees
◦ Nimodipine 60 mg every 4 hours for 21 days (prevents vasospasm)
◦ Maintenance of euvolemia and normal hemoglobin/hematocrit
◦ Surgical intervention
Giant Cell Arteritis
Aka Temporal arteritis
Subacute granulomatous inflammation of external carotid arterial system, particularly the
superficial temporal artery
Uncommon before age 50, increasing incidence with increasing age
◦ M:F 1:2

Headache
◦ Unilateral or bilateral
◦ Associated with scalp/skin tenderness over the temporal regions
◦ Jaw claudication
◦ Often associated with polymyalgia rheumatica
Giant Cell Arteritis
Complication
◦ Blindness
◦ Unusual presenting symptom but can occur within the first month
◦ Permanent
◦ 50% of untreated patients
◦ Bilateral in 25% of patients

Diagnosis
◦ ESR usually very elevated (~100)
◦ Temporal artery biopsy
◦ Vasculitis may be patchy so biopsy may be negative
◦ Thickened temporal artery may be visible on examination
Giant Cell Arteritis
Treatment
◦ Steroids are mainstay
◦ High-dose IV methylprednisolone (1000 mg/day x 5 days) or dexamethasone equivalent
◦ Prednisolone 60 mg/day x 2 months followed by slow taper (over months or 1-2 years)
◦ Titrate steroids to ESR
◦ Headache usually resolves within 2-3 days of starting steroids

◦ Do not withhold treatment waiting for biopsy or stop treatment if

biopsy is normal and there is a high clinical suspicion
Idiopathic Intracranial Hypertension
Formerly called: Pseudotumor cerebri or Benign Intracranial Hypertension
F >> M, peak incidence in 20s
Diffuse headache
◦ Often worse with lying down or may be non-positional
◦ Pulsatile tinnitus
◦ Transient visual obscurations
◦ Especially with sneezing, bending over, Valsalva maneuver
◦ Visual loss
◦ Constriction of visual fields followed by blindness
◦ Diplopia
Idiopathic Intracranial Hypertension
Risk Factors
◦ Obesity, rapid weight gain
◦ Most common

◦ Venous sinus thrombosis

◦ Withdrawal from steroid therapy/ steroid therapy
◦ Hormonal contraceptives
◦ Hypervitaminosis A
◦ 13-cis retinoic acid use (acne treatment)
◦ Tetracycline use
Idiopathic Intracranial Hypertension
Examination
◦ Bilateral papilledema
◦ 6th nerve palsies (unilateral or bilateral)
◦ Constriction of visual fields, enlargement of blind spot
◦ Decreased visual acuity
Diagnostic workup
◦ CT or MRI with venogram
◦ to exclude other causes e.g. CVST
◦ LP: elevated opening pressure with normal CSF studies
◦ >25cm H2O (normal 9-18cm H20)
Idiopathic Intracranial Hypertension
Treatment
◦ Maintenance
◦ Acetazolamide 1-2 grams/day or Topiramate 50-100mg BD
◦ Weight loss
◦ Transverse sinus shunting if transverse sinus stenosis is present

◦ Acute vision saving treatments

◦ Repeat LPs if worsening symptoms – not very effective
◦ Optic nerve sheath fenestration
◦ Lumber-peritoneal shunt
Take Home Points
Headaches are the some of the commonest neurological disorders
and reduce quality of life
Important to differentiate between primary and secondary
headaches
Important to understand the epidemiology and characteristics of the
different types of headaches
Secondary headaches can cause disability and death and must be
rapidly treated