This document provides an overview of approaches to headache. It begins with an introduction and classification of headaches as either primary or secondary. Common primary headaches include migraine, tension-type headache, and cluster headache. The document discusses the anatomy, physiology, pathophysiology, clinical evaluation, investigations and management principles of headache. A thorough history and physical exam are important for diagnosis. Brain imaging may be indicated depending on headache characteristics or warning signs. Primary headaches are disorders that occur in the absence of an underlying cause, while secondary headaches have an identifiable cause like head trauma or tumors.

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DEBREBIRHAN UNIVERSITY
Asrat weldeyes health science campus
Approach to Headache
Prepared by: Asebe Girma(C-II)
Shegaw Merkebu (C-II)
Zelalem Mekonnen (C-II)
Modulator: Dr.Zena (Internist)
December 2015 E.C

2. Outlines
2
 Introduction & classification of Headache
 Common Causes of Headache
 Anatomy and physiology of headache
 Pathophysiology of Headache
 Clinical evaluation
 Investigation and management principle

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4. Introduction
4
 DEFINITION: Pain or discomfort happening in the
structure between the orbit and the occiput and
arising from pain sensitive structures
 Headache is among the most common reasons
patients seek medical attention.
 Diagnosis and management are based on
understanding of:
 The anatomy, physiology & pharmacology of the
nervous system

5. Classification of Headache
5
1. Primary headaches : The primary
headaches are the ones with no
significant underlying neurologic
pathology.
2. Secondary headache : ones with
some cerebral or extracerebral pathology.

6. Epidemiology
6
 Lifetime prevalence of headache in population
based studies is >90% in males and>95 % in
females.
 severe headache has affected 1/3rd of people
in life.
 It accounts for 1-3% of emergency
department visits and and 4% of regular OPD
visits.
 In US the indirect cost of headache in lost
work days or productivity is 16 billion dollar
per year.

7. Common Causes of Headache
7

8. ANATOMY AND PHYSIOLOGY OF
HEADACHE
8
Pain usually occurs when:
 peripheral nociceptors are stimulated in
response to tissue injury, visceral distension,
or other factors.
 pain-producing pathways of the peripheral
or CNS are damaged or activated
inappropriately.

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 Relatively few cranial structures are pain producing;
these include:
 the scalp,
 meningeal arteries,
 Dural sinuses,
 falx cerebri, and
 proximal segments of the large pial arteries.
 The ventricular ependyma, choroid plexus, pial veins,
and much of the brain parenchyma are not pain
producing.

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The key structures involved in primary headache are
the following:
 The large intracranial vessels and dura mater, and
the peripheral terminals of the trigeminal nerve that
innervate these structures
 Rostral pain-processing regions, such as the
ventro-postero-medial thalamus and the cortex
 The pain-modulatory systems in the brain, such as
the hypothalamus & brainstem

11. Pathophysiology of Headache
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Headache results from:
 Distension, traction or dilation of intracranial or
extra-cranial arteries, large intracranial veins or their
dural veins & cranial and spinal nerves
 Spasm, inflammation or trauma to cranial and
cervical muscles
 Meningeal irritation & increased ICP
 Activation of brain structures

12. Clinical evaluation
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History
 Location
 Mode and time of onset
 Associated features, e.g., nausea, muscle spasm
 Quality and time-intensity attributes
 Duration
 Severity
 Provoking and relieving factors

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 Age of onset
 Family history of migraine
 Relationship with food/alcohol
 Response to any previous treatment,
change in character of headache
 State of general health (Medical illness,
Menstrual history)

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Mode of onset and duration
Patients with recent onset of pain require
prompt evaluation and appropriate treatment.
Serious causes to be considered include
 meningitis,
 subarachnoid haemorrhage,
 epidural or subdural hematoma,
 Tumor
 purulent sinusitis.

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Location of headache
Unilateral pain - cluster headache & in the majority of
migraine attacks.
Ocular or retroocular pain - primary ophthalmologic
disorder
 Headache from intracranial mass lesions may be focal ("it
hurts right here")
Para-nasal pain- acute infection or outlet obstruction of
Para-nasal pain structures.
Occipital localization- with meningeal irritation

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Quality of pain
 Ice pick-like pain (primary stabbing headaches)
- pts with migraine, cluster headache, or giant
cell arteritis.
 Sharp, lancinating pain - a neritic cause such
as trigeminal neuralgia.
 Pulsating, throbbing pain - migraine.
 Sensation of tightness or pressure - with
tension headache.
 Intracranial mass lesions is typically of dull &
steady headache

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Temporal pattern of the headache
Headaches from mass lesions - maximal on
awakening & increase in severity over time.
Cluster headaches frequently awaken
patients from sleep
 Tension headaches can develop whenever
stressful situations occur.
 Migraine headaches are episodic and may
be worse during menses

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Reliving and aggravating factors
 Migraine headaches are frequently relieved by
darkness, sleep, vomiting, or pressing on the
ipsilateral temporal artery, and their frequency
is often diminished during pregnancy.
 Post-lumbar-puncture are typically relieved by
recumbence positioning

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 Headaches caused by intracranial
mass lesions become less severe with
the patient standing.
 Cluster headache improve by activity
and exercise
 Stooping, bending forward, sneezing,
or blowing the nose characteristically
worsens the pain of sinusitis

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Associated symptoms
 Fever or chills, Myalgias, photophobia
 Visual disturbances, Ipsilateral
rhinorrhea and lacrimation
 Transient loss of consciousness
 Nausea/Vomiting
 Dyspnea or other symptoms of heart
disease
 ecent weight loss

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22. Headache Red Flags
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23. Physical examination
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Pulse
 Tachycardia can occur in a
tense, anxious patient with a
tension headache or
accompany any severe pain.
Respiratory rate
 Hypercapnea due to respiratory
failure increase ICP and result in
headache
Temperature
 fever suggests
systemic infectious
illness.
Blood pressure
 Hypertension rarely causes
headache unless the blood
pressure elevation is acute,
as with pheochromocytoma,
or very high, as with early
hypertensive encephalopathy
 SAH is commonly followed
by marked acute blood
pressure elevation
Vital signs

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General P/E
Weight change
 Weight loss or cachexia in a patient with headache
suggests the presence of cancer or chronic infection.
 Polymyalgia rheumatica of giant cell arteritis
syndromes can be accompanied by weight loss.

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1. Scalp, Face and Head
 SCALP tenderness with boring pain –paget’s
disease, myeloma, metastasis to the skull.
SCALP-for tenderness(migraine, SDH, Giant cell
arteritis, Postherpetic neuralgia).
 Nodularity, erythema, or tenderness over the
temporal artery
 Localized tenderness of the superficial temporal
artery
 Sinus tenderness
Lacerated tongue may suggest post ictal

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2. Neck
 Cervical muscle spasms occur with tension and
migraine headaches, cervical spine injuries, cervical
arthritis, or meningitis.
 Carotid bruits may be associated with cerebro-
vascular disease.
 Neck stiffness and meningeal signs
 -LISTEN to a bruit over the eye, neck and head
to rule out AVM.
3. HEART- to look for congenital or rheumatic heart
disease as a possible cause of brain abscess.

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3. Neurologic examination
Confusion, as is commonly seen with
SAH and meningitis.
Dementia may be the major feature of
 intracranial tumor, particularly one in the frontal
lobe
 chronic hydrocephalus

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Cranial nerve examination
Unilateral anosmia suggests a
frontal lobe tumor
 Bilateral anosmia could suggest
mild URTI or previous head injury
 Papilledema, may be seen in
 space-occupying intracranial lesions,
 carotid artery-cavernous sinus fistula,
 hypertensive encephalopathy

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Motor and sensory examination
Asymmetric motor function or gait ataxia –in
sub acute headache should exclude
intracranial mass lesions.
 Decreased sensation over the area of pain-
1st division of the trigeminal nerve in post-
herpetic neuralgia

30. Investigations
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The routine laboratory tests are done depending
on the clinical indications
 LFT, CBC, ESR, RFT, SEROLOGY, U/A, TFT,
S/E,…….
LP is urgently indicated in
SAH in the setting of a -Ve or normal head CT
scan.
an infectious or inflammatory etiology of
headache and

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Brain imaging
Is done for headache with the danger signs and any
of the following
 Recent significant change in the pattern, frequency
or severity of headaches
 Progressive worsening of headache despite
appropriate therapy
 Focal neurologic signs
 Onset of headache with exertion, cough, or sexual
activity
 Orbital bruit
 Onset of headache after age 50 years

32. Primary headache disorders
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Primary headaches are disorders in which
headache and associated features occur in the
absence of any exogenous cause.
The most common are:
 Migraine,
 Tension-type headache
 Cluster headache.

33. Migraine headache
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1. Common migraine – migraine without aura
 Location – fronto-temporal and uni- or – bilateral
 Mostly adolescents and young adults; more females
 Usually throbbing and pulsatile , scalp tender
 Onset – upon awakening or later in the day stays
for 4-24hrs
 Pattern – episodic with irregular intervals, weeks to
months

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 Frequency of attack tend to decrease with age
and pregnancy
 Aggravated by noise, bright light and alcohol but
relived by darkness and quite area with rest
 Associated symptoms – nausea and vomiting; No
AURA
 Treatment – Triptans & NSAIDs
 Prevention – Propanalol and TCA if it occur 4
times in 1 month

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2. Classic migraine – migraine with aura
 Associated with aura such as - Scintillating lights,
visual loss & visual illusions
 Location and distribution with age and sex is similar
with common headache
 Type - Throbbing (pulsatile); worse behind one eye
or ear
 Family history migraine headache is common
 Pattern and temporal course is similar with common
migraine

36. Cluster headache – Migrainous
neuralgia
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 Orbito-temporal, often unilateral
 Adolescent and adult males (90%)
 Intense, non-throbbing, could be throbbing
 Pattern – Usually nocturnal, 1–2 h after
falling asleep

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 Associated Sx – Lacrimation, stiffed nose,
conj. injected
 Prevention- Corticosteroids, verapamil,
valproate, and lithium in recalcitrant cases
 Treatment - O2, sumatriptan, ergotamine
before anticipated attack.

38. Tension headache
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 Generalized hedache
 Mainly adults, both sexes, more common in
women
 Pressure (non-throb-bing), tightness, aching

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 Pattern - Continuous, variable intensity, for
days, weeks, or months
 Course - One or more periods of months to
years
 Associated Sx - Fatigue and nervous strain
 Aggravated by - Depression, worry, anxiety
 Prophylaxis – Anti-anxiety and anti-
depressant drugs

40. Secondary headache
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1.Meningitis
Acute, severe headache with stiff neck
LP is mandatory.
Often there is striking accentuation of pain
with eye movement.

41. 2. Intracranial hemorrhage
41
Acute, maximal in 5 min with stiff neck but
without fever suggests SAH.
A ruptured aneurysm, or intraparenchymal
haemorrhage may also present with
headache alone.
LP may be required to diagnose definitively
SAH.

42. 3. Brain tumor
42
 The head pain is usually nondescript—an
intermittent deep, dull aching of moderate
intensity
 Sleep disturbance in about 10% of patients.
Vomiting that precedes the appearance of
headache by weeks is highly characteristic of
posterior fossa brain tumors.

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A history of amenorrhea or galactorrhea
should - whether a prolactin-secreting pituitary
adenoma or polycystic ovary syndrome
Head pain appearing abruptly after bending,
lifting, or coughing can be due to a posterior
fossa mass, a Chiari malformation

44. 4. Temporal arteritis
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 An inflammatory disorder of arteries that frequently
involves the extracranial carotid circulation.
 A common d/o of aged ≥50,
 About 1/2 of untreated Pts develop blindness due to
involvement of the ophthalmic artery and its branches.
 Rx with glucocorticoids is effective in preventing this
complication.

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 Typical presenting symptoms include
headache, polymyalgia rheumatica, jaw
claudication, fever, and weight loss.
 Head pain may be unilateral or bilateral and is
located temporally in 50% of Pts.
 Pain usually appears gradually; occasionally,
it is explosive in onset.

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 The quality of pain is almost invariably dull
and boring, with superimposed episodic
stabbing pains.
 Scalp tenderness
 Headache is usually worse at night and often
aggravated by exposure to cold.

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 ESR is often, although not always, elevated; a
normal ESR does not exclude giant cell arteritis.
 A temporal artery biopsy followed by immediate
treatment with prednisone 80 mg daily for the first
4–6wk should be initiated when clinical suspicion
is high.

48. 5. Glaucoma
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 Glaucoma may present with a prostrating
headache associated with nausea and vomiting.
 The headache often starts with severe eye pain.
 On physical examination, the eye is often red with
a fixed, moderately dilated pupil.

49. Chronic daily or near-daily
headache
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 CDH can be applied when a patient experiences
headache on 15 days or more per month.
 CDH is neither a single entity nor a diagnosis; it
encompasses a number of different headache
syndromes

50. Classification of Daily or Near-Daily
Headache
50

51. Management of CDH
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 Diagnose any secondary headache and treat that
problem.
 For pt with primary headaches, diagnosis of the
headache type will guide therapy.
 Preventive treatments such as TCA ( amitriptyline or
nortriptyline) at doses up to 1 mg/kg.

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 Tricyclics are started in low doses (10–25 mg
daily) and may be given 12 h before the expected
time of awakening.
 Medicines including topiramate, valproate,
propranolol, flunarizine, candesartan, if
underlying issue is migraine.

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The management of medically intractable
Headache:
Monoclonal antibodies to CGRP
Noninvasive neuromodulatory
 Single-pulse transcranial magnetic stimulation
 Noninvasive vagal nerve stimulation.

54. New daily persistent headache
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 Headache on most if not all days ,pt. recall the
moment of onset.
 The headache usually begins abruptly
 onset more gradual; evolution over 3 days
 The first priority is to distinguish between a primary
and a secondary cause of this syndrome.
 SAH is the most serious of the secondary causes

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56. Low CSF Volume Headache
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 Due to low CSF Volume rather than low pressure
 The a dull ache pain, which is occipitofrontal,
 Incidence 10% -30%.
 Caffeine may provide temporary relief
 Post-LP headache usually begins within 48 hr -12
days.

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Initial Rx for low CSF volume headache is bed
rest.
For persistent pain, IV caffeine 500 mg in 500
mL of saline administered over 2 hr
Because IV caffeine is safe and can be
curative
A blood patch is also effective for post-LP
headache
Intractable headache, oral theophylline

58. Raised CSF pressure headache
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 Raised CSF pressure is well recognized as a cause of
headache.
 Brain imaging can often reveal the cause, such as a
space-occupying lesion.
 It is most efficient to obtain an MRI
 An elevated opening pressure and improvement in
headache following removal of CSF are diagnostic in
the absence of fundal changes

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1st Rx is with acetazolamide (250–500 mg
bid), improve within weeks.
2nd line is topiramate if no respone
Pts. who do not respond to medical treatment
require ICP monitoring and may require
shunting.
 If appropriate, weight loss should be
encouraged.

60. Idiopathic intracranial hypertension
(pseudotumor cerebri)
60
 Pts. typically present with a hx of generalized
headache
 Headache present on waking and improves as the
day goes on.
 Present on awakening in the morning and is worse
with recumbency.
 Headache that occur in awakening ( obstructive sleep
apnea or poorly controlled hypertension) should ruled
out

61. Posttraumatic Headache
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 A traumatic event can trigger a headache process that
lasts for many months or years after the event.
 Complaints of dizziness, vertigo, and impaired
memory can accompany the headache.
 Symptoms may remit after several weeks or persist
for months and even years after the injury.

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 Typically, the neurologic examination is normal
and CT or MRI studies are unrevealing.
 Chronic subdural hematoma may on occasion
mimic this disorder.
 Posttraumatic headache may also be seen after
carotid dissection and SAH and after intracranial
surgery.

63. Treatment
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 TCAs, notably amitriptyline
 Anticonvulsants, such as topiramate, valproate,
candesartan, and gabapentin
 The headache usually resolves within 3–5 years, but
it can be quite disabling.

64. Headache mgt flow chart
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66. References
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1. Harrison’s principle of internal medicine 21st edition
2. Uptodate 2018

67. Thank you !!!
67