Aprroach to Headache

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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
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 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
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 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
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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
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 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
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8. ANATOMY AND PHYSIOLOGY OF
HEADACHE
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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
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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
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 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
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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)
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 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 !!!
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