Headache

Last updated: Sep 02, 2020

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Summary
Headache is a symptom commonly encountered in everyday clinical practice, and,
according to the WHO, one of the ten most common causes of functional disability. It
may be primary (e.g., tension-type headaches, migraine) or secondary (e.g.,
following head trauma or infections) in nature. Although most episodes of headache are
harmless, potentially life-threatening causes (e.g., subarachnoid
hemorrhage, meningitis) should always be considered. Identifying the cause of
headaches is often difficult and requires a detailed clinical history as well as a
thorough physical examination. Additional diagnostics, e.g., imaging, are only indicated
if headaches persist despite treatment or if specific clinical features are present that are
signs of an underlying disease. This article gives an overview of the most common
types of headache and serves as a guide to diagnosing different headache disorders.
NOTES
FEEDBACK
Approach
Red flags for headache  [1]

 Fever
 Focal neurological deficits
 Seizures
 Meningeal signs
 Signs of increased ICP (e.g., papilledema)
 impaired level of consciousness
NOTES
FEEDBACK
Epidemiology
 Most common forms of headache  [3]

o Tension-type headache: 40–80% of cases
o Migraine: 10% of cases
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Clinical features
History of present illness
 Nature of the headache
o Localization
o Character
 Triggers and exacerbating factors
o Stress
o oral contraceptives; menstruation
o Lying down or standing up
 Associated symptoms
o Nausea
o Aura
o Photopsia

Past medical history, social history, and family history

 hypertension
 Medications
 Substance use 
o Alcohol consumption
 Family history

Physical examination
 Vital signs
o Blood pressure
o Presence of fever
 HEENT
o Palpation of the temporal artery; jaw movement
o Palpation of the sinuses
o Direct fundoscopy
 Neurological
o Neurological examination for neurologic deficits
 Skin: rash
Consider secondary life-threatening causes if red flags for headache are present!
NOTES
FEEDBACK
Diagnostics
Risk stratification of headache  [4][5]

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Clinical features

Low-risk headache  Age < 30 years

 Features of primary headache

 Prior experience of similar headache

 Clinical features

 Absence of neurologic deficits

 Typical headache pattern 

 No recent history of cancer, HIV, or Lyme disease

 No red flags for headache

 Any red flags for headache

 Any features of secondary headache

 Horner syndrome

High-risk headache  Accompanying systemic illness (e.g., fever, myalgias)

 Triggered by cough, exertion, or sexual intercourse

 Tenderness over the temporal artery

 History of cancer, HIV, Lyme disease

Laboratory studies
 There are no routine recommended laboratory studies for headaches. Consider
the following based on clinical suspicion: 
o CBC
o TSH
o ESR, CRP

Imaging  [6]

 Test of choice 
o The initial test of choice is usually a head CT without contrast
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Recommended initial imaging modality for headache  [7]

Initial test of choice

Sudden-onset severe headache (i.e., thunderclap headache)  CT head without IV contrast

New headache with papilledema  MRI head 

o Without contrast

o Without and with IV

contrast
 Recommended initial imaging modality for headache  [7]

Initial test of choice

 CT head without IV contrast 

 CT head without IV contrast 

 MRI head 

New or worsening headache related to head trauma or accompanied by red flags o Without IV contrast 

o Without and with IV

contrast 

New primary headache suspected to be of trigeminal autonomic origin   MRI head without and with IV

(e.g., cluster headache)  contrast 

 MRI head 

o Without IV contrast
Chronic headache with new features or change in character, severity, or frequency
o Without and with IV

contrast

Additional diagnostics to consider  [6]

 Lumbar puncture (LP) with CSF analysis

The diagnostic modality should be determined by the patient history and clinical
presentation. Neuroimaging is usually not indicated for primary or low-risk headaches.
NOTES
FEEDBACK
Primary headaches
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Tension headache Migraine headache

Sex  ♂ < ♀  ♂ < ♀ 

 30 minutes to a couple of 
Duration  4–72 hours
days  
 Tension headache Migraine headache

 Occasionally to daily  Occasionally to several times a 

Frequency
 Episodic or chronic month 

Localization  Holocephalic or bifrontal  60% are unilateral. 

re

 Dull, nonpulsating, band- 

Character likeor vise-like pain  Pulsating, boring/hammering pain 

 Constant 


Intensity  Mild to moderate  Moderate to severe
re

na

 No autonomic  Nausea, vomiting

symptoms(vomiting, nausea,  Hyperacusis
sy
phonophobia, or photophobia)  Photophobia
Additional symptoms an
 Tightness in  Phonophobia

the posteriorneck muscles  Preceding aura
bu
 Pericranial tenderness  Prodrome

 Stress

 Stress  Fluctuation in hormone levels: oral

 Lack of sleep, fatigue contraceptives, menstruation

Triggers/exacerbating
 Routine activities (e.g.,  Certain types of food (e.g., those 
factors
climbing stairs) do not exacerbate containing tyramines or nitrates such as

symptoms. processed meat, chocolate, cheese)

 Exacerbated by exertion
The typical migraine headache can be remembered by “POUND”: pulsatile, one-
day duration, unilateral, nausea, disabling intensity.
NOTES
FEEDBACK
Secondary headaches
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Diagnosis Clinical features Diagnostic findings

Meningitis 
[12][13][14]
 Classic triad: fever,  ↑ WBC, ↑ procalcitonin (if bacterial)

headache, and neck  CSF analysis

stiffness (nuchal rigidity) o Bacterial: WBC ≥ 1000

 Diagnosis Clinical features Diagnostic findings

 Meningism (e.g., phot

ophobia) cells/μL (predominantly neutrophils),

 Dull, diffuse elevated protein, low glucose,

(holocephalic) headache that positive gram stain

worsens over hours/days o Viral: WBC 10-500

 Altered mental status cells/μL (predominantly lymphocytes), 

 Nausea, vomiting normal-elevated protein, normal glucose

 Seizures

 Acute, severe,

nonspecific headache

 Focal neurologic
 CT head without
Intracerebral signs and symptoms
contrast: hyperdense lesion with hypodense
hemorrhage [15][16]
 Nausea and vomiting
perifocal edema
 Confusion and loss of

consciousness

 Seizures

 Acute onset of

a thunderclap headache

 Focal neurologic

deficits
 CT head without contrast: blood
Subarachnoid  Meningism
in subarachnoid space(hyperdense)
hemorrhage [17]
 Impaired
 Lumbar puncture : ↑ RBC count
consciousness, rapidly

worsening neurological

status

 Seizures

Subdural  Diffuse headache  CT head without contrast: crescent-

hematoma (SDH
that is worst on the side of shaped, concave, hyperdensehemorrhage
)
 Diagnosis Clinical features Diagnostic findings

the hematoma

 Impaired

consciousness and confusio

 Focal neurologic

deficits (e.g., hemiparesis ,

gait, speech, visual

impairment, personality
that crosses suture lines but not the midline
changes, dilated pupil , or

nonreactive pupil )

 Signs

of increased intracranial

pressure

 Chronic subdural

hemorrhage : psychomotor

impairment, memory loss

Epidural  Headache localized to  CT head without

hematoma  [18]

the side of the hematoma contrast: biconvex, hyperdense lesion

 Contralateral focal

symptoms/hemiplegia

 Impaired mental

status, loss of

consciousness, seizures,

nausea, and vomiting

 Nearly half of patients

who lose consciousness will

have a lucid

interval followed by clinical

deterioration due to further

 Diagnosis Clinical features Diagnostic findings

expansion.

 Nonspecific headache

(acute, subacute, or chronic) 

 Cranial

nerve symptoms

(e.g., diplopia, tinnitus,

unilateral deafness, facial

palsy)

 Cavernous sinus  Labs: ↑ WBC , ↑ D-dimer

syndrome  Fundoscopy: papilledema

 Focal neurological  MRI/MRV or CT/CTV: direct or

Cerebral venous
deficits indirect signs of thrombus (see also
sinus
 Seizures “Diagnostics” in cerebral venous
thrombosis  [19]

 Impairment in thrombosis)  [20]

consciousness and awareness  Cerebral venography: filling

 Signs of increased defect  [19]

intracranial pressure (e.g.,

nausea, vomiting)

 Risk

factors: pregnancy, prothrom

botic states, vasculitis,

smoking, use of oral

contraceptives

Giant cell  Unilateral headache  Anemia, ↑ ESR ≥ 40–50

arteritis 
[21][22][23][24]

over the temporal/occipital mm/hour , ↑ CRP, ↑ IL–6

area  Temporal artery biopsy (gold

 Prominent, tender standard): segmental vasculitis with

temporal artery predominant mononuclear cells

 Jaw claudication, or granulomatous inflammation

 Diagnosis Clinical features Diagnostic findings

scalp tenderness

 Constitutional

symptoms: fever, malaise,

fatigue

 If temporal arteritis is

associated

with polymyalgia rheumatica  MRI with contrast: enhancement of

: shoulder/pelvic pain, the temporal artery

depression, tiredness, fever,

weight loss

 Partial or complete

vision loss (unilateral or

bilateral), amaurosis

fugax, diplopia

 Diffuse (sometimes  Clinical diagnosis: elevated BP

bifrontal), pulsating with or without signs of end-organdamage 

headache that is exacerbated o Labs: anemia, ↑ creatinine, 

by physical activity ↑ BNP, proteinuria, hematuria

Hypertensive  Hypertension > o ECG: left ventricular

crises 
[25][26]
180/120 mm Hg hypertrophy, signs of

 Signs of end- cardiac ischemia (e.g., ST

organ damage (e.g., chest depressions or elevations)

pain, dyspnea, oliguria, o Chest x-

altered mental status) ray: cardiomegaly, pulmonary edema

Ischemic  Tension-type  CT head without

stroke  [27][28]

headache contrast: hyperdense occluded

 Focal neurological vessels, hypodense parenchyma,

deficits effacement of the sulci and loss of

 Altered mental status corticomedullary differentiation

 Diagnosis Clinical features Diagnostic findings

 CTA head and neck: vessel

occlusion

 DW-MRI: T1 hypointense signal,

T2 hyperintense signal in the area of

the infarction

 A dull headache that is

usually bifrontal and worsens

Intracranial spa
ce-occupying les
ions (e.g., brain
tumors)  [29][30][31]
 T1-weighted MRI brain
over weeks/months 
with gadolinium: hypo-, hyper-,
 Signs of increased
or isointense mass lesion with
intracranial
peritumoral edema
pressure (e.g., papilledema)
 CT brain with IV contrast: mass
 Focal neurologic
lesion, commonly with contrast
deficits, altered mental
enhancement
status, seizures, nausea and

vomiting

 Headache of variable

intensity

 Confusion 

 Retrograde

amnesia and/or anterograde

Concussion (e.g. amnesia
 Clinical diagnosis
, mild traumatic  Nausea,
 CT head without contrast: usually
brain injury)  [32][33]
vomiting, dizziness
[34]
normal 
 Ageusia , anosmia, tin

nitus, photophobia, blurring

of vision

 Loss of consciousness

(rare)

 History of trauma 
 Diagnosis Clinical features Diagnostic findings

 Paroxysmal (seconds

to 2 minutes) and

stabbing pain

 Unilateral facial pain,

strictly localized to the

distribution of the branches

of the trigeminal nerve  Clinical diagnosis  [36]

Trigeminal
 Frequency and  MRI brain: vascular compression of
neuralgia 
[35][36]

intensity of episodes usually the trigeminal root

increase over time

 Tender trigger points

 Triggered by chewing,

talking, cold, and touching

specific areas of the face

 No neurologic deficits

 Headache with

variable characteristics

 History

Medication of analgesic overuse

overuse  Autonomic symptoms  Clinical diagnosis

headache
(e.g., nausea)

 Cognitive or

behavioral symptoms (e.g.,

comorbid depression)
NOTES
FEEDBACK
Differential diagnoses
Primary headache
 Migraine
 Tension-type headache
 cluster headaches
 Secondary headache
 Bleeding 
o Epidural hemorrhage
o Subdural hemorrhage
o Subarachnoid hemorrhage
 Vascular 
o Cerebral venous thrombosis
 Autoimmune 
o Temporal arteritis
 Drug/toxin-related 
o Medication overuse headache
 Infectious 
o Intracranial infections 
 Meningitis
 Encephalitis
 Brain abscess
 Other 
o Increased intracranial pressure
o post-lumbar puncture headache
o Glaucoma
o Brain tumors
o Trigeminal neuralgia
o Hypoxia and/or hypercapnia
o Hypertension
The differential diagnoses listed here are not exhaustive.
NOTES
FEEDBACK
Tips and Links
 The International Classification of Headache Disorders 3rd edition (pdf)
 Fact Sheet: Headache Disorders, WHO (2012)

Medication overuse headache

Last updated: Sep 02, 2020
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Summary
Medication-overuse headache (MOH) is a chronic secondary headache disorder caused
by regular overuse of analgesics that are used to treat a preexisting
chronic headache disorder. The most common underlying headache disorders
are migraine followed by tension-type headache.
Simple analgesics (e.g., acetaminophen, NSAIDs) alone or in combination
with caffeine, followed by triptans, are the most commonly overused medications.
Women aged 40–49 years are most commonly affected. The pathophysiology is not
completely understood but likely involves dependence processes, central sensitization,
and (possibly) genetic predisposition. The diagnosis is based on clinical criteria.
Diagnostic studies are usually not necessary unless indicated to investigate the cause of
the preexisting chronic headache. Treatment involves patient education, weaning of
overused medications, management of withdrawal symptoms, and relapse prevention.
MOH typically resolves with discontinuation of the overused medications.
NOTES
FEEDBACK
Clinical features

Pain localization in secondary headache

Certain pain characteristics and associated symptoms can help in the diagnosis of a secondary
headache:

– Temporal arteritis: unilateral headache, jaw claudication, tenderness of scalp or temporal artery,
constitutional symptoms, visual changes
– Hypertensive crisis: diffuse, often bifrontal, headache (Headache in the setting of hypertensive
crisis can be an isolated finding but may also be a manifestation of hypertensive encephalopathy,
which constitutes a hypertensive emergency)
– Sinusitis: Facial pain or pressure in the sinus cavity region, purulent rhinorrhea, flu-like symptoms
– Medication overuse headache: diffuse headache that can change in type and location within an
episode and has developed or worsened with pain medication overuse.
 Tension-type headache
(Tension headache)
Last updated: Apr 22, 2020
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Summary
Tension-type headache (TTH) is a primary headache disorder and the most common
type of headache overall. Tension-type headachesare characterized by a dull,
nonpulsating, band-like pain that is often bilateral. Autonomic symptoms
like photophobia, phonophobia, or nausea are usually not present. Depending on the
frequency and duration of episodes, tension-type headaches are classified as episodic or
chronic. Infrequent episodic tension-type headaches are treated with NSAIDs, while
chronic and frequent episodic forms may benefit from prophylactic amitriptyline.
Nonpharmacological treatment options include lifestyle modification (e.g., stress
reduction) and cognitive behavioral therapy.
NOTES
FEEDBACK
Epidemiology
 Most common type of headache
 Sex: ♀ > ♂
 Peak incidence: 30–40 years
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Etiology
 Exacerbating factors: fatigue, lack of sleep, poor posture, anxiety, stress,
depression
NOTES
FEEDBACK
Clinical features
 Episodic nature
 Headaches last 30 minutes to a couple of days.
 Holocranial or bifrontal, band-like headache
 Maximum of one autonomic symptom (nausea, phonophobia, or photophobia)
 No vomiting or aura
Tension headache fact sheet

Diagnostics
clinical diagnosis

Diagnostic criteria for tension-type headaches  [8][9]

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Classification of tension-type headache  [8]

Characteristics Infrequent episodic tension-type headache Frequent episodic tension-type headache

 ≥ 10 episodes on 1–14 days/month
 ≥ 10 episodes 
Frequency  For > 3 months (≥ 12 and< 180
 < 1 day/month or < 12 days/year 
days/year)

Duration  30 minutes to 7 days  30 minutes to 7 days 

 No nausea or vomiting
Autonomic symptoms
 No more than one of photophobia or phonophobia


 NOTES

FEEDBACK
Differential diagnoses
 See “Primary headaches” in differential diagnosis of headache.

Localization and additional symptoms of primary headaches

These three types of primary headache can be differentiated according to pain localization, intensity,
and additional symptoms.

– Tension headache: holocranial or bifrontal, dull headache; no autonomic symptoms

– Migraine: unilateral headache with autonomic symptoms (vomiting, nausea, phonophobia,
photophobia)
– Cluster headache: unilateral, periorbital headache with conjunctival injection, lacrimation,
rhinorrhea and swelling of nasal mucous membranes, Horner syndrome, forehead or facial sweating

The differential diagnoses listed here are not exhaustive.

NOTES
FEEDBACK
Treatment
 Pharmacological therapy
o Episodic tension-
type headache; NSAIDs (e.g., ibuprofen, aspirin); acetaminophen
o Chronic tension-type headache and frequent episodic type: consider
prophylactic therapy (e.g., with amitriptyline)
 Non-pharmacological therapy: Consider if there is a significant decrease in
patient's quality of life. 
o Lifestyle and behavioral modification
Avoid prolonged use (> 15 days/month) of NSAIDs for chronic tension headache, as
this may cause medication overuse headaches.  [8]

NOTES
FEEDBACK
References
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rebound.. Headache. 1998; 38(9): p.687-90. doi: 10.1046/j.1526-4610.1998.3809687.x.|
Open in Read by QxMD
27.
Krymchantowski AV, Moreira PF. Out-patient detoxification in chronic migraine:
comparison of strategies.. Cephalalgia. 2003; 23(10): p.982-93. doi: 10.1046/j.1468-
2982.2003.00648.x.| Open in Read by QxMD
28.
Pageler L, Katsarava Z, Diener H, Limmroth V. Prednisone vs. Placebo in Withdrawal
Therapy Following Medication Overuse Headache. Cephalalgia. 2007; 28(2): p.152-
156. doi: 10.1111/j.1468-2982.2007.01488.x.| Open in Read by QxMD
29.
Diener H-C, Bussone G, Oene JV, Lahaye M, Schwalen S, Goadsby P. Topiramate
Reduces Headache Days in Chronic Migraine: A Randomized, Double-Blind, Placebo-
Controlled Study. Cephalalgia. 2007; 27(7): p.814-823. doi: 10.1111/j.1468-
2982.2007.01326.x.| Open in Read by QxMD
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Rizzato B, Leone G, Misaggi G, Zivi I, Diomedi M. Efficacy and Tolerability of
Pregabalin Versus Topiramate in the Prophylaxis of Chronic Daily Headache With
Analgesic Overuse. Clin Neuropharmacol. 2011: p.74-
78. doi: 10.1097/wnf.0b013e318210ecc9.| Open in Read by QxMD
31.
Silberstein SD, Blumenfeld AM, Cady RK, et al. OnabotulinumtoxinA for treatment of
chronic migraine: PREEMPT 24-week pooled subgroup analysis of patients who had
acute headache medication overuse at baseline. J Neurol Sci. 2013; 331(1-2): p.48-
56. doi: 10.1016/j.jns.2013.05.003.| Open in Read by QxMD
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Agabegi SS, Agabegi ED. Step-Up To Medicine. Baltimore, MD, USA: Lippincott
Williams & Wilkins; 2013
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ed. UpToDate. Waltham,
MA: UpToDate.https://www.uptodate.com/contents/overview-of-follicular-thyroid-
cancer. Last updated January 16, 2014. Accessed January 25, 2017.
34.
Medication-overuse headache (MOH). url: https://ichd-3.org/8-headache-attributed-to-
a-substance-or-its-withdrawal/8-2-medication-overuse-headache-moh/ Accessed:
November 2, 2019. 
35.
 Tension-type headache (TTH). url: https://ichd-3.org/2-tension-type-
headache/. Accessed: November 2, 2019. 
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Rains JC, Penzien DB, McCrory DC, Gray RN. Behavioral Headache Treatment:
History, Review of the Empirical Literature, and Methodological Critique. Headache:
The Journal of Head and Face Pain. 2005; 45(s2): p.S92-S109. doi: 10.1111/j.1526-
4610.2005.4502003.x.| Open in Read by QxMD

Migraine
Last updated: Sep 02, 2020
QBANK SESSION
CLINICAL SCIENCES
CLINICIAN
LEARNED
Summary
Migraine is a primary headache characterized by recurrent episodes of unilateral,
localized pain that are frequently accompanied by nausea, vomiting, and sensitivity to
light and sound. In approximately 25% of cases, patients experience an aura preceding
the headache, which involves reversible focal neurologic abnormalities, e.g., visual
field defects (scotomas) or paresis lasting less than an hour. Migraine is a clinical
diagnosis and imaging is generally not indicated. Treatment of attacks consists of
general measures (e.g., minimizing light and sound) together with administration of
nonsteroidal anti-inflammatory drugs (e.g., aspirin)
and antiemetics (e.g., prochlorperazine) if nausea is present. In severe
cases, triptans may be added. Prophylactic treatment (e.g., beta blockers) may be
indicated if migraines are especially frequent or long lasting, or if abortive therapy fails
or is contraindicated.
NOTES
FEEDBACK
Epidemiology
 Peak incidence: 30–40 years
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Etiology
 Potential triggers 
o Emotional stress
o alcohol
o Poor sleeping habits
o oral contraceptive pills
NOTES
FEEDBACK
Pathophysiology
 The pathophysiology of migraine is not fully understood
 Vascular dysregulation
 Dysregulation of pain sensitization in the trigeminal system
NOTES

FEEDBACK
Clinical features
Migraine is characterized by recurrent attacks and may occur with aura (∼ 25% of
cases; headache

1. Prodrome (facultative)
 headache
 Sudden hunger or lack of appetite

2. Aura
headache
 Typical aura  [4][5]

o Visual disturbances; sensory and/or speech symptoms (positive and/or

negative ;) 
 Scintillating scotoma
 Central scotoma

3. Headache
 Localization
o Typically unilateral, but bilateral headache is possible
 Duration: usually 4–24 hours; rarely over 72 hours
 Course: progression of pulsating, throbbing, or pounding pain
 Exacerbated by physical activity
 Accompanying symptoms: photophobia, phonophobia, and nausea/vomiting

4. Postdrome (facultative)
The typical migraine headache is “POUND”: Pulsatile, One-
day duration, Unilateral, Nausea, Disabling intensity.

NOTES

FEEDBACK
Diagnostics
The most important step is to exclude red flags for headache
Migraine is a clinical diagnosis that is based on patient history and physical
examination!
 NOTES

FEEDBACK
Differential diagnoses
 See differential diagnoses of headache

The differential diagnoses listed here are not exhaustive.

NOTES

FEEDBACK
Treatment
Abortive therapy
All patients
 Limit stimuli (i.e., light, loud noises) and activity.
 Treat nausea/vomiting, if present.
o Parenteral antiemetics  [12]

 Prochlorperazine
Mild to moderate headache  [12][4]

 First-line treatment consists of NSAIDs, acetaminophen, acetylsalicylic acid, or

combinations including caffeine
 Children: ibuprofen and family counseling
Moderate to severe headache  [12][4]

 Start a migraine-specific agent: triptans (e.g., sumatriptan) or ergotamine (do

not combine these agents!)
o Second-line: consider one of the following 
 Butorphanol
Do not combine triptans and ergotamines (within a 24-hour period) because of
potentially dangerous drug interactions (e.g., coronary vasospasm and serotonin
syndrome).  [17]

Overview of migraine-specific agents

MAXIMIZE TABLETABLE QUIZ

Migraine-specific agents

Triptans E

 Ergotamine
Agents  Sumatriptan, zolmitriptan, almotriptan, rizatriptan
 Dihydroergotamine

 5-HT1B/1D receptor agonists that cause:

o Vasoconstriction of (dilated) cranial and

basilar arteries  Vasoconstriction by binding t

Mechanism of action
o Inhibition of trigeminal nerve nociception adrenergicreceptors  [18]

o Inhibition of vasoactive peptide secretion 

 Most effective if taken at the onset of headache

 Migraine headaches
Indications  Vascular headaches (i.e., mig
 Cluster headaches

 Vasospasm of coronary vessels →

coronary ischemia (rare)

 Paresthesia and sensation of cold in the extremities

 ECG changes
 Serotonin syndrome (if taken with other 5-
 Ischemia
HT agonists)
Side effects   Nausea/vomiting
 Temporary blood pressure increase (very common)
 Numbness, paresthesia, myalg
 Dizziness, malaise, flashes
 Ergot toxicity
 Frequent intake (≥ 10x/month) can lead

to headaches.

 Hypertension

Contraindications  Coronary artery disease  Pregnancy

 Vasospastic angina  Peripheral vascular disease

 Migraine-specific agents

Triptans E

 Peripheral artery disease  Coronary artery disease

 Hypertension  Hypertension

 Pregnancy and breastfeeding  Pharmacologic interactions 

Triptans and ergotamine have severe pharmacological interactions (e.g., coronary

spasm, serotonin syndrome) with one another and with other drugs
(e.g., SSRI, macrolides). ALWAYS take a detailed history of the patient's usual and
recent medications before selecting a drug.
Triptans and ergotamines are contraindicated in pregnancy.
A SUMo wrestler TRIPs ANd falls on his head: SUMaTRIPtANs are used
for headaches (cluster and migraine).

Prophylactic therapy
Nonpharmacological  [19]

 Lifestyle modifications
o Exercise
o Maintain a healthy diet 
o avoid potential triggers
o Follow a regular sleeping schedule
Pharmacological  [20]

 Indications [21][22]

o Severe disability regardless of frequency (e.g., hemiplegic migraine)

o ≥ 2 attacks/week regardless of severity
 General prophylaxis
o First-line  [20]

 Anticonvulsants (e.g., topiramate; valproate
 Beta blockers (e.g., propranolol
o Second-line  [20]

 Tricyclic antidepressant: amitriptyline
NOTES

FEEDBACK
References
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Krymchantowski AV, Moreira PF. Out-patient detoxification in chronic migraine:
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Diener H-C, Bussone G, Oene JV, Lahaye M, Schwalen S, Goadsby P. Topiramate
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Cluster headache
Last updated: Aug 10, 2020
QBANK SESSION
CLINICAL SCIENCES
CLINICIAN
LEARNED
Summary
Cluster headache (CH) is a type of primary headache that mostly affects adult men.
Patients present with recurrent, fifteen minute up to three hour attacks of agonizing,
strictly unilateral headaches in the periorbital and forehead region (areas innervated
by the trigeminal nerve). These attacks are associated with ipsilateral symptoms of
increased cranial autonomic activity, e.g., lacrimation, conjunctival
injection, rhinorrhea, or partial Horner syndrome. Cluster headaches tend to occur in
episodic patterns (“cluster bouts”) followed by months of remission, but are
considered chronic if remission between bouts lasts less than one month. Diagnosis is
based on the patient's history, in particular on the exact description and timing of
the headaches. Acute episodes are treated with 100% oxygen or triptans,
while verapamil is used for preventative treatment.
NOTES
FEEDBACK
Epidemiology
 Sex: ♂ > ♀ (3:1)
 Peak incidence: 20–40 years
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Etiology
 Risk factor: tobacco use
NOTES
FEEDBACK
 Clinical features
 Headache characteristics
o Agonizing pain
o Strictly unilateral, periorbital, and/or temporal
o Short, recurring attacks; usually occur in a cyclical pattern (“clusters”)
 Ipsilateral autonomic symptoms
o Conjunctival injections and/or lacrimation
o Rhinorrhea and nasal congestion
o Partial Horner syndrome: ptosis and miosis, but no anhidrosis
 Restlessness and agitation
While patients with migraine headaches tend to rest motionlessly in a quiet, dark
room, individuals with cluster headachepace around restlessly in excruciating pain!

NOTES
FEEDBACK
Differential diagnoses
 See article on “Headache”
 The differential diagnoses listed here are not exhaustive.

Treatment

Medical therapy
 Acute
o Oxygen therapy with   100%
FiO2

o First-line: triptans (e.g., sumatriptan) or zolmitriptan
NOTES
FEEDBACK
References
1.
Olesen J. The International Classification of Headache Disorders 3rd
Edition. https://www.ichd-3.org/. Updated: December 31, 2015. Accessed: April 1,
2017. 
2.
Blanda M. Cluster Headache. In: Ramachandran TS Cluster Headache. New York,
NY: WebMD.https://emedicine.medscape.com/article/1142459-overview. January 11,
2017. Accessed November 18, 2017.
3.
Lodi R, Pierangeli G, Tonon C, et al. Study of hypothalamic metabolism in cluster
headache by proton MR spectroscopy. Neurology. 2006; 66(8): p.1264-
1266. doi: 10.1212/01.wnl.0000208442.07548.71.| Open in Read by QxMD
4.
Foss-Skiftesvik J, Hougaard MG, Larsen VA, Hansen K. Clinical Reasoning: Partial Horner
syndrome and upper right limb symptoms following chiropractic
manipulation. http://www.neurology.org/content/84/21/e175.long. Updated: May 25,
2015. Accessed: April 1, 2017. 
5.
Matharu M. Cluster Headache. BMJ Clin Evid. 2010; 2010(1212). pmid: 21718584. |
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6.
Mendizabal JE, Umaña E, Zweifler RM. Cluster headache: Horton's cephalalgia
revisited. South Med J. 1998; 91(7): p.606-617. pmid: 9671830. | Open in Read by
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Weintraub JR. Cluster headaches and sleep disorders. Curr Pain Headache Rep. 2003;
7(2): p.150-156. pmid: 12628058. | Open in Read by QxMD
8.
Cittadini E, Matharu MS, Goadsby PJ. Paroxysmal hemicrania: a prospective clinical
study of 31 cases. Brain. 2008; 131(4): p.1142-1155. doi: 10.1093/brain/awn010.|
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9.
Headache Classification Committee of the International Headache Society (IHS). The
International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;
38(1): p.1-211. doi: 10.1177/0333102417738202.| Open in Read by QxMD
10.
Singh MK. Chronic Paroxysmal Hemicrania. In: Chronic Paroxysmal Hemicrania. New
York, NY: WebMD.http://emedicine.medscape.com/article/1142296-
overview#a6. December 7, 2014. Accessed April 1, 2017.
11.
Evers S, Husstedt IW. Alternatives in drug treatment of chronic paroxysmal
hemicrania. https://www.ncbi.nlm.nih.gov/pubmed/8783475. Updated: June 30,
1996. Accessed: April 1, 2017. 
12.
Silberstein SD. Short-Lasting Unilateral Neuralgiform Headache With Conjunctival
Injection and Tearing
(SUNCT). https://www.msdmanuals.com/professional/neurologic-
disorders/headache/short-lasting-unilateral-neuralgiform-headache-with-conjunctival-
injection-and-tearing-sunct. Updated: March 31, 2020. Accessed: May 11, 2020. 
13.
Pareja JA, Álvarez M, Montojo T. SUNCT and SUNA: Recognition and Treatment. Curr
Treat Options Neurol. 2012; 15(1): p.28-39.doi: 10.1007/s11940-012-0211-8.| Open in
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International Headache Society. The International Classification of Headache Disorders,
3rd edition (beta version). Cephalalgia. 2013; 33(9): p.629-
808. doi: 10.1177/0333102413485658.| Open in Read by QxMD
15.
NHS. Cluster Headache. http://www.nhs.uk/conditions/cluster-
headaches/Pages/Introduction.aspx. Updated: March 31, 2017. Accessed: April 1,
2017. 
16.
National Clinical Guideline Centre. Headaches: Diagnosis and Management of
Headaches in Young People and
Adults. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0078140/. Updated: June
30, 2012. Accessed: November 18, 2017. 
17.
Beck E, Sieber WJ, Trejo R. Management of cluster headache.. Am Fam
Physician. 2005; 71(4): p.717-24. pmid: 15742909. | Open in Read by QxMD
18.
Wei DY, Khalil M, Goadsby PJ. Managing cluster headache. Pract Neurol. 2019; 19(6):
p.521-528. doi: 10.1136/practneurol-2018-002124.| Open in Read by QxMD
19.
Burish MJ. Cluster Headache: History, Mechanisms, and Most Importantly, Treatment
Options. Practical Neurology. 2017: p.34-
36.url: https://practicalneurology.com/articles/2017-may/cluster-headache-history-
mechanisms-and-most-importantly-treatment-options.
20.
Robbins MS, Starling AJ, Pringsheim TM, Becker WJ, Schwedt TJ. Treatment of Cluster
Headache: The American Headache Society Evidence-Based Guidelines. Headache: The
Journal of Head and Face Pain. 2016; 56(7): p.1093-1106. doi: 10.1111/head.12866.|
Open in Read by QxMD
21.
Francis GJ, Becker WJ, Pringsheim TM. Acute and preventive pharmacologic treatment
of cluster headache. Neurology. 2010; 75(5): p.463-
473. doi: 10.1212/wnl.0b013e3181eb58c8.| Open in Read by QxMD
22.
May A. Cluster headache: pathogenesis, diagnosis, and management. Lancet. 2005;
366(9488): p.843-855. doi: 10.1016/s0140-6736(05)67217-0.| Open in Read by QxMD
23.
Mazzoni P, Pearson T, Rowland LP. Merritt's Neurology Handbook. Lippincott Williams
& Wilkins; 2006
24.
Mayo Clinic Staff. Cluster Headache. http://www.mayoclinic.org/diseases-
conditions/cluster-headache/home/ovc-20206295.Updated: December 31,
2016. Accessed: April 1, 2017. 
25.
Blanda M. Cluster Headache: Treatment & Management. In: Cluster Headache:
Treatment & Management. New York,
NY: WebMD.http://emedicine.medscape.com/article/1142459-treatment#d9. January
11, 2017. Accessed April 1, 2017.
26.
Goadsby PJ. Pathophysiology of cluster headache: a trigeminal autonomic
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+2002%3B+1(4)%3A251-7.
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of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education /
Medical; 2018
28.
Matharu MS, Levy MJ, Meeran K, Goadsby PJ. Subcutaneous octreotide in cluster
headache: Randomized placebo-controlled double-blind crossover study. Ann
Neurol. 2004; 56(4): p.488-494. doi: 10.1002/ana.20210.| Open in Read by QxMD
29.
Ferri FF. Ferri's Clinical Advisor 2015 E-Book. Elsevier Health Sciences; 2014
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Otolaryngologic Clinics of North America,. Elsevier Health Sciences; 2014
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2.| Open in Read by QxMD
33.
Goadsby PJ, Dodick DW, Leone M, et al. Trial of Galcanezumab in Prevention of
Episodic Cluster Headache. N Engl J Med. 2019; 381(2): p.132-
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14(1). doi: 10.1186/1129-2377-14-48.| Open in Read by QxMD

Idiopathic intracranial hypertension

(Pseudotumor cerebri, Benign intracranial hypertension)
Last updated: May 11, 2020
QBANK SESSION
CLINICAL SCIENCES
LEARNED
Summary
Idiopathic intracranial hypertension (IIH), often referred to as pseudotumor cerebri or
benign intracranial hypertension, is a condition of unknown etiology that manifests
with chronically elevated intracranial pressure (ICP). It predominantly
affects obese women, especially such who have gained significant weight over a short
period of time, but certain drugs (growth hormones, tetracyclines, excessive vitamin A)
 are also associated with the condition. The most common symptoms are
diffuse headaches, although various visual symptoms and pulsatile tinnitus are also
common. Ophthalmologic examination is crucial for confirming the diagnosis and
usually reveals bilateral papilledema and possibly loss of vision. MRI is often done to
rule out other causes of increased ICP. Lumbar puncturetypically shows an elevated
opening pressure. Acetazolamide is the first-line therapy, whereas surgery is only used
as a last resort. Even with treatment, the condition often worsens over the course of
months to years, and permanent symptoms are common.
NOTES
FEEDBACK
Epidemiology
 Predominantly affects obese women aged 15–45 years
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Etiology
 Risk factors
o Obesity
o Certain medications, including: 
 Growth hormone
 Tetracyclines
 Excessive vitamin A or derivatives
NOTES
FEEDBACK
Pathophysiology
A mismatch between production and resorption of CSF (cause unknown) → ↑ ICP →
damage to structures of the CNS and especially to the optical nerve fibers
NOTES
FEEDBACK
Clinical features
 Diffuse headaches
 Visual symptoms
o Transient vision loss
o Diplopia
o Retrobulbar pain
 Pulsatile tinnitus
 Cranial nerve disorders (especially CN VI)
NOTES
FEEDBACK
Diagnostics
 Ophthalmologic examination
o Opthalmoscopy: bilateral papilledema
o peripheral loss of vision
 MRI
o Unremarkable brain parenchyma
o Empty sella
 Lumbar puncture
o Elevated opening pressure >20–25 cm H O 2

o Normal CSF analysis with no signs of inflammation or bleeding

Papilledema in intracranial hypertension

Fundoscopy of a 43-year-old patient with bilateral visual impairment due to intracranial

hypertension.

The left side shows the characteristic fundoscopic finding of papilledema prior to treatment:
obscured disk margins with venous stasis and small hemorrhage.
The right image shows resolution of papilledema after treatment.

© AMBOSS. This image was adapted from the image “A 43-year-old woman on triptorelin presenting with
pseudotumor cerebri: a case report” by Uday Kumar Bhatt, Imran Haq, Venkata S. Avadhanam und Kim
Bibby, PubMed Central, licensed under CC BY 2.0.

NOTES
FEEDBACK
Treatment
 Discontinue any offending agents
 Weight loss
 Medical therapy (first line)
o Acetazolamide
o Add furosemide if acetazolamide alone is not sufficient
 Surgery: if conservative measures fail
o Optic nerve sheath fenestration
o CSF shunt
NOTES
FEEDBACK
References
1.
Lee AG, Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri):
Epidemiology and pathogenesis. In: Post TW, ed. UpToDate. Waltham,
MA: UpToDate.https://www.uptodate.com/contents/idiopathic-intracranial-
hypertension-pseudotumor-cerebri-epidemiology-and-pathogenesis. Last
updated August 24, 2015. Accessed April 4, 2017.
2.
Biousse V, Bruce BB, Newman NJ. Update on the pathophysiology and management of
idiopathic intracranial hypertension. J Neurol Neurosurg Psychiatr. 2012; 83(5): p.488-
494. doi: 10.1136/jnnp-2011-302029.| Open in Read by QxMD
3.
Jensen RH, Radojicic A, Yri H. The diagnosis and management of idiopathic intracranial
hypertension and the associated headache. Ther Adv Neurol Disord. 2016; 9(4): p.317-
326. doi: 10.1177/1756285616635987.| Open in Read by QxMD
4.
Lee AG, Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical
features and diagnosis. In: Post TW, ed. UpToDate. Waltham,
MA: UpToDate.https://www.uptodate.com/contents/idiopathic-intracranial-
hypertension-pseudotumor-cerebri-clinical-features-and-diagnosis. Last updated June
16, 2015. Accessed April 4, 2017.
5.
Gans MS. Idiopathic Intracranial Hypertension. In: Idiopathic Intracranial
Hypertension. New York,
NY: WebMD.http://emedicine.medscape.com/article/1214410-overview. January 27,
2016. Accessed February 28, 2017.
6.
Thurtell MJ, Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri):
recognition, treatment, and ongoing management. Curr Treat Options Neurol. 2013;
15(1): p.1-12. doi: 10.1007/s11940-012-0207-4.| Open in Read by QxMD
7.
Julayanont P, Karukote A, Ruthirago D, Panikkath D, Panikkath R. Idiopathic intracranial
hypertension: ongoing clinical challenges and future prospects. J Pain Res. 2016; 9:
p.87-99. doi: 10.2147/JPR.S60633.| Open in Read by QxMD
8.
Desai PK, et al. Idiopathic intracranial
hypertension. https://radiopaedia.org/articles/idiopathic-intracranial-hypertension-
1.Updated: April 4, 2017. Accessed: April 4, 2017. 
9.
Lee AG, Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri): Prognosis
and treatment. In: Post TW, ed. UpToDate. Waltham,
MA: UpToDate.https://www.uptodate.com/contents/idiopathic-intracranial-
hypertension-pseudotumor-cerebri-prognosis-and-treatment. Last updated June 16,
2015. Accessed April 4, 2017.
 Trigeminal neuralgia
(Tic douloureux, Prosopalgia)
Last updated: Jun 22, 2020
QBANK SESSION
CLINICAL SCIENCES
CLINICIAN
LEARNED
Summary
Trigeminal neuralgia, or tic douloureux, is a condition characterized by attacks of
facial pain in the area of one or more branches of the trigeminal nerve. The pain is
typically very severe in intensity, has a sharp, stabbing quality, and lasts for several
seconds. Attacks can occur without provocation but are sometimes triggered by
innocuous stimuli like chewing. It is a rare condition that typically manifests in patients
above the age of 60 years and affects women more often than men. Trigeminal
neuralgia is a clinical diagnosis. Neuroimaging (preferably MRI) is used for further
classification. Classical trigeminal neuralgia (CTN) is caused by neurovascular
compression of the trigeminal nerve root, while secondary trigeminal neuralgia (STN) is
caused by an underlying condition (e.g., multiple sclerosis). If there is no identifiable
cause, it is referred to as idiopathic trigeminal
neuralgia (ITN). Anticonvulsants (especially carbamazepine) are the mainstay of
therapy. Surgery may be indicated if pharmacological treatment is insufficient. Options
include microvascular decompression (MVD) and transcutaneous procedures that aim
to lesion sensory fibers of the trigeminal nerve root or ganglion.
NOTES
FEEDBACK
Epidemiology
 Peak incidence: 60–70 years
Epidemiological data refers to the US, unless otherwise specified.
NOTES
FEEDBACK
Clinical features
 Unilateral facial pain: paroxysmal, severe shooting or stabbing (like an electric
shock), followed by a burning ache
o Lasts several seconds; may occur up to 100 times per day
o Typically shoots from mouth to the angle of the jaw on the affected side
o triggered by movements such as chewing, talking, or
touch (e.g., brushing teeth, washing face); becomes worse with stimulation
Trigeminal neuralgia

The colors here indicate the areas innervated by different branches of the trigeminal nerve (V1 =
blue; V2 = green; V3 = yellow). In trigeminal neuralgia, there is shooting pain in the areas
innervated by the affected branch that occurs several times daily and often last only a few seconds.
Pain is triggered by various factors (e.g., touching the face, chewing, sneezing). Reflectory facial
spasms may occur. The trigeminal nerves V2 and V3 are usually affected. Pain attacks can be
accompanied by vegetative symptoms such as erythema, lacrimation, and sweating in the areas
innervated by the nerves affected.

© AMBOSS
 Cutaneous innervation of the trigeminal nerve

Branches of the trigeminal nerve (CN V) and the foramina in which they exit the skull.

© AMBOSS

NOTES
FEEDBACK
Diagnostics
clinical diagnosis
NOTES

FEEDBACK
Treatment

Medical therapy  [12][10][13][5]

Chronic therapy
 First-line treatment: choose from one of the following  [12][10]

o Carbamazepine
NOTES
FEEDBACK
References
1.
Singh MK. Trigeminal Neuralgia. In: Egan RA Trigeminal Neuralgia. New York,
NY: WebMD.http://emedicine.medscape.com/article/1145144-overview. November
27, 2016. Accessed November 18, 2017.
2.
Bajwa Zh, Ho CC, Khan SA. Trigeminal Neuralgia. In: Post TW, ed. UpToDate. Waltham,
MA: UpToDate.https://www.uptodate.com/contents/trigeminal-neuralgia?
source=search_result&search=Trigeminal%20Neuralgia&selectedTitle=1~150#H3. Last
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Headache Classification Committee of the International Headache Society (IHS). The
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38(1): p.1-211. doi: 10.1177/0333102417738202.| Open in Read by QxMD
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Cohen J. Trigeminal Neuralgia. https://rarediseases.org/rare-diseases/trigeminal-
neuralgia/. Updated: December 31, 2016. Accessed: April 1, 2017. 
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Bennetto L, Patel NK, Fuller G. Trigeminal neuralgia and its management. BMJ. 2007;
334(7586): p.201-205. doi: 10.1136/bmj.39085.614792.be.| Open in Read by QxMD
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Gronseth G, Cruccu G, Alksne J, et al. Practice Parameter: The diagnostic evaluation
and treatment of trigeminal neuralgia (an evidence-based review): Report of the
Quality Standards Subcommittee of the American Academy of Neurology and the
European Federation of Neurological Societies. Neurology. 2008; 71(15): p.1183-
1190. doi: 10.1212/01.wnl.0000326598.83183.04.| Open in Read by QxMD
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Policeni B et al.. ACR Appropriateness Criteria ® Cranial Neuropathy. J Am Coll
Radiol. 2017; 14(11): p.S406-S420. doi: 10.1016/j.jacr.2017.08.035.| Open in Read by
QxMD
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Matthew T. Whitehead, et al. American College of Radiology ACR Appropriateness
Criteria® Headache. https://acsearch.acr.org/docs/69482/Narrative/. Updated:
December 31, 2018. Accessed: January 12, 2020. 
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Cruccu G, Finnerup NB, Jensen TS, et al. Trigeminal neuralgia. Neurology. 2016; 87(2):
p.220-228. doi: 10.1212/wnl.0000000000002840.| Open in Read by QxMD
10.
Bendtsen L, Zakrzewska JM, Abbott J, et al. European Academy of Neurology guideline
on trigeminal neuralgia. European Journal of Neurology. 2019; 26(6): p.831-
849. doi: 10.1111/ene.13950.| Open in Read by QxMD
11.
Cruccu G, Biasiotta A, Galeotti F, Iannetti GD, Truini A, Gronseth G. Diagnostic accuracy
of trigeminal reflex testing in trigeminal neuralgia. Neurology. 2006; 66(1): p.139-
141. doi: 10.1212/01.wnl.0000191388.64530.8f.| Open in Read by QxMD
12.
Cruccu G, Gronseth G, Alksne J, et al. AAN-EFNS guidelines on trigeminal neuralgia
management. European Journal of Neurology. 2008; 15(10): p.1013-
1028. doi: 10.1111/j.1468-1331.2008.02185.x.| Open in Read by QxMD
13.
Obermann M. Treatment options in trigeminal neuralgia. Therapeutic Advances in
Neurological Disorders. 2010; 3(2): p.107-115. doi: 10.1177/1756285609359317.|
Open in Read by QxMD
14.
Moore D, Chong MS, Shetty A, Zakrzewska JM. A systematic review of rescue analgesic
strategies in acute exacerbations of primary trigeminal neuralgia. Br J Anaesth. 2019;
123(2): p.e385-e396. doi: 10.1016/j.bja.2019.05.026.| Open in Read by QxMD
15.
Kaufmann AM, Price AV. A history of the Jannetta procedure. J Neurosurg. 2020;
132(2): p.639-646. doi: 10.3171/2018.10.jns181983.| Open in Read by QxMD
16.
Asplund P, Blomstedt P, Bergenheim AT. Percutaneous Balloon Compression vs
Percutaneous Retrogasserian Glycerol Rhizotomy for the Primary Treatment of
Trigeminal Neuralgia. Neurosurgery. 2015; 78(3): p.421-
428. doi: 10.1227/neu.0000000000001059.| Open in Read by QxMD
17.
Di Muzio B. Trigeminal Neuralgia. https://radiopaedia.org/articles/trigeminal-
neuralgia. Updated: December 31, 2016. Accessed: April 1, 2017. 
18.
NIH. Trigeminal Neuralgia Fact Sheet. https://www.ninds.nih.gov/Disorders/Patient-
Caregiver-Education/Fact-Sheets/Trigeminal-Neuralgia-Fact-Sheet. Updated:
December 31, 2016. Accessed: April 1, 2017. 
19.
Singh MK. Trigeminal Neuralgia: Practice Essentials. In: Trigeminal Neuralgia: Practice
Essentials. New York, NY: WebMD.http://emedicine.medscape.com/article/1145144-
overview#showall. November 27, 2016. Accessed April 1, 2017.
20.
Bajwa Zh, Ho CC, Khan SA, Garza I, Swanson JW, Dashe JF. Overview of Craniofacial
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21.
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