Markovchick Vincent J., Pons Peter T., Bakes Katherine M.(ed.) Emergency medicine secrets. 5th ed

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Chapter 15 HEADACHE98

CT, computed tomography; CVST, cerebral venous sinus thrombosis; ESR, erythrocyte sedimentation rate;

LP, lumbar puncture; SAH, subarachnoid hemorrhage.

Headache Characteristics Differential Diagnosis

Possible Work-Up

(beyond history and

physical examination)

Headache begins after age 50 Mass lesion, temporal

arteritis, stroke

ESR, neuroimaging

Sudden onset of headache SAH, pituitary apoplexy,

hemorrhage into a mass

lesion or vascular malforma-

tion, mass lesion (especially

posterior fossa), vascular

dissection and CVST

Neuroimaging, LP if CT is

negative

Headaches increasing in

frequency and severity

Mass lesion, subdural hema-

toma, medication overuse

Neuroimaging, drug screen

New-onset headache in

patient who has risk factors

for HIV, cancer

Meningitis (chronic or carci-

nomatous), brain abscess

(including toxoplasmosis),

metastasis

Neuroimaging, LP if

neuroimaging is negative

Headache with fever,

meningismus, rash, or

altered mentation

Meningitis, encephalitis, Lyme

disease, systemic infection,

collagen vascular disease

Neuroimaging, LP, serology

Focal neurologic symptoms

or signs of disease (other

than typical aura)

Mass lesion, vascular

malformation, stroke,

Neuroimaging

Papilledema Mass lesion, pseudotumor,

meningitis

Neuroimaging, LP

Headache that worsens with

standing up

Spontaneous intracranial

hypotension, postdural

puncture headache

(if following an LP)

For the former—LP with

opening pressure, MRI

Headache with ocular

or visual symptoms

Pseudotumor cerebri, acute

narrow angle glaucoma,

temporal arteritis

LP for pseudotumor,

tonometry for glaucoma, ESR

and biopsy for arteritis

Headache after head trauma Intracranial hemorrhage,

subdural hematoma, epidural

hematomas, post-traumatic

headache

Neuroimaging of brain, and

possibly cervical spine

TABLE 15-1. RED FLAGS IN PATIENTS WITH HEADACHES

Chapter 15 HEADACHE 99

headaches, requires close evaluation. A sudden, severe onset, commonly described as “the

worst headache I have ever had,” is classic for a SAH. Associated fever requires evaluation for

infection, tumor, or drug use. A careful history is usually the diagnostic element that helps

decide which headaches to evaluate beyond history and physical examination. Any headache

associated with new focal neurologic signs should be investigated.

6. Why are age and context important in the history of a patient with a

headache?

Migraines most commonly begin before age 30. Tension-type headaches usually begin before

age 50. Headaches that begin after age 55 are much more likely to have a serious cause, such

as a mass lesion, giant cell arteritis, or cerebrovascular disease. Headaches occurring in the

peripartum period may be caused by cortical vein or cerebral venous sinus thrombosis. In

general, if a patient has a long history of previous similar attacks, a serious cause is less

likely. If a patient reports numerous identical attacks treated at home, it is important to

understand why this particular episode led to an ED visit.

7. What questions in the history are most important to ask in evaluating a

patient with a headache?

a. Do you get headaches frequently? Have you ever needed to go to an ED for one? Is this

current headache the same as prior ones that you have had? If not, how does it differ?

These questions are aimed at assessing the quality of pain.

b. How bad is this headache? Have you had headaches this severe in the past? These

questions assess the severity.

c. Did the headache start suddenly or gradually? If sudden, what were you doing at the time it

began? These questions go after the onset.

d. What symptoms accompany the headache? Did you vomit? Was there any fainting, seizure,

photophobia, or double vision? Did you have these same associated symptoms with prior

episodes or not? (for patients with a prior history of headache). These associated

symptoms can suggest secondary causes. For example, a patient with migraines, who has

never had photophobia or vomiting with prior episodes, and now does, ought to undergo

further evaluation. On the other hand, if this headache is similar to prior episodes, it is

most likely due to that same etiology.

e. Have you had any recent head trauma? Note that this includes even minor trauma for elderly

patients, who are more susceptible to chronic or delayed presentation subdural hematomas.

f. What treatment have you used at home and was it helpful? This can also help if a headache has

responded in the past the same as it does for the current visit. But be careful; see Question 13.

8. Does the physical examination add any information?

The history often leads to the correct diagnosis or at least a short list of possible diagnoses.

The physical ﬁndings may support or refute those diagnoses or change the likelihood of

various possibilities. Fever may reﬂect infection. Hypertension may cause headache, be a sign

that there is increased intracranial pressure, or simply be caused by the headache or anxiety

of an ED visit. Abnormal pulse or respiration may be due to infection or toxins.

Palpate the temporal arteries, sinuses (see Question 21), temporo-mandibular joints, and

the scalp for tenderness.

Examine the fundi for papilledema and spontaneous venous pulsations.

Check for nuchal rigidity and photophobia.

Perform a neurologic examination as indicated by the patient’s history and general physical

examination.

9. What is the sensitivity of a noncontrast, head computed tomography (CT) for

detection of a SAH?

Even with advances in imaging technology, only approximately 90% to 95% of SAHs are

detected on CT scans of the head. This number is higher in patients scanned within the ﬁrst

12 to 24 hours but declines rapidly with time from the onset. This is due to cerebrospinal ﬂuid

Chapter 15 HEADACHE100

(CSF) circulation. A lumbar puncture (LP) and CSF analysis will rule out SAH in a patient with

a normal CT scan with close to 100% sensitivity.

10. What are the CSF ﬁndings in a SAH?

As with CT, the ﬁndings on LP evolve with time. Even in the ﬁrst hours after SAH, the large

numbers of red blood cells are found in the lumbar theca. Over days, these numbers fall due to the

circulation of CSF and the breakdown of the red blood cells and hemoglobin. Thus, red cells are

nearly always present early, and xanthochromia (the yellow color due to hemoglobin catabolism) is

almost always found later (until about 2 weeks post-SAH, depending on the method one uses for

detection). Measuring the opening pressure can help too because it is often elevated in SAH.

11. How do I differentiate between a traumatic tap and a SAH?

There are many tests, but none is perfect. Clearing of blood from earlier- to later-collected

tubes is commonly used and is helpful, but unless the last tube contains zero cells, SAH is

still a possibility. Wasting a few milliliters of CSF between the ﬁrst and last tubes facilitates

this. An elevated opening pressure suggests a SAH and not a traumatic tap. Xanthochromia is

almost always present if blood has been in the CSF for 12 hours or longer and conﬁrms an

intracranial bleed. As with CT, one must factor in the timing of the LP (with respect to the

onset of the headache) in interpreting the LP results.

12. If the CT and LP are both normal, do I need to pursue the diagnosis of SAH

with some form of angiography?

The data strongly support, and American College of Emergency Physicians (ACEP) clinical policy

recommends, stopping the work-up if both tests are negative. However, this assumes that SAH is

the major consideration. Rarely, an unruptured aneurysm that is acutely expanding, dissecting, or

thrombosing can cause an acute headache. Furthermore, there are other causes of acute, severe,

sudden-onset headache associated with a normal CT and LP. These include (see Table 15-2):

Pituitary apoplexy.

Cervical artery dissections.

Cerebral venous sinus thrombosis.

Posterior reversible encephalopathy syndrome (related to eclampsia).

Acute stroke (especially posterior fossa).

13. What are migraine headaches?

Although people may refer to any severe headache as a migraine, a migraine is a speciﬁc type of

headache. Migraines tend to be familial and affect women twice as often as men. The underlying

pathophysiology is thought to be vasogenic inﬂammation. The ﬁrst headache usually occurs in an

individual in the teens or twenties. Headaches typically are described as unilateral, severe,

throbbing, and are commonly associated with photophobia and nausea. The headache may also

be non-throbbing. Variations on all of the symptoms occur, but each patient tends to experience a

similar constellation of symptoms with each headache. Patients who experience an aura will often

have positive symptoms (e.g., ﬂashing lights or zig-zag patterns in vision, tingling of the face or

arm or shaking of a limb) as opposed to negative symptoms (e.g., absence of vision, anesthesia

or absence of movement of a limb), which are more common with brain ischemia or infarction.

Occasional migraine patients will have weakness, however. Patients will often use the word

migraine to describe any severe headache, so if a patient says they have a history of migraines,

get more details about their duration, frequency, and what work-up has been done. Make sure

that their headaches are truly migraines.

14. If a headache patient improves or the pain completely resolves with

sumatriptan or ketorolac, does that mean that the diagnosis is migraine

(or some other primary headache cause)?

The answer to this question is an emphatic “no.” Because the ﬁnal common pathway for most

pain in the head is limited, and vasogenic inﬂammation probably plays a role, the response to

any analgesic or antimigraine medication is of no etiologic signiﬁcance. This includes triptans,

Chapter 15 HEADACHE 101

CT, computed tomography; CVA, cerebrovascular accident; LP, lumbar puncture; MRI, magnetic resonance

imaging.

Pathologic Process Clinical Characteristics Work-Up

Subarachnoid

hemorrhage

Headache worst of life CT; if normal, do LP

Headache abrupt, effort related

Normal neurologic examination to focal

deﬁcit or coma

Cervical artery

dissections

History of trauma, Marfan syndrome,

collagen disorders

Headache is ipsilateral

Carotid: neck or head pain, Horner

syndrome, stroke

Vertebral: occipital-nuchal pain and

posterior circulation stroke

Magnetic resonance or

CT angiography

Vascular ultrasound and

conventional angiography

Intracerebral

hemorrhage

History of hypertension CT

History of brain tumor

Severe headache with signs of elevated

intracranial pressure and depressed

mental status

Cerebral venous

thrombosis (superior

sagittal sinus or

transverse sinus)

Postpartum, hypercoagulable states,

and abrupt, dull, constant headache

MRI, magnetic resonance

venography, or conventional

angiography; CT angiography

shows promise

Sixth nerve palsy, seizures

Signs of raised intracranial pressure

Pituitary apoplexy Abrupt severe headache, progressive

visual loss with subsequent signs of

pituitary insufﬁciency

CT or MRI with coronal views of

the pituitary

TABLE 15-2. DIFFERENTIAL DIAGNOSIS AND WORK-UP FOR ACUTE, SEVERE HEADACHE

which have been documented to improve the headaches of patients with SAH and cervical

artery dissections.

15. What speciﬁc entities must be considered in patients with a headache and a

history of cancer or immunosuppression?

In a patient with a history of cancer, consider brain metastases, or infections related to

immunosuppression. In patients who are HIV positive, especially if they have low CD4

counts or high viral loads, opportunistic infections, such as cryptococcal meningitis or

Chapter 15 HEADACHE102

toxoplasmosis, brain abscess, and primary lymphoma of the central nervous system, should

be considered.

16. What speciﬁc diagnosis should be considered in older patients with a new

onset headache and general malaise or other systemic symptoms?

Temporal arteritis is a systemic arterial vasculitis that is rare before age 50 and dramatically

increases in incidence afterward. Also known as giant cell arteritis, temporal arteritis should be

suspected in any patient older than age 50 who has a new onset headache or a change in an

established pattern of headache. It is associated with localized scalp tenderness (anywhere in the

scalp), malaise, myalgias, arthralgias, polymyalgia rheumatica, low-grade fevers, or other

constitutional symptoms. Untreated, temporal arteritis can result in blindness or stroke. Jaw

claudication, if present, is strongly suggestive of the disorder. Erythrocyte sedimentation rate

(ESR) is usually greater than 50 mm/hour, and biopsy is required to establish the diagnosis.

Treatment should be initiated in the ED, based on the clinical presumption and results of the ESR

and not delayed by biopsy. The initial doses of prednisone range from 60 to 80 mg daily. Finally,

because primary headaches start less commonly after the age of 50, many of the other serious

etiologies become more common in this age group, conditions such as stroke and tumors.

17. What is a sentinel bleed?

Up to 50% of patients with aneurysmal SAH will have experienced a warning or sentinel hemorrhage

before their catastrophic bleed. These small hemorrhages occur days to months before the major

event. These events are still characterized by abrupt onset of severe, unusual headache and, if

worked up with CT and LP, should be diagnosable in the vast majority of cases. Note that these

headaches resolve over days to weeks because of the circulation of CSF mentioned previously.

Unfortunately, these episodes are often not worked up and are misdiagnosed as migraine, sinusitis,

or tension-type headache, however, and the patients are discharged from medical care.

18. How do I treat a migraine headache?

Patients who are unable to control their headache at home often present to the ED for better

pain control or supportive therapy. The choice of treatment is based on case presentation,

prior medications used, time elapsed since onset, patient’s prior response to therapy,

existence of comorbid conditions, and severity of the current attack. Narcotics should be used

as a last resort (Table 15-3).

19. How are cluster headaches different from migraines? How are they treated?

These are nonfamilial headaches predominantly affecting men. Excruciating, unilateral pain

lasting 30 to 90 minutes occurs multiple times a day for weeks, followed by a pain-free

interval. During the attacks, autonomic signs of rhinorrhea and lacrimation frequently

occur ipsilateral to the headache. Attacks may be induced by smoking or alcohol. Oxygen

sometimes relieves 90% of cluster headaches within 15 minutes. Other treatments include

corticosteroids, calcium channel blockers, lithium, intranasal lidocaine, and methysergide.

20. How do I treat tension headaches?

If the diagnosis is secure, treatment starts with reassurance and education. Because these

headaches are usually chronic, they should be treated with nonaddictive analgesics.

Biofeedback and acupuncture may be beneﬁcial. All patients with this diagnosis should be

screened for mood disorders because depression is a common cause of tension headaches.

21. Which toxin may bring in entire families complaining of headache?

Carbon monoxide poisoning. See Chapter 72.

22. Does sinusitis commonly cause headache? If a CT scan shows sinusitis, is

that the likely cause of a patient’s headache?

Acute bacterial sinusitis can certainly cause headache, but headache from sinusitis is not

nearly as common as some patients and doctors think. Patients will often use the term sinus

headache just as inaccurately as they use the term migraine. When sinusitis causes headache,

Chapter 15 HEADACHE 103

CAD, coronary artery disease; GI, gastrointestinal; HTN, hypertension; IM, intramuscularly; IV, intravenously;

PVD, peripheral vascular disease; SQ, subcutaneously.

*Assumes average-size adult patient.

Medication Dose and Route* Comments

Mild to moderate

Acetaminophen 500–1000 mg Avoid in patients with liver disease

Aspirin 650–1000 mg GI upset

Ibuprofen 600–800 mg GI upset

Naproxen sodium 275–550 mg GI upset

Indomethacin 50 mg rectal suppository

Moderate to severe

Dihydroergotamine 1 mg IV or IM May be repeated in 1 hour but not if

triptans used already

Contraindicated in HTN, PVD, CAD,

and pregnancy

Sumatriptan 6 mg SQ May be repeated in 1 hour but not if

ergots used already

Contraindicated in HTN, PVD, CAD,

and pregnancy

Metoclopramide 10 mg IV or IM Sedation and dystonic reaction

Prochlorperazine 10 mg IV or IM Sedation and dystonic reaction

Ketorolac 30–60 mg IM or 15–30 mg IV GI upset; caution in elderly and

patients at risk for renal failure

Morphine sulfate 0.1 mg/kg Opioids should be used as last resort

Hydromorphone 0.5–2 mg IV (note: 1 mg

hydromorphone 5 8–10 mg

of morphine)

Opioids should be used as last resort

Butorphanol 2 mg IV Opioids less efﬁcacious than other

medications

Refractory attack, status migrainosus

Dihydroergotamine 1 mg IV Use in conjunction with antiemetic

Steroids Various regimens Controversial; based on anecdotal

evidence

TABLE 15-3. SELECTED MEDICATIONS FOR ACUTE MIGRAINE ATTACKS

Chapter 15 HEADACHE104

there are generally other symptoms and signs of sinusitis (e.g., nasal congestion, fever, boggy

nasal mucosae), and the pain is generally unilateral. Tenderness over a sinus is non-speciﬁc

and may be a function of how hard one is pressing. Finally and very importantly, CT ﬁndings

of chronic sinusitis, such as mucosal thickening, retention cysts, or ostial narrowing, should

never be considered the cause of a patient’s acute headache.

23. What special diagnostic considerations must be given to a patient with AIDS

and headache?

Headache is a frequent complaint among AIDS patients, occurring in 11% to 55% of patients, and

may occur in many AIDS-related conditions. Acute lymphocytic meningitis can be seen in patients

at the time of acute HIV infections, sometimes associated with fever, lymphadenopathy, sore

throat, and myalgias. Toxoplasma gondii produces multiple brain abscesses and bilateral,

persistent headaches. The diagnosis of toxoplasmosis is made by CT, magnetic resonance

imaging (MRI), or brain biopsy. Other central nervous system lesions include B-cell lymphoma

and progressive multifocal leukoencephalopathy. Cryptococcal meningitis is a common cause of

headache in AIDS patients, occurring in 10% of patients. Meningitis is characterized by fever,

headache, and nausea. The presence of meningismus, or mental status changes, is uncommon.

Patients who have HIV and who present to the ED with persistent headache usually require

neuroimaging and, if imaging is normal, LP should be done.

24. What rapidly progressive infectious entity presents with headache, fever, and

altered mental status?

Herpes simplex encephalitis, the most common form of sporadic encephalitis, is a necrotizing,

hemorrhagic infection that results in brain destruction that mandates early aggressive

treatment with antiviral therapy. LP with polymerase chain reaction of the CSF and gadolinium-

enhanced MRI are the diagnostic methods of choice. On imaging, there is a predilection for

temporal lobe involvement. Note that there are other viral encephalitides (e.g., West Nile,

Eastern Equine) but there is currently no speciﬁc treatment for them.

25. What is idiopathic intracranial hypertension, and what is the complication if

not treated appropriately?

Also known as benign intracranial hypertension or pseudotumor cerebri, this entity presents

classically in obese young women with recurrent headaches that are constant or intermittent

and that may present with bilateral papilledema and loss of spontaneous venous pulsations.

Transient pulsatile tinnitus and visual symptoms are common. Occasionally, sixth nerve palsy

is found. Note that a sixth nerve palsy has no localizing value; it is the cranial nerve with the

longest intracranial course and is thus sensitive to pressure and inﬂammation. Brain imaging

should be done to rule out a mass lesion and, if negative, LP is done; this not only is

diagnostic but also commonly therapeutic. High opening pressure (25 to 40 cm H

O) and a

suggestive clinical scenario are diagnostic. It is important to consider the diagnosis of cerebral

venous sinus thrombosis because these two entities can mimic one another. Without

treatment, there is a risk of visual loss. Treatment is with serial LPs, acetazolamide, and

diuretics such as furosemide. Optic nerve fenestration is indicated in refractory cases.

26. Which cranial nerves pass through the cavernous sinus?

Cranial nerves III, IV, V1, and V

1-2

. Cavernous sinus disease may present as only a retro-orbital

headache. Any combination of involvement of the nerves passing through the cavernous sinus is

suggestive of the diagnosis, however, and warrants further evaluation. Invasion by tumor, vascular

disease such as aneurysm or carotid cavernous sinus ﬁstula, and clot (either bland or infection

related) are the more common causes. Patients with other cerebral venous sinus thromboses will

often present with isolated headache, seizure, and elevated intracranial pressure.

27. How common are headaches in children?

As with adults, headaches are also common in children. The history and physical examination

are paramount in sorting out who needs a work-up and who does not. Treatment can start

Chapter 15 HEADACHE 105

with acetaminophen or ibuprofen. Ruling out signiﬁcant pathology is crucial in children. SAH,

primary cerebral tumors, stroke, metabolic conditions, and toxicologic causes should be

considered in the appropriate setting.

28. What is a blood patch?

One third of patients experience headaches within hours of a diagnostic LP. This is due to a

persistent CSF leak from the dural rent that results in low CSF pressure, dilation of intracranial

vessels, and traction on intracranial contents. This postdural puncture headache is worse

when the patient sits or stands up and improves with bed rest. Treatment includes bed rest,

ﬂuids, and analgesia. Some practitioners use intravenous (IV) caffeine. If conservative

methods fail, autologous blood clot is used, the so-called blood patch. Blood is drawn from

the patient and injected into the soft tissue at the site of the LP. In most institutions, this is

performed by an anesthesiologist. Data suggest that using a small caliber LP needle and a

noncutting tip can decrease the incidence of postdural puncture headache.

29. Are there other forms of low pressure spinal headache?

In the absence of a prior LP, patients can still get a low pressure headache, a condition known

as spontaneous intracranial hypotension. The headache is positional (worse with standing,

better with lying down), similar to a post-dural puncture headache. Occasionally, patients will

develop neurological deﬁcits. Diagnosis is by imaging and LP. This is another diagnosis, albeit

an uncommon one, that supports measuring the opening pressure when doing an LP.

30. In the pregnant (or recently postpartum) woman, are there particular causes

of headache that I should worry about?

Pregnant women can get any kind of headache that nonpregnant women can get; however,

some headache disorders that occur more commonly, or exclusively, in this situation are

cerebral venous sinus thrombosis, eclampsia, pituitary apoplexy, SAH, and posterior reversible

leukoencephalopathy syndrome (PRES). Added to this list in the postpartum patient who has

had an epidural anesthetic are postdural puncture headache and the additional complication of

a postpuncture subdural hematoma. As for imaging, MRI has certain obvious advantages

during pregnancy, but one should get the tests that are needed to make the diagnosis, trying

to balance radiation exposure with accurate diagnosis.

31. Is high blood pressure causing my patient’s headache?

One potential mistake is to diagnose hypertensive urgency in headache patients who have a

high blood pressure. Coexistent headache and hypertension can occur for several reasons.

Probably the most common is that pain and anxiety are elevating the blood pressure.

A second cause is that the problem causing the headache is also causing some degree of

raised intracranial pressure, and the body is raising the arterial blood pressure to preserve

cerebral perfusion pressure. If hypertension is primarily causing the symptoms (the third

possibility), then end organ dysfunction is occurring (in this case, the end organ is the brain).

Lowering the blood pressure about 25% below the peak in this situation, using rapidly acting,

titratable agents, will both treat and help establish the diagnosis because the headache ought

to improve dramatically. In patients with acute ischemic stroke and headache, one should be

cautious about pharmacologically treating high blood pressure because it is likely that the high

pressure is simply due to the brain autoregulating.

32. When should I be concerned about a brain tumor?

Isolated headache is rarely caused by a brain tumor. Only about half of all patients with brain

tumors have headache and the pain characteristics are not speciﬁc. The classic early morning

headache is uncommon. Localization (other than neck pain with posterior fossa tumors) does

not usually occur. One risk for patients with brain tumors is to have a headache that is

different from their previous headaches. Therefore, a careful history and physical examination

are most important in deciding which patients need a work-up for a tumor as they are for any

other secondary cause of headache.

Chapter 15 HEADACHE106

BIBLIOGRAPHY

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3. Cumurciuc R, Crassard I, Sarov M, et al: Headache as the only neurological sign of cerebral venous

thrombosis: a series of 17 cases. J Neurol Neurosurg Psychiatr 76(8):1084–1087, 2005.

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being wrong? Eur J Neurol 15(12):1257–1258, 2008.

5. Edlow JA, Caplan LR: Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med

342(1):29–36, 2000.

6. Edlow JA, Malek AM, Ogilvy CS: Aneurysmal subarachnoid hemorrhage: update for emergency physicians.

J Emerg Med 34(3):237–251, 2008.

7. Edlow JA, Newman-Toker DE, Savitz SI: Diagnosis and initial management of cerebellar infarction. Lancet

Neurol 7(10):951–964, 2008.

8. Edlow JA, Panagos PD, Godwin SA, et al: Clinical policy: critical issues in the evaluation and management of

adult patients presenting to the emergency department with acute headache. Ann Emerg Med 52(4):407–436,

2008.

9. Edlow JA, Wyer PC: How good is a negative cranial computed tomographic scan result in excluding

subarachnoid hemorrhage? Ann Emerg Med 36(5):507–516, 2000.

10. Goldstein JN, Camargo CA Jr, Pelletier AJ, et al: Headache in United States emergency departments:

demographics, work-up and frequency of pathological diagnoses. Cephalalgia 26(6):684–690, 2006.

11. Jordan YJ, Lightfoote JB, Jordan JE: Computed tomography imaging in the management of headache in the

emergency department: cost efﬁcacy and policy implications. J Natl Med Assoc 101(4):331–335, 2009.

12. Lewis DW: Pediatric migraine. Neurol Clin 27(2):481–501, 2009.

13. Pope JV, Edlow JA: Favorable response to analgesics does not predict a benign etiology of headache.

Headache 48(6):944–950, 2008.

14. Savitz SI, Levitan EB, Wears R, et al: Pooled analysis of patients with thunderclap headache evaluated by

CT and LP: is angiography necessary in patients with negative evaluations? J Neurol Sci 276(1–2):123–125,

2009.

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27(8):904–911, 2007.

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of cervical artery dissection. AJNR Am J Neuroradiol 29(9):1753–1760, 2008.

KEY POINTS: HEADACHE

1. A response to analgesics does not exclude life-threatening causes of headache.

2. Even with modern CT, scanners will miss 5% to 10% of SAHs. LP is needed if SAH is a

major diagnostic concern.

3. HIV-positive patients presenting with headache should have a CT head scan with contrast to

exclude opportunistic infections, including toxoplasmosis.

4. A careful history and physical examination, including neurologic examination, will identify

most patients who need further evaluation.

107

CHAPTER 16

SYNCOPE, VERTIGO, AND DIZZINESS

William F. Young, Jr., MD

1. Do I need to be concerned by a complaint of dizziness?

Yes. There are over 25 million ED visits a year for dizziness; it is the most common

complaint in patients older than 75 years and may herald a stroke.

2. How do I approach this vague and ill-deﬁned complaint?

Start your history with an open-ended question that allows the patient to describe the

symptoms. Dizzy can describe a sensation of vertigo (the illusion of motion);

lightheadedness (presyncope or frank syncope); or disequilibrium (imbalance). Those

with disequilibrium often describe imbalance while walking, especially in the dark.

3. How does one know his or her position in space?

A combination of visual clues and vestibular input determine our spatial orientation.

When they don’t agree or are asymmetric, we feel dizzy.

4. How does the vestibular system work?

The semicircular canals use the principle of liquid inertia to determine angular

acceleration. The canals, oriented in three planes to encompass all aspects of space, are

ﬁlled with a ﬂuid, endolymph. When the head turns, the ﬂuid stimulates hair cells in

response to this relative movement, sending impulses to the brain via cranial nerve VIII.

5. How do you deﬁne central versus peripheral vertigo?

It is an anatomical deﬁnition. Peripheral vertigo is caused by a dysfunction of the inner

ear or vestibular nerve, whereas central vertigo is from etiologies of the brain and a

brain stem. Benign paroxysmal positional vertigo (BPPV), vestibular neuritis, and

Ménière disease are common etiologies of peripheral vertigo, whereas vertebrobasilar

ischemia, multiple sclerosis, cerebellar infarction/hemorrhage, and basilar migraine are

central causes.

6. What are the characteristics of peripheral vertigo?

DR FLIP. This mnemonic reminds you that the Epley maneuver, which ﬂips the patient,

helps BPPV.

Deafness (unilateral hearing loss)

Ringing in the ears (tinnitus)

Fatigable on repeated testing

Latency after Dix-Hallpike maneuver

Intense symptoms

Positional in nature

7. What are the characteristics of central vertigo?

Cranial nerve deﬁcits

Vertical nystagmus (not seen in peripheral vertigo)

Ataxia (with gait impairment)

8. What are the key points for the main causes of peripheral vertigo?

See Table 16-1.