Headache Emergencies

Headache Emergencies
a b a,
David Kopel, MD , Crandall Peeler, MD , Shuhan Zhu, MD *
KEYWORDS
Thunderclap headache Subarachnoid hemorrhage Elevated intracranial pressure
Intracranial hypotension Venous sinus thrombosis
Reversible cerebral vasoconstriction syndrome Giant cell arteritis Papilledema
KEY POINTS
The majority of patients who seek care for headache have primary headache; a small sub-
set have secondary causes associated with high morbidity and mortality.
A systematic history assessing for “red flag” features along with a careful neurologic ex-
amination is required to appropriately diagnose secondary causes.
Secondary causes include subarachnoid hemorrhage, reversible cerebral vasoconstric-
tion syndrome, elevated intracranial pressure, hydrocephalus, cerebral venous sinus
thrombosis, arterial dissection, central nervous system infection, and inflammatory
vasculitis.
Patients who are pregnant, immunocompromised, elderly, or have known malignancy
have higher risks of secondary disorders therefore.
Clinicians should have a different threshold to obtain additional diagnostic evaluations in
high-risk patients.
INTRODUCTION
Nontraumatic headache is responsible for approximately 2% of all emergency depart-

ment (ED) visits.1 With roughly 145 million total ED visits per year,2 this means an
average of nearly 8000 patients visit an ED for headache each day. Although the ma-
jority of nontraumatic headaches are benign, a small fraction (about 3%)3 are due to
underlying causes associated with significant morbidity and mortality.
The most common cause of ED visits for nontraumatic headache is migraine head-
aches, which, despite their severity and significant impact on quality of life, are not in
and of themselves dangerous. Yet migraine is important because the symptoms of
migraine headaches overlap with those caused by far more dangerous secondary
conditions such as aneurysmal subarachnoid hemorrhage (SAH), reversible cerebral
State on conflict of interest: The authors listed have no relevant conflicts of interest related to
information and topics reviewed within this article.
a
Department of Neurology, 725 Albany Street, Suite 7B, Boston, MA 02118, USA;
b
Department of Ophthalmology and Neurology, 85 East Concord Street 8th Floor, Boston, MA
02118, USA
* Corresponding author.
E-mail address: shuhan.zhu@bmc.org
Neurol Clin 39 (2021) 355–372

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356 Kopel et al
vasoconstriction syndrome (RCVS), elevated intracranial pressure (ICP), hydrocepha-

lus, cerebral venous sinus thrombosis (CVST), arterial dissection, central nervous sys-
tem (CNS) infection, and inflammatory vasculitis, which can carry high morbidity and
mortality if not appropriately diagnosed and treated. Additionally, because primary
headaches are very common, they often coexist with secondary causes.
The keystone of evaluation begins with thorough history taking. Without a guiding
history, the physical examination, imaging, and other studies that are obtained may
be inappropriate for the diagnosis at hand and can lead to false reassurance with
normal results. This review provides clinicians with the knowledge needed to appro-
priately and confidently distinguish patients with headache emergencies from the
more common yet superficially similar patients with benign causes of headache.
THE ROLE OF HISTORY AND NEUROLOGIC EXAMINATION
Owing to significant overlap in symptoms of benign and dangerous causes of head-

ache, and the fact that most patients with headache ultimately have primary causes,
clinicians must use a systematic approach each time to avoid misdiagnosis in the pa-
tients with dangerous secondary causes. Because the causes of secondary head-
aches range from intracranial bleeding to altered ICP to CNS inflammatory disease,
clinicians must first be guided by history to obtain the appropriate diagnostic studies.
Various mnemonics have been developed to assist the clinician in efficiently obtain-
ing a headache history aimed at identifying dangerous secondary etiologies. When
consistently used, the SNOOP4 mnemonic4 can be quite effective at this task. Each
component of the mnemonic represents a red flag that, when present, can signify
the presence of a dangerous secondary cause. Diagnoses such as SAH, RCVS,
elevated ICP, hydrocephalus, CVST, arterial dissection, CNS infection, and inflamma-
tory vasculitis would all trigger multiple red flags using this mnemonic.
This review discusses the clinical application of key red flags and how to evaluate for
their possible causes. We focus on thunderclap headache, positional headache, pa-
tients with abnormal physical examinations, and special very high-risk patient popula-
tions because we believe these are the most important to an efficient emergency
headache evaluation. We also recommend that the reader review the original publica-
tion by Dr Dodick for additional guidance on the use of SNOOP4. For the readers’
reference, we have summarized the SNOOP4 mnemonic in Table 1.
A prospective, observational study with 90 patients5 from Thailand using SNOOP4
for detection of serious causes of secondary headaches showed a high negative pre-
dictive value (96.4%) but a low positive predictive value (25.9%) for serious causes
such as intracerebral hemorrhage, infarction, CNS infection, or neoplasm. The low
positive predictive value is likely a reflection of the fact that only a small percentage
of all patients with nontraumatic headaches have a dangerous underlying cause. Pa-
tients who do not have any of the SNOOP4 red flags are unlikely to have a dangerous
secondary cause; patients who do have a red flag require additional evaluation or
consideration to further delineate whether a dangerous secondary cause may be
present.
Although clinical guides can be very helpful, it is also important to keep in mind that
no single guideline or mnemonic can capture all the clinical variations of a particular
condition or provide all relevant evaluations and possible causes. In particular, pa-
tients who are pregnant, immunocompromised, elderly, or have known malignancy
have higher risks of secondary disorders. Therefore, clinicians should have a higher
a priori clinical suspicion for a dangerous secondary headache etiology and a different
threshold to obtain additional diagnostic evaluations in such patients.
Headache Emergencies 357
Table 1
SNOOP4 mnemonic (Dodick 2010)
Symptoms to Assess for Secondary Causes to Consider:

Systemic symptoms Fever, chills, night sweats, Vasculitis, CNS infection,
myalgias, weight loss, metastatic malignancy
malignancy history,
immunocompromised state
Neurologic symptoms Unilateral weakness, diplopia, CNS neoplasm, inflammatory
gait changes, speech changes, lesion, infection or vascular
personality/behavior changes disease
Sudden Onset Sudden severe pain SAH, RCVS, venous thrombosis,
(“thunderclap”) arterial dissection
Onset after age 50 New headaches later in life CNS neoplasm, vasculitis,
inflammatory disease,
infection
Pattern change/ Worsening of previous headache Base on review of other
progressive patterns SNOOP4 symptoms
Valsalva Precipitation Headache triggered with CSF flow obstruction, elevated
straining or coughing intracranial pressure
Postural aggravation Worse with lying down Elevated intracranial pressure
Papilledema Transient visual obscurations, Elevated intracranial pressure,
double vision, visual field loss hydrocephalus, CSF flow
obstruction
Adapted from Dodick DW. Pearls: headache. Semin Neurol. 2010;30(1):74-81.
The role of the neurologic examination is often emphasized in the evaluation of

headache and other neurologic problems, but it should be noted that a detailed exam-
ination without an appropriate history for context is rarely helpful. The examination
should be guided and informed by the history, and the findings should be interpreted
in the context of the history. The history can help clinicians to hone in on the most
important examination components to perform and appreciate subtle findings that
may be missed otherwise. In addition to the general neurologic examination, physi-
cians should also perform a fundoscopic examination to assess for papilledema. In
some patients with an elevated ICP, this may be the only abnormal examination
finding.
In cases for which there are no red flags and the history is consistent with a primary
headache disorder, a careful neurologic examination should still be performed with the
goal of demonstrating normal findings and, thus, supporting the diagnosis made
based on history. Neurologic abnormalities that are unexplained should alert the clini-
cian to further review the patient’s history and/or reassess in the context of the pa-
tient’s history and presentation.
THUNDERCLAP HEADACHE
The most well-known worrisome headache pattern is the thunderclap headache, typi-
cally associated with aneurysmal SAH. Given the high degree of morbidity and mortality
associated with SAH, the emphasis is appropriately placed on its rapid and accurate
diagnosis. However, it is important to highlight several more subtle components of
the headache history that may guide management in cases of thunderclap headache,
as well as to highlight some other possible causes that should not be missed.
358 Kopel et al
Subarachnoid Hemorrhage
The majority of patients presenting with SAH in a recent study reported that their head-
ache reached peak intensity within 1 second of onset, a so-called apoplectic head-
ache.6 Eighty percent of patients with a SAH stated that their headache had peaked
in intensity within 1 minute. In contrast, of patients presenting with headaches unre-
lated to SAH, 10% and 17% reported peak intensity within 1 second and 1 minute,
respectively. Other clinical features in this study that were significantly associated
with SAH as a headache etiology included occipital location, a stabbing quality, and
the presence of meningismus.
A clinical decision rule known as the Ottawa SAH (OSAH) rule has been proposed in
a study of more than 1000 patients with an acute headache and externally validated in
several subsequent studies of hundreds of patients.7–9 The aim of this rule is to stratify
patients with nontraumatic headache peaking within 1 hour (without impaired con-
sciousness, focal deficits, or historical features such as past aneurysmal bleeding
placing them at high risk) as high or low risk for aneurysmal SAH. According to the
OSAH rule, one should look for the following features: age greater than 40 years,
neck pain, neck stiffness, limitations in neck flexion, apoplectic headache onset,
headache onset during exertion, or loss of consciousness at any point. The absence
of all these features had a sensitivity and negative predictive value of essentially 100%
to rule out SAH.7–9 Although the OSAH rule has been validated for other types of intra-
cerebral bleeding,9 the absence of these features should not reassure a provider
against other dangerous causes of headache.
We recommend the use of the OSAH rule to rule out SAH in patients presenting with
acute onset headache who have none of the red flags. For those who do have one of
these concerning features, further history taking and examination are required before
deciding on imaging. This practice is in line with the American College of Emergency
Physicians’ guidelines, which state that the OSAH rule should be used to rule out SAH,
but owing to low specificity, should not be used to rule in this disorder.10 A computed
tomography (CT) scan of the brain is nearly 100% sensitive and specific for SAH if
done within 6 hours of headache onset. However, sensitivity decreases to 93% by
24 hours and continues to decrease after that.11 The sensitivity of lumbar puncture
(LP) to look for xanthochromia is poor in the first 2 hours or so after headache onset
and peaks at about 12 hours from headache onset.12 Thus, we recommend LP for
all patients under investigation for SAH with a negative head CT scan more than
6 hours after symptom onset. When the head CT scan is negative within the first
6 hours, other diagnoses should be considered.
Reversible Cerebral Vasoconstriction Syndrome

RCVS should be considered in all patients presenting with thunderclap headache,
especially if the headache is recurrent. The headache onset can be very rapid, as in
SAH, but the headaches tend to be shorter, lasting 1 to 3 hours13 and often include
a moderate headache between recurrent exacerbations, as opposed to the head-
ache of SAH, which often persists for days or weeks in our clinical experience.
Traditionally, the headache of RCVS is posterior and bilateral at onset, then be-
comes holocranial, although significant variations exist.14 It can be triggered by
exertion or a Valsalva maneuver. About one-half of the time, there is a history of
exposure to vasoactive compounds (some are listed in Table 2) or the patient is
recently post partum.14 There may be focal neurologic deficits or seizures. Women
are at greater risk and are less likely to have a clear vasoactive trigger identified
than men.13
Table 2
Vasoactive compounds associated with RCVS
Drug Categories Examples of Offending Drugs

Drugs of abuse Cannabis, cocaine, amphetamines, LSD
Antidepressants Selective serotonin reuptake inhibitors and selective
norepinephrine reuptake inhibitors like fluoxetine,
paroxetine, duloxetine and venlafaxine
Alpha sympathomimetics Enteral or nasal decongestants like ephedrine and
pseudoephedrine, norepinephrine
Triptans Sumatriptan, rizatriptan, frovatriptan
Ergot alkaloid derivatives Methergine, bromocriptine, lisuride
Others Intravenous immunoglobulin, interferon, nicotine
patches, ginseng, binge drinking, phenytoin
RCVS can cause ischemic and hemorrhagic stroke and is associated with sulcal
SAH at the convexity. Brain edema and posterior white matter changes resembling
the posterior reversible encephalopathy syndrome (PRES) can occur and these 2 dis-
orders may have related pathophysiology.13 In a retrospective case series, although
55% of patients had normal imaging at the time of presentation, 39% developed in-
farcts, 34% had convexity SAH, 20% had lobar hemorrhage, and 38% had brain
edema on reimaging later in the disease course.15 Conventional angiography is the
best test to look for the characteristic segmental narrowing and dilatation of multiple
vessels.13
CT angiography and MR angiography have about 70% of the sensitivity of conven-
tional angiography,14 and reimaging is key because it is thought that vasoconstriction
begins with small distal vessels that may not be seen on angiography and progresses
proximally with maximum MCA branch vasoconstriction seen about 16 days after clin-
ical onset.13 On diagnosis, vasoactive medications are stopped, patients are advised
to avoid exertion, and they are often treated with nimodipine, the early administration
of which significantly improves headaches.13 It is not yet clear whether treatment with
nimodipine helps to prevent the neurologic complications of RCVS.
Cerebral Venous Sinus Thrombosis

CVST is traditionally associated with subacutely progressive headache, but can pre-
sent with a thunderclap headache in a minority of cases. Risk factors for CVST include
an underlying hypercoagulable state, head injury, exogenous estrogens through con-
traceptive pills, and pregnancy.16
Occlusion of the cortical and deep veins disrupts normal blood flow, leading to
venous infarct and/or hemorrhage, which can cause focal neurologic deficits or alter-
ation in mental status in about one-half of the cases.16 Occlusion of the sinuses im-
pairs cerebral spinal fluid (CSF) outflow leading to an increased ICP, headache, and
papilledema. Hemorrhages or infarcts that do not respect expected arterial vascular
territories raise concern for a venous stroke. When there is intracranial hemorrhage,
substantial early perihematomal edema can suggest a venous source; studies have
shown that decreased venous drainage is associated with an increase in edema
around a parenchymal bleed.17 Although a thrombus may appear hyperintense on
T1- and T2-weighted MRI, dedicated MR venography or CT venography is often help-
ful in making the diagnosis. Diagnostic angiography is rarely necessary, but can be
useful in subtle cases. CVST should be treated with anticoagulation, even if there is
360 Kopel et al
intracerebral hemorrhage present, because studies have indicated that such treat-
ment helps to prevent death and dependency.18 Anticoagulation arrests the growth
of the thrombus and helps to prevent pulmonary embolism.16 The role of endovascular
treatment is uncertain, and the current practice is to reserve it for refractory cases that
would otherwise have a poor prognosis.
Arterial Dissection
Another diagnosis to consider in patients presenting with rapid onset headache, espe-
cially after trauma or exertion, is arterial dissection of the cervical portions of the ca-
rotid and/or vertebral arteries. Less commonly, dissection of large intracranial arteries
can also cause sudden headache.19 Although there are clear cases with head or neck
trauma followed by neck pain, headaches, and focal neurologic deficits, most cases
are more subtle.
Carotid dissection usually causes a unilateral headache. When it is unilateral, the
sidedness of the headache is almost always ipsilateral to the location of the dissec-
tion.20 Carotid dissection can present without any pain or with isolated headache
and orbital or facial pain; however, in most cases there are some neurologic manifes-
tations such as transient ischemic attacks or strokes, ipsilateral Horner syndrome,
transient monocular vision loss, pulsatile tinnitus (corresponding to carotid bruit on ex-
amination), and dysgeusia.20
Vertebral dissection usually presents with unilateral or bilateral posterior headache,
but the pain can be more diffuse. Migraineurs are less likely to confuse this headache
for a typical migraine compared with that of carotid dissection.20 Neurologic findings
can be transient or permanent and symptoms are variable depending on the location
of the ischemia or infarct. These symptoms can include complete or partial Wallenberg
syndrome, visual field deficits, cranial neuropathies, and area postrema syndrome,
among others.20
Conventional or noninvasive (CT angiography, MR angiography) angiography can
be used to diagnose a dissection. In centers with radiologists who are experienced
in its interpretation, MR vessel wall imaging is a technique that may detect small, sub-
adventitial dissections with greater sensitivity than traditional imaging modalities by
demonstrating thrombus in the false lumen.21 Fig. 1 shows carotid dissection with
thrombus seen on vessel wall imaging (T1 fat saturation).There is controversy
regarding the use of anticoagulation or antiplatelet therapy for treatment and a recent
randomized clinical trial did not find a significant difference between the 2 in stroke
prevention.22 In our experience, anticoagulation is usually reserved for cases with
intraluminal thrombus, where one can definitively rule out intracranial extension of
the dissection.
POSITIONAL HEADACHE
Headaches with a strong positional component should raise clinicians’ suspicion for
altered ICP, which may be due to serious underlying causes. Classically, patients
with increased ICP report more and/or worsening headaches (which may be accom-
panied by nausea) on first waking in the morning, with the Valsalva maneuver, or with
lying down, which improve or resolve with sitting or standing. Patients with decreased
ICP owing to CSF leak typically report the opposite, with headaches that improve or
resolve with reclining and the onset of headaches with sitting or standing, although
some patients with intracranial hypotension have paradoxic worsening while supine.
Assessing a patient’s headache symptomatology for high or low pressure features
can be challenging, because many primary headache disorders can have a positional
Fig. 1. MR vessel wall imaging. Vessel wall imaging (A) with a T1 fat-saturation sequence
demonstrates hyperintense crescent of intramural hematoma (arrow) within the dissection,
which is not visualized on usual time of flight vascular imaging (B).
component. A diagnostic feature of migraine is “aggravation by or causing avoidance

of routine physical activity (eg, walking or climbing stairs)”23; in these cases, the
migraine pain is worsened by stimulus in general, which includes physical activity
(as well as other forms of stimulus such as noise and/or light). Additionally,
morning-predominant headaches may also be seen in other settings, such as obstruc-
tive sleep apnea and migraine, because approximately 25% of migraineurs report
headaches starting overnight.24
Elevated Intracranial Pressure

Although both high and low ICP can result in headaches, the causes of elevated ICP
are more likely to be associated with significant morbidity and mortality than the
causes of decreased ICP.
Some conditions associated with elevated ICP, such as mass lesions, CNS infec-
tions, or hydrocephalus (which can be due to many different etiologies) carry a risk
for coma and death if left untreated. Others, such as idiopathic intracranial hyperten-
sion (IIH), are not acutely life threatening but can be associated with significant
morbidity, such as permanent loss of vision. In cases of suspected high ICP, initial
brain imaging with a CT scan can offer rapid information on whether acutely
dangerous conditions such as hydrocephalus, mass lesions, diffuse edema, or
CVST may be present. The absence of overt hydrocephalus on an initial CT scan
does not always exclude an elevated ICP, because hydrocephalus is a relative finding
that is subject to the baseline degree of brain and CSF volume; mild hydrocephalus
may be difficult to diagnose on imaging, particularly in patients who are elderly or
have a preexisting brain injury with encephalomalacia. A comparison with prior imag-
ing is critical if it is available.
A clear understanding of the patient’s medical background and risk factors can be
very helpful because the pretest probability of a potential ICP disorder is highly depen-
dent on such information. Table 3 reviews the major groups of disorders that can lead
to elevated ICP with additional considerations and risk factors to assess for in each
patient.
362 Kopel et al
Table 3
Major groups of disorders leading to altered ICP
Secondary Evaluations/
Immediate Causes Considerations
Elevated ICP
Obstructive Mass-occupying lesion(s) owing to Assess patients for systemic
hydrocephalus tumor or infectious lesion cancer diagnoses and
immunosuppressed status
Nonobstructive Inadequate CSF resorption by Assess for systemic
hydrocephalus arachnoid granulations owing to inflammatory disorders,
inflammation, hemorrhage in immunosuppression or
subarachnoid space or obstruction hypercoagulable state
in dural venous sinuses
Diffuse edema CNS infection, hypoxic injury, Assess for risk factors
metabolic derangement for CNS infection,
(hyponatremia, hyperammonemia) immunosuppressed
status and risks for fluid/
electrolyte imbalances
Normal imaging Idiopathic increased ICP (IIH) Assess for risk factors based
on age, gender, body mass
and medication exposures
Decreased ICP
Iatrogenic Dural defect from medical Assess for epidural
procedure or overshunting procedures, ENT surgeries,
spinal surgeries and
evaluate for overshunting
Traumatic Dural defect owing to traumatic head Assess for recent head injury
injury in previous days to weeks
Spontaneous Dural defect owing to tear from Assess for underlying
perineural nerve root cyst tear or connective tissue disorders
calcified disc leading to dural that may predispose to
puncture spontaneous dural defects
A fundoscopic examination for papilledema is required when evaluating patients for

possible elevation of ICP. The presence of papilledema can help to confirm the diag-
nosis of an elevated ICP. The severity of papilledema is measured by the Frisen grade
(Fig. 2), with higher grades reflecting effects of higher ICP. In patients with papilledema
(of any Frisen grade) accompanied by features such as altered mental status or thun-
derclap headache, an emergent evaluation must be conducted because these find-
ings are worrisome for SAH, CVST, rapid expansion of a mass lesion, or a severe
CNS infection.
It must also be noted that the absence of papilledema does not exclude the pres-
ence of an elevated ICP, particularly in cases of an acutely elevated ICP, because
the finding of papilledema itself can take several days to develop. In acute cases,
when papilledema may not be a reliable feature, the absence of spontaneous retinal
venous pulsations (SVP) may be a more sensitive marker for an elevated ICP.25,26 In
healthy individuals, SVPs are seen as rhythmic pulsations in the diameter of the retinal
veins as they cross the optic disc and are the result of the interplay between the pulse
pressure in the intraocular space and the CSF. SVPs are detectable in approximately
90% of healthy individuals and cease to be present when ICP is greater than 19 mm
H2O26; they may be absent in some healthy individuals owing to anatomic variations
Fig. 2. Frisen grading of papilledema. Frisen grading of papilledema. (A) Grade 1 shows
nasal blurring of the disc margin with sparing of the temporal edge. (B) Grade 2 shows
circumferential disc blurring. (C) Grade 3 papilledema leading to partial obscuration of ma-
jor vessels as they pass over the disc margin. (D) Grade 4 papilledema leading to obscuration
of major vessel centrally over the disc.
within the optic disc and vasculature.26 The presence of SVPs (along with absence of
papilledema) can be helpful clues to the patient’s ICP; however, the absence of SVP
must be interpreted within the clinical context because this can be a normal finding.
The use of ultrasound examination to measure the optic nerve sheath diameter has
been studied as a noninvasive method to assess for elevated ICP in patients with IIH24
and severe brain injury.27 Although these studies showed an association between a
larger optic nerve sheath diameter and increased ICP, this technique is not yet
routinely applied in clinical practice owing the lack of consensus on an acceptable op-
tic nerve sheath diameter cut-off value, perhaps in part because of baseline variations
in optic nerve sheath anatomy across normal patient populations.28
In cases of elevated ICP owing to obstructive hydrocephalus or supratentorial
masses where an LP is contraindicated, ventricular shunting may be performed to
divert CSF and prevent coma and/or vision loss. Surgical or medical treatment of
the underlying lesion(s) varies depending on the nature of the lesion.
In patients with IIH, those with severe papilledema (Frisen grade 3 or 4) are at higher
risk for vision loss from irreversible optic nerve injury and warrant urgent treatment. An
364 Kopel et al
LP should be performed urgently, and the opening pressure should be measured with
the patient in the lateral decubitus position. CSF drainage during the LP can be tempo-
rarily therapeutic by decreasing the CSF pressure. In cases when an LP cannot be ob-
tained urgently either owing to a contraindication (such as anticoagulation) or technical
limitation, intravenous methylprednisolone in conjunction with acetazolamide29 may
provide a temporizing measure to decrease the risk of vision loss. The long-term
use of steroids for IIH, however, is not recommended owing to other risks of chronic
steroid exposure. After acute ICP control, patients should be initiated on treatments to
maintain ICP reduction with agents such as acetazolamide or topiramate30 in addition
to long-term treatments of weight loss and dietary management. In patients who are
refractory to these treatments, surgical procedures such as optic nerve fenestration,
venous sinus stenting, or ventricular shunting may be required to prevent vision
loss. The selection of the procedure depends on the procedural availabilities and pro-
cedurals risks based on individual patient characteristics owing to a lack of random-
ized controlled data comparing these different modalities.31,32
Decreased Intracranial Pressure

Decreased ICP can occur spontaneously (more commonly in at-risk patients such as
those with connective tissue disorders), owing to trauma, or owing to iatrogenic
causes such as postprocedural complications from an LP, epidural injection, surgeries
(skull base, ENT, or spinal) or CSF shunt overdrainage. The pathognomonic, and
oftentimes only, feature is orthostatic headache owing to decreased buoyancy of
the brain leading to traction on pain-sensitive structures, such as the dura and vascu-
lature when patients are upright. The orthostatic headache is often accompanied by
neck pain, nausea, and dizziness or vertigo; patients may also report muffled hearing
or tinnitus with orthostatic stress.
The neurologic examination and imaging are typically normal, which can make this a
very difficult diagnosis, particularly in cases of spontaneous leaks. Although generally
not an acutely life-threatening condition, in some cases of rapid leaks, a severely
decreased ICP lead to disorders of consciousness or coma from brain sag with
compression of the brainstem.33–35 This diagnosis should be considered in patients
who do not otherwise have an explanation for coma or cranial nerve palsies. Special
care should be used during the examination of vision and eye movements as associ-
ated cranial nerve palsies frequently include the sixth, fourth, or third nerves and can
be subtle.
Imaging may show supportive features, although normal findings do not entirely
exonerate this diagnosis owing to the positioning of the patient during imaging (supine)
and lack of imaging sensitivity by any 1 criteria alone. The changes seen on imaging
are related to the physical effects of brain sag and compensatory vascular
changes.36,37 With brain sag, imaging may show ventricular collapse, decreased
mamillopontine distance, decreased prepontine cisterns, posterior fossa crowding
or secondary Chiari malformation, subdural hematoma, and/or hygroma may be
seen if bridging vein tear occurs. Compensatory increases in blood flow to the intra-
cranial space may result in an enlargement of the venous sinuses, engorgement of
the pituitary vasculature, and pachymeningeal enhancement on MRI. A classification
system published by Dobrocky and associates38 in JAMA Neurology in 2019 stratifies
imaging findings into 3 major criteria scored as 2 points each (pachymeningeal
enhancement, engorgement of venous sinuses, effacement of suprasellar cistern)
and 3 minor criteria scored at 1 point each (subdural fluid collection, effacement of
the prepontine cisterns and reduced mamillopontine distance) showed that a high
score of 5 or higher was associated with a very high probability of CSF leak (78.6%
sensitivity and 98.3% specificity) and should be referred quickly for epidural blood
patch. In patients with a low score of 2 or less, the probability of CSF leak is very
low (92.9% sensitivity and 93.3% specificity) additional noninvasive imaging with
MRI of the spine to assess for epidural CSF collections should be performed before
consideration for invasive diagnostic procedures.
In patients who are suspected to have spontaneous CSF leaks, an empiric spinal
epidural blood patch39 can be performed because most spontaneous leaks occur in
the spinal column (thoracic being most common). In patients who are refractory to
the initial patch, MR imaging of the whole spinal column (with sagittal and axial T2 se-
quences for better visualization of possible epidural spinal fluid collections) can be
performed to attempt to identify the site of the leak to guide additional targeted treat-
ment. For patients with persistent leaks despite empiric blood patching, CT scan or
radioisotope myelography may be obtained to assess for the source of leak. Rapid
leaks are more difficult to detect on CT myelopathy owing to the rapid equilibration
of contrast between the intradural and extradural CSF spaces; in these cases, the
use of digital subtraction myelography may be required.40,41
In iatrogenic cases, when the dural puncture is small as in subarachnoid block, LP,
or epidural injection and there are no indwelling devices, the majority of patients will
recover with conservative care after several days (rarely, an epidural blood patch is
necessary). Patients with orthostatic headaches who have had larger surgical access
should have investigation to determine the site of the leak to assess the risk for CNS
infection or need for surgical revision.
HEADACHE WITH ABNORMAL EXAMINATION
Patients with headache accompanied by symptoms such as persistent fever, hemiple-

gia, or diplopia generally undergo further diagnostic testing, but probing for more sub-
tle abnormalities with an eye toward potentially devastating causes is essential in
evaluating and triaging patients with a headache. It is worth noting that migraine
can be associated with hemiparesis, brainstem aura, hemianesthesia, visual field ab-
normalities, and other neurologic symptoms. However, when such findings are pre-
sent, migraine is a diagnosis of exclusion and should only be made with confidence
in patients diagnosed with migraines associated with those features consistently in
the past. A high index of suspicion should be maintained to avoid the morbidity asso-
ciated with intracranial pathology.
Although intracerebral hemorrhage is known to cause headache, ischemic stroke
can also cause headache in about 14% of cases.42 Ischemia is more likely to cause
headache when it involves the cerebellum, is not lacunar, and when the patient is fe-
male, young, and has a history of migraine.43 This finding highlights the importance
of a thorough cerebellar examination screening for appendicular dysmetria, dysdia-
dochokinesia, truncal ataxia, and gait abnormalities in all patients presenting with
headache associated with dizziness or nausea, even if there is a history of migraine
(particularly considering that patients suffering from migraine with aura are at a
greater risk of stroke).44 Cerebellar strokes are frequently misdiagnosed and pitfalls
in the initial history and examination have been shown to be a major cause of these
errors.45
Altered mentation, presenting as new onset confusion, lethargy, or behavioral alter-
ations, is not commonly associated with primary headache and should always raise
suspicion for secondary headache owing to an intracranial process such as CNS
infection or increased ICP. Patients suspected to have meningitis should undergo a
CT of the brain before an LP if they have papilledema, focal deficits, a Glasgow
366 Kopel et al
Coma Scale score of less than 10, new-onset seizures, or if they are immunocompro-
mised.46 Empiric treatment should be initiated with haste to cover Streptococcus
pneumoniae and Neisseria meningitidis in all patients and Listeria monocytogenes in
neonates, pregnant women, the elderly, and the immunocompromised.46 Coverage
for herpes simplex meningoencephalitis should be considered when the patient has
seizures, altered consciousness, or language/behavioral disturbances.46 In herpes
simplex virus meningoencephalitis, imaging may show abnormalities of the temporal
lobes (MRI is most sensitive and can show diffusion restriction early in the course of
illness) and the initial CSF tests may show lymphocytic pleocytosis, increased red
blood cells, and a positive polymerase chain reaction test for herpes simplex virus
(even if treatment with acyclovir has been initiated).46
SPECIAL POPULATIONS
In addition to headaches that raise red flags owing to their semiology or associated
examination abnormalities, any new headache in patients with certain demographic
risk factors should cause concern. Although primary headache disorders can occur
in patients who are pregnant, immunocompromised, elderly, or have a known malig-
nancy, special care should be taken in these groups before ascribing a benign diag-
nosis to new headaches.
Pregnant Patients
About 87% of women with migraines report improvement in their headaches in the
third trimester, 83% in the second trimester, and 47% in the first trimester.47 Notably,
this trend may not apply to patients who have migraine with aura or chronic migraine.
Accordingly, new or changing headaches (including longer headache duration) during
pregnancy or the postpartum period is unusual and should always be a cause for
concern because several secondary headaches are more likely during this time.
Patients with migraines are at increased risk for eclampsia, and other headache eti-
ologies to consider in a pregnant or postpartum patient with new headache include
CVST, RCVS, PRES, intracranial hypotension, and pneumocephalus (especially after
dural puncture for epidural anesthesia), SAH, arterial dissection, pituitary apoplexy,
and ischemic stroke.
Hypertension may raise concern for preeclampsia, but should also prompt evalua-
tion for overlapping vasculopathies including PRES or RCVS leading to ischemic or
hemorrhagic stroke. A thunderclap pattern may raise concern for SAH, but can also
be due to RCVS, arterial dissection, CVST, or pituitary apoplexy. Papilledema sug-
gests increased ICP and, although IIH is possible, CVST and space-occupying lesions
need to be ruled out. This point is especially true when a headache is brought about by
a Valsalva maneuver during delivery (which should also prompt investigation for arte-
rial dissection and aneurysmal SAH).
Bitemporal hemianopia suggests pituitary apoplexy, but this diagnosis can present
with less classical visual field alterations48 that may include vision loss in 1 eye more
than the other owing to asymmetric optic nerve and chiasm compression.49 There is
usually a sudden headache that can be associated with nausea, vomiting, ophthalmo-
plegia, and severe endocrine dysfunction, such as hemodynamic instability and dia-
betes insipidus.50 Vision alterations or loss in a pregnant patient with headache can
also suggest preeclampsia, PRES, or CVST. MRI is typically recommended over a
CT scan in pregnant patients to limit fetal radiation exposure and, depending on the
headache semiology and associated examination findings, there should be a low
threshold for arterial and venous imaging as well.51
Immunosuppressed Patients
Patients at risk for an infectious etiology of acute headache include those with cranial
trauma, recent neurosurgery, endocarditis, chronic and/or recent ear infection, sinus-
itis, and those who are immunocompromised such as patients with human immuno-
deficiency virus infection, cancer, or who are on immunosuppressive medications.
Etiologies to consider include viral, bacterial, parasitic, and fungal infections of the
meninges and brain parenchyma, as well as space-occupying lesions, such as sub-
dural empyema, brain abscess, and granulomas, which can cause an increased
ICP. A chronic headache in immunosuppressed patients can be owing to meningeal
or parenchymal infection with slow-growing pathogens including fungi like Crypto-
coccus and mycobacteria like tuberculosis. Cryptococcal infection is often associated
with a dramatically elevated ICP and papilledema. CSF studies are critical after ruling
out obstructive hydrocephalus in immunocompromised patients with acute or chronic
headache.
Patients with Underlying Malignancies

Patients with known malignancy who present with headache should undergo appro-
priate studies to assess for intracranial metastasis (particularly in those with sites of
primary malignancy that have a tendency to metastasize to the brain or meninges
such as breast, lung, kidney, and melanoma). Other crucial diagnoses to consider in
patients with cancer with acute headache include CVST, ischemic stroke owing to hy-
percoagulable state, and infection owing to immunosuppression from the malignancy
or its treatment. Brain metastases or primary brain cancer can cause headache owing
to meningeal irritation without significantly increasing ICP. In these cases, there may
not be features such as papilledema or headache intensity that is worse in the morn-
ing. In cases of known malignancy presenting with new headache and normal imaging,
CSF cytology should be done to evaluate for leptomeningeal metastasis.48 Patients
who have received cerebral radiation therapy may develop stroke-like migraine at-
tacks after radiation therapy syndrome years later, characterized by unilateral
migraine headache with stroke-like symptoms and signs and imaging showing dra-
matic contrast enhancement in the affected hemisphere.52
Older Patients
Patients presenting with new or changing headaches after the age of 50 should be
evaluated for vascular and oncologic etiologies. In addition to an increased risk of
stroke, there is risk in these patients for arteritis, most notably giant cell arteritis. Giant
cell arteritis classically presents with constant unilateral or bilateral temporal head-
ache refractory to analgesia, scalp tenderness, jaw claudication, transient vision
loss, and/or systemic symptoms such as fever, weight loss, and myalgias.53 Its inci-
dence increases with advancing age.53 A feared complication is vision loss owing to
arteritic ischemic optic neuropathy or central retinal artery occlusion. Physical exam-
ination may demonstrate temporal artery tenderness, an absence of temporal artery
pulse, or a prominent, enlarged temporal artery, although it should be noted that
absence of these findings does not exonerate giant cell arteritis, because early exam-
ination is often normal. The finding of prominent, enlarged temporal artery is the most
specific54 and occurs more commonly when the patient is presenting with a nonhead-
ache chief complaint (65% of the time vs 20% in those presenting with headache).55
The erythrocyte sedimentation rate and C-reactive protein should be checked and
although neither is specific, the C-reactive protein is more sensitive (95%–98% vs
77%–86%).56 Color-coded duplex ultrasound examination can show stenoses and
368 Kopel et al
occlusions as well as hypoechoic wall thickening that indicates sites of inflammation,

which may be good candidates for biopsy.53 Providers should not delay therapy while
awaiting biopsy because it can still be diagnostic up to 14 days after the initiation of
treatment.53 To prevent vision loss, steroids should be started early if giant cell arteritis
is considered. Patients often need prolonged steroid therapy to avoid recurrence;
agents that can decrease the necessary steroid maintenance dose include metho-
trexate, azathioprine, and tocilizumab.53,57
SUMMARY
Consistent and systematic application of an appropriate history and neurologic exam-

ination in patients with headache can help clinicians to appropriately diagnose
dangerous secondary conditions for optimal clinical outcomes. Owing to the overlap-
ping symptoms of primary and secondary causes of headache, a systematic
approach is required when obtaining history to identify patients with dangerous sec-
ondary causes. The SNOOP4 mnemonic provides a rapid and systematic approach to
obtaining history, which can guide triage, examination, and additional clinical studies.
Physical examination, particularly with attention to mental status and funduscopic
findings, can offer additional clues to the presence of secondary causes. The history
and examination should be used to guide appropriate imaging and laboratory studies
and interpretations of their results.
SAH carries very high morbidity and mortality if not diagnosed appropriately and
rapidly. Other secondary causes with significant risks if not diagnosed in timely fashion
include RCVS, elevated ICP, CVST, arterial dissection, CNS infection and inflamma-
tory vasculitis. In addition to the history, physical examination, and laboratory studies,
the patient’s medical background can offer key clues when evaluating for these
possible disorders. Patients who are pregnant are at an increased risk for CVST,
and patients who are older and immunocompromised are at greater risk for CNS infec-
tion and inflammatory vasculitis. Patients with underlying cancer and new headaches
should be evaluated for cerebral metastasis and vascular etiologies arising from a hy-
percoagulable state.
KEY CLINICAL POINTS

The majority of patients who seek care for headache have primary headache, but
a small subset have secondary causes associated with high morbidity and
mortality.
A systematic history assessing for red flag features along with a careful neuro-
logic examination is required to appropriately diagnose secondary causes
such as SAH, RCVS, elevated ICP, hydrocephalus, CVST, arterial dissection,
CNS infection, and inflammatory vasculitis.
Patients who are pregnant, immunocompromised, elderly, or have known malig-
nancy have higher risks of secondary disorders therefore, clinicians should have
a different threshold to obtain additional diagnostic evaluations in these patients.
CLINICS CARE POINTS
Headaches with thunderclap onset always require close evaluation for dangerous underlying
etiologies such as SAH, RCVS, and elevated ICP that, if left untreated, are associated with a
high degree of morbidity and mortality.
A CT scan of the brain is nearly 100% sensitive and specific for SAH if performed within
6 hours of headache onset. However, sensitivity decreases to 93% by 24 hours and
continues to decrease after that; therefore, an LP is recommended for patients who are
suspected of having SAH, especially if it has been more than 6 hours since the onset of the
headache.
Altered mentation, presenting as new onset confusion, lethargy, or behavioral alterations, is
not commonly associated with primary headache and should always raise suspicion for
secondary headache owing to an intracranial process such as CNS infection or an increased
ICP.
Headaches with a strong positional component should raise clinicians’ suspicion for altered
ICP, which may be due to serious underlying causes. Although both high and low ICP can
result in headaches, the causes of elevated ICP are more likely to be associated with
significant morbidity and mortality than the causes of decreased ICP. A fundoscopic
examination for papilledema is required when evaluating patients for possible elevation of
the ICP.
Although generally not an acutely life-threatening condition, in some cases of rapid leaks, a
severely decreased ICP leads to disorders of consciousness or coma from brain sag with
compression of the brainstem. This diagnosis should be considered in patients who do not
otherwise have an explanation for coma or cranial nerve palsies.
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Headache Emergencies

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Headache Emergencies

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Headache Emergencies

Nontraumatic headache is responsible for approximately 2% of all emergency depart-

Neurol Clin 39 (2021) 355–372

vasoconstriction syndrome (RCVS), elevated intracranial pressure (ICP), hydrocepha-

THE ROLE OF HISTORY AND NEUROLOGIC EXAMINATION

Owing to significant overlap in symptoms of benign and dangerous causes of head-

Symptoms to Assess for Secondary Causes to Consider:

Adapted from Dodick DW. Pearls: headache. Semin Neurol. 2010;30(1):74-81.

The role of the neurologic examination is often emphasized in the evaluation of

Reversible Cerebral Vasoconstriction Syndrome

Drug Categories Examples of Offending Drugs

Cerebral Venous Sinus Thrombosis

component. A diagnostic feature of migraine is “aggravation by or causing avoidance

Elevated Intracranial Pressure

A fundoscopic examination for papilledema is required when evaluating patients for

Decreased Intracranial Pressure

HEADACHE WITH ABNORMAL EXAMINATION

Patients with headache accompanied by symptoms such as persistent fever, hemiple-

Patients with Underlying Malignancies

occlusions as well as hypoechoic wall thickening that indicates sites of inflammation,

Consistent and systematic application of an appropriate history and neurologic exam-

KEY CLINICAL POINTS

CLINICS CARE POINTS

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