Current Neurology and Neuroscience Reports (2020) 20: 7

https://doi.org/10.1007/s11910-020-01030-w

HEADACHE (R. H. SINGH, SECTION EDITOR)

Emergency Department and Inpatient Management

of Headache in Adults
Jennifer Robblee 1 & Kate W. Grimsrud 2

Published online: 18 March 2020

# Springer Science+Business Media, LLC, part of Springer Nature 2020

Abstract
Purpose of Review This article reviews treatment options for patients presenting with headache in the emergency department
(ED) and for inpatients, including red flags and status migrainosus (SM).
Recent Findings Most patients presenting with headache in the ED will have migraine, but red flags must be reviewed to rule out
secondary headaches. SM refractory to home treatment is a common reason for ED presentation or inpatient admission, but high-
quality treatment evidence is lacking. Common treatments include intravenous fluids, anti-dopaminergic agents with diphenhy-
dramine, steroids, divalproex, nonsteroidal anti-inflammatory drugs, intravenous dihydroergotamine, and nerve blocks. Other
therapies (e.g., ketamine and lidocaine) are used with limited or inconsistent evidence. There is evidence for inpatient behavioral
management therapy.
Summary This article details red flags to review in the workup of headache presentation in the ED and provides a step-wise
approach to ED and inpatient management. However, more studies are needed to better optimize care.

Keywords Emergency . Headache . Inpatient . Migraine . Red flags . Status migrainosus

Abbreviations Introduction
AHS American Headache Society
DHE Dihydroergotamine Neurologic disorders account for at least one-tenth of presen-
ED Emergency department tations to the emergency department (ED) with approximately
EFNS European Federation for Neurological Sciences one-fourth of these presentations being headache related
IV Intravenous [1–3•]. The vast majority, over 95%, of these patients will
IVF Intravenous fluid have migraine [2, 3•]. We lack guidelines for acute treatment
NSAID Nonsteroidal anti-inflammatory drug of migraine in infusion centers, urgent care clinics, EDs, and
RCT Randomized controlled trial inpatient settings. Patients presenting to the ED with primary
SM Status migrainosus headaches frequently get workups despite the majority having
migraine without red flags. One study showed that half of
these patients with migraine received unnecessary neuroimag-
ing [4]. As migraine attack frequency increases in the general
population, so does the burden of disease, healthcare utiliza-
This article is part of the Topical Collection on Headache
tion, and cost, which includes inappropriate workup and ED
utilization [5]. Presentation to the ED for migraine, especially
* Jennifer Robblee
Neuropub@barrowneuro.org if concurrent with opioid or triptan overuse, is associated with
even higher all-cause healthcare cost [6]. Currently, satisfac-
1
tion with ED treatment of headache is low, and evidence-
Jan and Tom Lewis Migraine Treatment Program, Department of
Neurology, Barrow Neurological Institute, St. Joseph’s Hospital and
based treatment options are often quite limited [7•].
Medical Center, Phoenix, AZ, USA Status migrainosus (SM) is a common reason for presenta-
2
Cerebrovascular and Hospital Neurology, Penrose Neuroscience,
tion to the ED and may represent nearly one-fifth of headache-
Colorado Springs, CO, USA related ED presentations [2, 3•]. The true incidence of SM is
7 Page 2 of 9
unknown and may even be complicated by other diagnoses
such as episodic status migrainosus or new daily persistent
headache [8–10]. An 11-year retrospective study in France
that found only 24 cases of SM out of 8821 patients concluded
that SM is rare [11•]. However, in clinical practice, SM-like
presentations are frequently seen as severe migraine attacks
lasting greater than 72 h overlying a baseline chronic daily
headache; this makes true diagnosis of status migrainosus less
clear despite patients having symptoms that are often managed
as SM. Interestingly, most patients with SM have a low rate of
frequency of attacks, and their frequency of SM attacks does
not appear to increase after an episode of SM resolves [11•].
Recurrence of SM is not uncommon and may evolve into
episodic SM [8, 12]. The average duration of SM is 4.8 weeks
[11•]. It confers high disability, including a 1.81-fold risk of
attempting suicide [13]. In those admitted as inpatients for
SM, prolonged stay is predicted by female gender, African
American race, presence of mood disorder, obesity, opioid
overuse, congestive heart failure, and chronic renal failure
[14].
Identifying Secondary Headaches
Nye and Ward [15•] provided an excellent overview of
red flags to consider in the ED that includes the
SNOOP4 criteria, age < 5 years, and headache worsening
under observation. SNOOP4 was originally described by
Dodick [16] and stands for systemic sign/symptoms,
neurologic signs/symptoms, onset thunderclap, onset >
50 years of age, and 4 pattern changes. The pattern chang-
es are progressive, cough/Valsalva precipitation, postural,
and papilledema, with a fifth “P” often added for
pregnancy. All patients with headache need funduscopic
examination performed specifically for consideration of
papilledema. See Table 1 for details on applying the dif-
ferential diagnosis of headache to these red flags [16].
The decision of when and how to investigate headache
is based on concern for a specific secondary headache,
which guides appropriate investigation into potential dif-
ferential diagnoses. The American Headache Society’s
guide “Choosing Wisely” does not recommend neuroim-
aging in patients with stable headache meeting criteria for
migraine [17]. If there is concern for a secondary head-
ache, magnetic resonance imaging should always be cho-
sen over computed tomography when available, except
for situations that require immediate imaging such as
thunderclap headache or stroke. Furthermore, deciding
what imaging test to use also depends on concern for an
underlying vascular abnormality such as venous sinus
thrombosis requiring venous imaging or vasospasm re-
quiring arterial imaging.
Curr Neurol Neurosci Rep (2020) 20: 7
Aura and Mimics
Another important component of headache evaluation in the
ED is differentiating migraine aura from stroke. Khan et al.
[18] reviewed 105 patients who received tissue plasminogen
activator, and found that 25% were stroke mimics. From this
sample, they devised a stroke mimic scoring system with
100% specificity if the score is more than 5, but a sensitivity
of only 15% [18]:
& Age:
< 50 years = 2 points
50–70 years = 1 point
> 70 years = 0 points
& Stroke risk factors: hypertension, hyperlipidemia, diabe-
tes, atrial fibrillation (AF)
No risk factors = 3 points
1 risk factor other than AF = 2 points
≥2 risk factors other than AF = 1 point
AF = 0 points
& Other factors:
Migraine = 2 points
Epilepsy = 1 point
Psychiatric illness = 1 point
Lebedeva et al. [19] also looked at differentiating aura from
a transient ischemic attack and proposed diagnostic criteria for
transient ischemic attack with a sensitivity of 99% and a spec-
ificity of 95–96%:
A. Sudden onset of fully reversible neurologic or retinal
symptoms (e.g. hemiparesis, hemi-numbness, apha-
sia, neglect, amaurosis fugax, hemianopia,
hemiataxia)
B. Duration < 24 h
C. At least 2 of the following:
a. At least 1 symptom is maximal in < 1 min without
gradual spread
b. ≥ 2 symptoms occur simultaneously
c. Symptoms are deficits (no irritative symptoms like
photopsia, paresthesia)
d. No headache within 1 h of symptoms
D. None of the following isolated symptoms: shaking spells,
diplopia, dizziness, syncope, decreased level of con-
sciousness, confusion, hyperventilation-associated pares-
thesia, unexplained falls, amnesia
E. No acute infarct in relevant territory on imaging
Curr Neurol Neurosci Rep (2020) 20: 7 Page 3 of 9 7

Table 1 Clues to secondary headache diagnoses—SNOOP4 criteria

Clues Considerations

S = Systemic symptoms of signs or disease

Anticoagulation ICH
Awakens from sleep Cluster headache, CSF leak, hypnic headache, increased ICP, migraine,
sleep apnea headache
Coronary artery disease Cardiac cephalgia, stroke
Dialysis Dialysis headache, migraine
Eye pain ± red eye Acute angle-closure glaucoma, iritis/uveitis, optic neuritis, TAC
Fall, head trauma, whiplash Concussion with post-traumatic headache, CSF leak, ICH, skull fracture
Fever Acute sinusitis, GCA, HaNDL, infection (meningitis, encephalitis, brain abscess),
NDPH, neoplasm
Hypermobility CSF leak, dissection, migraine, SAH (aneurysm)
Hypertensive emergency ICH, pheochromocytoma, pre-eclampsia, PRES
Illicit drug use Infection, RCVS, stroke
Immunosuppression Infection (meningitis, encephalitis, brain abscess), medication (e.g. tacrolimus), neoplasm
Jaw pain GCA, migraine, persistent idiopathic facial pain, TMD, trigeminal neuralgia
Neck pain Cervicogenic headache, craniocervical dystonia, dissection, migraine, myofascial pain, TTH
Shunt Infection, over-shunting, under-shunting
Tachycardia POTS
Tooth pain Dental issue, trigeminal neuralgia

N = Neurologic symptoms or signs

Diplopia/ophthalmoparesis GCA, IIH, ischemic cranial nerve III palsy, neoplasm, recurrent painful ophthalmoplegic
neuropathy, Tolossa-Hunt syndrome
Horner syndrome Carotid dissection, ICH, neoplasm, stroke, TAC
Loss of consciousness Brainstem aura, carbon monoxide, colloid cyst of third ventricle, concussion, epilepsy,
glossopharyngeal neuralgia, infection, POTS
Progressive vision loss IIH, increased ICP, RVCL
Pulsatile tinnitus CSF leak, IIH, vascular lesion
Seizure ICH, ictal or postictal headache, infection, neoplasm, stroke
Sudden vision loss or TVOs Acute angle closure glaucoma, aura, carotid dissection, GCA, ICH, IIH, increased ICP, stroke
Weak, numb, aphasia, etc. Aura, carbon monoxide, focal lesion, genetic vasculopathy, HaNDL, hemiplegic migraine,
ICH, infection, inflammatory (e.g. neurosarcoidosis, aseptic meningitis), neoplastic
(mass or leptomeningeal), RCVS, stroke

O = Onset thunderclap
Single thunderclap headache SAH/ICH, unruptured aneurysm (sentinel headache), CVST, RCVS, dissection, CSF leak
Recurrent thunderclap headaches RCVS

O = Onset > 50 years of age

> 50 years GCA, ICH, infection, neoplasm, stroke

P = 4 Pattern changes*
Progressive headache
Progression to daily Chronic migraine, medication-overuse headache, neoplasm, vasculitis
New onset daily from day 1 CSF leak, NDPH, status migrainosus
Precipitated by Valsalva/cough
Cough/Valsalva trigger Chiari malformation, CSF leak, DAVF, increased ICP, migraine (exacerbates only),
neoplasm (especially posterior fossa), primary cough headache
Postural aggravation
Headache better supine Cervicogenic headache, intracranial hypotension/CSF leak, over-shunting, POTS
Headache worse supine IIH, increased ICP, under-shunting
Papilledema
Papilledema CVST, IIH, increased ICP, neoplasm, optic neuritis
Pregnancy
Pregnancy/post-partum CSF leak/post-epidural headache/intracranial hypotension, CVST, migraine, pituitary
apoplexy, pre-eclampsia/eclampsia, RCVS, stroke

*A fifth “P” for pregnancy is often added to the original 4 “Ps” proposed by Dodick [16]
CSF cerebrospinal fluid, CVST cerebral venous sinus thrombosis, DAVF dural arteriovenous fistula, GCA giant cell arteritis, HaNDL syndrome of
transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis, ICH intracranial hemorrhage, ICP intracranial pressure, IIH idiopathic
intracranial hypertension, NDPH new daily persistent headache, POTS postural orthostatic tachycardia syndrome, PRES posterior reversible encepha-
lopathy syndrome, RCVS reversible cerebral vasoconstriction syndrome, RVCL retinal vasculopathy with cerebral leukoencephalopathy, SAH subarach-
noid hemorrhage, TAC trigeminal autonomic cephalgia, TMD temporomandibular joint disease, TTH tension-type headache, TVO transient visual
obscurations
7 Page 4 of 9 Curr Neurol Neurosci Rep (2020) 20: 7

Ultimately, clinic judgment is still required until tools like
these are validated, but using the type of reasoning these tools
provide may help guide diagnosis.
Management
SM and severe headache attacks not responding to acute treat-
ment at home are a common reason for presentation to the ED,
with patients often requiring admission. The research on op-
timal treatment is limited, but many options do exist. See
Fig. 1 for a potential approach to management.
As a first step, treatment often includes intravenous fluid
(IVF), anti-dopaminergic agents with diphenhydramine, ste-
roids, and nonsteroidal anti-inflammatory drugs (NSAIDs).
Intravenous (IV) dihydroergotamine (DHE) is a common
medication added to this list and has long been used with
one of the original approaches to the management of SM
described by Raskin [20] in 1990, who used primarily IV
DHE. However, even now years after the Raskin protocol
was published, we do not have clear guidance on optimal
ED treatment for SM or severe migraine not responding to
home treatment. This section outlines the current evidence
and provides guidance on one approach to managing severe
migraine attacks including SM in the ED and inpatient setting.
Step 1—Initial Treatment
As part of step 1, many protocols include IVF based on the
belief that dehydration may be a component of the attack.
Unfortunately, two randomized controlled trials (RCTs) and
post hoc analysis of metoclopramide RCTs in which 20% of

Step 1 – initial treatment:

IVF ± prochlorperazine 10 mg ± diphenhydramine
25 mg IV ± dexamethasone 10 mg IV ± ketorolac 30 mg IV
Consider DHE 0.5 mg-1 mg IV

If poor response

Step 2 – second-line options: Considerations if significant aura:

Prochlorperazine 10 mg IV* Divalproex 500 mg-1000 mg IV
Acetaminophen 1 g IV Magnesium sulfate 1 g-2 g IV
Divalproex 500 mg IV Furosemide 20 mg IV
Magnesium sulfate 1 g IV Ketamine 25 mg IN or 0.1 mg/kg/h IV
Ondansetron 4 mg IV Levetiracetam 500 mg-1500 mg IV
Nerve block Acetazolamide 500 mg-1000 mg PO BID
100% oxygen 12-15 L using NRB Lamotrigine 100 mg PO BID (outpatient)
*may repeat (frequency/duration not well established) *Rule out stroke if relevant*

If poor response

Step 3 – consider inpatient admission:

DHE IV every 8 h over 3-6 days
Prochlorperazine 10 mg IV*
Ketamine IV continuous over 4-6 days (max 1 mg/kg/h)
Lidocaine bolus then IV continuous over 4-6 days (max 2 mg/min)
Levetiracetam 500 mg-1500 mg IV*
Lacosamide 400 mg load then 200 mg-400 mg IV daily
Fosphenytoin 20 mg/kg IV*
Mannitol 250 mg IV BID
Droperidol 2.5 mg-8.25 mg IM*
Ziprasidone 10 mg-40 mg IM*
Propofol IV 30 mg loading dose then bolus 10 mg boluses
Suprazygomatic SPG block
Inpatient behavioral treatments
*may repeat (frequency/duration not well established)

Fig. 1 Approach to status migrainosus and severe headache management mask, PO oral, SPG sphenopalatine ganglion. Used with permission from
in the ED. BID twice daily, DHE dihydroergotamine, IM intramuscular, Barrow Neurological Institute, Phoenix, Arizona
IN intranasal, IV intravenous, IVF intravenous fluid, NRB nonrebreather
Curr Neurol Neurosci Rep (2020) 20: 7
subjects also had IVF showed no benefit from IVF in SM
[21–23]. However, because IVF is a benign treatment with
occasional success, it is often still used.
Another mainstay in the treatment of SM is administration
of anti-dopaminergic drugs, which have better evidence than
IVF. In fact, a 2008 systematic review recommended IV
prochlorperazine even after IV ketorolac was ineffective
[24]. Prochlorperazine has even shown benefit over IV
hydromorphone [25••]. Other anti-dopaminergic agents have
been studied including RCT support for metoclopramide and
prospective study support for chlorpromazine [26–28]. These
are good options given that they treat headache and nausea.
Awareness of potential adverse effects, however, is important;
these include extrapyramidal symptoms such as akathisia or
dystonic reaction [29]. Particularly, if providing an anti-
dopaminergic agent as a bolus rather than infusion, diphenhy-
dramine should be given to reduce extrapyramidal symptoms
[30]. It is important to also consider these treatment options if
using IV DHE given its common adverse effect of nausea.
IV DHE can be provided in the ED or may be used repeat-
edly over several days as part of inpatient treatment [12, 21,
31–36]. The European Federation for Neurological Sciences
(EFNS) task force recommends DHE for SM [37], and the
American Headache Society (AHS) gave it level B evidence
[38••]. Patients naïve to DHE may require low starting doses
of 0.5 mg, and all patients of child-bearing potential should
undergo a pregnancy test. Physicians should ensure that the
patient has not used triptans in the preceding 24 h. Similar to
the Raskin protocol [20], IV DHE can be provided every 8 h
as part of a 3- to 5-day admission [20]. The Ford protocol [39]
for IV DHE also showed good tolerance of continuous IV
DHE in patients with intractable headache while withdrawing
excessively used analgesia over 3 days. Some centers will
discharge patients with a short-course nasal DHE or even oral
methylergonovine maleate to prevent relapse [40].
Another consideration as part of step 1 is the use of ste-
roids. Importantly, a systematic review from 2015 that includ-
ed 25 studies on the use of corticosteroids for migraine
showed that steroids improve headache and the response to
nonsteroidal treatment [41•]. The EFNS task force recom-
mends steroids for SM; however, the AHS only gave it level
C evidence [37]. It has been shown that dexamethasone 10 mg
(range 4–24 mg) IV is useful for severe or refractory migraine
attacks with a number needed to treat of 9 for preventing
recurrence [38••, 41•]. Predictors of benefit from steroids in-
clude high disability, prolonged attack, SM, incomplete pain
relief, and recurrence. Repetitive IV therapy in an outpatient
setting with 10–20 mg of dexamethasone may help prevent
relapses and increase prolonged remission with remission
times shortened when combined with an anti-dopaminergic
agent like prochlorperazine 3.5 mg [42]. The AHS assessed
chlorpromazine, droperidol, metoclopramide, and
prochlorperazine to have level B evidence [38••].
Page 5 of 9 7
NSAIDs are often used in the treatment of SM. Agents that
have been studied in RCTs with results showing a benefit over
placebo include dexketoprofen 50 mg and lysine-
acetylsalicylic acid (IV aspirin) 1000 mg [43, 44].
Dexketoprofen and ketorolac have also demonstrated benefits
in systematic reviews [45, 46]. Only ketorolac 30–60 mg IV/
intramuscular has been assessed by the AHS as a parental
NSAID with level B evidence [38••].
Step 2—Second-line Option
If IVF, anti-dopaminergic agents, NSAIDs, dexamethasone,
and DHE provide insufficient relief, the next step is to repeat
doses of medications already tried such as prochlorperazine or
DHE to perform nerve blocks or to consider other treatments
with less evidence. These other treatments may include mag-
nesium sulfate, anti-epileptics (e.g., divalproex), IV acetamin-
ophen, ondansetron, and high-flow oxygen.
Magnesium sulfate has been shown in a systematic review
to benefit pain after 1 h, reduce aura duration, and reduce need
for analgesia [47]. Adverse events may include hypotension
and diarrhea [48]. Intravenous anti-epileptics are often includ-
ed in treatment, most commonly IV divalproex. Other anti-
epileptics including levetiracetam, lacosamide, and
fosphenytoin are used, though no headache studies exist for
some of these agents. Dosing for divalproex includes bolus,
intermittent dosing, continuous infusion with bolus, and con-
tinuous infusion. Continuous infusion is optimal for reaching
steady state, whereas bolus has the fastest response [35, 49,
50]. Parental acetaminophen dosed at 1000 mg IV is often
used despite a lack of evidence or guideline support [38••,
51]. High-flow oxygen has also been shown to be beneficial
in the acute treatment of migraine in a Cochrane review, al-
though the quality of evidence is poor [52].
Nerve blocks have demonstrated benefits for the treatment
of many types of headache including occipital neuralgia, clus-
ter headache, and migraine. Most studies have looked at long-
term benefit, but a few studies have shown benefit for SM.
Nerve blocks may be used in an outpatient clinic, in the ED, or
as part of inpatient treatment. Friedman et al. [53•] presented
an RCT of bilateral occipital nerve block with bupivacaine in
acute migraine patients who were refractory to
metoclopramide in the ED. The rate of headache freedom
was 31% at 30 min and 23% at 48 h, compared with no
freedom from pain seen in any of the sham patients [53•].
Another RCT of occipital nerve block with bupivacaine found
the treatment equivalent to IV treatments such as those de-
scribed above in step 1 [54]. In addition to nerve blocks,
another simple procedure that can be done in the ED is a
sphenopalatine ganglion block. Catheters are marketed specif-
ically for this procedure, but a cheap alternative is to use an
angiography catheter in its place.
7 Page 6 of 9
Considerations for Significant Aura
If aura is a significant component of the presenting attack,
especially migraine aura status or prolonged aura, there is
limited evidence to guide a more tailored treatment approach.
Studies have suggested that magnesium may be beneficial
because of low cerebral magnesium and that magnesium
may be most beneficial for migraine with aura in particular
because of the mineral’s ability to block cortical-spreading
depression, which suggests a benefit for protocols for mi-
graine aura status [55•]. The AHS gave magnesium sulfate
1–2 g IV level B evidence for acute treatment of migraine with
aura. Other options include divalproex [55•, 56, 57], acetazol-
amide [58–60], lamotrigine [60–64], levetiracetam [65], furo-
semide [60, 66, 67], and ketamine [68]. Other options from
step 1 may be considered for management of associated head-
ache, and workup should be considered to rule out stroke.
Step 3—Consider Inpatient Admission
If a patient is still refractory after the first 2 steps, treating physi-
cians should consider admission and reassess patient history to
ensure another secondary diagnosis or factor has not been
missed. Inpatient treatments may last 3 to 5 days and may result
from refractoriness to ED treatment or may be an elective admis-
sion for treatment, often in a patient known to respond to the
therapy. Patients with severe chronic refractory pain are also
occasionally admitted for these treatments when other extensive
medication trials have been ineffective. DHE 0.5–1.0 mg IV
every 8 h is a common option with good evidence. Other anti-
epileptics as described above may be tried, although evidence for
their use is more limited. Anti-dopaminergic agents may be re-
peated to target sleep. Continuous infusions may include lido-
caine or ketamine, although evidence is varied [69–73].
Ketamine is generally started at a dose of 0.2 mg/kg and in-
creased by 0.05–0.1 mg/kg/h every 1–4 h as tolerated with max-
imum dose of 1 mg/kg/h [69, 70, 73]. Adverse effects like nys-
tagmus, confusion, and hallucinations can be treated with loraz-
epam or by lowering the dose [70]. One recommended protocol
for IV lidocaine is a 1 mg/kg bolus followed by infusion at
2 mg/min [71]. Propofol has been tried as a 30–40 mg IV loading
dose with repeated boluses of 10–20 mg aimed at reducing the
level of alertness [74–78]. Mannitol has even been tried dosed at
250 mg IV twice daily [79–81], and intramuscular ziprasidone
has support from a retrospective study [82]. There is even a case
report of a patient with refractory 5-day SM responding to induc-
tion and general anesthesia [83, 84].
Additional Options
Beyond pharmacologic treatment, evidence also supports be-
havioral management using inpatient programs [85–89].
These programs may include mindfulness, cognitive
Curr Neurol Neurosci Rep (2020) 20: 7
behavioral therapy, and biofeedback among other non-
pharmacologic options such as massage and aromatherapy.
These programs may be provided in combination with phar-
macologic treatment, detoxification for medication overuse,
and/or as pure behavioral management. Typically, they are
used as part of inpatient management for refractory patients.
Follow-up Plan
A final consideration as part of headache management in the
ED and for inpatients is the discharge plan. Questions to ask
include: Is this person on preventive medication? Should they
be, and who will follow-up their presentation? Patients should
not be prescribed opioids or butalbital-containing medication
as the use of such medications can ultimately worsen the con-
dition [17]. In fact, opioids should not be used for acute treat-
ment of migraine except as a last resort. Similarly, prolonged
and frequent use of over-the-counter medications is not rec-
ommended. Analgesia use should be counseled with a good
general rule being no more than twice a week to prevent
medication-overuse headache. Patients prone to recurrent
SM should consider backup home treatments like oral dexa-
methasone or subcutaneous NSAIDs in limited doses.
Upcoming migraine treatments such as the IV monoclonal
antibody eptinezumab may eventually provide new options
to offer in the ED or to inpatients, but further research is
needed.
Conclusions
Headache is a cause of significant disability worldwide and is
a common reason for presentation to the ED. The vast major-
ity will be migraine, but red flags must be carefully reviewed
to rule out secondary headaches requiring targeted investiga-
tions and treatment. SM or severe migraine attacks refractory
to home treatment are common reasons for presentation with
headache to the ED or for inpatient admission. However, high-
quality evidence is lacking to guide treatment. This article
reviews the currently available evidence to provide a step-
wise approach, but more studies are needed to better guide
management in these settings. Furthermore, patients who are
refractory to outpatient treatments often receive recurrent in-
patient treatment with little evidence-based guidance as far as
combined pharmacologic and behavioral management.
Emergency and inpatient management of headache is an im-
portant area with much room for improvement.
Acknowledgments The authors thank the staff of Neuroscience
Publications at Barrow Neurological Institute for assistance with manu-
script preparation.
Author Contributions Robblee: literature review, writing, figure creation,
and table creation. Grimsrud: writing and table creation.
Curr Neurol Neurosci Rep (2020) 20: 7
Compliance with Ethical Standards
Conflict of Interest Jennifer Robblee and Kate W Grimsrud each declare
no potential conflict of interest.
Human and Animal Rights and Informed Consent This article does not
contain any studies with human or animal subjects performed by any of
the authors.
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