The Journal of Emergency Medicine, Vol. 59, No. 3, pp. 392–395, 2020
Ó 2020 Elsevier Inc. All rights reserved.
0736-4679/$ - see front matter

https://doi.org/10.1016/j.jemermed.2020.06.008

Selected Topics:
Neurological Emergencies

THE TROUBLE WITH SWALLOWING: DYSPHAGIA AS THE PRESENTING SYMPTOM
IN LATERAL MEDULLARY SYNDROME
Meaghan Frederick, MD,* Abhinav Rajpal, MD, MPH,* Charles Kircher, MD,*† and Kiran A. Faryar, MD, MPH*
*Department of Emergency Medicine, University of Cincinnati, Cincinnati, Ohio and †University of Cincinnati Gardner Neuroscience Institute,
Cincinnati, Ohio
Reprint Address: Kiran A. Faryar, MD, MPH, University of Cincinnati, Department of Emergency Medicine, Medical Sciences Building Room
1654, 231 Albert Sabin Way, PO Box 670769, Cincinnati, OH 45267-0769

, Abstract—Background: Posterior circulation strokes
account for approximately one-fourth of all ischemic
strokes, but are frequently misdiagnosed by emergency providers. Current standard stroke screening tools such as the
National Institutes of Health Stroke Scale and the Cincinnati
Prehospital Stroke Scale are weighted toward anterior circulation stroke diagnosis. Lateral medullary syndrome, a
type of posterior circulation stroke, can be particularly challenging to diagnose due to nonspecific presenting symptoms,
such as dysphagia. Case Report: This report describes a 65year-old man who presented with dysphagia, dizziness, and
hoarseness. An initial neurological examination did not
reveal any gross deficits, and imaging to evaluate for posterior circulation stroke was not obtained. The patient presented the following day with worsening symptoms,
prompting imaging that revealed a large cerebellar ischemic
infarction. Why Should an Emergency Physician Be Aware
of This?: Although dysphagia frequently occurs in lateral
medullary syndrome, it is rarely the presenting symptom
in the emergency department. In patients with cerebrovascular risk factors who present with dysphagia, a complete
neurological examination should be performed and noncontrast computed tomography (CT) of the head should be obtained if a neurological deficit is appreciated. Due to their
poor sensitivity, CT scans can frequently miss posterior circulation strokes, therefore magnetic resonance imaging
should be considered if provider suspicion remains high.
Emergency providers are encouraged to have a high level
of suspicion for this rare but debilitating stroke syndrome

to avoid misdiagnosis and delayed care.
Inc. All rights reserved.

Ó 2020 Elsevier

, Keywords—posterior circulation stroke; lateral medullary syndrome; Wallenberg syndrome; dysphagia; dizziness

INTRODUCTION
Appropriate and timely recognition of posterior circulation strokes by emergency medicine providers is critical.
Posterior circulation strokes account for 20–25% of all
ischemic strokes (1). They are more than twice as likely
to be misdiagnosed as anterior circulation strokes, with
a misdiagnosis rate of up to 37% (2,3). Posterior circulation stroke symptoms are frequently misdiagnosed as
dehydration, vestibular neuritis, benign positional vertigo, gastroenteritis, or various metabolic disorders (4).
Standard stroke screening tools such as the National Institutes of Health Stroke Scale and Cincinnati Prehospital
Stroke Scale are weighted toward symptoms commonly
found in anterior circulation strokes (5,6).
Wallenberg syndrome, caused by infarction of the
lateral medulla, is a posterior circulation stroke syndrome
that typically arises due to occlusion of the vertebral artery or posterior inferior cerebellar artery (7). This syndrome can be difficult to differentiate among posterior
circulation strokes. Key vestibulocerebellar features
include dysphagia, hoarseness, gait abnormalities, dysmetria, dysarthria, dizziness, lethargy, headache, nausea,

RECEIVED: 7 December 2019; FINAL SUBMISSION RECEIVED: 18 May 2020;
ACCEPTED: 1 June 2020
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Dysphagia as the Presenting Symptom in Lateral Medullary Syndrome

and vomiting (2,8). Classic sensory signs and symptoms
include loss of pain and temperature sensation to the ipsilateral face and contralateral trunk and limbs due to
involvement of the spinothalamic tract (9). This report
provides recommendations for emergency medicine providers as they approach high-risk patients presenting with
nonspecific symptoms, specifically dysphagia, dizziness,
and hoarseness, which are frequently associated with posterior circulation stroke syndromes such as lateral medullary syndrome.

393

the soft palate. NP scope performed by the resident physician with attending supervision at bedside revealed
diffuse mild edema of the posterior oropharynx with a
thick white plaque. The uvula was midline, and epiglottis
and vocal cords were normal in appearance. The patient
was diagnosed with esophageal candidiasis, prescribed
nystatin suspension, and instructed to follow up with an
ear, nose, and throat specialist and his primary care physician.
ED Presentation #2 and Hospital Course

CASE REPORT
ED Presentation #1
A 65-year-old white man presented to the Emergency
Department (ED) with 2 days of ‘‘throat congestion and
fullness,’’ cough, and dizziness. He reported similar episodes nearly every 6 months for the last 10 years, which
typically lasted < 24 h and resolved with over-the-counter
decongestants. He reported difficulty swallowing and
voice changes. His dizziness was described as lightheadedness with standing, which he attributed to decreased
oral intake secondary to dysphagia. He denied vertiginous symptoms. A comprehensive review of symptoms
was otherwise noncontributory. He denied exposure to
any reported allergens. Past medical history was significant for allergic rhinitis, migraines, and chronic back
pain. He was a nonsmoker.
In the ED, vital signs were only significant for hypertension with a systolic blood pressure in the 160s (mm
Hg), heart rate 70 beats/min, and oxygen saturation in
the mid 90s. On examination he was alert and oriented,
and in no acute distress. He had no asymmetry of the
external face or neck, oral or labial swelling, tongue
edema, or oral erythema. There was no appreciated asymmetry or erythema of the posterior oropharynx, and his
uvula was midline. There was no palatal or submental
fullness. The patient had nasal voice but no stridor or
notable upper airway noises, and his respirations were unlabored. No gross cranial nerve (CN) deficits, dysarthria,
or aphasia were appreciated on examination. There was
no tracheal deviation, neck tenderness, or thyromegaly.
He had no gross sensory or motor deficits, and his gait
was grossly intact by observing him ambulate unassisted
to the restroom in the ED. The patient received 1 L of
intravenous (i.v.) lactated Ringer solution, i.v. diphenhydramine, i.v. solumedrol, and i.v. famotidine, with
improvement in symptoms, and was able to tolerate
oral intake. Renal panel demonstrated a glucose of
161 mg/dL, but was otherwise unremarkable. The resident and attending physician discussed performing a nasopharyngoscopy (NP scope) to rule out any significant
pharyngeal edema, obstruction, or abnormality deep to

The patient returned to the ED the following day for
persistent symptoms, with new-onset inability to tolerate
oral intake and the prescribed nystatin due to dysphagia
and odynophagia, which resulted in gagging upon attempted swallowing. He also endorsed continued dizziness with new-onset difficulty standing and assistance
with ambulation. Vital signs on ED arrival showed he
was hypertensive, afebrile, and without tachycardia or tachypnea. His examination was remarkable for bilateral
submandibular gland swelling and cervical adenopathy,
but no tonsillar erythema or exudate. Cardiac, pulmonary,
and abdominal examinations were unremarkable. A brief
neurological examination showed no gross motor or sensory deficits in his upper or lower extremities; however,
CN and cerebellar functions were not initially tested.
The patient received i.v. fluids, diphenhydramine, famotidine, guaifenesin, and sublingual atropine drops without
improvement of symptoms. Laboratory work demonstrated a mild leukocytosis with a white blood cell count
of 11.4 K/uL, but was otherwise unremarkable. At this
time, the management plan was focused on identifying
pharyngeal or laryngeal soft tissue edema, infection, or
mass. A computed tomography angiography scan
(CTA) of the neck was obtained to identify structural abnormalities, but incidentally revealed a large left cerebellar infarct with left vertebral artery occlusion at the
level of C1–C2. Tissue plasminogen activator (tPA) was
contraindicated given the time since onset of symptoms
and established infarct present on CT. A comprehensive
neurologic examination performed in the ED revealed
left upper and lower extremity ataxia, left miosis,
nystagmus on leftward gaze, left-sided facial weakness,
and dysarthria. The patient was admitted to the intensive
care unit for cerebellar infarct with lateral medullary syndrome. An urgent magnetic resonance imaging (MRI)
scan was performed, which showed large-volume infarct
in the left cerebellar hemisphere with extension into the
posterolateral medulla (Figure 1). He was intubated for
hypoxic respiratory failure and aspiration pneumonia.
He received a tracheostomy due to prolonged intubation
and failed extubation. A percutaneous endoscopic gastrostomy tube was placed for poor feeding due to significant

394

M. Frederick et al.

dysphagia. He was discharged to inpatient rehabilitation
and has since been discharged home. To date, the patient
does not eat by mouth due to persistent dysphagia and
aspiration risk; his tracheostomy tube has been decannulated and capped, and his modified Rankin Score is 4.
DISCUSSION
Posterior circulation strokes frequently present with
nonspecific symptoms, which contributes to their high
misdiagnosis rate (10). Our patient was a 65-year-old
man with acute lateral medullary infarction, or Wallenberg syndrome, who initially presented with a primary
complaint of dysphagia, with associated hoarseness and
nonvertiginous dizziness. Dysphagia is common in lateral
medullary syndrome due to impaired swallowing function, and may be present in up to 94% of lateral medullary
strokes (8,11). However, dysphagia is a presenting symptom in < 15% of all posterior strokes and is frequently
transient or mild (11,12). Although several prior case reports have discussed cases of lateral medullary syndrome
presenting with dysphagia, this report is unique because
the authors outline specific diagnostic considerations
for the emergency physician to mitigate future misdiagnosis (13–15).
Brainstem strokes, such as the one our patient suffered, will typically present with numerous crossed
symptoms due to the density of tracts within the brainstem that are affected by relatively small infarcts. However, posterior strokes can present with one to two isolated
complaints and deficits (16). Dysphagia is typically
affected in lateral medullary syndrome because swallowing is controlled by several anatomical regions in the medulla (17,18). These include the dorsal region, which
contains the nucleus solitarius, and the middle and ventral

regions, which include the reticular formation and the nucleus ambiguous (17,18). In patients with cardiovascular
risk factors presenting with dysphagia, it is crucial to
maintain a high level of suspicion for cerebrovascular
causes.
Patients with dysphagia should undergo a detailed
neurological examination, including cranial nerve and
cerebellar testing, to identify a potential posterior circulation stroke. When evaluating a patient with dysphagia,
structural causes (e.g., masses, infection, lymphadenopathy, food boluses) must first be excluded. After these have
been ruled out, the following physical examination maneuvers are recommended to evaluate for neurological
causes: bedside swallow test; examination of the uvula,
specifically looking for contralateral deviation (as CN 9
and 10 are affected in lateral medullary syndrome); hypoesthesia of the face from CN 7 (although this is higher in
the brainstem), loss of gag reflex, or tongue deviation to
suggest CN 12 involvement. With regards to the patient’s
dizziness, a more detailed gait test (looking for specifically wide-based gait) as well as Romberg test could
have differentiated a more concerning neurological cause
of dizziness from a more benign orthostatic cause secondary to dehydration. The HINTS examination (Head-Impulse, Nystagmus, Test-of-Skew) has gained significant
traction in both the emergency medicine and neurology
literature as a tool to aide in the diagnosis of posterior
strokes (19). The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric
gaze, or skew deviation have been proven to be highly
sensitive and specific for vertebrobasilar strokes (19).
Failure to perform the above testing during the initial
ED visits could have contributed to misdiagnosis, had
the CTA of the neck not been ordered for other diagnostic
purposes. If both dysphagia and a neurological deficit are

Figure 1. Diffusion-weighted imaging (left) and fluid-attenuated inversion recovery (right) magnetic resonance imaging of the
brain during hospitalization illustrating large-volume infarct in the left cerebellar hemisphere with extension into the posterolateral medulla.

Dysphagia as the Presenting Symptom in Lateral Medullary Syndrome

appreciated on examination, standard noncontrast CT imaging of the head should be obtained. Patients presenting
with acute symptoms should be considered for thrombolysis, if eligible. However, CT scans frequently miss acute
posterior strokes, and MRIs offer superior sensitivity
when compared with CT scans (3,8,20).
Diffusion-weighted imaging (DWI) can also aid in
early demonstration of infarction, if suspected (3).
Despite the superiority of MRI DWI, there is still a
considerable false-negative rate (anywhere from 6–12%
quoted in the literature) of acute-onset posterior circulation strokes missed on MRI (3,19,21). Selected patients
who present > 4.5 hours from when last seen well may
be candidates for thrombolysis on the basis of DWIfluid-attenuated inversion recovery mismatch on acute
MRI, although this is not the standard of care for tPA
and the decision should be made on a case-by-case basis
in conjunction with Neurology (22). We recommend that
patients with cerebrovascular risk factors who present
with dysphagia and objective cranial nerve impairment
receive urgent MRI despite a negative CT of the head if
the level of suspicion is high. Additionally, emergency
medicine providers can advocate for admission for
repeated imaging and frequent neurological examinations
despite initial negative imaging, if symptoms persist.
Posterior circulation strokes are diagnostically challenging to emergency medicine providers. They
frequently present with nonspecific symptoms common
in benign diagnoses. A detailed neurologic examination
should accompany any patient with cardiovascular risk
factors presenting with dysphagia to identify subtle
neurologic findings. If standard stroke imaging is negative and provider concern remains high, evaluation of
these patients may be further enhanced by early utilization of MRI. Overall, early diagnosis of posterior stroke
requires a high level of suspicion among emergency physicians.

WHY SHOULD AN EMERGENCY PHYSICIAN BE
AWARE OF THIS?
Although dysphagia frequently occurs in lateral medullary syndrome, it is rarely the presenting symptom in
the ED. In patients with cerebrovascular risk factors
who present with dysphagia, a complete neurological examination should be performed and noncontrast CT head
should be obtained if a neurological deficit is appreciated.
Due to their poor sensitivity, CT scans can frequently
miss posterior circulation strokes, therefore MRI should
be considered if provider suspicion remains high. Emergency providers are encouraged to have a high level of
suspicion for this rare but debilitating stroke syndrome
to avoid misdiagnosis and delayed care.

395

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