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J. M. Baratta
when rapid neurological decline leads to respiratory compromise. As with other
autoimmune diseases, Guillain–Barré syndrome predominantly affects females. It
is the most common paralytic neuropathy, estimated to affect 100,000 per year
across the globe [4]. The syndrome can be heterogeneous and further complicated
by disease variants, thereby raising the risk of misdiagnosis particularly in early
stages of the illness.
This case presents a man who was evaluated for acute neurological ndings.
Initial workup was most consistent with posterior circulation stroke, and management was initiated accordingly. It was not until the patient’s neurological status
decompensated that Guillain–Barré syndrome became a concern. Guillain–Barré
syndrome was conrmed with further neurological workup including lumbar puncture and electrodiagnostic studies.
Clinical Case Presentation
“A 53-year-old man presented with left-arm weakness, glossolalia, and right eyelid
droop for a duration of 3 h. He had a sore throat and stuffy nose 10 days earlier.
Other than having hypertension and gout, his medical history was unremarkable.
None of his family members had experienced similar symptoms. On admission, his
vital signs were normal, and his higher mental functions were appropriate for his
age. Neurological examination showed dysarthria, right eyelid droop, left facial
droop, and a left-held tongue. No nystagmus, ophthalmoplegia, ataxia, or hearing
loss was noticed. His muscle strength was 4/5in the left upper limb (in both the
proximal and distal muscles). There was no sensory function decit. Deep tendon
reexes were present and symmetrical. The results of coordination tests and gait
tests were normal, and plantar responses were normal bilaterally. The results of the
rest of his physical examination were normal. The results of his brain CT examination were normal. In summary, he was managed as having a posterior circulation
infarct. The patient and his family did not agree to intravenous thrombolysis because
of the risk of bleeding. Eight hours after he was admitted, his condition deteriorated,
with quadriplegia and bilateral peripheral facial palsy. Immediately, cranial magnetic resonance imaging (MRI) with magnetic resonance angiography was performed, but no abnormal manifestations were found. Cervical and thoracic spinal
MRI were also performed, and the results were normal. Because of his unremarkable neuroimaging results, Guillain–Barré became the primary working diagnosis.
The following day, he developed bilateral ophthalmoplegia, dysphagia, dyspnea,
and numbness in all extremities, and he underwent tracheotomy to prevent a worsening of his acute respiratory failure. Lumbar puncture was performed, and cerebrospinal uid (CSF) analysis showed that the protein level was 0.87 g/L (normal
values: 0.25–0.47g/L), while the white blood cell count was 5×106/L (normal
values: 0–8× 106/L). Anti-ganglioside antibody analysis of the serum and CSF
revealed high levels of anti-GQ1b. The blots for other anti-gangliosides (anti-GM1,
anti-GM2, anti-GM3, anti-GD1a, anti-GD1b, and anti-GT1b) were negative. Nerve
53 Guillain–Barré Syndrome Misdiagnosed asPosterior Circulation Stroke
conduction study (NCS) results showed that the amplitudes of the bilateral facial,
median, ulnar, and right peroneal (bular) motor nerves were reduced; the occurrence rates of the F wave in the left median nerve and ulnar nerve were reduced; the
F wave was absent in the right median nerve; and the rest of the testing revealed
normal results. Unfortunately, the H wave could not be detected in either leg due to
the limitations of the patient’s posture. According to the NCS results, mild to moderate damage to multiple motor nerves was considered. The patient received intravenous immunoglobulin (0.4kg/day) for 5 days. Three weeks after admission, at
discharge, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and
leg weakness had recovered almost completely, but his arms were still moderately
impaired, with a power of 4/5 (in both the proximal and the distal muscles). When
the patient was discharged, he no longer needed a ventilator and could breathe normally. The patient had to be own home, and due to safety concerns, the patient was
discharged with a tracheotomy. Fortunately, the patient recovered well without any
sequelae after two years of follow-up.” [5]
Case taken verbatim from source, which is open access: “Copyright © 2021 Sun,
Gao, Chi, Cao, Ning and Nan. This is an open-access article distributed under the
terms of the Creative Commons Attribution License (CC BY). The use, distribution
or reproduction in other forums is permitted, provided the original author(s) and
the copyright owner(s) are credited and that the original publication in this journal
is cited, in accordance with accepted academic practice. No use, distribution or
reproduction is permitted which does not comply with these terms.”
385
Differential Diagnosis
• Stroke
• Brain tumor
• Seizure
• Conversion disorder
• Complicated migraine
• Metabolic derangement
• Vestibular dysfunction
• Polyneuropathy
What WasMisdiagnosed inThis Case andWhy?
The patient in this case was diagnosed with a posterior circulation stroke after
appropriate initial workup which included general and neurological physical exam
and CT imaging of the head. The results of this initial evaluation were most consistent with stroke. It was not until the patient subsequently declined that an alternate
diagnosis of atypical Guillain–Barré syndrome became more apparent.
386
J. M. Baratta
Discussion
The heterogenous presentations Guillain–Barré syndrome and variant conditions
can lead to diagnostic challenges for clinicians. While the syndrome classically
presents with progressive, ascending accidity and loss of reexes, symptoms can
be variable particularly early in the disease process. Numerous disease variants further complicate the diagnosis. For example, the Miller–Fisher variant often presents
with prominent ophthalmoplegia in addition to limb ataxia and loss of deep tendon
reexes [6]. The pharyngeal-cervical-brachial variant can be seen with progressive
oropharyngeal and cervicobrachial weakness accompanied by upper extremity areexia [7].
Diagnosis of Guillain–Barre syndrome is made with careful history-taking and
examination. A history of progressive, ascending loss of strength and sensation
accompanied by diminished reexes is convincing [8]. Lumbar puncture should be
performed on all patients with suspected Guillain–Barre and typically demonstrates
albuminocytologic dissociation dened as an elevation of CSF protein without an
elevation in white blood cells [9]. Electrodiagnostic studies, including nerve conduction study and electromyography, can be helpful for diagnosis, often showing
delay of nerve transmission through an absent or reduced H response, F wave, and
abnormal upper extremity sensory nerve action potential combined with a normal
sural sensory nerve action potential [10].
Treatment is multipronged and frequently includes high-dose steroids, intravenous immunoglobulin, and plasmapheresis. Supportive care is necessary for those
with nutritional and respiratory deciencies, potentially involving provision of parenteral feeding and mechanical ventilation [11]. Mortality typically involves respiratory failure and is estimated at 3–10%. Symptoms typically peak at 4weeks after
disease onset and gradually remit with time. At 6months after disease onset, 20%
of patients are still unable to ambulate [12]. Pain, fatigue, and other functional
impairments may continue for months or years.
Conclusion
Guillain–Barré syndrome is the most common paralytic neuropathy globally. While
initial symptoms classically include ascending weakness and areexia, the presentation can be heterogeneous leading to diagnostic challenges. A thorough history
and physical examination along with frequent re-evaluation are critical for patients
presenting with acute neurological concerns. Appropriate diagnosis is necessary for
timely administration of immunomodulating treatments to minimize disease
progression.
53 Guillain–Barré Syndrome Misdiagnosed asPosterior Circulation Stroke
387
References
1. Shahrizaila N, et al. Guillain-Barré syndrome. Lancet (London, England).
2021;397(10280):1214–28. https://doi.org/10.1016/S0140- 6736(21)00517- 1.
2. Jasti AK, et al. Guillain-Barré syndrome: causes, immunopathogenic mechanisms and
treatment. Expert Rev Clin Immunol. 2016;12(11):1175–89. https://doi.org/10.108
0/1744666X.2016.1193006.
3. Caress JB, etal. COVID-19-associated Guillain-Barré syndrome: the early pandemic experience. Muscle Nerve. 2020;62(4):485–91. https://doi.org/10.1002/mus.27024.
4. Fujimura H.The Guillain-Barré syndrome. Handb Clin Neurol. 2013;115:383–402. https://
doi.org/10.1016/B978- 0- 444- 52902- 2.00021- 7.
5. Sun J, Gao Y, Chi L, Cao Q, Ning Z, Nan G.Case report: early-onset Guillain-Barre syndrome
mimicking stroke. Front Neurol. 2021;12:525699. https://doi.org/10.3389/fneur.2021.525699.
6. Al Othman B, etal. Update: the Miller Fisher variants of Guillain-Barré syndrome. Curr Opin
Ophthalmol. 2019;30(6):462–6. https://doi.org/10.1097/ICU.0000000000000611.
7. Wakerley BR, Yuki N. Pharyngeal-cervical-brachial variant of Guillain-Barre syndrome. J
Neurol Neurosurg Psychiat. 2014;85(3):339–44. https://doi.org/10.1136/jnnp- 2013- 305397.
8. Florian IA, et al. To be, or not to be… Guillain-Barré Syndrome. Autoimmun Rev.
2021;20(12):102983. https://doi.org/10.1016/j.autrev.2021.102983.
9. van den Berg B, etal. Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol. 2014;10(8):469–82. https://doi.org/10.1038/nrneurol.2014.121.
10. Gordon PH, Wilbourn AJ.Early electrodiagnostic ndings in Guillain-Barré syndrome. Arch
Neurol. 2001;58(6):913–7. https://doi.org/10.1001/archneur.58.6.913.
11. Liu S, et al. Immunotherapy of Guillain-Barré syndrome. Hum Vacc Immunotherapeut.
2018;14(11):2568–79. https://doi.org/10.1080/21645515.2018.1493415.
12. van Doorn PA. Diagnosis, treatment and prognosis of Guillain-Barré syndrome (GuillainBarre). Presse medicale (Paris, France : 1983). 2013;42(6 Pt 2):e193–201. https://doi.
org/10.1016/j.lpm.2013.02.328.
Chapter 54
Stroke Misdiagnosed asBenign Positional
Paroxysmal Vertigo
JohnMichaelBaratta
Introduction
Stroke is a leading cause of disability and death both in the United States and globally. Efcient and accurate evaluation of a person with suspected stroke is particularly important given the rapid destruction of neurons, lending to the saying “time is
brain.” [1] Newer interventions for stroke, including intravenous tissue-type plasminogen activator (IV tPA) and mechanical thrombectomy, can dramatically
improve mortality as well as neurological and functional outcomes.
In the United States, it is estimated that 800,000 people suffer a stroke annually,
with a total cost exceeding 40 billion dollars. Stroke is classically associated with
facial droop, arm or leg weakness, and speech difculties; however in many cases
stroke does not present typically. There are often nonspecic symptoms such as dizziness or transient numbness that increase the risk of misdiagnosis. In the United
States, it is estimated that there are up to 165,000 missed stroke diagnoses annually.
Inability to diagnose stroke in the emergency department may lead to failure of
acute intervention and secondary prevention therapy resulting in higher risk of mortality and morbidity. The risks of a missed stroke diagnosis are higher for younger,
female, and non-White patients [2, 3].
Most frequently error occurs in posterior circulation infarcts with presenting
symptoms such as nausea, headache, and dizziness. Identifying symptoms like these
that are not specic but accompanied by neurologic signs such as ataxia and Horner
syndrome will reduce the rate of misdiagnosis. Additional symptoms which can help
J. M. Baratta (*)
Department of Physical Medicine and Rehabilitation, Medical Director of Stroke
Rehabilitation, University of North Carolina School of Medicine, Chapel Hill, NC, USA
e-mail: john_baratta@med.unc.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_54
389
390
J. M. Baratta
with stroke identication include crossed motor sensory problems, oculomotor nerve
palsies, and visual eld defecits [2].
Initial presentation of stroke can be variable and can include arm or leg weakness, facial droop, slurred speech, gait instability, confusion, and headache. Due to
the complex nature of the central and peripheral nervous systems, stroke mimics are
a frequent concern. Stroke mimics can vary widely and include seizure, metabolic
derangement, complicated migraine, vestibular dysfunction, and polyneuropathy. A
thorough review of the history, physical examination, and diagnostic studies is critical to achieving the proper diagnosis and initiating appropriate, timely management. In this case, the 50-year-old patient checked himself into the emergency
department for a 3-week history of frequent episodes of gait imbalance, nausea,
blurred vision, and tinnitus.
Learning Objectives
By the end of this presentation, the clinician will be able to:
1. Articulate ideas about the signs and symptoms of case presentation in this
condition.
2. Discuss an alternative diagnosis of stroke.
3. Enumerate the various diagnostic techniques used in the investigation of this
condition.
4. Discuss why this condition is often misdiagnosed with presentation of its
symptoms.
Clinical Case Presentation
A 50-year-old male with a history of smoking and alcohol use presented to the
emergency department with recurring episodes of gait imbalance, nausea, blurred
vision, and tinnitus. Episodes had occurred for approximately 3 weeks, lasting for
several seconds to minutes, and resolved spontaneously. The patient underwent
thorough physical examination. A head computed tomography was done showing
normal ndings. He was discharged from the emergency department with a diagnosis of benign positional paroxysmal vertigo. Over the following weeks, his condition deteriorated instead of improving, with progressive development and worsening
of diplopia and dysgraphia. Repeat brain computed tomography demonstrated multiple bilateral cerebellar infarctions, and he was subsequently admitted to the hospital for further evaluation and management.
On hospital day 1, the patient developed left rapid phase nystagmus which progressed to rapid right phase and then bilateral nystagmus. He also had left-sided
dysmetria that became right-sided and then bilateral. He also expressed concerns
about dysgraphia. On hospital day 3, the patient developed dysarthria and later was
started on a statin and dual antiplatelet therapy containing aspirin and clopidogrel.
54 Stroke Misdiagnosed asBenign Positional Paroxysmal Vertigo
During the admission, he underwent carotid Doppler ultrasound and blood testing, including cholesterol, hemoglobin A1C, and autoimmunity labs, which were
unrevealing. A transesophageal echocardiogram was normal, ruling out a patent
foramen ovale and intracardiac thrombus. Computed tomography angiography ndings revealed bilateral vertebral artery (VA) occlusions. The patient underwent
interventional angiography for atheromatous stenosis greater than 50% at the right
V4 segment and VA ostium. Retrograde ow with total occlusion of the distal left
VA segment was noted. A vascular stent was placed in the right V4 segment with
30% of residual stenosis.
After the procedure, the patient’s status improved substantially. He was noted to
have substantial reductions in nystagmus and balance impairment. The patient
improved to the point that he could return to walking and performing activities of
daily living independently. He was discharged with dual antiplatelet therapy. After
1 year he had recovered well with minor residual effects of mild dysgraphia and
slowed cognition.
[Case source: Costa, Ana et al. “A Patient With (Initially) Non-Persistent
Vertigo - A Posterior Circulation Stroke Case.” Cureus vol. 14,1 e21468. 21 Jan.
2022, doi:10.7759/cureus.21468]
391
Differential Diagnosis
1. Benign paroxysmal positional vertigo
2. Brain tumor
3. Functional neurological disorder
4. Seizures
5. Migraine
What WasMisdiagnosed inThis Case andWhy?
The patient was diagnosed with a benign paroxysmal positional vertigo after initial
workup which included computed tomography head which was negative for stroke.
More sensitive imaging, such as magnetic resonance imaging brain, was not performed during the initial workup. Further diagnostic testing was completed when
the patient’s symptoms worsened over the following weeks. Interventional angiography demonstrated bilateral vertebral artery stenosis which had resulted in substantially reduced ow and was likely the source of thromboembolic events.
392
J. M. Baratta
Discussion
Stroke is a heterogeneous disease as well as a leading cause of death and disability
[4]. Depending on its etiology and location, acute stroke can present with a variety
of symptoms including arm or leg weakness, facial droop, slurred speech, gait instability, confusion, and headache [5]. The challenging nature of acute stroke presentations and numerous stroke mimics can lead even experienced clinicians to a
misdiagnosis [6].
Efcient and accurate evaluation is critical for optimal stroke management, as
key acute ischemic stroke interventions, such as intravenous tissue-type plasminogen activator and mechanical thrombectomy, are time-limited [7]. For this reason,
many medical centers have developed acute stroke management pathways to minimize wait times for patients with stroke-like symptoms to undergo critical components of the evaluation, such as head imaging and neurology consultation [8].
Implementation of acute stroke interventions can provide the patient a substantial
benet in acute survival rates and long-term neurological sequelae [9]. Evaluation
of patients with acute stroke-like symptoms should include emergent head imaging
[8]. This is most often done with computed tomography as it is faster and less
expensive to perform than other modalities but still sufcient to evaluate for a hemorrhagic event. It should be noted, however, that a negative head computed tomography in the acute phase does not rule out an acute ischemic event given the poor
sensitivity of this test in the acute phase of stroke [10]. In patients with unclear or
uctuating symptoms, magnetic resonance imaging or contrasted imaging modalities may be better able to determine the source of symptoms [11, 12]. In this case, it
was not until magnetic resonance imaging and angiography were performed that the
correct diagnosis of vertebral artery occlusion leading to posterior circulation stroke
was made.
Conclusion
Evaluation of people with stroke-like symptoms can pose diagnostic challenges due
to the heterogeneous nature of presentations. Initial workup should include head
imaging such as computed tomography; however it should be noted that negative
initial computed tomography should not rule out acute ischemic stroke. Other diagnostic imaging modalities, such as magnetic resonance imaging and angiography,
should be considered for further evaluation of patients with an initial negative workup.
54 Stroke Misdiagnosed asBenign Positional Paroxysmal Vertigo
393
References
1. Saver JL.Time is brain—quantied. Stroke. 2006;37(1):263–6.
2. Newman-Toker DE, Moy E, Valente E, Coffey R, Hines AL.Missed diagnosis of stroke in
the emergency department: a cross-sectional analysis of a large population-based sample.
Diagnosis (Berl). 2014;1(2):155–66. https://doi.org/10.1515/dx- 2013- 0038.
3. León Cejas L, Mazziotti J, Zinnerman A, Nofal P, Fernández Pardal M, Bonardo P,
Reisin R. Misdiagnosis of acute ischemic stroke in young patients. Medicina (B Aires).
2019;79(2):90–4.
4. Costa A, etal. A patient with (initially) non-persistent vertigo- a posterior circulation stroke
case. Cureus. 2022;14(1):e21468. https://doi.org/10.7759/cureus.21468.
5. Guzik A, Bushnell C.Stroke epidemiology and risk factor management. Cerebrovascular Disease
Continuum (Minn). 2017;23(1):15–39. https://doi.org/10.1212/CON.0000000000000416.
6. Pare JR, Kahn JH.Basic neuroanatomy and stroke syndromes. Emerg Med Clin North Am.
2012;30(3):601–15. https://doi.org/10.1016/j.emc.2012.05.004.
7. Buck B, etal. Stroke mimics: incidence, aetiology, clinical features and treatment. Ann Med.
2021;53(1):420–36. https://doi.org/10.1080/07853890.2021.1890205.
8. Powers WJ, etal. Guidelines for the early management of patients with acute ischemic stroke:
2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a
guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2019;50(12):e344–418. https://doi.org/10.1161/STR.0000000000000211
9. Herpich F, Rincon F. Management of acute ischemic stroke. Crit Care Med.
2020;48(11):1654–63. https://doi.org/10.1097/CCM.0000000000004597.
10. Hasan TF, etal. Overview of acute ischemic stroke evaluation and management. Biomedicine.
2021;9(10):1486. https://doi.org/10.3390/biomedicines9101486.
11. Smajlović D, Sinanović O.Sensitivity of the neuroimaging techniques in ischemic stroke. Med
Arh. 2004;58(5):282–4.
12. Simonsen CZ, etal. Which imaging approach should be used for stroke of unknown time of
onset? Stroke. 2021;52(1):373–80. https://doi.org/10.1161/STROKEAHA.120.032020.
Chapter 55
Primary Amoebic Meningoencephalitis
Misdiagnosed asPyogenic Meningitis
SathishVenugopal
Learning Objectives
By the end of this presentation, the clinician will be able to:
1. Demonstrate an appropriate understanding of the condition and its causative
organism.
2. Describe the conditions that present with a similar pattern as primary amoebic
meningoencephalitis.
3. Articulate the knowledge of symptomatology and proper history of the patient to
narrow down the diagnosis.
4. Discuss the course of disease, management techniques, and various treatment
modalities to help patients recover quickly.
5. Enumerate the various diagnostic techniques from laboratory tests done to techniques like next-generation sequencing and polymerase chain reaction.
Introduction
This disease was rst identied in 1899 caused by a protist pathogen called
Naegleria fowleri. It causes fatal infection of the central nervous system that has
acute phase infection and rapid progression. This condition arises when the organism, Naegleria fowleri, is accidentally introduced via nasal route. Through the crib-
riform plate, amoeba enters the central nervous system and advances along the
cribriform plate, following the olfactory nerve. Naegleria fowleri is a thermophile,
S. Venugopal (*)
St. Martinus University Faculty of Medicine, Willemstad, Curacao
e-mail: sathish.venugopal@martinus.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_55
395