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Case Report

A case of COVID-19 with multiple cranial neuropathies

Bhanu GogiaDepartment of Neurology, University of Texas Medical Branch, Galveston, Texas, USACorrespondencebhgogia@utmb.edu
,
Andrea Gil GuevaraDepartment of Neurology, University of Texas Medical Branch, Galveston, Texas, USA
,
Prashant K. RaiDepartment of Neurology, University of Texas Medical Branch, Galveston, Texas, USA
&
Xiang FangDepartment of Neurology, University of Texas Medical Branch, Galveston, Texas, USA
Received 25 Jul 2020
Accepted 10 Nov 2020
Accepted author version posted online: 29 Dec 2020
Published online: 30 Dec 2020

Case Report

A case of COVID-19 with multiple cranial neuropathies

Abstract

Abstract

Various neurological manifestations involving the central and peripheral nervous system have been reported in association with COVID-19. Most common associations reported are encephalopathy, headache, ischemic, hemorrhagic stroke and transient ischemic attack, Miller Fisher syndrome, cranial neuropathies and Guillain-Barre syndrome. Of the cranial neuropathies, anosmia, and dysgeusia are the most common reported symptoms. This is a case of COVID-19 with ipsilateral fifth and seventh cranial nerve involvement with complete resolution of symptoms over a period of 3 weeks. The neurological symptoms started within 5 days of respiratory symptoms. We conclude that isolated cranial neuropathies can be the manifestations of SARS-CoV-2 infection.

Introduction

With the continued surge in the COVID-19 across the world in the past several months, various neurological symptoms in association with COVID-19 have emerged. Amongst the long list of manifesting symptoms of COVID, loss of smell and taste sensation has been one of the commonly associated symptoms (86% and 84%) per a European study. During the initial phase of the pandemic, studies from Wuhan and Spain reported neurological involvement in about 36.4% and 57.4% of the patients respectively [1,2]. With growing literature in regards to SARS-CoV-19, there is a wide spectrum of neurological manifestations of COVID-19 involving both CNS and peripheral nervous system (PNS). Some of the possible mechanisms reported are neurotropism towards angiotensinogen converting enzyme (ACE2) receptors present in the central nervous system (CNS), autoimmunity, and cytokine storm and hypercoagulable state [3–6]. The common neurological manifestations include encephalopathy, headache, ischemic, hemorrhagic stroke and transient ischemic attack, Miller Fisher syndrome (MFS), cranial neuropathies and Guillain-Barre syndrome (GBS) [7–11]. Cerebrospinal fluid (CSF) analysis in patients with MFS or GBS showed elevated protein, whereas, in other patients, CSF has reportedly been normal [11]. As per the authors’ knowledge, there are a few reported cases of cranial nerve (CN) involvement in cases with suspected Guillain Barre syndrome or Miller fisher variant, and a case report of Bell’s palsy with COVID-19 [8–14]. However, no case of multiple cranial neuropathies is reported in a COVID patient We hereby report the very first case of COVID-19 with ipsilateral fifth and seventh CN involvement with complete resolution of symptoms over a period of 3 weeks.

Case description

The patient is a 58-year-old Caucasian male right-handed with a past medical history of chronic obstructive pulmonary disease, hypertension, non-obstructive coronary artery disease, facial trauma with no residual deficits or pain, who presented to our hospital with chest pain at the beginning of June 2020. The patient also had nausea, vomiting, shortness of breath, abdominal pain, and fever that started 5 days before the admission. Notably, the patient was tested positive for SARS-CoV-2 at an outside institution and then transferred to our hospital for a higher level of care. Twelve hours prior to the arrival the patient reported a new onset left-sided facial numbness for which neurology was consulted. Additionally, he reported dribbling through the left side of the face and mild dysphagia. Otherwise, the patient denied any other neurological symptoms such as new weakness, numbness in arms, legs, difficulty speaking, dysphagia, and diplopia. Vital signs were significant for an elevated temperature of 103.8 F, blood pressure was within normal limit, pulse in the range between 97 and 110 and oxygen saturation SpO2 > 90 in room air. The neurological examination confirmed the decreased sensation in V1-V3 distribution (cranial nerve V) and lower motor neuron type of facial palsy (cranial nerve 7) on the left side but no diminished gag reflex or objective evidence of CN IX and X involvement. Laboratory tests revealed a positive PCR test for SARS-CoV-2, D-Dimer: 0.31 µg/ml, WBC 2.65 * 103/µL, Hgb 16.4 g/dL, basal metabolic profile within normal limit, lactate dehydrogenase (LDH) 1654 U/L, C reactive protein 6.4 mg/dl; ferritin 990 ng/ml, ALT/AST: 107/179 U/L and troponin was negative. Magnetic resonance images (MRI) of the brain demonstrated no acute intracranial findings, such as acute ischemia, intracranial hemorrhage, or mass effect. No significant abnormality identified along the course of the trigeminal and 7th/8th nerve complexes (Figure 1(A–D)). Unfortunately, the patient refused a lumbar puncture. Following a clinical impression of an acute peripheral 7th nerve palsy secondary to a viral infection, the patient received a course of valacyclovir 1 gram three times a day for 7 days total with improvement. Of note, for his COVID due to a decline in his respiratory status, the patient was started on Remdesivir for five days followed by convalescent plasma, and dexamethasone.

Figure 1. A–D: shows normal MR images T2 FLAIR (A-B) and T1 + C (C–D) without any abnormal enhancement or hyperintensity noted in the supratentorial as well as in the brainstem region.

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Discussion

To date, there are several published articles on neurological associations of COVID-19. The manifestations are classified based on central versus peripheral nervous system involvement. The most common presentation of CNS involvement remains encephalopathy 69% [12,15], followed by cerebrovascular events. Of the CN, anosmia, and dysgeusia have been the most common reported symptoms with the proposed mechanism being neurotropism [7]. Gutiérrez-Ortiz et al, have described two patients with MFS and polyneuritis cranialis and others have reported GBS with bilateral CN VII involvement in the presence of GD1b antibodies [9–13]. To the authors’ knowledge, at the time of writing this manuscript, there was a single case report of facial paresis in a COVID-19 patient [14]. This is the first case of multiple cranial neuropathies (ipsilateral V and VII and possibly cranial nerve) in a patient with COVID-19 without any clinical suspicion for acute peripheral neuropathies such as Guillain Barre and its variants.

The patient described in this article only presented with unilateral facial and trigeminal nerve involvement, with no ataxia, ophthalmoplegia, weakness, and intact reflexes. The symptoms started after around five days after the onset of respiratory symptoms. Unlike other cases in the literature where CSF analysis showed elevated protein in cases of GBS or MFS, a lumbar puncture was not pursued as there was no clinical suspicion for GBS and its variants and the patient refused. MRI brain with contrast was completely unremarkable with no evidence of enhancement of the involved cranial nerves. Following a seven-day course of prednisone and valacyclovir, there was complete resolution of symptoms over 3 weeks, hence, IVIG was not considered.

From the existing literature, it is evident that a large proportion of COVID-19 patients exhibit neurological manifestations likely due to predilection of the coronavirus to the central nervous system [16]. Activation of peripheral trigeminal nerve endings by SARS-CoV2 directly or indirectly has also been postulated [17, 18]. Our patient developed symptoms within 5 days of onset of respiratory symptoms. From this case and the other cases in the literature, it can be postulated that the isolated cranial neuropathies can also be the manifestations of SARS-CoV-2 infection especially with the brainstem being a part of proposed route for viral entry as described in one study [19]. The natural history of the disease suggests that 80% of the patients with COVID-19 infection recover spontaneously, therefore it remains unclear if a course of prednisone and valacyclovir given in our patient had any contribution in the resolution of the symptoms. The patient did have respiratory complications from COVID-19 infection and was monitored in the hospital for 6 weeks with no further neurological complications.

Conclusion

We can conclude that isolated cranial neuropathies in patients with COVID-19 infection should be carefully followed through with serial neurological examinations, neuroimaging, CSF analysis, neurophysiologic testing, and possible biopsy to understand the pathogenesis of this virus. Patients with these symptoms should be monitored carefully since subtle initial neurological deficits could be a predictor of further CNS/PNS involvement.

Disclosure statement

None of the authors have any conflicts of interest.

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