Content uploaded by Pradip Bhattacharya
Author content
All content in this area was uploaded by Pradip Bhattacharya on Sep 16, 2021
Content may be subject to copyright.
Acta Scientific Neurology (ISSN: 2582-1121)
Volume 4 Issue 8 August 2021
Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report
Pushpanjali R Ojha1*, Mohd Saif Khan2, Pradip Kumar Bhattacharya3,
Aneesha Thomas4 and Kritika Raj5
1Assistant Professor (Pathology), Trauma Center, RIMS, Ranchi, Jharkhand, India
2Associate Professor, Department of Critical Care Medicine, RIMS, Jharkhand, India
3Professor and HOD, Department of Critical Care Medicine, Trauma Center, RIMS,
Jharkhand, India
4Assistant Professor, Department of Neurology, RIMS, Ranchi, India
5Junior Resident, Department of Anaesthesia, RIMS, Ranchi, India
*Corresponding Author: Pushpanjali R Ojha, Assistant Professor (Pathology),
Trauma Center, RIMS, Ranchi, Jharkhand, India.
Case Study
Received: July 08, 2021
Published: July 28, 2021
© All rights are reserved by Pushpanjali R
Ojha., et al.
Abstract
Background:
reported were stroke, GBS, ADEM and encephalitis. A rare case of sensory motor polyneuropathy (SMPN) in COVID 19 was reported
in our institute.
Methods: A COVID19 diseased patient without any previous neurological disorders was admitted and during the course of treatment
developed neurological complications. After complete radiological and pathological evaluation he was diagnosed as a case of SMPN
- a new manifestation of SARS - CoV2 infection.
Results: HRCT chest shows COVID 19 related ARDS, MRI (T2W) at D6-10 spines shows subtle patchy intramedullary high signal
intensity and Nerve conduction study revealed asymmetrical sensory-motor polyneuropathy. He had leucocytosis with neutrophilia,
lymphopenia, raised Neutrophil-lymphocyte ratio, D-Dimer and ferritin.
Conclusion: SMPN is relatively rare but acute manifestation of SARS-CoV2 infection which need immediate management and long
term follow up to diagnose chronic complication related with it.
Keywords: Guillain - Barre Syndrome; Sensory Motor Polyneuropathy; Nerve Conduction Study
Abbreviations
RT-PCR: Reverse Transcriptase Polymerase Chain Reaction; ARDS:
Acute Respiratory Distress Syndrome; HRCT: High Resolution
Computed Tomography; T2W MRI: T 2 Weighted Magnetic Reso-
nance Imaging; PT: Prothrombin Time; SGOT: Serum Glutamic
Oxalo-Acetic Transaminase; SGPT - Serum Glutamate Pyruvate
Transaminase; ALP: Alkaline Phosphatase; LDH: Lactate Dehydro-
genase; CMAP: Compound Muscle Action Potential
Introduction
SARS-CoV2 virus show neurotropism in addition to cytotropism
with cells of multiple organs. Several recent studies had reported
CNS manifestations that range from encephalitis, myelitis, radicu-
litis, plexitis, Guillan-Barrè syndrome (GBS), Acute disseminated
encephalomyelitis (ADEM) and sensory-motor polyneuropathy
case from east India, which was a diagnostic challenge and require
a multispecialty approach for management.
Citation: Pushpanjali R Ojha., et al. “Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report". Acta Scientific Neurology 4.8
(2021): 68-71.
Case History
A 27-year-old male admitted with fever for last 18 days with a
pre-admission diagnosis of Malaria. He was treated for the same
-
tive for SARS - CoV2 by RT-PCR. He had tachypnea with SpO2 of 92%
on room air, bilateral basal crepitation and hypertension He had
no associated complaints of anosmia, dysguesia or gastrointestinal
symptoms. He was known diabetic. HRCT chest shows features of
ARDS (Figure 1). His laboratory investigations showed leukocyto-
sis with neutrophilia (90%), lymphocytopenia (7%), Neutrophil
- Lymphocyte ratio of 12.86, platelets -1.57 lacs/cmm, D - Dimer
> 10000, PT - 17.8 sec, S. Urea - 52 mg/dl, Total Bilirubin - 7.35
mg/dl, Direct Bilirubin - 6.83 mg/dl, Total protein - 6.40gm/dl, S.
Albumin - 2.70 gm/dl, SGOT - 72 U/L, SGPT - 57 U/L, S. ALP - 379
U/L, S. LDH - 624 U/L, S. C-reactive protein - 138.05, S. Ferritin - >
mg/dl and HbA1C - 14.3%. Toxicology screening was negative. He
was managed and treated as per the COVID 19 management proto-
-
gen therapy, shows clinical improvement and became SARS- CoV2
negative on RT-PCR after 10 days of admission.
He developed gradually progressive profound bilateral lower
and right upper limb weakness and tremors within 20 days of
Figure 1: HRCT Chest - Bilateral lungs show ground-glass
opacities, a large consolidation with air bronchogram in left
inferior lingula along with left pleural effusion.
S. No. Name of drugs Dosage
1 Ramdesivir 200 mg stat i.v. followed by 100 mg
i.v. OD for 5 days
2 Enoxaparin sodium 60 mg s.c. injection OD
3 Regular Insulin 18 Units i.v. infusion
4 Insulin Glargine 16 Unit s.c. after dinner
5 Potassium chloride 1 ampule in 500 ml Normal saline
i.v. BD
6 Dexamethasone 60 mg i.v. OD
7 Meropenem loading dose of 2 gm followed by 1
gm i.v.TDS
8 VitaminC 1 gm i.v. BD
9 Tablet Ivermectin 6 mg BD for 7 days
10 Tablet Doxycycline 200 mg BD for 7 days
11 Tablet
N-Acetyl-Cysteine 600 mg TDS
12 Tablet Multivitamin 1 tab OD
Table 1: List of drugs administered to the patient.
which neurological consultation was advised. He had Glasgow
Coma Scale of E4V2M6, reduced tone, 3/5 power in both lower limbs,
absent knee and ankle jerk, plantar bilateral extensors and normal
neither facial or ocular muscles involvement nor bladder dysfunc-
tion. A differential diagnosis of ADEM or GBS was made and CSF ex-
amination, MRI brain, cervical and dorso-lumbar spine and Nerve
CSF examination shows mildly raised protein and three lympho-
cytes suggestive of albumino-cytological dissociation. MRI brain
-
verse myelitis (Figure 2). NCS from upper and lower limbs show
reduced motor nerve conduction velocities and CMAP’s over both
peroneals and prolonged latencies over both tibials. Sensory nerve
conduction velocities were reduced over both sural nerves with
prolonged latencies. F wave latencies were prolonged over-tested
nerves (Table 2). NCS suggested asymmetrical sensory-motor poly-
with Dexamethasone and IV Ig started with which clinical improve-
ment noted.
Discussion
SARS-CoV2 causes COVID 19 disease and most commonly pre-
sented with symptoms of ARDS, thromboembolic events or gastro-
intestinal dysfunctions. Recent studies report cases in which CNS
69
Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report
Citation: Pushpanjali R Ojha., et al. “Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report". Acta Scientific Neurology 4.8
(2021): 68-71.
one-third of patients with SARS-CoV-2 develop neurological mani-
festations [1]. The pathological spectrum of the disease include
encephalitis, plexitis, radiculitis, encephalopathy, ischemic stroke,
GBS, Multiple sclerosis, transverse myelitis and sensory-motor
polyneuropathy. SARS-CoV-2 attacks the olfactory bulb and then
affect the CNS through the olfactory tract in the early stages of in-
fection [2]. Neurological impairment and demyelinating reaction
appear as complications in case of severe COVID-19 [1].
Neurotropism may occur via trans-lamina cribrosa to reach the
brain through the olfactory tract [3]. The SARS -CoV2 spike pro-
tein binds with host ACE 2receptor, expressed in the CNS capillary
endothelium and allows the virus to penetrate the neuronal cells
[4]. Budding of Virus particle lead to the onset of symptoms such
as anosmia and dysguesia in the early phase of infection [1]. The
-
kine storm, and sustained neurological damage by delayed immune
response may be responsible for the activation of glial cells with
subsequent demyelination [5].
Zhao described a case report of GBS during SARS-CoV-2 infec-
tion [6]. GBS is an acute autoimmune fulminant demyelinating
70
Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report
Citation: Pushpanjali R Ojha., et al. “Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report". Acta Scientific Neurology 4.8
(2021): 68-71.
Upper limb
Nerve Side Site Distal latency
(mS) Duration (mS) Amp (mV) NCV
(m/s)
F wave mean latency
(mS)
Median
Right
Left Wrist 16.15 13.02 9.4 57.08
Elbow 18.96 11.46 6.2
Wrist 12.81 10.42 6.8 53.42
Elbow 17.08 10.00 6.9
Ulnar
right
left Wrist 15.94 13.75 4.6 50.10
Elbow 20.52 13.54 4.6
Wrist 14.38 12.08 3.4 50.10 49.7
Elbow 18.65 11.56 2.9
Lower limb
Nerve Side Site Distal latency (mS) Duration(mS) Amp (mV) NCV (m/s) F wave mean
latency (mS)
Peroneal
Right
Knee
Ankle 17.19 12.50 2.2 38.63 49.2
25.42 11.67 1.2
Left
Knee
Ankle 16.04 11.56 0.7 39.55 52.9
25.31 11.98 1.0
Tibial
Right
Knee
Ankle 18.96 12.50 5.7 50.10
28.02 12.92 5.5 46.30
Left
Knee
Ankle 18.75 12.50 5.2 45.71
27.50 12.50 5.8
Table 2: Results of nerve conduction study (Motor) of the patient.
Figure 2: MRI Dorso-lumbar spine - Subtle patchy
intramedullary high signal intensity on T2W seen at D 6 to D 10.
polyradiculopathy. It appears within 1-3 weeks of any viral infec-
disturbance is mildly involved, and autonomic involvement is com-
mon. The clinical presentations in our patient are not of typical
GBS, but a variant of GBS can be considered. We have limitations
the diagnosis of GBS. The recent studies had described less than
30 cases to date of GBS as CNS manifestation of COVID 19 disease;
however, the pathophysiology of the same is still not clear.
ADEM is a syndrome of multifocal demyelination, developing
weeks after an infection, presents generally with focal neurologi-
cal symptoms and often with encephalopathy. There are two cases
of ADEM reported to date. One have progressive dysphagia, dysar-
thria, and encephalopathy nine days after the onset of headache
and myalgia [7]. The other presented with seizures and reduced
consciousness and required intubation for respiratory failure [8].
Both patients had normal CSF and high signal intensities on MRI,
typical of acute disseminated encephalomyelitis. Both of them
show clinical improvement after treatment with IV Ig and steroids
respectively. Symptoms of our case resemble very similar to this;
hence we cannot exclude the possibility of the same.
In investigating patients with limb weakness and sensory
change, it is crucial to distinguish between the disease of the pe-
[9]. CSF examination, neurophysiological studies, and spinal imag-
ing are essential.
Conclusion
CNS manifestations in SARS - CoV2 infection is probably the re-
sult of direct cytolytic activity of virus itself or the indirect effect
of altered hemodynamic milieu secondary to cytokine storm that
result in acute CNS disorders, some of which are entirely reversible
whereas few of them may progress gradually in a dormant form
and reappear in future. Possibilities of psychomotor dysfunction
cannot be ruled out. Hence it will be suggested that these patients
must be followed up for several years at frequent intervals to as-
sess the long term effect of the virus.
Key Messages
Sensory motor polyneuropathy is an immediate COVID 19 asso-
ciated complication which will be completely reversible provided
diagnosed and treated as early as possible.
Acknowledgement
in the manuscript are mentioned below. We acknowledge the De-
partment of Neurology, Critical care medicine, Pathology, Radiol-
ogy and Laboratory Medicine for providing their support in the
diagnosis of disease. We also acknowledge the effortless work of
nursing staffs, technicians and physiotherapist in the management
of patient and due to their effort patient is recovering very fast.
Bibliography
1. Mao L., et al. “Neurologic manifestations of hospitalized pa-
tients with coronavirus disease 2019 in Wuhan, China”. JAMA
Neurology 77.6 (2020): 683-690.
2. Desforges M., et al. “Human coronaviruses and other respira-
tory viruses: underestimated opportunistic pathogens of the
central nervous system?” Viruses 12.1 (2019): 14.
3. Baig AM., et al. “Evidence of the COVID-19 virus targeting the
CNS: tissue distribution, host-virus interaction, and proposed
neurotropic mechanisms”. ACS Chemical Neuroscience 11.7
(2020): 995-998.
4. Wrapp D., et al. “Cryo-EM structure of the 2019-nCoV spike in
the prefusion conformation”. Science 367.6483 (2020): 1260-
1263.
5. Mehta P., et al. “COVID-19: consider cytokine storm syndromes
and immunosuppression”. Lancet 395.10229 (2020): 1033-
1034.
6. Zhao H., et al. “Guillain-Barrè syndrome associated with SARS-
CoV-2 infection: causality or coincidence?” Lancet Neurology
19.5 (2020): 383-384.
7. Zhang T., et al. “COVID-19-associated acute disseminated en-
cephalomyelitis: a case report”. MedRxiv (2020).
8. Zanin L., et al. “SARS-CoV-2 can induce brain and spine demy-
elinating lesions”. Acta Neurochirurgica (2020).
9.
paralysis”. Current Opinion in Infectious Diseases 16 (2003):
375-381.
Volume 4 Issue 8 August 2021
© All rights are reserved by Pushpanjali R Ojha., et al.
71
Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report
Citation: Pushpanjali R Ojha., et al. “Sensory Motor Polyneuropathy in a COVID 19 Patient: An Interesting Case Report". Acta Scientific Neurology 4.8
(2021): 68-71.