COVID-19-associated myelitis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Musadiq Ali M.B.B.S.[2] Tayebah Chaudhry[3]
Synonyms and keywords:
Overview
In the current pandemic state, COVID-19 should be considered as a differential diagnosis in a patient presenting with acute myelitis. Acute Transverse Myelitis is a neurological condition characterized by inflammation and injury of the spinal cord. In a confirmed or newly diagnosed patient of COVID-19, it is thought to be either a direct consequence of viral infection or a sequalae of autoimmune-mediated response. COVID-19-associated myelitis is diagnosed based on the hallmark symptoms of acute myelitis and confirmed with changes on spinal MRI, after ruling out other possible etiologies of myelitis. The symptoms show marked improvement after treatment with steroids and plasma exchange.
Historical Perspective
- First case of acute myelitis as a COVID-19 complication was reported in February 2020 in Wuhan by Kang Zhao et al, in a 66 year old male patient. [1]
- The second case was reported in Boston by Sarma et al in a 28 year old female patient who developed acute myelitis 7 days after symptoms of upper respiratory tract infection. [2]
- As of now, only few case reports have been published in literature showing an association of COVID-19 with acute myelitis as a neurological complication.
Classification
- There is no established system for the classification of COVID-19-associated myelitis.
Pathophysiology
- The pathogenesis of the disease behind this manifestation is not fully understood yet.
- There is a strong evidence suggesting that COVID-19 virus uses angiotensin-converting enzyme2 (ACE2) as its receptor to interact with host cells.
- This evidence is based on the previous extensive SARS-CoV structural analyses that showed interactions between the SARS-CoV virus and ACE2 receptors and because of the marked sequence similarities between Covid-19 and the SARS-CoV virus it is hypothesized that COVID 19 virus pathogenesis is comparable.
- The ACE2 receptors are expressed on alveolar epithelial cells, intestinal enterocytes and arterial and venous endothelial cells.
- The brain only the vascular cells were expressing ACE2 as a cell receptor not the neurons; yet this could be a potential mechanism for dissemination of the virus into the brain by the blood circulation[3].
- It is also hypothesized that the virus can disseminate into the nervous system through the olfactory bulb in which sensory neurons connect the nasal cavity to the central nervous system by the axons, which terminate in the olfactory bulb and passes through the cribriform plate[4].
- Early‐phase COVID‐19‐affected patients who exhibit loss of smell and taste[5].
- Advanced stages of the disease the neurological signs and symptoms observed in the COVID‐19 cases could be due to the effects of hypoxia, respiratory, and metabolic acidosis[6].
Causes
Apart from COVID-19 other causes of viral myelitis include[7]:
- Herpes viruses, including the one that causes shingles and chickenpox (zoster)
- Cytomegalovirus
- Epstein-Barr
- HIV
- Enteroviruses such as poliovirus and coxsackievirus
- West Nile
- Echovirus
- Zika
- Influenza
- Hepatitis B
- Mumps, measles and rubella
Other causes of myelitis are:
- Bacterial myelitis
- Fungal myelitis
- Parasitic myelitis
- Multiple Sclerosis
- Transverse Myelitis
- Autoimmune disorders like SLE and Sjogren’s Syndrome
- Sarcoidosis
- Vaccinations
Differentiating COVID-19-associated myelitis from other Diseases
COVID-19-associated myelitis must be differentiated from other diseases that may cause hypotonia, muscle weakness, or paralysis:[8][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]
| Diseases | History and Physical | Diagnostic tests | Other Findings | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Motor Deficit | Sensory deficit | Cranial nerve Involvement | Autonomic dysfunction | Proximal/Distal/Generalized | Ascending/Descending/Systemic | Unilateral (UL)
or Bilateral (BL) or No Lateralization (NL) |
Onset | Lab or Imaging Findings | Specific test | ||
| Transverse myelitis | + | + | + | + | Proximal > Distal | Systemic | BL or UL | Sudden | MRI & Lumbar puncture | MRI | History of chronic viral or autoimmune disease (e.g. HIV) |
| Adult Botulism | + | - | + | + | Generalized | Descending | BL | Sudden | Toxin test | Blood, Wound, or Stool culture | Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis |
| Infant Botulism | + | - | + | + | Generalized | Descending | BL | Sudden | Toxin test | Blood, Wound, or Stool culture | Flaccid paralysis (Floppy baby syndrome), possible respiratory paralysis |
| Guillian-Barre syndrome[24] | + | - | - | - | Generalized | Ascending | BL | Insidious | CSF: ↑Protein
↓Cells |
Clinical & Lumbar Puncture | Progressive ascending paralysis following infection, possible respiratory paralysis |
| Eaton Lambert syndrome[25] | + | - | + | + | Generalized | Systemic | BL | Intermittent | EMG, repetitive nerve stimulation test (RNS) | Voltage gated calcium channel (VGCC) antibody | Diplopia, ptosis, improves with movement (as the day progresses) |
| Myasthenia gravis[26] | + | - | + | + | Generalized | Systemic | BL | Intermittent | EMG, Edrophonium test | Ach receptor antibody | Diplopia, ptosis, worsening with movement (as the day progresses) |
| Electrolyte disturbance[27] | + | + | - | - | Generalized | Systemic | BL | Insidious | Electrolyte panel | ↓Ca++, ↓Mg++, ↓K+ | Possible arrhythmia |
| Organophosphate toxicity[28] | + | + | - | + | Generalized | Ascending | BL | Sudden | Clinical diagnosis: physical exam & history | Clinical suspicion confirmed with RBC AchE activity | History of exposure to insecticide or living in farming environment. with : Diarrhea, Urination, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating |
| Tick paralysis (Dermacentor tick)[29] | + | - | - | - | Generalized | Ascending | BL | Insidious | Clinical diagnosis: physical exam & history | - | History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area) |
| Tetrodotoxin poisoning[30] | + | - | + | + | Generalized | Systemic | BL | Sudden | Clinical diagnosis: physical exam & dietary history | - | History of consumption of puffer fish species. |
| Stroke[31] | +/- | +/- | +/- | +/- | Generalized | Systemic | UL | Sudden | MRI +ve for ischemia or hemorrhage | MRI | Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation. |
| Poliomyelitis[32] | + | + | + | +/- | Proximal > Distal | Systemic | BL or UL | Sudden | PCR of CSF | Asymmetric paralysis following a flu-like syndrome. | |
| Neurosyphilis[33][23] | + | + | - | +/- | Generalized | Systemic | BL | Insidious | MRI & Lumbar puncture | CSF VDRL-specifc | History of unprotected sex or multiple sexual partners.
History of genital ulcer (chancre), diffuse maculopapular rash. |
| Muscular dystrophy[35] | + | - | - | - | Proximal > Distal | Systemic | BL | Insidious | Genetic testing | Muscle biopsy | Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. Gower sign positive. |
| Multiple sclerosis exacerbation[36] | + | + | + | + | Generalized | Systemic | NL | Sudden | ↑CSF IgG levels
(monoclonal) |
Clinical assessment and MRI [37] | Blurry vision, urinary incontinence, fatigue |
| Amyotrophic lateral sclerosis[38] | + | - | - | - | Generalized | Systemic | BL | Insidious | Normal LP (to rule out DDx) | MRI & LP | Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity). |
| Inflammatory myopathy[39] | + | - | - | - | Proximal > Distal | Systemic | UL or BL | Insidious | Elevated CK & Aldolase | Muscle biopsy | Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations. |
To view the differential diagnosis of COVID-19, click here.
Epidemiology and Demographics
- As of now, the incidence of acute myelitis associated with Covid-19 infection in unknown. [40][41]
- To view epidemiology and demographics for COVID-19, click here.
Risk Factors
- There are no established risk factors for COVID-19-associated myelitis. However, since this condition is a direct consequence of infection by the novel coronavirus, risk factors for COVID-19 should be considered.
- To view the risk factors of COVID-19, click here.
Screening
- Screening for COVID-19-associated myelitis is not currently done.
- To view screening for COVID-19, click here.
Natural History, Complications, and Prognosis
Natural History
- Myelitis associated with COVID-19 is an acute condition. The first case of COVID-19 associated myelitis developed the symptoms 5 days after the onset of fever. [1]The second case developed symptoms of myelitis 7 days after the upper respiratory symptoms. [2]
Complications
- Lack of prompt recognition and management may result in lasting neurological complications (such as residual loss of sensation in lower extremities) after novel corona virus infection. [2]
Prognosis
- Exact prognosis of COVID-19-associated myelitis is not known.
- Marked improvement in symptoms is seen with steroids and plasma exchange.
Diagnosis
Diagnostic Study of Choice
- Diagnosis of COVID-19-associated myelitis is based on the hallmark symptoms of acute myelitis in a known case of COVID-19 or a positive PCR nasal swab for COVID-19 in a new patient. And classic contrast-enhancing lesions on MRI spine.
- Hallmark symptoms of acute myelitis include bilateral symmetric weakness and sensory changes in extremities, urinary retention and lower back pain.
- Absence of visual symptoms such as eye pain or vision loss ( classically seen in Multiple Sclerosis or Neuromyelitis optica), negative immunoglobulin G auto-antibodies or oligoclonal bands, negative anti-nuclear antibody (ANA) test (very sensitive test for autoimmune diseases such as lupus), absence of other system involvement (such as skin rash, nodules, cardiac arrhythmias or arthritis seen in lupus or sarcoidosis) rule out other possible etiologies. [40]
History and Symptoms
Symptoms of COVID-19-associated myelitis include:
- Urinary retention [40]
- Lower back pain [2]
- Weakness in lower extremities [40]
- Paresthesias in lower extremities with possible ascension to upper extremities [2]
- Numbness in lower extremities with possible ascension to upper extremities[2]
- Numbness in tip of tongue [2]
Physical Examination
Vitals:
Abnormal vitals can be seen due to COVID-19 association. These include:
- Decreased O2 saturation
- Tachycardia
- Tachypnea
Abdominal exam:
- Palpable distended bladder
Neurological exam:
Neurological findings are symmetric and more severe in lower extremities. [1] [2] [40]
- Wide based gait
- Decreased muscle strength
- Decreased sensation
- Decreased proprioception
- Hyporeflexia
- Paresthesias
- Positive Lhermitte's sign
- Positive Babinski's sign bilaterally.
Laboratory Findings
Nasal swab:
Other Viral Screening:
- Viral PCR screening including Adenovirus, Herpes Simplex Virus (Type 1&2), Epstein Barr Virus, Cytomegalovirus, Human Immunodeficiency Virus (HIV) will yield negative results.
- Viral serology for Influenza Virus A and B, Parainfluenza 1-4, Respiratory Syncytial virus, Enterovirus and Rhinovirus with negative results.
- Negative antibody results for bacteria such as Chlamydia Pneumoniae, Bordetella Pertussis, Mycoplasma Pneumoniae and Borrelia.
MRI spine:
- MRI findings consistent with Acute Transverse Myelitis (involving more than three spinal cord segments) are seen. This includes widespread elongated signal changes throughout the gray matter of spinal cord, with no disc pathology or spinal canal narrowing. [2]
Urinary retention:
- Foley catheter insertion will show and relieve retained urine.
Lumbar Puncture (LP):
- CSF analysis may show lymphocytic pleocytosis and elevated protein level. [42]
To view the laboratory findings on COVID-19, click here
Electrocardiogram
- There are no ECG findings associated with COVID-19-associated myelitis.
- To view the electrocardiogram findings on COVID-19, click here.
X-ray
- Chest X-ray may or may not show opacities in lungs depending on the degree of lung damage caused by COVID-19.
- To view the x-ray finidings on COVID-19, click here.
Echocardiography or Ultrasound
- There are no echocardiography findings associated with COVID-19-associated myelitis.
- Abdominal ultrasound may show bladder distension due to urinary retention.
- To view the echocardiographic findings on COVID-19, click here.
CT scan
- CT scan exclude other causes that can cause myelitis.
- To view the CT scan findings on COVID-19, click here.
MRI
- MRI may be used to exclude other causes.
- MRI findings consistent with Acute Transverse Myelitis (involving more than three spinal cord segments) are seen.
- This includes widespread elongated signal changes throughout the gray matter of spinal cord, with no disc pathology or spinal canal narrowing.
- T2-weighted fast spin-echo and short-tau inversion recovery (STIR) are the best sequences to view the spinal cord lesions[43].
- To view other imaging findings on COVID-19, click here.
Treatment
Medical Therapy
- Oxygen inhalation treatment with high-flow nasal catheters.
- Ganciclovir ( 0.5g once daily) for 14 days, Lopinavir/ritonavir (500mg twice daily) for 5 days. "Coronavirus Disease 2019 (COVID-19) Treatment Guidelines".
- Moxifloxacin (400mg once daily) for 6 days.(Treatment with arbidol and moxifloxacin could be helpful in reducing viral load and inflammation during SARS-CoV2 infection, especially for negatively regulating fatal inflammation in severe COVID-19 patients)[44].
- Glutathione (1.8g once daily) for 14 days. (Glutathione inhibits replication of various viruses at different stages of the viral life cycle and decreasing viral load. It also prevents the massive release of inflammatory cells into the lung “cytokine storm”)[45].
- Dexamethasone (10mg once daily) for 10 days[46]. (NIH COVID-19 Treatment Guidelines Panel recommends using dexamethasone (at a dose of 6 mg per day for up to 10 days) in patients with COVID-19 who are mechanically ventilated and in patients with COVID-19 who require supplemental oxygen but who are not mechanically ventilated. And recommends against using dexamethasone in patients with COVID-19 who do not require supplemental oxygen.
- Human immunoglobulin (15g once daily) for 7 days.
- Pantoprazole (80mg once daily) for 10 days.
- Mecobalamin (1000ug once daily) for 14days.[47] (Vitamin B12 may inhibit RNA-dependent-RNA polymerase activity of nsp12 protein from the COVID-19 Virus).
- Plasma exchange.
- Foley's catheter to relieve urinary retention
Surgery
- Surgical intervention is not recommended for the management of COVID-19-associated myelitis.
Primary Prevention
- Effective measures for the primary prevention of COVID-19-associated myelitis are the same as of COVID-19.
Secondary Prevention
- Effective measures for the secondary prevention of COVID-19-associated myelitis are the same as of COVID-19.
References
- ↑ 1.0 1.1 1.2 "www.medrxiv.org" (PDF).
- ↑ Manji H, Carr AS, Brownlee WJ, Lunn MP (2020). "Neurology in the time of COVID-19". J Neurol Neurosurg Psychiatry. 91 (6): 568–570. doi:10.1136/jnnp-2020-323414. PMID 32312872 Check
|pmid=value (help). - ↑ Wan Y, Shang J, Graham R, Baric RS, Li F (2020). "Receptor Recognition by the Novel Coronavirus from Wuhan: an Analysis Based on Decade-Long Structural Studies of SARS Coronavirus". J Virol. 94 (7). doi:10.1128/JVI.00127-20. PMC 7081895 Check
|pmc=value (help). PMID 31996437. - ↑ Baig AM (2020). "Neurological manifestations in COVID-19 caused by SARS-CoV-2". CNS Neurosci Ther. 26 (5): 499–501. doi:10.1111/cns.13372. PMC 7163592 Check
|pmc=value (help). PMID 32266761 Check|pmid=value (help). - ↑ Pastor Bandeira, Isabelle; Machado Schlindwein, Marco Antônio; Breis, Leticia Caroline; Schatzmann Peron, Jean Pierre; Magno Gonçalves, Marcus Vinicius (2020). doi:10.20944/preprints202004.0304.v1. Missing or empty
|title=(help) - ↑ Pekcevik Y, Mitchell CH, Mealy MA, Orman G, Lee IH, Newsome SD; et al. (2016). "Differentiating neuromyelitis optica from other causes of longitudinally extensive transverse myelitis on spinal magnetic resonance imaging". Mult Scler. 22 (3): 302–11. doi:10.1177/1352458515591069. PMC 4797654. PMID 26209588.
- ↑ 8.0 8.1 Kira R (February 2018). "[Acute Flaccid Myelitis]". Brain Nerve (in Japanese). 70 (2): 99–112. doi:10.11477/mf.1416200962. PMID 29433111.
- ↑ Hopkins SE (November 2017). "Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations". Curr Treat Options Neurol. 19 (12): 48. doi:10.1007/s11940-017-0480-3. PMID 29181601.
- ↑ Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR (September 2016). "Acute flaccid myelitis: A clinical review of US cases 2012-2015". Ann. Neurol. 80 (3): 326–38. doi:10.1002/ana.24730. PMC 5098271. PMID 27422805.
- ↑ Chong PF, Kira R, Mori H, Okumura A, Torisu H, Yasumoto S, Shimizu H, Fujimoto T, Hanaoka N, Kusunoki S, Takahashi T, Oishi K, Tanaka-Taya K (February 2018). "Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015". Clin. Infect. Dis. 66 (5): 653–664. doi:10.1093/cid/cix860. PMC 5850449. PMID 29028962.
- ↑ Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters H, Tyler KL, Abzug MJ, Dominguez SR (August 2018). "Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality". Lancet Infect Dis. 18 (8): e239–e247. doi:10.1016/S1473-3099(18)30094-X. PMID 29482893. Vancouver style error: initials (help)
- ↑ Chen IJ, Hu SC, Hung KL, Lo CW (September 2018). "Acute flaccid myelitis associated with enterovirus D68 infection: A case report". Medicine (Baltimore). 97 (36): e11831. doi:10.1097/MD.0000000000011831. PMC 6133480. PMID 30200066.
- ↑ "Botulism | Botulism | CDC".
- ↑ McCroskey LM, Hatheway CL (May 1988). "Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract". J. Clin. Microbiol. 26 (5): 1052–4. PMC 266519. PMID 3290234.
- ↑ Lindström M, Korkeala H (April 2006). "Laboratory diagnostics of botulism". Clin. Microbiol. Rev. 19 (2): 298–314. doi:10.1128/CMR.19.2.298-314.2006. PMC 1471988. PMID 16614251.
- ↑ Brook I (2006). "Botulism: the challenge of diagnosis and treatment". Rev Neurol Dis. 3 (4): 182–9. PMID 17224901.
- ↑ Dimachkie MM, Barohn RJ (May 2013). "Guillain-Barré syndrome and variants". Neurol Clin. 31 (2): 491–510. doi:10.1016/j.ncl.2013.01.005. PMC 3939842. PMID 23642721.
- ↑ Walling AD, Dickson G (February 2013). "Guillain-Barré syndrome". Am Fam Physician. 87 (3): 191–7. PMID 23418763.
- ↑ Gilhus NE (2011). "Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy". Autoimmune Dis. 2011: 973808. doi:10.4061/2011/973808. PMC 3182560. PMID 21969911.
- ↑ Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA (May 2004). "Transverse Myelitis: pathogenesis, diagnosis and treatment". Front. Biosci. 9: 1483–99. PMID 14977560.
- ↑ Amato AA, Greenberg SA (December 2013). "Inflammatory myopathies". Continuum (Minneap Minn). 19 (6 Muscle Disease): 1615–33. doi:10.1212/01.CON.0000440662.26427.bd. PMID 24305450.
- ↑ 23.0 23.1 Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
- ↑ Talukder RK, Sutradhar SR, Rahman KM, Uddin MJ, Akhter H (2011). "Guillian-Barre syndrome". Mymensingh Med J. 20 (4): 748–56. PMID 22081202.
- ↑ Merino-Ramírez MÁ, Bolton CF (2016). "Review of the Diagnostic Challenges of Lambert-Eaton Syndrome Revealed Through Three Case Reports". Can J Neurol Sci. 43 (5): 635–47. doi:10.1017/cjn.2016.268. PMID 27412406.
- ↑ Gilhus NE (2016). "Myasthenia Gravis". N Engl J Med. 375 (26): 2570–2581. doi:10.1056/NEJMra1602678. PMID 28029925.
- ↑ Ozono K (2016). "[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]". Clin Calcium. 26 (2): 215–22. doi:CliCa1602215222 Check
|doi=value (help). PMID 26813501. - ↑ Kamanyire R, Karalliedde L (2004). "Organophosphate toxicity and occupational exposure". Occup Med (Lond). 54 (2): 69–75. PMID 15020723.
- ↑ Pecina CA (2012). "Tick paralysis". Semin Neurol. 32 (5): 531–2. doi:10.1055/s-0033-1334474. PMID 23677663.
- ↑ Bane V, Lehane M, Dikshit M, O'Riordan A, Furey A (2014). "Tetrodotoxin: chemistry, toxicity, source, distribution and detection". Toxins (Basel). 6 (2): 693–755. doi:10.3390/toxins6020693. PMC 3942760. PMID 24566728.
- ↑ Kuntzer T, Hirt L, Bogousslavsky J (1996). "[Neuromuscular involvement and cerebrovascular accidents]". Rev Med Suisse Romande. 116 (8): 605–9. PMID 8848683.
- ↑ Laffont I, Julia M, Tiffreau V, Yelnik A, Herisson C, Pelissier J (2010). "Aging and sequelae of poliomyelitis". Ann Phys Rehabil Med. 53 (1): 24–33. doi:10.1016/j.rehab.2009.10.002. PMID 19944665.
- ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients". J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
- ↑ Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
- ↑ Falzarano MS, Scotton C, Passarelli C, Ferlini A (2015). "Duchenne Muscular Dystrophy: From Diagnosis to Therapy". Molecules. 20 (10): 18168–84. doi:10.3390/molecules201018168. PMID 26457695.
- ↑ Filippi M, Preziosa P, Rocca MA (2016). "Multiple sclerosis". Handb Clin Neurol. 135: 399–423. doi:10.1016/B978-0-444-53485-9.00020-9. PMID 27432676.
- ↑ Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). "Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group". Arch Neurol. 51 (1): 61–6. PMID 8274111.
- ↑ Riva N, Agosta F, Lunetta C, Filippi M, Quattrini A (2016). "Recent advances in amyotrophic lateral sclerosis". J Neurol. 263 (6): 1241–54. doi:10.1007/s00415-016-8091-6. PMC 4893385. PMID 27025851.
- ↑ Michelle EH, Mammen AL (2015). "Myositis Mimics". Curr Rheumatol Rep. 17 (10): 63. doi:10.1007/s11926-015-0541-0. PMID 26290112.
- ↑ 40.0 40.1 40.2 40.3 40.4 40.5 AlKetbi, Reem; AlNuaimi, Dana; AlMulla, Muna; AlTalai, Nouf; Samir, Mohammed; Kumar, Navin (2020). "Acute Myelitis as a Neurological Complication ofCovid-19:A Case Report and MRI Findings". Radiology Case Reports. doi:10.1016/j.radcr.2020.06.001. ISSN 1930-0433.
- ↑ Munz M, Wessendorf S, Koretsis G, Tewald F, Baegi R, Krämer S; et al. (2020). "Acute transverse myelitis after COVID-19 pneumonia". J Neurol. doi:10.1007/s00415-020-09934-w. PMC 7250275 Check
|pmc=value (help). PMID 32458198 Check|pmid=value (help). - ↑ "Acute transverse myelitis after COVID-19 pneumonia".
- ↑ Scotti G, Gerevini S (2001). "Diagnosis and differential diagnosis of acute transverse myelopathy. The role of neuroradiological investigations and review of the literature". Neurol Sci. 22 Suppl 2: S69–73. doi:10.1007/s100720100038. PMID 11794482.
- ↑ Yu, Dongshan; Sun, Shuilin; Li, Yanhua; Xi, Wenna; Jin, Di; Sun, Ke; Yu, Rongyan; Yao, Xuebing; Song, Zhiying; Yang, Aoyu; Luo, Ruixia; Zou, Biaoshu; Liu, Yun (2020). doi:10.1101/2020.05.30.20117598. Missing or empty
|title=(help) - ↑ De Flora, S.; Grassi, C.; Carati, L. (1997). "Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment". European Respiratory Journal. 10 (7): 1535–1541. doi:10.1183/09031936.97.10071535. ISSN 0000-0000.
- ↑ Sotoca, Javier; Rodríguez-Álvarez, Yensa (2020). "COVID-19-associated acute necrotizing myelitis". Neurology - Neuroimmunology Neuroinflammation. 7 (5): e803. doi:10.1212/NXI.0000000000000803. ISSN 2332-7812.
- ↑ nair, deepak t; narayanan, naveen. doi:10.35543/osf.io/p48fa. Missing or empty
|title=(help)