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      Acute inflammatory transverse myelitis post-Pfizer-BioNTech-COVID-19 vaccine in 16-year-old

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          Coronavirus disease 2019 (COVID-19) originated in China in early March 2019. Saudi Food and Drug Authority approved the registration of the Pfizer-BioNTech COVID-19 vaccine in Saudi Arabia on December 10, 2020, and on May 10, 2021, Pfizer-BioNTech was given an authorized emergency use in 12–15-years-old children. Saudi Arabia’s Ministry of Health started Pfizer-BioNTech COVID-19 vaccination for 12–18-years-old on June 27, 2021. Here, we have a case of a 16-year-old female admitted to the medical ward diagnosed with acute inflammatory transverse myelitis after 2 weeks from second dose of the Pfizer-BioNTech COVID-19 vaccine. The diagnosis was based on normal laboratory workup but significant radiological findings. She was discharged after a full recovery. There are multiple cases of post-vaccine acute inflammatory transverse myelitis shared by medical journals, but due to lack of literature review for the teenager population, we think our case may be the first case of acute inflammatory transverse myelitis following second dose of Pfizer-BioNTech COVID-19 vaccine in this population.

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          Covid-19: European countries suspend use of Oxford-AstraZeneca vaccine after reports of blood clots

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            Acute Transverse Myelitis (ATM):Clinical Review of 43 Patients With COVID-19-Associated ATM and 3 Post-Vaccination ATM Serious Adverse Events With the ChAdOx1 nCoV-19 Vaccine (AZD1222)

            Introduction Although acute transverse myelitis (ATM) is a rare neurological condition (1.34-4.6 cases per million/year) COVID-19-associated ATM cases have occurred during the pandemic. Case-finding methods We report a patient from Panama with SARS-CoV-2 infection complicated by ATM and present a comprehensive clinical review of 43 patients with COVID-19-associated ATM from 21 countries published from March 2020 to January 2021. In addition, 3 cases of ATM were reported as serious adverse events during the clinical trials of the COVID-19 vaccine ChAdOx1 nCoV-19 (AZD1222). Results All patients had typical features of ATM with acute onset of paralysis, sensory level and sphincter deficits due to spinal cord lesions demonstrated by imaging. There were 23 males (53%) and 20 females (47%) ranging from ages 21- to 73- years-old (mean age, 49 years), with two peaks at 29 and 58 years, excluding 3 pediatric cases. The main clinical manifestations were quadriplegia (58%) and paraplegia (42%). MRI reports were available in 40 patients; localized ATM lesions affected ≤3 cord segments (12 cases, 30%) at cervical (5 cases) and thoracic cord levels (7 cases); 28 cases (70%) had longitudinally-extensive ATM (LEATM) involving ≥4 spinal cord segments (cervicothoracic in 18 cases and thoracolumbar-sacral in 10 patients). Acute disseminated encephalomyelitis (ADEM) occurred in 8 patients, mainly women (67%) ranging from 27- to 64-years-old. Three ATM patients also had blindness from myeloneuritis optica (MNO) and two more also had acute motor axonal neuropathy (AMAN). Conclusions We found ATM to be an unexpectedly frequent neurological complication of COVID-19. Most cases (68%) had a latency of 10 days to 6 weeks that may indicate post-infectious neurological complications mediated by the host’s response to the virus. In 32% a brief latency (15 hours to 5 days) suggested a direct neurotropic effect of SARS-CoV-2. The occurrence of 3 reported ATM adverse effects among 11,636 participants in the AZD1222 vaccine trials is extremely high considering a worldwide incidence of 0.5/million COVID-19-associated ATM cases found in this report. The pathogenesis of ATM remains unknown, but it is conceivable that SARS-CoV-2 antigens –perhaps also present in the AZD1222 COVID-19 vaccine or its chimpanzee adenovirus adjuvant– may induce immune mechanisms leading to the myelitis.
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              Acute transverse myelitis after COVID-19 pneumonia

              Background Neurological complications of SARS-CoV2 infection are increasingly recognized [1]. Recently, a SARS-CoV2 induced focal encephalitis was reported [2]. Here we describe a case of multifocal transverse myelitis following acute COVID-19 pneumonia. Case A 60-year-old patient was first admitted to our hospital with typical respiratory symptoms of COVID-19 infection without neurological symptoms. The polymerase chain reaction (PCR) test of the throat swab was positive for SARS-CoV2. A chest x-ray showed mild bilateral ground-glass opacification. Laboratory findings revealed elevated C-reactive protein but normal white blood cell count. The patient’s previous medical history was unremarkable other than hypertension (treated with ramipril and felodipine), mild fatty liver, and ureterolithiasis. Patients and family history revealed no signs of neurological disorders and he received no vaccination in the months before. He recovered rapidly from COVID-19 pneumonia and was discharged home 5 days later without any symptoms. Three days after discharge, he developed bladder dysfunction and progressive weakness of the lower limbs. He was unable to micturate or walk unaided. On re-admission two days later, clinical examination revealed hypesthesia below the Th9 level and a moderate spastic paraparesis. Babinski’s sign was positive bilaterally. Cognition and cranial nerves were unaffected. General lab results were unremarkable including a nearly normalized c-reactive protein. A repeated throat swab showed a negative SARS-CoV2 PCR. Magnetic resonance imaging (MRI) of the spine revealed T2 signal hyperintensity of the thoracic spinal cord at Th9 level suggestive of acute transverse myelitis rather than multiple sclerosis [3] (Fig. 1a). Brain MRI showed no inflammatory changes. Cerebrospinal fluid (CSF) analysis was abnormal with lymphocytic pleocytosis (16/µl) and elevated protein level (793 mg/l). SARS-CoV2-PCR in the CSF and oligoclonal bands were negative. Further work-up was unremarkable including PCR for herpes simplex virus, varicella-zoster virus, antibodies against human herpesvirus 6, Epstein-Barr virus, and Hepatitis E, antineuronal antibody panel, Aquaporin-4, and myelin oligodendrocyte glycoprotein antibodies. Follow-up MRI on day 6 further showed a patchy hyperintensity of the thoracic myelon at Th9-10 and at Th3-5 level (Fig. 1d), suggestive of transverse myelitis. Repeated CSF analysis showed a slight increase in CSF lymphopleocytosis (27/µl) and protein levels (1177 mg/l). Repeated SARS-CoV2-PCR in the CSF was negative. There was no specific intrathecal synthesis of Anti-SARS-CoV IgG. Fig. 1 MRI of the spine. a Day 1 (admission). T2 weighted axial imaging shows central hyperintensity on Th9 level. b Day 1: Axial T1 weighted image on the same level showed no enhancement after gadolinium. c Day 6: T2 axial slice on level Th9 with hyperintense edema. d Day 6: Longitudinal view of upper thoracic spine shows central hyperintensity on level Th3 (arrow) Initial treatment with aciclovir and ceftriaxone intravenously was discontinued on day 8 after negative CSF results for respective infective agents. The patients’ clinical status slightly improved 3 days after admission. Because of persisting symptoms and after negative workup for active infection, methylprednisolone was started on day 7 at a dose of 100 mg/d. During the further course, the patient improved rapidly. Follow-up CSF on day 12 showed normalization of cell count (3/µl) and regressing protein levels (734 mg/l), no oligoclonal bands. The patient was discharged home on day 13 with a slight spastic paraparesis and hypesthesia below Th9 level, but normal bladder function. He was able to walk independently. A steroid taper scheme was initiated. Discussion This case describes multifocal myelitis occurring shortly after COVID-19 infection. No other causes of myelitis could be identified after extensive workup. We assume a post-infectious etiology in terms of secondary immunogenic overreaction. Previously, others suggested a direct infection of the central nervous system by human coronaviruses like SARS or MERS [4]. The affection of the peripheral nervous system and muscles was described for SARS-CoV-1 [5]. Cases of Guillain-Barré Syndrome in association with severe COVID-19 infections were reported [6]. In a series of 58 severely affected COVID-19 patients, 67% showed clinical corticospinal tract signs but received no spinal MRI [7]. Only one other case with suspected focal myelitis without imaging or serological confirmation is reported from Wuhan [8]. This patient improved with empiric multiple treatments including intravenous immunoglobulins, prednisolone, and antiviral agents. Our case shows that improvement might also occur with moderate steroid treatment, avoiding high doses because of uncertain effects on the immunogenic elimination of SARS-CoV2. It remains unclear at present whether post-infectious myelitis after COVID-19 behaves differently from other virus infections. Increased awareness of spinal symptoms following COVID-19 is recommended.

                Author and article information

                Journal of Medical Research and Innovation
                Scientific Scholar
                November 26 2021
                : 0
                : 1-4
                [1 ]Department of Internal Medicine, Hera General Hospital, Makkah, Saudi Arabia,
                © 2021


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