Diagnosing Severe Acute Respiratory Syndrome Coronavirus 2-Associated Encephalomyelitis and Radiculitis Requires Verification of the Virus.

Abstract

To the Editors: We read with interest the article by Khera et al (1) about an 11-year-old female who developed acute-onset quadruparesis and respiratory insufficiency shortly after onset of fever but without coughing or dyspnea. Neurologic abnormalities were attributed to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)–associated myelitis and radiculitis, as the patient tested positive for SARS-CoV-2 antibodies.1 The study is appealing but raises concerns. We do not agree with the diagnosis “longitudinal extensive transverse myelitis.”1 The patient had at least 3 cerebral lesions which were hyperintense on fluid-attenuated inversion recovery and diffusion weighted imaging.1 However, there is no discussion about the etiology of these lesions. To further assess their etiology, we need to know the results of ADC maps and magnetic resonance angiography and if these lesions represent a cytotoxic or a vasogenic edema. Asymmetric, subcortical, fluid-attenuated inversion recovery hyperintense lesions are typical for acute, disseminated encephalomyelitis (ADEM).2 ADEM lesions may be hyperintense on diffusion weighted imaging and may even enhance upon contrast medium.2 Thus, we suggest diagnosing rather ADEM than longitudinal extensive transverse myelitis. The patient presented with quadruparesis with lower limb predominance.1 However, myelitis extended only between D7 and D10, which does not explain upper limb muscle weakness. Thus, we should know the results of nerve conduction studies of the upper limbs including results of F-wave studies. Assuming that upper limb weakness was due to radiculitis of cervical nerve roots and in the light of the diagnosis “motor axonal polyradiculopathy,” we can expect increased F-wave latencies, normal nerve conduction velocity and reduced compound muscle action potentials of the radial, ulnar and median nerves. An argument against radiculitis, however, is that tendon reflexes on the upper limbs were preserved. Did cervical nerve roots enhance on cervical magnetic resonance imaging as did lumbar nerve roots? Arguments against the central nervous system lesion as cause of upper limb weakness are that the lesions were unilateral and in the postcentral areas. The discrepancy between the location of the central nervous system lesions and absence of sensory disturbances requires clarification. It is unclear if respiratory insufficiency was muscular (ie, because of affection of the respiratory muscles in GBS), because of myelitis or because of pneumonia from the virus. Thus, we should know the results of thoracic computed tomography scans to confirm or rule out coronavirus disease 2019 pneumonia respectively acute respiratory distress syndrome. It would be interesting to know if nerve conduction studies of the phrenic nerve were carried out and if neuropathy had also affected this nerve. Missing in Table 11 are reference limits for cerebrospinal fluid protein, why it cannot be assessed if cerebrospinal fluid protein was elevated, which is crucial for diagnosing GBS according to the Brighton criteria. We should know how many days after onset of fever the patient tested positive for SARS-CoV-2 antibodies (become positive 1–3 weeks after onset). If the interval was >3 weeks, it is unlikely that SARS-CoV-2 was responsible for the neurologic compromise. In this case, the patient had experienced the viral infection already before onset of fever, suggesting that SARS-CoV-2 was not causative for ADEM with polyradiculitis, an association which has been previously reported.3 We should know if dural arteriovenous fistula was excluded.4 Overall, this interesting study has several limitations which challenge the results and their interpretation.