Dr. Anwar Ali Alshukami. Dr. Ahmed Atef Soliman.Patient
57 years, male
Our patient was known diabetic and was in close contact with a COVID patient that’s why he presented to our dedicated clinics where PCR was done and the result came out positive and as the patient was clinically free he was sent for home quarantine and to follow up if any new manifestations appeared.
6 days later he presented to the ER with confusion, unsteadiness, memory impairment, disoriented to time and unsteady gait. On examination, the patient was vitally stable with no fever, or signs of meningeal irritation, ataxic gait, and left-sided hemiparesis grade 4, the patient was admitted for evaluation.
Chest X-ray was done showed bilateral peripheral patchy areas of faint lung opacities with no pleural effusion. (Figure 1)
CT showed bilateral patchy areas of low attenuation involving both middle cerebellar peduncles in addition to bilateral patchy areas of similar densities involving white matter of both cerebral hemispheres. (Figure 2)
MRI showed Ovoid-shaped restricted areas seen on diffusion-weighted images corresponding to abnormal hyperintense T2/FLAIR signal, iso-/hypointense T1 signal, involving both middle cerebellar peduncles and centre of the splenium of the corpus callosum associated.
The supra-tentorial periventricular, deep and subcortical white matter of both cerebral hemispheres showed multiple scattered tiny nodular foci of restricted diffusion corresponding to abnormal hyperintense T2/FLAIR foci on a background of extensive white matter abnormal hyperintense T2/FLAIR signal with no diffusional restriction. (Figure 3)
Since December 2019, about 20 million cases worldwide and just less than 300,000 cases in KSA of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have been reported (According to WHO situation report). Although the respiratory system complications of coronavirus disease 19 (COVID-19) have been the most frequent and life-threatening, there are increasing reports of central and peripheral nervous system (PNS) involvement that most probably appears later on in the disease process.
The neurological complications of SARS-CoV2 show some similarities to those described in the other coronavirus epidemics, especially severe acute respiratory syndrome (SARS) and the Middle East acute respiratory syndrome (MERS), including encephalopathy, meningoencephalitis, ischaemic stroke, acute necrotizing encephalopathy, and Guillain-Barré Syndrome (GBS). However, overall number of SARS-CoV2 infected individuals is currently much higher than previous coronavirus epidemics. 
Though Mechanisms of CNS involvement in COVID-19 remains unclear yet many possibilities were described in literature including primary encephalopathy with direct viral injury, a secondary hyper-inflammatory syndrome with what is called as a cytokine storm with the IL-6 considered as the main factor, Coagulopathies/vasculopathy or sort of oxygen deprivation of the brain as sequelae of the generalized hypoxia causing hypoxic/anoxic changes, post-infectious inflammatory process including autoantibody production to neuronal antigens and finally iatrogenic etiologies, with any of those could occur separately or in combination. [2,3]
Recent MRI studies found different patterns of CNS involvement, which could occur separately or in combination. the most frequent finding include an altered signal in the form of Raised FLAIR / T2 signal with diffusional restriction involving the mesial temporal lobe on one side followed by micro-hemorrhagic foci that could be associated with non-confluent patchy areas of raised FLAIR signal involving the supra-tentorial WM or either appear separately as isolated findings, less frequently other findings were reported like focal areas of raised FLAIR signal and diffusional restriction seen involving splenium of corpus callosum or the middle cerebellar peduncle, necrotizing encephalopathy, patchy areas of contrast uptake. Whether these patterns represent the same pathology over different timelines, different pathologies or combinations, that is still unclear at the present time but could be considered as a major factor for patients’ condition evaluation and upon which management decisions could be taken. For example, haemorrhagic lesions were considered as indicator of severe disease. 
 Paterson RW, Brown RL, Benjamin L, Nortley R, Wiethoff S, Bharucha T, et al. The emerging spectrum of COVID-19 neurology: clinical, radiological and laboratory findings. Brain [Internet]. 2020;(2020):2–37. Available from: http://www.ncbi.nlm.nih.gov/pubmed/32637987
 Lang M, Buch K, Li MD, Mehan WA, Lang AL, Leslie-Mazwi TM, et al. Leukoencephalopathy Associated with Severe COVID-19 Infection: Sequela of Hypoxemia? Am J Neuroradiol. 2020;1–5.
 Jaunmuktane Z, Mahadeva U, Green A, Sekhawat V, Barrett NA, Childs L, et al. Microvascular injury and hypoxic damage: emerging neuropathological signatures in COVID-19. Acta Neuropathol [Internet]. 2020;(0123456789):1–4. Available from: https://doi.org/10.1007/s00401-020-02190-2
 Kremer S, Lersy F, de Sèze J, Ferré J-C, Maamar A, Carsin-Nicol B, et al. Brain MRI Findings in Severe COVID-19: A Retrospective Observational Study. Radiology. 2020;202222.
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