A 25-year-old female came with the complaints of headache. Cerebellar examination demonstrated ataxic gate with incoordination and left motor neuron facial nerve weakness. No complaints of nausea, delirium, she had no focal sensory/ motor deficit. History of being diagnosed COVID positive RT -PCR 8 months back.
CT brain revealed an ill-defined relatively hypodense lesion occupying the left middle cerebellar peduncle with no significant mass effect on the pons. (Figures 1A and B)
MRI brain plain study showed a well-defined homogeneously T1 iso intense (Figure 2C), T2/FLAIR hyperintense lesion (Figure 2 A and B) measuring ~ 1.5 X 1.1X 1.0 cm (TRXCCXAP) without blooming as evident on T1 FFE(Figure 3), SWI(Figure 4), Phase(Figure 5) sequences and hyperintense on ADC (Figure 6) involving the left middle cerebellar peduncle mildly abutting the fourth ventricle medially. No evidence of perilesional oedema noted. T2 Spine screening reveals no abnormality (Figure 7)
On post-contrast images (Figure 8), there is mild incomplete peripheral enhancement predominantly in the posterior & medial aspect of the lesion. No enhancing mural nodule noted within the lesion. MRS shows elevated choline peak (choline/creatine ratio ~ 1.4) & mildly reduced NAA peak. No lipid/ lactate peak(Figure 9)
MR angiogram and MR venogram appeared normal.
Based on the clinical suspicion and history of covid in a young patient with no other comorbidities. These findings were in keeping with possible post-COVID demyelination.
Follow-up MR images show the shows reduction in the size and FLAIR hyperintensity signals after 6 months post-treatment in keeping with our diagnosis. (Figure 10)
Neurological involvement in COVID-19 was initially suggested by multiple case reports showing encephalitis/acute necrotizing encephalopathy in MRI of affected patients.
Many possible mechanisms of Cerebral manifestations of COVID are suggested based on various studies.
One mechanism state that infection directly enters the brain through the blood circulation. 
Another mechanism describes the virus infecting cells via binding of its spike protein to the ACE2 receptors and also causes inflammation of endothelium thus leading to vasoconstriction and a prothrombotic state prone for arterial and venous thromboses leading to stroke and stroke-like radiological features. [1,2]
COVID induced demyelination, however, is a rarer presentation
Diffuse leukoencephalopathy - MRI findings of diffuse leukoencephalopathy in some patients demonstrate diffuse, confluent, and symmetric T2 hyperintensities and restricted diffusion of the bilateral deep and subcortical white matter following delayed post-hypoxic insult with subsequent demyelination, possibly due to an indirect inflammatory response post-COVID. 
ADEM like imaging findings usually in the pediatric and young adult population with few case reports describing lesions in the periventricular, deep, and juxtacortical white matter that showed variable enhancement and a case report with multiple lesions were also identified in the cervical and thoracic spinal cord  seen after COVID infection respiratory infection.
MRI findings of covid induced demyelination in posterior fossa.
Case reports like a 69-year-old diabetic with post-Covid encephalopathy showed bilaterally symmetric middle cerebellar peduncles with areas of restricted diffusion and increased T2 signal in the corticospinal tracts (bilateral internal capsule) without microbleeds. 
Wong et al described another case where there was a lesion with T2/ FLAIR increased signal in the right inferior cerebellar peduncle, extending to involve a small portion of the upper cord. There was swelling at the affected tissue and associated micro-haemorrhage. The supratentorial region of the brain was normal; this was diagnosed as a case of post-COVID rhombencephalitis .
Although few cases with posterior fossa involvement post-COVID are documented with signs of neurological deficit and cranial nerve involvement, limited cases of isolated posterior cranial fossa like this have been documented.
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