ADEM in COVID-19
Neurological symptoms were the main presentation of COVID-19, which did not correlate with the severity of respiratory symptoms. The high incidence of ADEM with hemorrhage is striking. Brain inflammation is likely caused by an immune response to the disease rather than neurotropism. CSF analysis was not indicative of an infectious process, neurological impairment was not present in the acute phase of the infection, and neuroimaging findings were not typical of classical toxic and metabolic disorders. The finding of bilateral periventricular relatively asymmetrical lesions allied with deep white matter involvement, that may also be present in cortical gray-white matter junction, thalami, basal ganglia, cerebellum, and brainstem suggests an acute demyelination process. Additionally, hemorrhagic white matter lesions, clusters of macrophages related to axonal injury and ADEM-like appearance were also found in subcortical white matter. Causes
Since the discovery of the anti-MOG specificity against multiple sclerosis diagnosis it is considered that ADEM is one of the possible clinical causes of anti-MOG associated encephalomyelitisAbout how the anti-MOG antibodies appear in the patients serum there are several theories:

A preceding antigenic challenge can be identified in approximately two-thirds of people. Some viral infections thought to induce ADEM include influenza virus, dengue, enterovirus, measles, mumps, rubella, varicella zoster, Epstein–Barr virus, cytomegalovirus, herpes simplex virus, hepatitis A, coxsackievirus and COVID-19. Bacterial infections include Mycoplasma pneumoniae, Borrelia burgdorferi, Leptospira, and beta-hemolytic Streptococci.
The factors that are being implicated in this trend are the relative deterioration and muscle weakness that occur during the off-season.The hamstrings undergo a complex dynamic process during gait, making it unsurprising that they are frequently injured. They must first contract concentrically during the end of the stance phase in order to bend the knee and allow the foot (along with dorsiflexion at the ankle) to clear the ground. At the end of the swing phase, the hamstrings must eccentrically contract while applying a braking moment to knee extension, then immediately change functions to again concentrically contract and produce hip extension. Studies have shown that "the hamstring group reaches peak elongation and acts eccentrically at the hip and knee during the late swing phases of running" and that "the hamstrings are most active and develop the greatest torques at the hip and knee during the late swing through midstance phase of running." Thus, the hamstrings reach their maximum length while attempting to forcefully contract eccentrically and switch functions to immediately produce a concentric contraction, which makes the terminal part of swing phase the most vulnerable for injury. There have been many other proposed predisposing factors to injury. These include muscle weakness, muscle imbalance, poor flexibility, fatigue, inadequate warm up, poor neuromuscular control, and poor running technique. One of the few predisposing factors that most researchers agree upon however is previous hamstring injury. Brokett et al.