A 9-year-old girl with newly diagnosed Type 1 DM, DKA, brain oedema, multifocal vasogenic brain lesions and lower limb paresis was presented for treatment. She had reported polyuria and polydipsia over the past week and a weight loss of 3 kg over the previous month prior to admission. The blood glucose level initially was found to be 1136 mg/dL, and severe acidosis was also present (pH 7.1; BE-25.9). Intravenous fluid therapy and insulin therapy did not show any improvement in her medical and neurological state. Glasgow Coma Scale (GCS) scores depleted from 13 points to 7 points. She experienced agitation and motor restlessness followed by upper limb spasms. Computed tomography scan revealed brain oedema and a hypodense lesion in the left temporal region. An anti-edematous treatment helped improve her medical condition, but she had developed symmetric lower limbs paresis. Brain magnetic resonance imaging (MRI) and nerve conduction studies revealed numerous, diffuse lesions and damaged motor neurons in both lower limbs with dysfunctional both peroneal nerves and the right tibial nerve respectively. She reported improvement in her health after therapeutic regimen intensive physiotherapy.
What will most likely explain the pathogenesis of acute neuropathy in this case?