multiple theories have been advanced to explain the pathophysiology of this disease, namely: 1) increased dopamine receptor sensitivity that could trigger the hyperkinesia under certain conditions; 2) striatal infarction, given that petechial hemorrhages have been described in some cases; 3) increased gamma-aminobutyric acid (GABA) metabolism, resulting in decreased GABA levels and a reduction of the epileptic seizure threshold; 4) a disruption of the blood-brain barrier caused by the hyperglycemia and the consequent
