A 27-year-old woman attempted suicide and was diagnosed with acute carbon monoxide (CO) poisoning. Neurological examinations were normal except for confusion. Initial brain images showed no acute lesions (Fig. 1A) on the next day of admission. Twelve days after CO intoxication, severe headache, choreic movement of both upper extremities, and impaired visual acuity with optic ataxia, oculomotor apraxia, and simultanagnosia were observed. Cerebrospinal fluid findings showed pleocytosis (white blood cell, 135/mm³) with elevated protein level (134.8 mg/dL). From the follow-up brain magnetic resonance imaging, she was diagnosed with posterior reversible encephalopathy syndrome (PRES) as delayed neurologic sequelae (DNS) after CO intoxication (Fig. 1B). With steroid pulse therapy, she had clinical improvement (Fig. 1C). During the acute phase of CO poisoning, brain MRI shows signal changes in the bilateral globus pallidus (GP) with cytotoxic edema [1]. PRES shows distinctive MRI findings of the parieto-occipital lesions with either vasogenic or cytotoxic edema or both [2]. A patient with DNS with PRES was reported without GP involvement [3]. However, in this case, DNS after CO intoxication affected not only the basal ganglia but also the parieto-occipital regions as PRES. Therefore, it is the reason that the patient presented with both chorea and Balint’s syndrome simultaneously.