Jee Hyun Kim

TL;DR: The cerebral perfusion patterns of mTLE suggest interictal hypofunction and ictal activation of the cortico-thalamo-hippocampal-insular network and ictsal hypoperfusion of the anterior frontal cortex.

TL;DR: The distribution of abnormal cerebral perfusion is concordant with the pathway of the cerebral hypocretin system and may explain the characteristic features of narcolepsy, i.e., cataplexy, emotional lability, and attention deficit.

TL;DR: It is suggested that brain regions showing a postoperative increase in glucose metabolism appear to represent the propagation pathways of ictal and interictal epileptic discharges in MTLE, whereas the postoperative decrease in glucose metabolic may be related to a permanent loss of afferents from resected anterior-mesial temporal structures.

TL;DR: C cerebral glucose hypometabolism of the hypothalamus‐thalamus‐orbitofrontal pathways in the narcoleptic brain was showed, with small volume correction.

TL;DR: Cerebral perfusion abnormality of bilateral caudate nuclei is present in idiopathic PKC, showing that the basal ganglia or thalamus is involved in the pathogenesis of paroxysmal kinesigenic choreoathetosis.