“…Aging FD of the cortex early in fetal life and childhood into adulthood [39][40][41] human entropy production from birth to age 18 [77] human entropy production after early adulthood [77] and entropy production correlates with and in VO 2 max in childhood and early adulthood, respectively [80] entropy production-decreased glucose metabolism in frontal and temporal lobes with normal healthy aging [72,81,82] FD of the cortex and white matter in late adulthood [28,42,43] Epilepsy FD of white matter in half the patients with frontal lobe epilepsy [24] Abnormal FD of the cortex in half the patients with cryptogenic epilepsy [23] entropy production -interictal glucose hypometabolism correlates with epileptogenic region [83,85] entropy production-glucose hypometabolism of the cerebral cortex, subcortical nuclei, supratentorial white matter, infratentorial structures, superior mesial frontal cortex, superior dorsolateral frontal cortex, mesial occipital cortex, lateral occipital cortex, deep parietal white matter and pons [86,87] Degree of cerebral hypometabolism number of relapses [88] Thalamic and cerebellar glucose hypometabolism total lesion volume [89] entropy production-increased cerebral glucose metabolism in the parietal and frontal cortex located close to areas of hypometabolism [89] FD of grey matter [46] Alzheimer's FD of anterior tip of the temporal lobe, mammillary bodies, superior colliculus, posterior edge of the corpus callosum, inferior colliculus and midthalamus [42] FD of cortical ribbon significantly different from control subjects [48] entropy production-cerebral glucose hypometabolism including the posterior cingulate cortex, parieto-temporal lobe and prefrontal cortex [90][91][92][93][94][95][96]…”