Cortical demyelination in CNS inflammatory demyelinating diseases is reviewed in an editorial and in a study by Moll NM et al [1]. Cortical demyelination occurs in 3 different patterns: 1) leukocortical lesions, affecting both gray and white matter; 2) small perivenous intracortical lesions; and 3) widespread subpial demyelination. Type 3 is most abundant in multiple sclerosis (MS) and is related to chronic inflammation of the meninges. Cortical lesions in progressive multifocal leukoencephalopathy (PML) are similar to those in MS but are absent in HIV-encephalitis and adrenoleukodystrophy. T-cell inflammation is sparse in MS and PML cortical lesions in contrast to white matter lesions. Widespread subpial demyelination may be pathognomonic for MS and related inflammatory demyelinating diseases. [2]

COMMENT. Subpial cortical lesions in MS are related to an inflammatory process in the meninges. Cortical demyelination occurs mostly in progressive MS, and is invisible by conventional MRI.

Abnormal T-cell reactivities in childhood inflammatory demyelinating disease [3]. Peripheral T-cell proliferative responses to self-, dietary, and control antigens were evaluated in children with CNS inflammatory demyelination, recent-onset type 1 diabetes mellitus, nonautoimmune neurologic disorders, and healthy children. Those with inflammatory demyelination, CNS injury, and diabetes showed heightened T-cell reactivities to self-antigens. Nonspecific T-cell dysregulation is an early feature of childhood onset MS and diabetes. The study highlights the possible relation between dietary antigens (eg cow-milk reactivities) and autoimmune diseases. High milk consumption and early weaning to foreign protein diets have been proposed as a possible MS risk factor [4]. In the present study, the incidence of MS and diabetes was not different in patients exposed to infant formula and those breast-fed exclusively, but the analysis was limited.