RESUMO
Crossed Cerebellar Diaschisis (CCD) describes a depression of oxidative metabolism and blood flow in the cerebellum secondary to a supratentorial lesion in the contralateral cerebral hemisphere. The pathophysiology is not clear but appears to be caused by abnormal neuronal connection of the primary to the remote site. The diagnosis is usually done using positron emission tomography (PET) and singlephoton emission CT (SPECT) scans. Almost all the reported cases of CCD are caused by acute ischemic stroke in adults. Hence, CCD secondary to status epilepticus, extremely rare and there is limited literature available on it. This is important because it's findings can easily be confused with acute ischemic stroke and similar concurrent diseases. Correct diagnosis can also help localize the cause of the seizures and significantly influence surgical decisions. We present a case of CCD in a child with status epilepticus using MRI of the brain with DWI.
Assuntos
Isquemia Encefálica , Doenças Cerebelares , Diásquise , Estado Epiléptico , Acidente Vascular Cerebral , Adulto , Cerebelo , Criança , Humanos , Acidente Vascular Cerebral/diagnóstico por imagemRESUMO
In vitiligo, chronic loss of melanocytes and consequent absence of melanin from the epidermis presents a challenge for long-term tissue maintenance. The stable vitiligo patches are known to attain an irreversible depigmented state. However, the molecular and cellular processes resulting in this remodeled tissue homeostasis is unclear. To investigate the complex interplay of inductive signals and cell intrinsic factors that support the new acquired state, we compared the matched lesional and non-lesional epidermis obtained from stable non-segmental vitiligo subjects. Hierarchical clustering of genome-wide expression of transcripts surprisingly segregated lesional and non-lesional samples in two distinct clades, despite the apparent heterogeneity in the lesions of different vitiligo subjects. Pathway enrichment showed the expected downregulation of melanogenic pathway and a significant downregulation of cornification and keratinocyte differentiation processes. These perturbations could indeed be recapitulated in the lesional epidermal tissue, including blunting of rete-ridges, thickening of stratum corneum and increase in the size of corneocytes. In addition, we identify marked increase in the putrescine levels due to the elevated expression of spermine/spermidine acetyl transferase. Our study provides insights into the intrinsic self-renewing ability of damaged lesional tissue to restore epidermal functionality in vitiligo.
