Glucocortioids affect several cellular structures and functions, which may explain the observed adverse effects. Glucocorticoids can impair neuronal glucose uptake, decrease excitability, cause atrophy of dendrites, compromise development of myelin-producing oligodendrocytes and disturb important cellular structures involved in axonal transport, long-term potentiation and neuronal plasticity.
Therefore, we can speculate that the co-occurrence of CAH and central nervous system demyelination could in fact be nonrandom. First, validation of this alternative hypothesis would depend on a plausible reason as to why the CAH-MS co-occurrence has been described in only one case and why all the previous CAH patients with white matter abnormalities, perhaps interpretable as demyelinating lesions, had no clinical neurological signs. A possible explanation derives from the interplay between MS-inducing immunopathological processes and the particular “hormonal environment” that characterizes CAH patients. These latter patients are indeed exposed before and after birth to high levels of dehydroepiandrosterone and progesterone, which can have anti-inflammatory effects and a protective role for myelin.7- 8 The dual-signal hypothesis on MS pathogenesis holds that 2 concomitant (but possibly unrelated) inflammatory events, respectively occurring in the central nervous system and in the periphery, constitute the crucial elements in the disease’s development.9 Accordingly, in those CAH patients who are prone to develop MS, hormonal factors could modulate the peripheral MS-promoting autoimmune events and prevent these patients from exceeding the clinical threshold of the disease. In this scenario, the patients could show only mild pathological signs, not overt clinical manifestations.
civickiller wrote:the 2 mri pics for Anonymoose and euphoniaa both have scaring around the ventricles suggesting csf leakage so a blockage somewhere which is usually at the C1 and/or C2 levels in your spine
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