Overview
Building on previous findings regarding microglial immune function and the immunosuppressive effects of glucocorticoids, this project centers on the cerebellum's role in cognitive science. Using Cushing's syndrome-induced cerebellar atrophy leading to CCAS as a model, we aim to elucidate the pathogenic mechanisms governed by the neuro-adrenal-immune network and to uncover the molecular basis by which a novel minimally invasive brain-machine fusion system ameliorates cerebellar ataxia and cognitive impairment.
Eligibility
Inclusion Criteria:
- 1. Clinically and biochemically confirmed ACTH-dependent or ACTH-independent Cushing syndrome (loss of serum cortisol circadian rhythm, elevated 24-hour urinary free cortisol, and failure to suppress on low-dose dexamethasone suppression test). 2. Cranial MRI demonstrating unequivocal cerebellar atrophy (CCAS imaging criterion: cerebellar hemisphere or vermian volume ≥1.5 SD below age-matched normative data). 3. Established clinical diagnosis of CCAS (meets Schmahmann criteria, CCAS-S total score ≥20). 4. Cerebellar ataxia rating scale (SARATA) ≥10, indicating at least moderate motor ataxia. 5. Positive cognitive impairment screen (MoCA <26, or Z-scores ≤-1.5 in at least two cognitive domains). 6. Willingness to undergo minimally invasive epidural cerebellar stimulation and provision of written informed consent.
Exclusion Criteria:
Patients with significant systemic disease; occurrence of major complications or irreproducible, critical deviations in data collection or experimental procedures; or any circumstance rendering continued participation inappropriate-including clinical deterioration, serious adverse events, or poor compliance-will result in discontinuation of the subject's enrollment.