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.

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.

Patients aged 18-80 years who have documented hypercortisolism (Cushing syndrome) on clinical testing and are assessed as having decision-making capacity.