Short answer:

• No evidence that selegiline fixes or shrinks basal ganglia PVS in humans. If anyone claims that, they’re extrapolating pretty aggressively.
• High dopamine turnover / HVA could theoretically contribute via oxidative stress, but there’s no direct data tying “high HVA → BG ePVS” in people.

Let’s walk through it without turning this into a Reddit biohacking thread.

1. What actually drives BG PVS in the literature

Current mainstream view: BG ePVS are basically a small-vessel / clearance phenotype, not a “dopamine metabolite storage error.”

Large reviews put the main mechanisms as:

• Arterial stiffening and pulsatility changes
• Protein aggregation & impaired glymphatic drainage
• Brain / tissue atrophy changing geometry of the spaces

Epidemiology-wise, BG ePVS track with:

• Hypertension, arterial stiffness, and other cerebral small vessel disease (CSVD) markers
• Aging & vascular risk, not “people with high CSF HVA.”

There are PD papers showing perivascular changes in dopaminergic regions (midbrain, BG) and linking PVS burden / distribution to PD phenotypes.

But that’s more like “degenerating dopamine system ↔ lousy clearance ↔ PVS changes,” not “HVA ate your basal ganglia arterioles.”

2. Selegiline & PVS: what we actually know