If PFS is classified as persistent hormonal changes after cessation then the mice must have had PFS as a testicular adenoma is tissue which autonomously hyper-produces hormones. So their hormone levels must have been altered persistently. Alterations in hormonal levels means changes in behavior.
We do not know the actual mechanisim which fin causes the adenoma. It is proposed that it happens with LH changes but there has been no real proof given for this apart from the fact mice taking higher doses of fin were more likely to get it. Higher doses of fin increased LH.
Some of us crashed after quiting, some before. I do not think that matters too much it could have been that the fluxuations in hormones or lh set it off or made it worse or even that the metabolite created via the adenoma was being blocked by 5ar inhibition, but this may be unlikely.
Here is the abstract.
ncbi.nlm.nih.gov/pubmed/8005373
If you want the full study which goes into a lot of detail and really needs to be read, send me a message.