It seems that bica actually crosses the blood-brain barrier. Following quote is from Cockshott 2004, Bicalutamide: Clinical Pharmacology and Metabolism:
Bicalutamide is a competitive and pure androgen receptor antagonist in vitro and a potent anti- androgen in vivo. In laboratory animals, bicalu- tamide is a peripherally selective antiandrogen, but in man, elevations of LH, testosterone, oestradiol and, to a lesser degree, follicle-stimulating hormone have been observed.[4,7,15,92-96] From an efficacy per- spective, increases in androgens are of particular importance as the human androgen receptor binding affinity of 5α-dihydrotestosterone is approximately 100-fold higher than that of bicalutamide. During daily administration of bicalutamide 10–200mg to prostate cancer patients, serum testosterone concen- trations increased to reach a plateau at between 4 and 12 weeks. However, the magnitude of the in- crease was relatively small (up to about 80%) and was independent of dose (figure 9), and mean testos- terone concentrations remained within the normal range at all dosage levels. These data indicate that, in man, bicalutamide does not display the peripheral selectivity observed in rats. The observed selectivity in rats may be a consequence of its poor penetration across the blood-brain barrier, as indicated by tissue distribution data, whereas the lack of peripheral selectivity in man suggests that bicalutamide may be blocking androgen receptors within the hypothalamic pituitary axis.