A review of the literature on the bovine spastic paresis (sp. P.) reve
als i) a clinical diversity, ii) a genetic determinism incompatible wi
th a simple mode of inheritance either dominant or recessive. The freq
uency of the early form of the sp. P., in the progeny of an A I bull o
f the Belgian Blue breed known as a transmitter of the disorder was co
mpared to that of other bulls of the same breed used in the same pedig
ree herds. These frequencies were 13,6 % and 1,0 % respectively (P < 0
.001). Mated to daughters and grand-daughters of an other A I sire kno
wn to have transmitted the so-called <<straight hocks>> the first bull
fathered 55 % of affected offspring against 7 % with mates of differe
nt ancestry (P = 0.0014). An hereditary contribution is unquestionable
. The fitting of a monogenic model which takes account of a mean incid
ence of 1 % and of 13,6 % affected in the random progeny of an homozyg
ous (heterozygous) bull led to the estimation of the following paramet
ers: gene frequency: 4,3 % (1,94 %) penetrance of the homozygote: 98 %
(94 %), penetrance of the heterozygote 10 % (27 %). According to this
model, affected animals are expected in the progeny of any bull whate
ver its genotype but with different frequencies. Moreover, 39 % (38 %)
of affected progeny are expected from affected parents. This model ex
plains 25 % (30 %) of the phenotypic variation. In the discussion of t
he results of this investigation, are considered : the possible influe
nce of non-genetic factors and the possible existence of acquired form
s of the disease, its ubiquity, its human equivalent, its possible gen
etic heterogeneity, the question of gene expression against a polygeni
c background, the fate of a carrier sire and of its sons, the perspect
ives of a diagnosis of the carrier state at the DNA level.