Lions are known to reproduce well in captivity but high incidence of morbidity and mortality has been reported in young captive lions .
A sizable number of these cases have been attributed to bone malformations, primarily of the skull, that include thickening of the tentorium cerebelli and occipital bone, and narrowing of the foramen magnum (FM) [ 3,5–12]. These changes apply pressure on the nervous tissue at the caudal fossa, causing severe, and potentially fatal, neurologic abnormalities [5, 7, 8].
Based on our previous studies the occurrence of the described bone malformation occurs primarily in captivity. Significantly higher incidences of this pathology was detected in lion skulls from captivity. It is still possible though, that genetic predisposition exists in lions or in specific groups of lions, and that under certain environmental settings this pathology may be introduced to the wild lion populations .
Although circumstantial evidence suggest that Vitamin A deficiency plays the main role in the pathogenesis of skull malformations and concurrent neurologic abnormalities in captive lion populations, conclusive reports have yet to prove its existence. In addition, genetic variation may also play a role in the predisposition of certain families of lions to skull malformations, with or without association to the availability of dietary Vitamin A .