Chronic Bovine Hypo- and Hypervitaminosis A and Cerebrospinal Fluid Pressure

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Abstract
In experimental vitamin A deficiency of the calf, cerebrospinal fluid pressure was elevated and the magnitude of the elevation was directly related to the degree of the deficiency. Upon addition of adequate dietary vitamin A to the hypovitaminotic A animal, cerebrospinal fluid pressure decreased in 2–4 weeks to, or approaching, normal levels. Employing ventriculocisternal perfusion, it was determined that rates of formation of cerebrospinal fluid were unaffected in hypovitaminosis A, but resistance to bulk absorption of cerebrospinal fluid was greater. In the vitamin A-deficient calf, the dura was thicker and, in the region of the tentorium cerebelli where arachnoid villi are abundant, it contained greater concentrations of mucopolysaccharides and ribonucleic acid, but essentially the same concentrations of hydroxyproline and deoxyribonucleic acid. While there was less cerebrospinal fluid space in the hypovitaminotic A growing animal due to faulty bone growth, the contribution of the restricted space to the elevated cerebrospinal fluid pressure is not known. Unlike the elevated cerebrospinal fluid pressure reported in hypervitaminosis A of humans, in experimentally produced chronic vitamin A toxicity of calves, young pigs, and puppies, decreased cerebrospinal fluid pressure occurred. In a longitudinal study of 24 days duration during development of chronic hypervitaminosis A, cerebrospinal fluid pressure did not increase and in calves fed a very toxic intake it did decrease at the rate of 1.4% per day. In animals exhibiting lowered cerebrospinal fluid pressure due to feeding a relatively mild toxic vitamin A intake, cerebrospinal fluid pressure had returned to normal levels after withdrawal of the vitamin for a 12-week period. In chronic vitamin A toxicity, the rate of formation of cerebrospinal fluid was decreased and resistance to bulk absorption of cerebrospinal fluid was slightly less. The permeability of the membranes of the tissues surrounding the ventriculocisternal space was apparently altered as evidenced by a greater creatinine clearance. Due to faulty bone growth, cerebrospinal fluid space in chronic vitamin A toxicity was greater, but its relationship to the lowered cerebrospinal fluid pressure was not ascertained.

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