Cerebellar hypoplasia/atrophy is a relatively rare neurological disease of cats.
In cats, the most common diffuse cerebellar disorder is a congenital malformation. Postnatal cerebellar cortical abiotrophy has been observed but is uncommon in cats. Primary developmental cerebellar malformations are uncommon. The congenital malformation that is most common consists of a varying degree of hypoplasia and atrophy caused by a perinatal infection with feline panleukopenia virus. This parvovirus has a predilection for rapidly dividing cells, and therefore exposure to this virus at the time of birth puts the cerebellar external germinal layer at risk. Destruction of this layer prevents the formation of the granular layer; thus the name granuloprival hypoplasia. In some kittens, extensive destruction to the parenchyma occurs, with loss of all layers of the cerebellar cortex and much of the cerebellar medulla and nuclei. The loss of previously formed cerebellar components is referred to as atrophy. These severe lesions may be the result of an earlier in utero infection with this virus. The lesions can be experimentally induced by in utero inoculation of virus during gestation.
This disease has an interesting history. It was first recognized as early as the 1880s and until the 1960s was thought to be an inherited disorder, one that was very common in families of unvaccinated farm cats. In 1965, Drs. Kilham and Margolis at Dartmouth Medical College were studying a viral-induced cerebellar disorder in the rat and hamster that caused a cerebellar ataxia in the newborn animals. When the veterinarian in charge of the laboratory animals informed them of this congenital cerebellar ataxia in kittens that he often saw on local farms, they proved that the cat disorder was also viral induced. With the help of Dr. Johnson in the United Kingdom, they showed that the virus was the feline panleukopenia parvovirus. Subsequent studies at Cornell University by Dr. Charles Csiza further confirmed this viral agent as the cause of this congenital cerebellar lesion.
Whether the natural infection occurs in utero before birth or at or shortly after birth is not known. Using molecular biologic techniques, Dr. Scott Schatzberg reported in 2002 on polymerase chain reaction amplification of parvoviral DNA from archived brain tissues of cats with this cerebellar lesion. This perinatal infection is limited to the developing brain, with most of the lesions being in the cerebellum. No multisystem infection is observed with this virus, as occurs after a few weeks of age. No direct correlation exists between the severity of the clinical signs and the extent of the cerebellar lesions. This viral-induced feline disorder can be prevented by vaccination of queens before pregnancy.
Clinical signs are observed when the kitten first attempts to stand and try to walk. By that time, the development of the cerebellar lesion is completed. Although the disease process does not progress, as the kitten grows and is capable of making more vigorous voluntary movements, the clinical signs may be more obvious. Little compensation occurs, and these clinical signs will be present for the life of the cat. These cats make great pets. They have an excellent quality of life but just need an environment in which they will not get injured when they fall.
Because of the congenital nature of the disease, and its invariably terminal nature, treatment is not warranted and euthanasia recommended.
- Résibois A, et al (2007) Naturally occurring parvovirus-associated feline hypogranular cerebellar hypoplasia-- A comparison to experimentally-induced lesions using immunohistology. Vet Pathol 44(6):831-841
- Kilham L, Margolis G. (1974) Intrauterine infections induced by mumps virus in hamsters. Lab Invest 31(1):34-41
- de Lahunta, A & Glass, EN (2009) Veterinary Neuroanatomy and Clinical Neurology. Elsevier Saunders, Philadelphia. pp:370
- Schatzberg, S et al (2002) Polymerase chain reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia. J Vet Intern Med 17(4):538-544