Feline patients are rapidly becoming a major portion of the small animal clinician's case load. In neurology, the most
common etiologies for particular spinal cord lesions do not mirror canine cases. In the past, authors have discussed the various
causes of feline spinal cord disease in detail, but without an indication of the respective prevalence of these disease entities
(Fenner, W.R. in the second edition of The Cat, Diseases and Clinical Management, Churchill Livingstone, New York, 1994, pgs.1507-68,
editor Robert Sherding). Now the clinician has a current reference to suggest the likelihood of a particular disease state
when faced with a feline with a neuroanatomic localization of spinal cord disease. A recent retrospective study including
205 cats, published by Marioni-Henry et al, divides the feline spinal cord diseases into seven categories (Table 1, p. 16S).
Their order of decreasing prevalence was: inflammatory/infectious (32 percent), neoplastic (27 percent), traumatic (14 percent),
congenital/inherited (11 percent), vascular (9 percent), degenerative (6 percent) and metabolic (1 percent) [Prevalence of
Diseases of the Spinal Cord of Cats, Marioni-Henry at al, J Vet Intern Med 2004; 18:851-858].
Table 1: Disease categories in order of decreasing prevalence (Marioni-Henry, et al)
The most common spinal cord disorder was feline infectious peritonitis (FIP). FIP induces severe pyogranulomatous meningomyelitis
primarily affecting the cervical spinal cord segments. FIP is a surface-related disease, with prevalence in the inner and
the outer surfaces of the spinal cord with secondary involvement of the neuroparenchyma. Syringohydromyela is a possible sequellae
at any level of the spinal cord. Cats with FIP show multifocal or localized neurologic signs (ataxia, paresis, caudal fossa
signs) and they are often younger than 2 years of age.
The second most common spinal cord disorder and the most common spinal cord neoplasia was the lymphosarcoma (LSA). LSA is
usually found in the epidural space with rare invasion of the vertebrae, and it is rarely intradural in nature. In the study,
40 percent of LSA effected cats had multifocal cord involvement, 50 percent had brain involvement, and more than 80 percent
had LSA in other organ systems concurrently with the spinal cord lesion. LSA is common in all ages and often presents with
acute onset and rapid progression of the clinical signs. This may be explained by a relatively slowly-growing compressive
extramedullary mass with initial adaptation to the slow compressive forces. However, if the mass occludes a significant blood
vessel, it interferes with the spinal cord circulation and thus produces ischemic myelopathy. At this point the clinical signs
will become obvious. More than half of the cats with LSA had lesions localized to the lumbosacral segments with or without
other segments being affected. LSA causes asymmetric or symmetrical clinical signs such as mono, hemi, para or tetraparaparesis,
respectively. In the study, pain was noted in about one third of the LSA patients.
Vertebral column neoplasia was the third common spinal cord disorder in cats. The most common vertebral column neoplasia was
osteosarcoma, followed by fibrosarcoma.
Spinal cord disease secondary to trauma had the same prevalence as ischemia or infarct. Injury to the spinal cord can be sustained
from extrinsic or intrinsic causes. Extrinsic injury includes vertebral fractures/luxations, subdural hematomas and cellulitis/granulation
tissue formation. Examples of intrinsic injuries are intervertebral disc injury or vertebral malformation. Regardless of the
etiology, spinal cord injuries result in spinal cord concussion, contusion or laceration. In the case of concussion, the damage
may be only temporary. Contusion may cause loss of vascular integrity, hemorrhage and diffuse axonal injury. Laceration is
the most severe lesion, when the spinal cord is physically disrupted. Cats that had focal malacia of the spinal cord due to
unknown origin were categorized as the ischemic or infarct group. The clinical signs were frequently asymmetric in the study.
Fibrocartilaginous embolic myelopathy was not found in this histopathologic study, however sporadic cases are reported in
the literature in cats. Acute or peracute onset of the clinical signs were common in both of these groups.
Storage diseases and presumed bacterial infections were less prevalent. Cats in these groups were also commonly younger than
2 years of age.