Tetraparesis in a Cat With Fibrocartilaginous Emboli

Case Report

An 8-year-old, male neutered domestic shorthair cat was admitted to the University of Georgia’s Veterinary Teaching Hospital (UGA-VTH) with a 5-day history of acute-onset, progressive ataxia and weakness. The owners had initially noted incoordination in the pelvic limbs, which improved over a 24-hour period but then recurred and rapidly progressed to thoracic limb ataxia as well. Within 5 days of the initial sign of incoordination, the cat had become tetraparetic and was referred to UGA-VTH for further neurological evaluation. The cat had become completely anorectic on the morning of presentation but had otherwise maintained a normal attitude. There was no history of toxin exposure or heart disease in the patient. The cat had outdoor access; therefore, trauma could not be ruled out as a differential for the neurological signs. In the owners’ opinion, a 12-year-old housemate cat was neurologically normal.

On admission, the cat was bright and alert. He did not act painful when handled, and the owners had not noted pain or an abnormal mentation throughout the course of the cat’s illness. There were no external abrasions or any other evidence of trauma. No murmurs were audible on cardiac auscultation, and femoral pulses were bilaterally strong and regular. Mild iris atrophy was noted in the right, leading to incomplete constriction of the pupil in response to light. A neurological examination revealed normal cranial nerve function, with the exception of a mild anisocoria characterized by a constricted left pupil that was minimally responsive to direct and consensual light stimulation. A full ophthalmic examination was done, which revealed a very slight protrusion of the third eyelid on the left. The ocular signs on the left were felt to be compatible with a mild unilateral Horner’s syndrome. The cat was unable to withdraw his left thoracic limb, and the right thoracic limb had only a weak flexor-withdrawal reflex. Patellar and flexor-withdrawal reflexes were normal in both pelvic limbs, though there was an exaggerated crossed-extensor reaction present bilaterally. The cat required assistance to stand, and when held, conscious proprioception deficits were noted in all four limbs. There was no voluntary motor activity in any limb, and poor muscle tone was evident in the thoracic limbs. The cat’s bladder was noted to be of moderate size and was easily expressed. No pain could be elicited on palpation of the spinal column.

The clinical examination was suggestive of a caudal cervical to cranial thoracic spinal cord lesion (sixth cervical [C₆] to second thoracic [T₂]) that was more severe on the left. Differentials for the lesion localization included neoplasia, infectious meningomyelitis, trauma, discospondylitis, intervertebral disk disease (IVDD), or a vascular disease.

Preliminary blood work included a complete blood count (CBC), serum biochemical profile, and feline infectious disease panel (feline immunodeficiency virus [FIV]; feline leukemia virus [FeLV]; feline infectious peritonitis [FIP]; and Toxoplasma gondii). The only significant variations from normal were low blood urea nitrogen (BUN, 10 mg/dL; reference range, 20 to 30 mg/dL) and a low alanine aminotransferase (ALT, 17 U/L; reference range, 31 to 104 U/L). Feline leukemia virus, FIP, FIV, and Toxoplasma titers were all negative. No abnormalities of the soft tissue or bony structures in the cat were observed on thoracic or abdominal radiographs. The patient was hospitalized for supportive care measures that included maintenance intravenous (IV) fluid therapy (lactated Ringer’s solution [LRS] + 20 mEq/L potassium chloride), bladder expression q 6 hours, and rotation q 4 hours with passive range of motion exercises. Intravenous clindamycin^a (10 mg/kg body weight, tid) and enrofloxacin^b (5 mg/kg body weight, bid) were administered to address the possibility of underlying infectious etiologies. Due to continued anorexia, a nasogastric feeding tube was placed to administer nutritional requirements^c 3 days after admission. The anorexia was believed to be a complication of the stress of disability and hospitalization.

Cerebrospinal fluid (CSF) was collected from the cerebellomedullary cistern; the fluid was clear with an elevated white blood cell (WBC) count (36 cells/μL; reference range, 0 to 5 cells/μL) and a normal protein concentration (19.5 mg/dL; reference range, 15 to 35 mg/dL). The WBC differential after cytocentrifugation contained 98% neutrophils and 2% monocytes. There were many hypersegmented neutrophils. This indicated an acute inflammation of unknown origin. There were no infectious agents present in the CSF, and the infectious disease panel serology was negative, so anti-inflammatory doses of glucocorticoids were started. Methylprednisolone sodium-succinate^d was given (15 mg/kg body weight, IV), then repeated 8 hours later (10 mg/kg body weight, tid for 24 hours). This use and dosing regimen of methylprednisolone sodium-succinate was based on the current recommendations for animals with acute spinal cord trauma.¹ However, the doses were reduced because of the delay in initiation of medical treatment. The patient was then converted to oral prednisone^e (1 mg/kg body weight, bid) for treatment of potential spinal cord edema or neoplasia.¹

The owners declined further workup, including myelography and cervical computed tomography. Exactly 1 week after admission and 5 days after glucocorticoids were started, there was no improvement identified in the cat’s neurological status, and the owners opted for euthanasia.

Discussion

The results of the neurological examination in the cat of this report revealed a lesion localization to the C₆–T₂ spinal cord segment. The lesion seemed intrinsic and asymmetrical, with neurological signs worse on the left (as indicated by a total lack of withdrawal in the left thoracic limb), some reflex response remaining in the right thoracic limb, and the presence of a mild Horner’s syndrome in the left eye. The miosis in the left eye is believed to be due to a loss of sympathetic tone to the pupillary dilator muscles. The mild protrusion of the third eyelid of the left eye is believed to be secondary to a loss of sympathetic tone of the third eyelid. Sympathetic innervation to the ipsilateral eye is affected by lesions of the gray matter or spinal nerve roots in the cervical and thoracic areas where the cell bodies of the sympathetic second-order neurons are located.³ Over 40% of the cell bodies of sympathetic nerves that travel through the vagosympathetic trunk to the cervical sympathetic trunk (and cranially to the ipsilateral eye) are located in the caudal cervical and cranial thoracic region of the spinal cord. Thus, an injury to the spinal cord at this level may result in a lack of sympathetic innervation to the ipsilateral eye, as was seen in this case.⁴⁵

Though the initial differential list included trauma, intra- and extramedullary lymphoma, FIP, toxoplasmosis, discospondylitis, IVDD, and vascular injury, the lack of pain on direct spinal palpation made several of the differentials unlikely. Infection in the vertebrae, trauma, and extradural lesions such as disk disease are usually locally painful. Thus, these were placed lower on the differential list than intrinsic spinal lesions, which would be less likely to cause local pain.

Necropsy findings in this case resulted in a diagnosis of focally extensive infarction of the cervical spinal cord, caused by fibrocartilaginous emboli (FCE). The differential list for a canine with the presenting clinical signs and history seen in this case would have also included FCE. However, it was not initially considered likely in this case because of the rarity of the condition in the feline species, the slow progression of signs in this case, and the tetraparetic nature of the condition, which has not been previously published as a result of FCE in cats. The progression of signs over a 5-day period was possibly due to progressive ischemia and inflammation secondary to the initial embolic infarction. However, this finding has been rare in cases documented in other species. This is an interesting case, as there are only two published reports in the English language of FCE in cats,⁶⁷ and none yet reported that affect the C₆ to T₂ spinal cord segments in this species. The cats from both previous case reports were euthanized because of the severity of their spinal injuries.

Fibrocartilaginous embolization is not uncommon in the dog; it has been occasionally reported in other species such as sheep, horses, turkeys, pigs, and cats, as well as in humans.^28–14 In dogs, reports of up to 30% of confirmed FCE lesions are found in the cervical intumescence, and up to 47% are in the lumbar intumescence.¹¹ These areas are the only sites identified thus far in the feline species, with both prior reports from the lumbar intumescence and the current case localized to the cervical intumescence.

The CSF analysis in this case was consistent with acute inflammation expected with traumatic, infectious, or vascular injuries to the spinal cord. A retrospective study by Cauzinille and Kornegay in 1996 found that 46.2% of 36 dogs with confirmed FCE had abnormal CSF. Twenty-three percent had an elevated protein alone, and 23% had an elevated protein with increased cellularity.¹¹ The two previous case reports of feline FCE showed increased protein and cell counts that were predominantly neutrophilic.⁶⁷ In the case reported in this paper, the CSF analysis showed no elevation in protein but did demonstrate an elevation in cell count, indicative of acute inflammation. Another sample drawn at a later point in the disease process may have revealed more chronic changes, such as elevation in protein. In the same paper previously mentioned by Cauzinille and Kornegay, FCE were identified as strictly arterial in 40% of the cases, strictly venous in 36% of the cases, and both arterial and venous in 23% of the cases.¹¹ This case contributes to the number of cases reported with both arterial and venous involvement.

The cause of FCE in animal species is still unknown, but several theories exist.²¹² One theory involves mild trauma to the intervertebral disk, causing a fragment of nucleus pulposus to seep into damaged venous systems. Since the cat reported here was allowed outdoors unsupervised, the possibility of trauma to the cervical region cannot be ruled out, although there was no external evidence of trauma at the time of presentation and no internal trauma at the time of necropsy.

Other theories suggest that a small piece of intervertebral fibrocartilage may enter the vasculature through direct penetration of the arteries or veins, through arteriovenous communications, mechanical herniation through the vertebral end plate with subsequent entrance into the vertebral venous sinus, or the entrance into embryonic remnant vessels.¹³ Unfortunately, none of the postmortem investigations in cats diagnosed with this condition have examined the vertebral bodies, end plates, or intervertebral disks on a histopathological level to look for the underlying pathogenesis.

Conclusion

It is important to remember FCE as a possible differential for acute spinal injury in the cat as well as in the dog. This is particularly relevant when the lesion is asymmetric and not painful. It is also important to note that the clinical signs and anatomical location are not limited to the lumbosacral regions, as had been seen up until the present report. Since the etiology of this condition is still unknown, and it may be different for the cat than for the dog, it is important that future necropsy examinations investigate the vertebral bodies and intervertebral disks of dogs and cats presenting with possible FCE. It is also important to keep this disease in mind with feline patients so that a complete postmortem investigation can be performed and the underlying etiology of this condition can be discovered.