Fibrocartilaginous Embolic Myelopathy in Five Cats
Five cats had clinical signs, radiographic findings, and cerebrospinal fluid analyses consistent with fibrocartilaginous embolic myelopathy. All cats had an acute onset of nonpainful, asymmetrical spinal cord signs (paresis or paralysis of one or more limbs). Magnetic resonance imaging was performed in three cats. On T2-weighted images, an intramedullary lesion was revealed that was hyperintense to normal spinal cord gray matter. On T1-weighted images, the lesion was isointense. Three of the cats were euthanized, and postmortem examination confirmed myelomalacia with intralesional fibrocartilaginous emboli. Two cats survived and were clinically improved within 3 weeks.
Introduction
Fibrocartilaginous embolism is regarded as an uncommon cause of spinal cord dysfunction in the cat and has been reported only five times in this species.1–5 A recent retrospective study examining the frequency of spinal cord diseases in cats that were necropsied over a 15-year period failed to identify a single case with histologically confirmed fibrocartilaginous embolism.6 The disease is more commonly described in the dog and is often associated with an acute onset of nonpainful, nonprogressive, asymmetrical clinical signs.7
The route by which fibrocartilaginous material enters the vasculature of the spinal cord is unknown, although several theories have been proposed in man and animals.8–10 Some theories involve migration of disk material into the spinal arteries, persistence or neovascularization of a common blood supply to the spinal cord and the intervertebral disk, or mechanical herniation of fibrocartilaginous material into the vertebral body with subsequent entry into the vertebral venous sinus.10,11 Regardless of the mechanism, histopathological examination consistently reveals fibrocartilaginous material identical to nucleus pulposus within the lumen of spinal cord blood vessels, as well as an associated myelomalacia.1
The purpose of this study is to describe the case histories and diagnostic evaluations of five cats that were presented over a 2-year period with confirmed or suspected fibrocartilaginous embolism. Results of magnetic resonance imaging (MRI) are discussed in three cases.
Case Reports
Case No. 1
A 10-year-old, spayed female, domestic shorthaired cat was presented for acute onset of pelvic-limb ataxia that was worse on the left side. The cat was housed indoors and had no known history of trauma prior to the onset of clinical signs. The clinical signs progressed over 24 hours to nonambulatory paraparesis. Neurological examination revealed absent postural reactions in both pelvic limbs. Exaggerated segmental spinal reflexes and increased muscle tone were also detected in the pelvic limbs. The cutaneous trunci reflex was intact bilaterally. The cat was not painful on palpation of the thoracolumbar spine. The neurological examination suggested a third thoracic (T3) to third lumbar (L3) myelopathy.
A complete blood count (CBC), serum biochemical analyses, and thoracic radiography were unremarkable. Systolic blood pressure was 160 mm Hg.a Analysis of cerebrospinal fluid (CSF) collected from the cisterna magna was unremarkable [see Table]. Contrast myelography showed thinning of the subarachnoid space over the first lumbar (L1) vertebral body on the lateral projection, with no lateral compression noted on the ventrodorsal projection. These findings were consistent with an intramedullary lesion at L1 [Figure 1].
Given the clinical suspicion of intramedullary neoplasia (e.g., lymphoma) or myelitis (e.g., feline infectious peritonitis [FIP]), the owners elected euthanasia. Postmortem examination revealed no gross abnormalities. Histopathology showed severe, focally extensive malacia of the cranial lumbar spinal cord (predominantly involving the gray matter) with intravascular fibrocartilaginous emboli, Wallerian degeneration, and meningeal hemorrhage. The emboli were identified on histopathology slides stained with hematoxylin and eosin (H&E). Toluidine blue was used to stain the fibrocartilaginous emboli a more obvious purple hue for confirmation [Figures 2, 3].
Case No. 2
An 11-year-old, spayed female, domestic shorthaired cat was presented for acute onset of a left thoracic-limb lameness that progressed to nonambulatory left-sided hemiparesis over 12 hours. The cat was housed indoors and had no history of trauma prior to the onset of clinical signs. Neurological examination revealed miosis of the left eye and nonambulatory tetraparesis characterized by absent postural reactions and increased muscle tone in the left thoracic and left pelvic limbs. Segmental spinal reflexes were exaggerated in the left pelvic limb and were normal in the other three limbs. The cutaneous trunci reflex was intact. The cat was not painful on palpation of the thoracolumbar spine. The left pupil dilated 40 minutes after one drop of topical 10% phenylephrine,b suggesting a lesion of the first-order neuron of the sympathetic pathway controlling pupillary dilatation.12 The neurological examination suggested a left-sided first cervical (C1) to fifth cervical (C5) myelopathy.
A CBC, serum biochemical analyses, and thoracic radiography were unremarkable. Analysis of CSF collected from the cisterna magna was consistent with neutrophilic pleocytosis (i.e., 94% nondegenerate neutrophils) [see Table]. A serum immunoglobulin G (IgG) titer for Toxoplasma gondii was negative.
The cat was weaker in the right thoracic and pelvic limbs on the second day of hospitalization, and she vomited twice. The owners elected euthanasia. Upon necropsy, there were no gross abnormalities of the spinal cord; however, histopathology demonstrated fibrocartilaginous emboli predominantly affecting the gray matter at the fourth cervical (C4) vertebra. There was also severe regional myelomalacia of the ventral gray and white matter with foamy macrophages and Wallerian degeneration. Emboli were identified on histopathology slides stained with H&E and confirmed with toluidine blue [Figure 4].
Case No. 3
A 7-year-old, castrated male, Maine coon cat was presented for acute onset of pelvic-limb ataxia progressing to tetraparesis within several hours. The cat was housed indoors and had no history of trauma prior to the onset of clinical signs. Neurological examination revealed nonambulatory tetraparesis with absent postural reactions in the left thoracic limb and both pelvic limbs. Segmental spinal reflexes were diminished in the left thoracic limb and exaggerated in both pelvic limbs. The urinary bladder was large, turgid, and difficult to express. The cat was not painful on manipulation of the neck. The cutaneous trunci response was absent on the left side of the body. Neurological examination suggested a left-sided sixth cervical (C6) to second thoracic (T2) myelopathy.
A CBC, serum biochemical analyses, and cervical radiography were normal. Systolic blood pressure was 115 mm Hg.a Magnetic resonance imaging of the cervical spine revealed an intramedullary lesion from C6 to the seventh cervical (C7) vertebra, with associated spinal cord swelling and apparent dorsal displacement of the cranial end of C6 [Figures 5A, 5B].c The lesion was hyperintense to normal gray matter on T2-weighted imaging (Repetition time [TR] 2000 milliseconds [ms], Echo time [TE] 84 ms), isointense on T1-weighted imaging (TR 367 ms, TE 17 ms), and did not exhibit contrast enhancement after intravenous administration of gadodiamide (63.7 mg/kg).d On the T2-weighted images, the lesion primarily involved gray matter. The nucleus pulposus of the C5 to C6 intervertebral disk space was hypointense on the T2-weighted imaging, consistent with a degenerative disk. Analysis of CSF collected from the fifth lumbar (L5) to sixth lumbar (L6) cistern was consistent with neutrophilic pleocytosis (i.e., 98% nondegenerate neutrophils) [see Table]. A serum IgG titer for Toxoplasma gondii and CSF titers for Cryptococcus neoformans and FIP were negative. There was no growth on aerobic bacterial culture of the CSF.
The cat was discharged with a presumptive diagnosis of fibrocartilaginous embolism. Physical therapy was instituted, consisting of passive range-of-motion exercises and massage, and the urinary bladder was manually expressed three times daily. The cat was given oral phenoxybenzaminee (0.3 mg/kg q 12 hours) to decrease urinary sphincter tone and empirical oral prednisonef (0.8 mg/kg q 12 hours) for the possibility of spinal lymphoma or inflammatory disease.
At recheck examination 5 days later, the cat was anorexic and dehydrated, had a very large bladder that remained difficult to express, and had no improvement in neurological status. The owners elected euthanasia. Postmortem examination revealed no gross abnormalities; however, histopathology showed severe, regionally extensive necrosis of the dorsal and ventral gray matter at C6 to C7, intralesional fibrocartilaginous emboli, and foamy macrophage infiltration. Some changes extended into the adjacent white matter, where there was extensive Wallerian degeneration. The emboli were identified on histopathology slides stained with H&E and confirmed with toluidine blue.
Case No. 4
A 10-year-old, castrated male, domestic shorthaired cat was presented for acute onset of right pelvic-limb paresis, progressing to right thoracic-limb paresis over 2 hours. The cat was housed indoors and had no known history of trauma prior to the onset of clinical signs. Neurological examination revealed nonambulatory tetraparesis with absent postural reactions in both right limbs. Exaggerated segmental spinal reflexes and increased muscle tone were detected in the pelvic limbs. Muscle tone in the right thoracic limb was decreased. The cat was not painful on palpation of the cervical or thoracolumbar spine. Neurological examination suggested a right-sided C6 to T2 myelopathy.
A CBC, serum biochemical analyses, and cervical and thoracic radiographs were normal. Magnetic resonance imaging of the cervical spine showed an intramedullary lesion from C5 to C6, with associated spinal cord swelling [Figure 6]. The lesion was hyperintense to normal gray matter on T2-weighted imaging (TR 5116 ms, TE 50 ms), isointense on T1-weighted imaging (TR 633 ms, TE 18 ms), and did not exhibit contrast enhancement. The intervertebral disk space of the fourth thoracic (T4) to fifth thoracic (T5) vertebrae was hypointense, suggesting a dehydrated disk, although the remaining intervertebral disks appeared normal on T2-weighted imaging. Analysis of CSF collected from the cisterna magna was consistent with peripheral blood contamination [see Table]. A serum IgG Toxoplasma gondii titer was positive (1:128). Latex agglutination for Cryptococcus neoformans performed on the CSF was negative. Systolic blood pressure was 130 mm Hg,a and echocardiography was unremarkable. The cat was discharged on supportive care, and acupuncture was begun.
Three weeks later, the cat ambulated normally and only mild postural deficits of the right pelvic limb were noted on neurological examination. A convalescent Toxoplasma gondii titer performed at this time was unchanged (1:128).
Case No. 5
A 7-year-old, castrated male, domestic shorthaired cat was presented for acute onset of paraplegia. The cat was an indoor/outdoor cat with no recent history of trauma. Neurological examination revealed exaggerated spinal reflexes and decreased withdrawal in the pelvic limbs, suggestive of a caudal T3 to L3 or cranial fourth lumbar (L4) to second sacral (S2) myelopathy.
Packed cell volume, total solids, and serum biochemical analyses were unremarkable. Magnetic resonance imaging showed an intramedullary lesion that began within the dorsal columns at the caudal aspect of the second lumbar (L2) vertebra, widening to involve the gray matter by the midbody of L3 and the entire spinal cord at L3 to L4. The lesion was hyperintense to normal gray matter on T2-weighted imaging (TR 4400 ms, TE 116 ms), isointense on T1-weighted imaging (TR 700 ms, TE 31 ms), and exhibited mild contrast enhancement [Figures 7A, 7B, 7C]. No evidence of disk degeneration was seen in affected areas. Analysis of CSF collected from L5 to L6 was consistent with a neutrophilic pleocytosis (i.e., >50% neutrophils, with an occasional mature lymphocyte and macrophage) [see Table]. The owners declined serology for infectious diseases and culture of the CSF.
The cat was discharged with a presumptive diagnosis of fibrocartilaginous embolism. It began walking within 2 days and was neurologically normal at recheck examination 2 weeks after discharge.
Discussion
This case series describes five cats with confirmed or presumed fibrocartilaginous embolism. Diagnosis in three cases was confirmed by histopathology after postmortem examination. A presumptive diagnosis was made in the remaining two cases on the basis of compatible history, clinical signs, MRI findings, exclusion of other causes of myelopathy, and resolution of the clinical signs without specific therapy.
Previous reports of fibrocartilaginous embolism in cats described involvement of the cervical intumescence in two cats and the lumbosacral intumescence in two others.1–4 In dogs, a predilection for the cervical or lumbar intumescence has been reported; this may result from an increased blood supply to these regions.11,13 In affected humans, lesions are reported in the brain stem of 20%; however, this location has only been reported once in a dog.11,14 In the cases presented here, the lesions were not restricted to an intumescence, and no involvement of the brain stem was noted.
The cats in this case series were between 7 and 12 years of age, similar to the age range of 8 to 12 years in previous reports.1–4 The ages were older than the mean age of 7 years for cats with clinical intervertebral disk herniation.15 Dogs with fibrocartilaginous embolism tend to be younger. In one study, 79% of the dogs were between the ages of 3 and 6 years.13 All of the cats in this report, as well as the cats of the four previous reports, had acute onset of asymmetric clinical signs and an absence of pain on spinal palpation. One of the cats with confirmed fibrocartilaginous embolism in this case series, as well as one cat in a previous report, had clinical signs that continued to progress for >24 hours.4 Progression of neurological signs over 1 to 3 days has been reported in humans with fibrocartilaginous embolism and may occur from worsening of myelomalacia and spinal cord edema following the initial infarction.4,7,10,16
Results of CSF analysis were abnormal in four cats of this report. Three cats had a neutrophilic pleocytosis. In dogs with confirmed fibrocartilaginous embolism, CSF analyses were normal in 64% of confirmed cases in one study, and the remaining cases showed mild, nonspecific changes (e.g., hemorrhage, albuminocytological dissociation, pleocytosis).11 In previous reports of fibrocartilaginous embolism in cats, two had CSF analyzed, and an elevated white blood cell count and a neutrophilic pleocytosis were found in both.3,4 In this report, CSF was collected from the cisterna magna in three cases and from the lumbar cistern in two cases. Collection of CSF was performed within 24 to 48 hours after the onset of clinical signs in all five cases. Cerebrospinal fluid may be more likely to be abnormal if collected from a site closer to the lesion. One cat (case no. 1) with a lumbar lesion and collection of CSF from the cisterna magna had a normal CSF analysis. One cat (case no. 3) had a markedly elevated white blood count and total protein in the CSF, and this cat had particularly severe myelomalacia on necropsy. According to a previous report, the more inflammatory CSF analyses in dogs with fibrocartilaginous embolism may indicate more extensive spinal cord necrosis.7
Magnetic resonance imaging was performed on three cats in this case series—one of which had a diagnosis of fibrocartilaginous embolism confirmed on postmortem examination. In each case, an intramedullary lesion was detected on MRI that was hyperintense to normal gray matter on T2-weighted imaging and isointense on T1-weighted imaging. There was mild contrast enhancement in one case, possibly from breakdown of the blood-spinal cord barrier secondary to myelomalacia. The MRI characteristics in these cats were consistent with MRI findings in humans with histologically confirmed and clinically suspected fibrocartilaginous embolism.10,17 In one cat (case no. 3), the spinal cord lesion was located close to a degenerative disk. Intervertebral disk disease near the site of spinal cord infarction has been described in dogs and humans with fibrocartilaginous embolism.11,18,19 In two other cats (case nos. 4, 5) of this report, the spinal cord lesions on MRI were not associated with degenerative disks.
Physical activity or a Valsalva maneuver has been theorized to play an important role in the development of fibrocartilaginous embolism in dogs, humans, and turkeys.11,17,20 No cat in this case series, and none of the cats previously described with fibrocartilaginous embolism, had any known history or clinical evidence of trauma. Four of the five cats in this report were confined to the indoors. However, the maneuvers associated with fibrocartilaginous embolism in dogs and humans tend not to be associated with external evidence of trauma. No other common risk factors or potential causes were identified in these cats. Systemic blood pressure was measured in three cats, and hypertension was not identified. No structural abnormalities of the heart were noted in the three cats that underwent necropsy or in the cat that survived and had a normal echocardiogram.
Two cats in this case series recovered with only supportive care and physical therapy. The role of corticosteroids in the treatment of fibrocartilaginous embolism is controversial, and, to date, there have been no studies comparing the outcomes for animals with fibrocartilaginous embolism treated with corticosteroids and those not treated.11 Physiotherapy in dogs with fibrocartilaginous embolism has been advocated as a means to improve the recovery rate.7
In one cat (case no. 3) of this report, the owner elected euthanasia 1 week following initial presentation, because the cat became anorexic and dehydrated. Two cats from previous studies also became anorexic several days after the onset of clinical signs, which contributed to their euthanasia. Negative prognostic indicators for dogs with fibrocartilaginous embolism include lower motor neuron dysfunction, absence of deep pain perception, and no improvement within 2 weeks of the onset of clinical signs.7,11 The prognosis for recovery from fibrocartilaginous embolism in small dogs is thought to be better than for large dogs, because small animals are easier for owners to manage supportively.19 Cats are small enough to easily manage at home, and two cats in this case series had a complete neurological recovery.
Conclusion
A confirmed or presumed diagnosis of fibrocartilaginous embolism was made in five adult cats. Magnetic resonance imaging was a useful tool to localize the lesions of fibrocartilaginous embolism in these cats. Neurological recovery occurred in two cats that were provided appropriate supportive care. The mortality rate of three out of five cats indicated that the overall prognosis for fibrocartilaginous embolism may be guarded. Fibrocartilaginous embolism should be considered as a differential diagnosis in middle-aged to older cats with acute onset of a nonpainful asymmetrical myelopathy.
Ultrasonic Doppler Flow Detector Model 811-B; Parks Medical Electronics, Inc., Aloha, OR 97006
AK-Dilate; Akorn, Buffalo Grove, IL 60089
1.5-Tesla Signa 5X Magnetic Resonance system; General Electric, Fairfield, CT 06828
Omniscan; Amersham Health, Inc., Princeton, NJ 08540
Dibenzyline; WellSpring Pharmaceutical Corp., Neptune, NJ 07753
Prednisone; West-ward Pharmaceuticals, Eatontown, NJ 07724
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Citation: Journal of the American Animal Hospital Association 42, 3; 10.5326/0420226
Thoracolumbar myelogram of a 10-year-old, spayed female, domestic shorthaired cat (case no. 1) with fibrocartilaginous emboli confirmed histopathologically on postmortem examination. The contrast column is attenuated (black arrowhead) over the first lumbar (L1) vertebral body on the lateral projection.
Histopathological section of the midlumbar spinal cord from the cat in Figure 1, showing fibrocartilaginous emboli present in the vessels of the gray matter (small arrowheads). The central canal is normal (large arrowhead). Note the severe, focal malacia that involves the adjacent white matter (black arrow) (Hematoxylin and eosin stain, 10×; bar=50 μm).
Same histopathological section as Figure 2, stained with toluidine blue. The emboli (small arrowheads) in the vessels stain purple, which is compatible with fibrocartilaginous material (10×; bar=50 μm). The large arrowhead points to the central canal, and the black arrow indicates an area of severe, focal malacia.
Histopathological section of the midcervical spinal cord from an 11-year-old, spayed female, domestic shorthaired cat (case no. 2). The toluidine blue-stained image reveals fibrocartilaginous emboli (stained purple) within the spinal cord vessel (40×; bar=20 μm).
Magnetic resonance images from a 7-year-old, castrated male, Maine coon cat (case no. 3) with confirmed fibrocartilaginous emboli of the caudal cervical spinal cord. Sagittal (A) and axial (B) T2-weighted (TR=2000 ms, TE=84 ms) images are shown. On the sagittal view, there is a hyperintense intramedullary lesion from the sixth cervical (C6) to seventh cervical (C7) vertebrae (white arrowhead) and a degenerative disk at the fifth cervical (C5) to C6 vertebrae (white arrow). The hyperintense lesion primarily involves the gray matter of the spinal cord on the axial view (white arrow).
Magnetic resonance image from a 10-year-old, castrated male, domestic shorthaired cat (case no. 4) with presumptive fibrocartilaginous embolism of the caudal cervical spinal cord. On this T2-weighted (TR 5116 ms, TE 500 ms) axial image at the level of C5, there is an asymmetric, hyperintense lesion of the gray matter of the spinal cord that is worse on the right side (white arrowhead).
Magnetic resonance images from a 7-year-old, castrated male, domestic shorthaired cat (case no. 5) with presumptive fibrocartilaginous embolism of the lumbar spinal cord. Axial T2- (A) and T1-weighted, pre- (B) and post- (C) gadolinium contrast enhancement images are shown. On the T2-weighted image, there is a lesion of hyperintensity, relative to normal spinal cord parenchyma, of the gray and white matter (white arrowhead). This lesion is isointense on the T1-weighted precontrast image and shows mild contrast enhancement (white arrowhead) on the postcontrast image.
