A 7-year-old 6.9-kg (15.2-lb) neutered male Manx was evaluated because of a 3-day history of sudden onset severe nonambulatory hind limb paraparesis and hyperpathia. The cat had been examined previously by multiple veterinarians; findings included hind limb ataxia with hyperesthesia and mild dehydration. Referral abdominal radiography reportedly revealed no abnormalities. Medical management included a single dose of meloxicam (0.05 mg/kg [0.023 mg/lb], PO, q 24 h), 2 doses of dexamethasone (0.72 mg/kg [0.327 mg/lb], IM, q 24 h), and an SC isotonic crystalloid fluid bolus, none of which improved clinical signs. At the evaluation, the cat was quiet, but alert and responsive, and moderately overweight. Rectal temperature, heart rate, and respiratory rate were within reference limits; however, increased respiratory effort was noted. A splayed hind limb posture at rest was evident.
Etiologic diagnosis—Differential diagnoses considered for sudden onset, nonprogressive hind limb paraparesis and hyperpathia of the hind limb musculature in a middle-aged cat included spinal neoplasia (eg, lymphoma), aortic thromboembolic disease, myelitis, or intervertebral disk extrusion. The initial diagnostic plan included a CBC, serum biochemical analysis, assessment of both serum total thyroxine concentration and anti–Toxoplasma antibody titer, and urinalysis with urine culture (all to differentiate between localized and systemic disease). Planned diagnostic imaging included thoracic and thoracolumbar radiography, abdominal ultrasonography, echocardiography, and MRI of the lumbar and lumbosacral portions of the vertebral column (to assess for musculoskeletal problems).
Diagnostic test findings—The CBC results revealed mild neutrophilia (14,852 neutrophils/μL; reference range, 2,500 to 12,500 neutrophils/μL) and lymphopenia (790 lymphocytes/μL; reference range, 1,500 to 7,000 lymphocytes/μL) consistent with a stress leukogram. Serum biochemical analysis revealed mildly high alanine aminotransferase activity (96 U/L; reference range, 7 to 60 U/L) and severely high creatine kinase activity (3,250 U/L; reference range, 50 to 225 U/L). Serum thyroxine concentration was within reference range (2.5 μg/dL; reference range, 0.8 to 4 μg/dL). The cat's serum anti–Toxoplasma antibody (IgG) titer (1:256) was suggestive of recent Toxoplasma exposure or infection. A urinalysis revealed a urine specific gravity of 1.023 and mild proteinuria; urine culture results were negative.
Thoracic radiography revealed mild enlargement of the cardiac silhouette with diffuse patchy alveolar disease, consistent with pulmonary edema, and moderate pleural fissures. Consideration was given to chylous effusion or modified transudate associated with congestive cardiac failure. Echocardiography revealed mild bilateral atrial enlargement with mild asymmetric left ventricular free wall thickening consistent with hypertrophic cardiomyopathy. Abdominal ultrasonography revealed bilaterally isoechoic renal cortices consistent with normal renal tubular fat, nephropathy, or chronic renal disease. Thoracolumbar spinal radiography revealed multiple small, ovoid to linear (< 2 mm in height), irregular mineral opacities in the intervertebral disk spaces from L4 through L7, with narrowing of the L4–5 and L5–6 intervertebral disk spaces. The differential diagnosis list was narrowed to thromboembolic disease or acute intervertebral disk extrusion, and an MRI examination was considered to be the most reasonable next step pending results of pleurocentesis, pleural fluid cytologic examination, and diuretic therapy outcome. Examination of a pleural fluid sample revealed a modified transudate with no evidence of neoplastic cells or infectious agents. The cat was treated for congestive cardiac failure with 3 days of diuretic therapy. Recheck thoracic radiography prior to MRI revealed resolution of the pulmonary edema and pleural effusion without recurrence of respiratory difficulty.
Various dorsal plane MRI images of the caudal portion of the body of a cat that was evaluated because of sudden onset severe nonambulatory hind limb paraparesis and hyperpathia of 3 days’ duration. A—Two-dimensional time-of-flight MR angiography image prior to contrast agent administration. Notice the normal appearance of the aorta and caudal vena cava. The lack of hypointense filling defects and presence of normal branching patterns confirm that there are no thromboemboli within the vascular structures. B—T1-weighted fat-saturated echo planar image without contrast agent administration. Notice the heterogeneous, but predominantly hyperintense fusiform-shaped, right-sided extradural lesion at the L5–6 intervertebral disk space (right is to the left). The hyperintensity is most indicative of subacute hemorrhage or mineral material; fat was ruled out given the saturation techniques applied, and melanin was considered unlikely. C—T1-weighted fat-saturated echo planar image after contrast agent administration. Notice the strong enhancement (hyperintensity) of the displaced cauda equina, most consistent with myelitis.
Citation: Journal of the American Veterinary Medical Association 248, 1; 10.2460/javma.248.1.59
Additional sagittal plane MRI images obtained from the cat in Figure 1. A—Magnetic resonance myelogram from the thoracolumbar to caudal spinal segments. Notice the diffuse loss of the dorsal subarachnoid space from L3 to S1. Mild hydromyelia is present just cranial to L3. B—Sagittal plane short tau inversion recovery sequence. Notice the lesion's central hyperintensity, most consistent with combined edema, disk material, and hemorrhage. The inversion recovery sequence rules out the presence of fat. C—T1-weighted fluid attenuated inversion recovery image. There is a lack of fluid suppression with hyperintensity. This finding is most consistent with protein-rich fluids, hemorrhage (methemoglobin), or mineral material. D—T2* image. Notice the small multifocal (profoundly hypointense) signal voids and heterogeneity of the lesion. Although undistinguishable, the signal voids are most consistent with acute hemorrhage or calcified nucleus. Calcified bodies were not detected radiographically (not shown). Hemorrhage was considered most likely.
Citation: Journal of the American Veterinary Medical Association 248, 1; 10.2460/javma.248.1.59
Contrast-enhanced MRI of the vertebral region from L1 through S1 was performed with a 3-T magnet. The following sequences were acquired in multiple image planes: time-of-flight MR angiography, 3-D reconstructible single-shot turbo spin echo MR myelography, T2-weighted fast spin echo, 3-D reconstructible T2*, T1-weighted short tau inversion recovery, T1-weighted fat-saturated fluid-attenuated inversion recovery (FLAIR), and T1-weighted fat-saturated fast spin echo before and after IV administration of an MRI contrast agenta (0.2 mmol of gadolinium/kg [0.09 mmol/lb]). Normal signal intensity was observed in all lumbar intervertebral disks with the exception of L4 through L6. The L4–5 intervertebral disk demonstrated severe, homogenous, decreased T2-weighted signal intensity with signal loss and incidental mild thickening of the dorsal annulus at L4–5. The intervertebral disk signal loss was consistent with degenerative desiccation at these locations. Time-of-flight imaging of the aorta and caudal vena cava revealed no evidence of thromboembolism. The MR myelography revealed severe attenuation of the dorsal and ventral subarachnoid space from L3 through S1 and hydromyelia at and just cranial to L3. At L5 and L6, a poorly marginated, 13-mm-long, 4-mm-wide, 6-mm-deep ovoid, extradural, right-sided, fusiform, heterogenous lesion was present within the spinal canal. The lesion was centrally hyperintense on short tau inversion recovery images with peripheral T1-weighted fat-saturated hyperintensity, was iso- to hyperintense on T1-weighted FLAIR images, and had multifocal regions of T2* magnetic susceptibility artifact (signal voids) seen as black, or profoundly hypointense, areas throughout the lesion. Some of these areas of T2* signal void also displayed a lack of contrast enhancement. These MRI features were consistent with acute hemorrhage. The lesion caused severe extradural compression of the caudalmost portion of the spinal cord and cauda equina, with leftward displacement and avid (strong) enhancement of the neuronal parenchyma that spanned from L4 to S1. The short tau inversion recovery images confirmed lack of vertebral body involvement. Moderate bilateral contrast enhancement of the iliopsoas musculature was also noted.
The MRI findings were negative for aortic thromboembolic disease. Acute (extradural), Hansen type I intervertebral disk disease (IVDD) with areas of extradural hemorrhage (attributable to ventral vertebral sinus rupture or extruded mineralized nucleus pulposus) was considered likely. Secondary severe compressive myelopathy with myelitis from L3 through S1, attenuation of the subarachnoid space from L3 through L7, and hydromyelia at the level of L3 were also noted. Bilateral contrast agent enhancement of the iliopsoas musculature was attributed to the cat's splayed hind limb posture at rest.
Surgical intervention was proposed because of progression of the cat's severe paraparesis to lack of sensation and deep pain of the right hind limb and perineal region. Despite discussions regarding the increased anesthetic risk, the owners opted for surgery for quality of life reasons because the cat would be unable to urinate, defecate, or ambulate without decompression of the cauda equina. The cat underwent a L5–6 right-sided hemilaminectomy, which confirmed severe right-sided compression of the cauda equina. A large volume of dark red, gelatinous material admixed with smaller amounts of white gelatinous tissue was removed from the spinal canal and submitted for histologic examination. The cat was stable (mean heart rate, 160 beats/min; mean arterial blood pressure, 70 mm Hg) with controlled ventilation (12 respiratory cycles/min at 15 mm Hg) during the surgical procedure. During an attempt to recover the cat from anesthesia, cardiac arrest occurred with unsuccessful attempts at resuscitation.
A necropsy was not performed; however, histologic examination of the excised material revealed small, fragmented portions of degenerative fibrocartilaginous material surrounded by neutrophils and macrophages. These findings were consistent with a degenerative nucleus pulposus with hemorrhage.
Comments
Clinically relevant IVDD is rare in cats.1 Cats with clinical IVDD are frequently middle aged and of either sex.2 Clinical signs may be acute or chronic in nature and are dependent on the section of spinal cord affected.2 For the cat of this report, radiographic findings were consistent with those described for cats with IVDD1 and included narrowing of intervertebral disk spaces and mineralization of the intervertebral disks. The most common sites of disk protrusion in cats are the C6–7 and L4–5 intervertebral disk spaces.1 Extradural compressive lesions can be visualized by means of myelography.1 In affected cats, MRI findings may include reduced signal from the nucleus pulposus on T2-weighted images, suggestive of desiccation, and a compressive extradural lesion within the spinal canal that has an increased signal on T2-weighted images.3 Although not often performed routinely, T2* imaging of the vertebral column can provide additional information regarding the hemorrhagic component of lesions. Typically, gas, calcium, and blood degradation by-products have hypointense signal voids on T2* images.4 Given the T1-weighted fat-saturated hyperintensity of the lesion in the cat of this report, hemorrhage was suspected. Results of T2* imaging provided valuable information because regions of profound hypointensity, also known as signal loss due to magnetic susceptibility artifact, can be caused by blood degradation by-products (such as intra- or extracellular methemoglobin) and typically occur with acute hemorrhage or calcification.4 To the authors’ knowledge, this is the first report of the use of T2* imaging to evaluate Hansen type I IVDD in a cat. Acute hemorrhage seen as signal voids on T2* images has been reported for dogs with spinal extradural hematoma associated with IVDD, hemorrhagic myelomalacia, traumatic intramedullary spinal cord hemorrhage, ischemic myelopathy, acute noncompressive extrusions, or necrotizing myelopathy.5
With surgical treatment, cats with IVDD have a fair to good prognosis, with over half of the documented cases having excellent outcomes following removal of the compressive disk material.1 The cat of this report had hypertrophic cardiomyopathy and pleural effusion in addition to IVDD at L5–6. The clinical signs in this cat, along with the markedly high serum creatine kinase activity (not typically associated with feline IVDD), raised the suspicion for aortic thromboembolic disease. High serum creatine kinase activity is common in sick cats and can be caused by many disease processes, including cardiomyopathy; systemic bacterial, viral, or protozoal infections; trauma; arterial thromboembolism; and renal disease.6 Differential diagnoses for the cat's mildly high serum alanine aminotransferase activity, apart from isoenzyme leakage, could include underlying ischemic muscle damage or iliopsoas muscle trauma secondary to its splayed hind limb posture and nonambulatory status. Magnetic resonance imaging is an excellent technique for evaluating both the spinal cord and peritoneal vasculature and can easily distinguish compressive myelopathy from aortic thromboembolism, as highlighted by the case described in this report. Furthermore, the use of T2* imaging can aid in determining the hemorrhagic or calcific components of spinal lesions. The owners of the cat of this report declined necropsy; hence, the cause of the cat's death was presumed to be associated with hypertrophic cardiomyopathy in combination with anesthesia, which may have led to spontaneous cardiac arrhythmias or thromboembolic disease.7
Footnotes
Gadolinium (Omniscan), GE Healthcare, Princeton, NJ.
References
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