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What Is Your Neurologic Diagnosis?

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.

Neurologic examination
Observation
Mental
Posture
Gait
Paresis
Other

Alert X
Normal X
Normal
Pelvic limbs X

Depressed
Head tilt
Ataxia X
Tetra

Disoriented
Tremor
Pelvic limbs X
Hemi

Stupor
Falling
All 4
Mono

Coma
Circling

Key: 4 = exaggerated, clonus; 3 = exaggerated; 2 = normal; 1 = diminished; 0 = none; NE = not evaluated

Postural
reactions
Wheelbarrow
Hopping
Ext postural thrust
Proprioceptive pos
Hemistand/walk
Placingtactile
Placingvisual

Spinal reflexes
Quadriceps
Extensor carpi
Flexion
Crossed extensor
Perineal

LF
NE
2

RF
NE
2

2
NE
NE
NE

2
NE
NE
NE

LF

RF

2
2
2

2
2
2

Cranial nerves

II, VIIVision menace

II, IIIPupils resting
Stim L
Stim R
IIFundus
III, IV, VIStrabismus, resting
III, IV, VI, VIIIStrabismus, position

2
2
2
2
2
2
2

2
2
2
2
2
2
2

LR

RR

1
NE
1
NE

1
NE
1
NE

LR
1

RR
1

0
0
2

0
0
1

VIIINystagmus, resting
VIIINystagmus, change
VSensation
VIIFacial mm
V, VIIPalpebral flex
IX, XGag
XIITongue

2
2
2
2
2
2
2

2
2
2
2
2
2
2

Comments CN

All findings were

considered normal.

Sensation (Locate and describe abnormal)

Hyperesthesia 3
Superficial pain 2
Cutaneous reflex 2
Deep pain NE

Elicited bilaterally during palpation of the quadriceps femoris, gastrocnemius, semitendinosus, and semimembranosus muscles

Owing to the presence of superficial pain and motor function, it was not necessary to assess deep pain response

What is the problem? Where is the lesion? What are the most probable causes of this
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JAVMA Vol 248 No. 1 January 1, 2016

59

Assessment
Anatomic diagnosis
Rule out location

Problem
Sudden onset, nonprogressive, nonambulatory
hind limb paraparesis and hyperpathia. Bilaterally decreased patellar reflexes and bilaterally
absent withdrawal, flexor, and perineal reflexes

Focal or diffuse spinal cord lesion within the L4-S2 spinal cord segments

Likely location of 1 lesion

A lesion within the L4-S2 spinal cord segments was suspected

Etiologic diagnosisDifferential 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 antiToxoplasma 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 findingsThe CBC results revealed
mild neutrophilia (14,852 neutrophils/L; reference
range, 2,500 to 12,500 neutrophils/L) and lymphopenia (790 lymphocytes/L; reference range, 1,500 to
7,000 lymphocytes/L) 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 g/dL; reference range, 0.8 to 4 g/
dL). The cats serum antiToxoplasma 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
60

Figure 1Various 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. ATwo-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.

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,

JAVMA Vol 248 No. 1 January 1, 2016

Figure 2Additional sagittal plane MRI images obtained from

the cat in Figure 1. AMagnetic 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. BSagittal plane
short tau inversion recovery sequence. Notice the lesions
central hyperintensity, most consistent with combined edema,
disk material, and hemorrhage.The inversion recovery sequence
rules out the presence of fat. CT1-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. DT2* 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.

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.
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 subarach-

noid 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 cats
splayed hind limb posture at rest.
Surgical intervention was proposed because of
progression of the cats 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.

JAVMA Vol 248 No. 1 January 1, 2016

61

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; trau-

62

ma; arterial thromboembolism; and renal disease.6 Differential diagnoses for the cats 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 cats 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
a.

Gadolinium (Omniscan), GE Healthcare, Princeton, NJ.

References
1.
2.
3.
4.

5.
6.
7.

Marioni-Henry K. Feline spinal cord diseases. Vet Clin Small

Anim 2010;40:10111028.
Knipe MF, Vernau KM, Hornof WJ, et al. Intervertebral disc extrusion in six cats. J Feline Med Surg 2001;3:161168.
Lu D, Lamb CR, Wesselingh K, et al. Acute intervertebral disc
extrusion in a cat: clinical and MRI findings. J Feline Med Surg
2002;4:6568.
Hodshon AW, Hecht S, Thomas WB. Use of the T2*-weighted
gradient recalled echo sequence for magnetic resonance imaging of the canine and feline brain. Vet Radiol Ultrasound
2014;55:599606.
Ruth D. Optimal magnetic resonance imaging of the spine. Vet
Radiol Ultrasound 2011;52:S72S80.
Aroch I, Keidar I, Himelstein A, et al. Diagnostic and prognostic
value of serum creatine-kinase activity in ill cats: a retrospective study of 601 cases. J Feline Med Surg 2010;12:466475.
Payne JR, Borgeat K, Connolly DJ, et al. Prognostic indicators
in cats with hypertrophic cardiomyopathy. J Vet Intern Med
2013;27:14271436.

This report was submitted by Elizabeth C. Hiebert, DVM; Jennifer

Gambino, DVM; Darin Kepler, DVM; and Michaela Beasley, DVM, MS;
from the Department of Clinical Sciences, College of Veterinary
Medicine, Mississippi State University, Mississippi State, MS 39762.
Address correspondence to Dr. Hiebert (ehiebert2014@gmail.com).

This feature is published in coordination with the

American College of Veterinary Internal Medicine on
behalf of the specialty of neurology. Contributors to this
feature should contact Dr. Helen L. Simons (800-2482862, ext 6692) for case submission forms. Submissions
will be sent to Dr. Karen Kline, DVM, DACVIM, for her
review, except when Dr. Kline is an author.

JAVMA Vol 248 No. 1 January 1, 2016