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What Is Your Neurologic Diagnosis?

A

n 11-year-old 6-kg (13.2-lb) neutered male Yorkshire Terrier was evaluated for thoracolumbar
hyperesthesia and sudden-onset ambulatory paraparesis. A week prior, the referring veterinarian identified
signs of thoracolumbar discomfort during a routine
physical examination and NSAID treatment was instituted. At the referral examination, clinical signs had
progressed to bilateral hind limb ataxia and hyperesthe-

sia with vocalization. Historically, the dog had chronic

diabetes mellitus and had undergone bilateral cataract
phacoemulsification surgery. Current treatments included insulina (2.17 U/kg [0.99 U/lb], SC, q 12 h). Physical
examination revealed a pendulous abdomen with cranial abdominal organomegaly, bilaterally weak femoral
pulses, and symmetric mild ventral abdominal alopecia.
A neurologic examination was performed.

Neurologic examination
Observation
Alert X
Normal X
Normal
Para X

Mental
Posture
Gait
Paresis
Other

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

RF

NE
2

NE
2

2
NE
NE
NE

2
NE
NE
NE

LF

RF

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

LR

RR

1
NE
0
NE

1
NE
0
NE

LR

RR

1
2
2

1
2
2

2
2
2

2
2
2
2
2
2
2

2
2
2
2
2
2
2

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 Over T13 and L1 vertebrae
Superficial pain 2
Cutaneous reflex 2
Deep pain NE Owing to intact motor function

What is the problem? Where is the lesion? What are the most probable causes of this
problem? What is your plan to establish a diagnosis? Please turn the page.
JAVMA, Vol 246, No. 12, June 15, 2015

Vet Med Today: What Is Your Neurologic Diagnosis?

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Assessment
Anatomic diagnosis
Rule out location

Problem
Ambulatory paraparesis and ataxia with
bilaterally decreased postural reactions,
withdrawal deficits, and sudden-onset
thoracolumbar hyperesthesia (T13-L1 region of
the vertebral column)

Focal or diffuse spinal cord lesion within the T3-L3 region of the vertebral
column, L6-S2 spinal cord segments, or sciatic nerve

Weak femoral pulses

Cardiovascular (hypotension) or thromboembolic vascular disease

Likely location of one lesion

Considering the combination of signs, a lesion within the T3-L3 spinal cord segments was suspected. However, this did not
explain the dogs weak pulses and weak withdrawal reflex; thus, cardiovascular or thromboembolic disease was not definitively
excluded.

Etiologic diagnosisDifferential diagnoses considered for the dog of the present report were intervertebral disk disease with disk extrusion or protrusion,
neoplasia, or infectious or inflammatory myelitis. On
the basis of the dogs signalment, fibrocartilaginous
embolic myelopathy and diskospondylitis were considered less likely. Weak femoral pulses and hind limb
withdrawal responses were consistent with vascular occlusion cranial to the femoral arteries, underlying cardiovascular disease, or hypotension. Diagnostic testing
included a minimum database, CBC, serum biochemical analysis, and urinalysis (to evaluate for infection or
inflammation and ascertain general status) with survey
radiography of the thorax and abdomen (to assess for
vertebral abnormalities and neoplasia). Echocardiography was performed (to rule out a cardiogenic cause of
weakness). Hyperesthesia of the thoracolumbar region,
bilateral femoral hyperreflexia, and bilaterally reduced
withdrawal prompted an MRI examination of the T13S1 region of the vertebral column.
Diagnostic test findingsThe CBC results
revealed mild neutrophilia (12,348 neutrophils/L;
reference range, 3,000 to 11,500 neutrophils/L) with
a normal leukocyte count (14.7 X 103 cells/L; reference range, 7 X 103 cells/L to 22 X 103 cells/L), and
high plasma protein concentration (9 mg/dL; reference
range, 6 to 8 mg/dL). Serum biochemical analyses
revealed hyperglycemia (348 mg/dL; reference range,
75 to 125 mg/dL), high concentrations of BUN (39 mg/
dL; reference range, 8 to 24 mg/dL) and total protein
(8.5 g/dL; reference range, 5.5 to 8 g/dL), hyperglobulinemia (5.7 g/dL; reference range, 2.1 to 4.3 g/dL),
hypercholesterolemia (577 mg/dL; reference range, 140
to 360 mg/dL), mildly high activities of alanine aminotransferase (95 U/L; reference range, 10 to 90 U/L) and
alkaline phosphatase (227 U/L; reference range, 11 to
140 U/L), and severely high creatine kinase activity
(1,666 U/L; reference range, 50 to 300 U/L). Moderate
proteinuria with a normal urine specific gravity (1.039;
reference range, 1.035 to 1.045) was detected by urinalysis. All clinicopathologic findings (results of the
CBC, serum biochemical analysis, and urinalysis) with
the exception of high creatine kinase activity were
1294

Vet Med Today: What Is Your Neurologic Diagnosis?

attributed to dehydration and endocrinopathy. High

creatine kinase activity raised the suspicion of myopathy and an ischemic event. Results of thoracoabdominal imaging were consistent with endocrine system
related hepatomegaly and results of echocardiography
were consistent with mild mitral and tricuspid valve
regurgitation attributable to endocardiosis. Pre- and
postcontrast enhanced MRI of the T3-S1 region of the
vertebral column was performed (Figure 1). Image
sequences included T1-weighted (T1-W), T2-weighted
(T2-W), T1-fluid attenuated inversion recovery, T1-W
fast spoiled gradient echo, short tau inversion recovery
(STIR), 3-D reconstructable MR myelography, and 2-D
time of flight (TOF) MR angiography in multiple
planes. Magnetic resonance myelography revealed multifocal desiccated intervertebral disks throughout the
vertebral column with mild to moderate areas of com-

Figure 1Sagittal contrast-enhanced TI-weighted fast spoiled

gradient echo fat saturated (A) and T2-weighted (B) images of
the lumbar vertebral column, MR myelogram (C) of the C4-S3
region of the vertebral column, and transverse 3-D reconstructed MR myelogram of the L4 and L5 region of the vertebral
column (D) of a dog with thoracolumbar hyperesthesia and
sudden-onset ambulatory paraparesis. In panels A and B, notice
the large, ovoid, hypointense lesion within the aorta and ventral
to the L4-L7 region of the vertebral column. In panels C and D,
MR myelography clearly reveals multifocal intervertebral disk
protrusions (loss of the ventral and, to a lesser degree, the
dorsal subarachnoid columns). Notice the poorly defined area
of T2-weighted hyperintensity (indicative of edema, fluid stasis,
or proteinaceous fluid) in the region of the aorta, just ventral to
the L4 vertebral body.
JAVMA, Vol 246, No. 12, June 15, 2015

pressive myelopathy at the T12-13 and L7-S1 intervertebral disk spaces. A non-enhancing, heterogeneous,
ovoid (3.8 cm in length), sharply marginated luminal
structure (compared with the surrounding gray matter,
the structure was iso- to hyperintense on T2-W images,
hyperintense on STIR images, and hypointense on
T1-W images) was present in the abdominal portion of
the descending aorta caudal to the renal arteries. Time
of flight angiography of the abdominal aorta revealed
abrupt termination of flow extending from the level of
the L4 vertebra into the left external iliac artery. Findings of abdominal ultrasonography with color flow
Doppler evaluation agreed with MRI findings, in that
an echogenic thrombus was detected in the distal portion of the aorta and extended into the left external
iliac artery. Markedly reduced blood flow was evident,
as was bilateral adrenomegaly.
On the basis of the combined findings, a diagnosis
of aortic thromboembolic disease (ATE) and hind limb
ischemia was made. Other findings included chronic
intervertebral disk disease and subclinical mitral and
tricuspid valve endocardiosis. Adrenomegaly, thromboembolic disease, and biochemical abnormalities
prompted evaluation for hyperadrenocorticism. Results
of an ACTH stimulation test on the ninth day following
initial examination were consistent with hyperadrenocorticism (prestimulation cortisol concentration, 5.6
g/L [reference range, 0 to 9.9 g/L]; poststimulation cortisol concentration, 29.9 g/L [reference
range, 5.5 to 20 g/dL]). Pituitary-dependent hyperadrenocorticism was considered most likely given the
lack of MRI and ultrasonographic evidence of macroscopic adrenal gland tumors.
Comments
In dogs, aortic thrombosis and thromboembolism
are uncommon and have an underlying pathogenesis
that is different from ATE in cats. Cats with aortic
thrombosis and thromboembolism generally have cardiac disease with predispositions for left atrial blood
turbulence, thrombus formation, and subsequent
(usual) embolization to the aortic bifurcation.1 In dogs
with ATE, focal thrombosis of the distal portion of the
aorta is often seen as a result of underlying prothrombotic disease (eg, protein-losing nephropathy, endocrinopathy, cardiac disease) or paraneoplastic causes.13
Clinical signs in affected dogs include hind limb weakness or paresis, proprioceptive deficits, weak (or
absent) femoral pulses, altered hind limb reflexes, cold
extremities, and chronic hyperesthesia exacerbated by
physical activity.13 Laboratory abnormalities include
high serum creatine kinase activity and plasma D-dimer
concentration with variable clotting profiles.13 Treatment of dogs with ATE includes administration of tissue plasminogen activator, streptokinase, warfarin
sodium, heparin sodium, dalteparin sodium, aspirin, or
clopidogrel bisulphate, and thrombectomy. Response
to treatment varies, and prognosis depends on the
underlying cause and initial improvement with treatment.1,3 In most dogs, morbidity is not associated with
the initial thromboembolic event. A median diseaseJAVMA, Vol 246, No. 12, June 15, 2015

free period of 24.2 months is reported in a study1,3 of

dogs with ATE that were treated with oral administration of warfarin. The dog of this report was treated with
enoxaparin sodium (1 mg/kg [0.45 mg/lb], SC, q 6 h),
clopidogrel (1 mg/kg, PO, q 24 h), and aspirin (1 mg/
kg, PO, q 24 h). The dog was maintained on the previous dosage of insulin. Chronic intervertebral disk disease was conservatively managed with cage rest. The
dogs paraparesis gradually improved. Marked bilateral
proprioceptive placing deficits persisted 119 days after
the initial referral evaluation. Medical management
continued with the addition of trilostane (1.5 mg/kg
[0.68 mg/lb], PO, q 12 h) to manage hyperadrenocorticism and the hypercoagulable state, which was attributed to the loss of antithrombin III. Serial ultrasonographic assessments revealed gradual reduction of
thrombus size (decreased to 0.5 cm in length by day
119) with adequate blood flow around the thrombus.
The case described in the present report exemplifies a
clinical situation in which nonneurologic disease
affects neurologic function and highlights the importance of inclusion of the aorta within the field of view
on MRI images of the vertebral column of paraparetic
dogs for accurate diagnosis. The dog of this report had
multiple disease entities known to cause hypercoagulability.46 Vessel thrombi should be considered as a differential diagnosis in dogs with hind limb weakness
and neurologic deficits.
a. Humulin-N, Lilly USA LLC, Indianapolis, Ind.

References
1.
2.
3.
4.
5.
6.

Winter RL, Sedaca CD, Adams A, et al. Aortic thrombosis in

dogs: presentation, therapy, and outcome in 26 cases. J Vet
Cardiol 2012;14:333342.
Van Winkle TJ, Hackner SG, Liu SM. Clinical and pathological
features of aortic thromboembolism in 36 dogs. J Vet Emerg Crit
Care (San Antonio) 1993;3:1321.
Boswood A, Lamb CR, White RN. Aortic and iliac thrombosis
in six dogs. J Small Anim Pract 2000;41:109114.
Rose L, Dunn ME, Bedard C. Effect of canine hyperadrenocorticism
on coagulation parameters. J Vet Intern Med 2013;27:207211.
Pace SL, Creevy KE, Krimer PM, et al. Assessment of coagulation
and potential biochemical markers for hypercoagulability in canine
hyperadrenocorticism. J Vet Intern Med 2013;27:11131120.
Alzahrani SH, Ajjan RA. Coagulation and fibrinolysis in diabetes. Diab Vasc Dis Res 2010;7:260273.

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

Gambino, DVM; Kyle D. Hutcheson, DVM; and Gabriel A. Garcia,
DVM; from the Department of Clinical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS
39762.
The authors declare that no conflicts of interest or sources of funding
exist.
Address correspondence to Dr. Hiebert (hiebert@vt.edu).

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.

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