Objective—To characterize matrix metalloproteinase
(MMP)-2 and -9 in CSF of clinically normal dogs.
Sample Population—Samples of CSF collected from
Procedure—Dogs were anesthetized, CSF samples
were collected, and dogs were then euthanatized.
Each CSF sample was evaluated immediately for RBC
count, WBC count, and protein and glucose concentrations,
and cytologic examination also was performed.
Samples were considered normal when protein
concentration was < 25 mg/dL and CSF contained
< 6 WBCs/μL and < 25 RBCs/μL. Samples were stored
at –70°C. Sections of brain tissue were collected and
processed for histologic examination. The MMPs were
evaluated by use of gelatin zymography and a polyclonal
antibody-based sandwich ELISA.
Results—Mean WBC count for CSF samples was < 1
WBC/μL (range, 0 to 3 WBCs/mL). Mean protein concentration
was 12 mg/dL (range, 8 to 17 mg/dL). Mean
RBC count was 3.65 RBCs/μL (range, 0 to 21
RBCs/μL). All CSF samples generated a clear band on
zymography gels that corresponded to the human
commercial standard of proenzyme MMP-2. Other
major clear bands were not detected on zymography
gels. Bands correlating to MMP-9 were not detected in
any samples. The ELISA results revealed a mean ± SD
proenzyme MMP-2 concentration of 5.61 ± 1.92 ng/mL
(range, 3.36 to 10.83 ng/mL).
Conclusions and Clinical Relevance—The proenzyme
form of MMP-2 is detectable in CSF of clinically
normal dogs, whereas MMP-9 is not detectable.
Additional investigation of MMPs in CSF from dogs
with various diseases of the nervous system is indicated.
(Am J Vet Res 2002;63:1359–1362)
Objective—To evaluate clinical signs, risk factors, and outcomes associated with bromide toxicosis (bromism) in dogs with idiopathic epilepsy treated with potassium or sodium bromide.
Design—Retrospective case-control study.
Animals—83 clinically ill epileptic dogs with (cases; n = 31) and without (controls; 52) bromism.
Procedures—Medical records were reviewed for information regarding signalment, epilepsy history, treatment, diet, clinicopathologic test results, concurrent diseases, clinical signs, and outcome. Case and control dogs were matched by the veterinary hospitals from which they were referred and by month of admission. A presumptive diagnosis of bromism was made in case dogs when treatment for primary clinical signs was limited to induction of diuresis or reduction in the dose of bromide administered, and this diagnosis was supported by serum bromide concentrations. Potential risk factors for bromism were identified via univariate and subsequent multivariate logistic regression analyses.
Results—Common clinical signs of bromism included alterations in consciousness, ataxia, and upper and lower motor neuron tetraparesis and paraparesis. The multivariate analysis identified bromide dose at admission to the hospital as the only factor significantly associated with bromism. In all dogs with bromism, treatment via dose reduction or facilitated renal excretion of bromide resulted in rapid clinical improvement, although breakthrough seizures happened during treatment in 8 of 31 (26%) dogs.
Conclusions and Clinical Relevance—Bromism is a clinically heterogeneous, dose-dependent neurotoxicosis that is largely reversible with treatment. Regular serial monitoring of serum bromide concentrations is recommended to optimize anticonvulsant treatment in dogs with idiopathic epilepsy.
Objectives—To evaluate computed tomography (CT)
densitometry as a technique for quantifying contrast
enhancement of compressive soft tissues in the
canine lumbosacral vertebral canal and to determine
whether the degree of contrast enhancement can be
used to help predict tissue type or histopathologic characteristics.
Animals—29 large breed dogs with lumbosacral
Procedure—Contrast-enhanced CT of L5-S3 was performed
by use of a previously described protocol. At
each disk level, CT densities of a water-filled syringe,
epaxial muscles, and 4 vertebral canal locations were
measured. Mean tissue enhancement was calculated
by vertebral canal location, using water-filled syringe
enhancement as a correction factor. Corrected CT
enhancement was compared with tissue type,
degree of tissue inflammation, and degree of tissue
Results—Intravenous contrast administration of contrast
medium significantly increased CT densities of
water-filled syringes and epaxial muscles. Corrected CT
enhancement of vertebral canal soft tissues at stenotic
sites was greater than at nonstenotic sites. There was
no association between enhancement and tissue type
for any vertebral canal location. There was no correlation
between enhancement and degree of tissue inflammation.
There was a correlation between enhancement
and tissue activity in the dorsal vertebral canal only.
Conclusions and Clinical Relevance—A water-filled
syringe is a useful calibration tool for CT density measurements.
The degree of tissue contrast enhancement,
measured by CT densitometry, can be helpful for
predicting the location of compressive soft tissues in
dogs with lumbosacral stenosis. However, it is of limited
value for predicting compressive soft-tissue types or
histopathologic characteristics. (Am J Vet Res
Objective—To evaluate nonselective computed
tomographic (CT) venography for evaluating the cervical
internal vertebral venous plexus (IVVP), define the
diameter and area dimensions of the IVVP, and determine
the relationship between dimensions of the cervical
IVVP and other vertebral components in medium-sized dogs.
Animals—6 healthy dogs that weighed 18 to 27 kg.
Procedure—Helical CT scans were performed from
C1 to C7 before and after IV injection of contrast medium
(480 mg of iodine/kg) and a continuous infusion
(240 mg of iodine/kg). Image data were transferred to
a CT workstation, and measurements were performed
on displayed transverse images. Diameter and area
measurements of the vertebral canal, dural sac, IVVP,
and vertebral body were obtained at C3 to C7.
Results—Opacification of vertebral venous structures
was achieved in all dogs with no adverse reactions.
Sagittal diameters of the IVVP for C3 to C7 ranged
from 0.6 to 3.2 mm. Transverse diameters ranged
from 2.32 to 5.74 mm. The IVVP area represented
12.4% of the mean vertebral canal transverse area
and 30.61% of the mean vertebral epidural space
area. Area measurements of the IVVP were significantly
correlated with vertebral canal area and dural
Conclusions and Clinical Relevance—Results indicated
that nonselective CT venography is a safe, sensitive
method for performing morphometric assessments
of the cervical IVVP in dogs. Findings support
the theory that there may be a physiologic or developmental
relationship between cervical vertebral canal
components. (Am J Vet Res 2005;66:2039–2045)
Objective—To study the effects of experimentally induced hypothyroidism on skeletal muscle and characterize any observed myopathic abnormalities in dogs.
Animals—9 female, adult mixed-breed dogs; 6 with hypothyroidism induced with irradiation with 131 iodine and 3 untreated control dogs.
Procedures—Clinical examinations were performed monthly. Electromyographic examinations; measurement of plasma creatine kinase, alanine aminotransferase, aspartate aminotransferase, lactate, and lactate dehydrogenase isoenzyme activities; and skeletal muscle morphologic-morphometric examinations were performed prior to and every 6 months for 18 months after induction of hypothyroidism. Baseline, 6-month, and 18-month assessments of plasma, urine, and skeletal muscle carnitine concentrations were also performed.
Results—Hypothyroid dogs developed electromyographic and morphologic evidence of myopathy by 6 months after treatment, which persisted throughout the study, although these changes were subclinical at all times. Hypothyroid myopathy was associated with significant increases in plasma creatine kinase, aspartate aminotransferase, and lactate dehydrogenase 5 isoenzyme activities and was characterized by nemaline rod inclusions, substantial and progressive predominance of type I myofibers, decrease in mean type II fiber area, subsarcolemmal accumulations of abnormal mitochondria, and myofiber degeneration. Chronic hypothyroidism was associated with substantial depletion in skeletal muscle free carnitine.
Conclusions and Clinical Relevance—Chronic, experimentally induced hypothyroidism resulted in substantial but subclinical phenotypic myopathic changes indicative of altered muscle energy metabolism and depletion of skeletal muscle carnitine. These abnormalities may contribute to nonspecific clinical signs, such as lethargy and exercise intolerance, often reported in hypothyroid dogs.
Objective—To determine clinical features, diagnostic
imaging abnormalities, underlying disease, disease
progression, and outcome in dogs with bilateral cavernous
Procedure—Dogs were included if clinical signs consistent
with bilateral cavernous sinus syndrome (ie,
deficits of the third, fourth, and sixth cranial nerves
and at least 1 of the first 2 branches of the fifth cranial
nerve) were present and a lesion of the cavernous
sinus was identified by means of diagnostic imaging
or postmortem examination.
Results—5 dogs were evaluated because of problems
referable to abnormal ocular motility or pupillomotor
dysfunction, and 1 dog was evaluated because
of partial motor seizures involving the face and bilateral
mydriasis. Four dogs had neurologic signs referable
to an extrasinusoidal lesion at the time of initial
examination, and the remaining 2 dogs eventually
developed extrasinusoidal signs. Besides neuroanatomic
location, the only consistent neuroimaging
feature was variably intense, heterogeneous
enhancement of cavernous sinus lesions. Neoplasia
was histologically confirmed as the underlying cause
in 5 of the dogs and was suspected in the remaining
dog. Median survival time for the 4 dogs that were
treated was 199 days (range, 16 to 392 days).
Conclusions and Clinical Relevance—Results suggest
that bilateral cavernous sinus syndrome is rare in
dogs but should be suspected in dogs with compatible
clinical signs. Affected dogs have a poor prognosis, and
dogs with clinical signs of bilateral cavernous sinus syndrome
should be systematically evaluated for neoplastic
disease. (J Am Vet Med Assoc 2005;226:1105–1111)