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.
Objective—To quantitatively evaluate expression of vascular endothelial growth factor (VEGF) in intracranial tumors in dogs and determine whether relationships exist between circulating and intratumoral VEGF concentrations and tumor type and grade.
Animals—27 dogs with primary intracranial neoplasms and 4 unaffected control dogs.
Procedures—Plasma and brain tumor samples were obtained from each dog, and plasma and intratumoral concentrations of VEGF were measured by use of an ELISA.
Results—Dogs with meningiomas (n = 11) were significantly older than dogs with oligodendrogliomas (7) or astrocytomas (9). Measurable VEGF was detected in all tumors, and a significant negative correlation between age and intratumoral VEGF concentration was detected. Age-adjusted comparisons identified significant differences in intratumoral VEGF concentrations among all tumor types; the highest VEGF concentrations were associated with astrocytomas. Within each tumor type, increasing tumor grade was significantly associated with increasing VEGF expression. Plasma VEGF concentrations were detectable in 9 of 27 dogs; the proportion of dogs with astrocytomas and a detectable circulating VEGF concentration (7/9 dogs) was significantly higher than the proportion of dogs with meningiomas (1/11 dogs) or oligodendrogliomas (1/7 dogs) with a detectable circulating VEGF concentration.
Conclusions and Clinical Relevance—Overexpression of VEGF appears common in canine astrocytomas, oligodendrogliomas, and meningiomas. In the neoplasms examined, intratumoral VEGF concentrations correlated well with tumor malignancy. The VEGF expression patterns paralleled those of analogous human tumors, providing evidence that dogs are a suitable species in which to study angiogenesis and intracranial neoplasia for human application.
Objective—To analyze survival time and identify prognostic factors associated with outcome following discharge in dogs with primary brain tumors treated palliatively.
Design—Prospective case series.
Animals—51 dogs with 5 histopathologic types of brain tumors.
Procedures—Owners with dogs examined from 2004 to 2008 were invited to participate if dogs had CT or MRI evidence of a brain mass that was histopathologically confirmed as a neoplasm upon death, dogs survived for ≥ 48 hours after hospital discharge, and treatments following discharge were limited to administration of prednisone or phenobarbital. Prognostic factors, including signalment, clinical signs (including duration), tumor type, tumor location, degree of peritumoral edema, lesion burden, and prescribed treatment, were evaluated. Survival time was estimated and animal- and tumor-specific variables evaluated as potential prognostic factors.
Results—The median survival time in all dogs was 69 days (95% confidence interval [CI], 18 to 201 days). Multivariate analyses identified neuroanatomic location as the only significant prognostic variable, with the survival time of dogs with infratentorial tumors (n = 18) being significantly shorter (median, 28 days; 95% CI, 19 to 68 days) than survival time of dogs with supratentorial (33) tumors (median, 178 days; 95% CI, 119 to 270 days). Seizures were the most common clinical sign associated with supratentorial tumors (24/33 [73%]) and central vestibular dysfunction with infratentorial tumors (12/18).
Conclusions and Clinical Relevance—Dogs with palliatively treated primary brain tumors, particularly those with tumors in the cerebellum, pons, or medulla, had a poor prognosis. However, dogs with supratentorial tumors had survival times > 3 months.
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)