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Abstract

Objective—To determine the prevalence of ischemic stroke in Greyhounds and determine whether affected dogs had coagulation abnormalities and hypertension.

Design—Multi-institutional, retrospective study.

Animals—21 dogs.

Procedures—Medical records (including diagnostic testing results) and MRI images of the brain were reviewed for Greyhounds with ischemic stroke that had been evaluated at 4 institutions. The proportion of Greyhounds with ischemic stroke was compared with the proportion of non-Greyhound dogs with ischemic stroke. Demographic information for dogs evaluated at each institution was obtained to determine the proportion of Greyhounds in the hospital populations.

Results—21 Greyhounds with ischemic stroke were identified. Abnormalities in coagulation were not identified in the 14 Greyhounds that underwent such testing. Systemic hypertension was identified in 6 of 14 Greyhounds that underwent such testing. No other abnormalities were identified by means of other routine diagnostic tests for Greyhounds. For all institutions combined, the prevalence of ischemic stroke in Greyhounds was 0.66% (21/3,161 Greyhounds). Greyhounds were significantly more likely to be evaluated because of ischemic stroke, compared with all other dog breeds combined (OR, 6.6; 95% confidence interval, 4.2 to 10.2).

Conclusions and Clinical Relevance—Results of this study suggested that Greyhounds were predisposed to ischemic stroke, compared with all other breeds combined. Coagulation abnormalities did not seem to contribute to ischemic stroke. Hypertension may have contributed to the development of ischemic stroke. Greyhounds with ischemic stroke should undergo measurement of systolic arterial blood pressure. Antihypertensive treatments may be warranted for such dogs.

Full access
in Journal of the American Veterinary Medical Association

Abstract

CASE DESCRIPTION

3 dogs were examined because of a sudden onset of signs of pain (1 dog) or paraparesis (2 dogs).

CLINICAL FINDINGS

Neurologic findings consisted of myelopathy affecting the lumbar intumescence (1 dog) and T3-L3 myelopathy (2 dogs). In all dogs, MRI revealed spinal cord compression caused by L3-4 disk herniation. All dogs underwent routine surgical decompression of the intervertebral disk herniation. During MRI and decompressive surgery, physiologic variables were monitored. Immediately after surgery, all dogs were paraplegic with pelvic limb neurologic dysfunction consistent with myelopathy affecting the L4 through caudal spinal cord segments.

TREATMENT AND OUTCOME

Within 24 hours after surgery, repeated MRI in all dogs revealed hyperintensity in the spinal cord gray matter of the lumbar intumescence on T2-weighted images. In the absence of neurologic improvement, dogs were euthanized at 3, 91, and 34 days after surgery. Postmortem microscopic examination of each dog's spinal cord at the lumbar intumescence revealed necrosis of the gray matter with relative white matter preservation suggestive of an ischemic injury.

CLINICAL RELEVANCE

Dramatic neurologic deterioration following decompressive surgery for intervertebral disk herniation in dogs may be associated with the development of poliomyelomalacia secondary to ischemia. In these 3 dogs, ischemia developed despite probable maintenance of normal spinal cord blood flow and perfusion during anesthesia. To exclude other causes, such as compression or hemorrhage, MRI was repeated and revealed hyperintensity of the spinal cord gray matter on T2-weighted images, which microscopically corresponded with ischemic neurons and neuronal loss.

Full access
in Journal of the American Veterinary Medical Association

Abstract

Case Description—A 10-month-old Boxer was evaluated for fever and signs of cervical pain.

Clinical Findings—Physical examination revealed lethargy, fever, and mucopurulent ocular and preputial discharge. On neurologic examination, the gait was characterized by a short stride. The dog kept its head flexed and resisted movement of the neck, consistent with cervical pain. Clinicopathologic findings included neutrophilic leukocytosis, a left shift, and monocytosis. Cervical radiographs were unremarkable. Cerebrospinal fluid analysis revealed neutrophilic pleocytosis and high total protein content. On the basis of signalment, history, and clinicopathologic data, a diagnosis of steroid-responsive meningitis-arteritis was made.

Treatment and Outcome—The dog was treated with prednisone (3.2 mg/kg [1.45 mg/lb], PO, q 24 h), for 3 weeks with limited response. Consequently, azathioprine (2 mg/kg [0.9 mg/lb], PO, q 24 h) was administered. Three weeks later, the dog was evaluated for tachypnea and lethargy. Complete blood count revealed leukopenia, neutropenia, and a left shift. Thoracic radiography revealed a diffuse bronchointerstitial pattern. The dog subsequently went into respiratory arrest and died. On histologic evaluation, amoebic organisms were observed in the lungs, kidneys, and meninges of the brain and spinal cord. A unique Acanthamoeba sp was identified by use of PCR assay.

Clinical Relevance—This dog developed systemic amoebic infection presumed to be secondary to immunosuppression. The development of secondary infection should be considered in animals undergoing immunosuppression for immune-mediated disease that develop clinical signs unrelated to the primary disease. Although uncommon, amoebic infection may develop in immunosuppressed animals. Use of a PCR assay for identification of Acanthamoeba spp may provide an antemortem diagnosis.

Full access
in Journal of the American Veterinary Medical Association