Vertebral stabilization using positively threaded profile pins and polymethylmethacrylate, with or without laminectomy, for spinal canal stenosis and vertebral instability caused by congenital thoracic vertebral anomalies.

OBJECTIVE: To describe diagnostic findings, surgical technique, and outcome in dogs with thoracic spinal canal stenosis and vertebral instability secondary to congenital vertebral anomalies. STUDY DESIGN: Retrospective clinical study. ANIMALS: Dogs (n=9) with thoracic spinal canal stenosis. METHODS: Medical records (1995-1996; 2000-2006) of 9 dogs with a myelographic diagnosis of spinal canal stenosis and/or vertebral instability secondary to congenital vertebral anomaly that were surgically managed by vertebral stabilization with or without laminectomy were reviewed. Data on pre- and postoperative neurologic status, diagnostic findings, surgical techniques, and outcomes were retrieved. Follow-up evaluations were performed at 1, 2, and 6 months. Long-term outcome was assessed by means of clinical examination or owner telephone interviews. RESULTS: Spinal cord compression was confirmed by myelography, and in 2 dogs, dynamic compression by stress myelography. Eight dogs regained the ability to ambulate postoperatively. One dog with a partial recovery regained voluntary movement but did not become ambulatory. CONCLUSIONS: Spinal cord injury secondary to congenital vertebral anomaly may have a good outcome when treated by vertebral stabilization with or without laminectomy. Adequate stabilization of the vertebrae and improved neurologic outcome were achieved in most dogs. CLINICAL RELEVANCE: Vertebral stabilization using positively threaded profile pins and polymethylmethacrylate with or without laminectomy is an effective treatment for spinal canal stenosis and vertebral instability secondary to congenital thoracic vertebral anomalies.

Polymerase chain reaction screening for DNA viruses in paraffin-embedded brains from dogs with necrotizing meningoencephalitis, necrotizing leukoencephalitis, and granulomatous meningoencephalitis.

The objective of this investigation was to determine whether or not herpesvirus (herpes-), adenovirus (adeno-), or canine parvovirus DNA is present in the brains of dogs with necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalitis (GME). Paraffin-embedded brain specimens from 12 histopathologically confirmed dogs with NME, 3 with NLE, and 7 with GME were screened for viral DNA with degenerate herpes- and adenovirus polymerase chain reaction (PCR) and a canine parvovirus-specific PCR. Positive-control specimens included genomic viral DNA and paraffin-embedded tissues from dogs with confirmed herpes-, adeno-, or canine parvovirus infections. Herpes-, adeno-, or canine parvovirus DNA was amplified by PCR from the corresponding positive-control specimens. Negative controls included 7 dogs with various brain disorders and produced no viral amplicons. The 22 dogs with NME, NLE, and GME were negative for viral DNA. Additional studies testing for other viruses or inherited genetic mutations are warranted to gain insight into the etiologies of NME, NLE, and GME. We discuss potential etiologies and provide a clinical and histopathologic overview of these common canine encephalitides.

Use of a multiplex polymerase chain reaction assay in the antemortem diagnosis of toxoplasmosis and neosporosis in the central nervous system of cats and dogs.

OBJECTIVE: To develop a multiplex polymerase chain reaction (PCR) assay for the detection of Toxoplasma gondii and Neospora caninum DNA in canine and feline biological samples. SAMPLE POPULATION; Biological samples from 7 cats with systemic (n = 4) or CNS (3) toxoplasmosis, 6 dogs with neospora- or toxoplasma-associated encephalitis, and 11 animals with nonprotozoal disease. PROCEDURE: Primers for T gondii, N caninum, and the canine ferritin gene (dogs) or feline histone 3.3 gene (cats) were combined in a single PCR assay. The DNA was extracted from paraffin-embedded brain tissue, CSF, or skeletal muscle. The PCR products with positive results were cloned, and sequence identity was confirmed. RESULTS: Of 7 cats and 4 dogs with immunohistochemical or serologic evidence of toxoplasmosis, PCR results were positive for all cats and 3 dogs for T gondii, and positive for T gondii and N caninum for 1 dog. Another dog had negative PCR results for both parasites. Of 2 dogs with immunohistochemical or serologic evidence of neosporosis, PCR results were positive for 1 for N caninum and positive for the other for T gondii. All negative-control samples yielded negative results for T gondii and N caninum on the PCR assay. CONCLUSIONS AND CLINICAL RELEVANCE: Standard tests for toxoplasmosis or neosporosis associated with the CNS rely on serologic, histologic, or immunohistochemical analysis and can be difficult to interpret. The multiplex PCR assay with built-in control reactions could be a complementary clinical tool for the antemortem diagnosis of toxoplasmosis or neosporosis associated with the CNS.

Polymerase chain reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia.

Cerebellar hypoplasia in cats is caused most commonly by an in utero or perinatal infection with feline panleukopenia virus (parvovirus). Cerebellar hypoplasia has been reported infrequently in dogs, but no viral etiology has been identified to date. DNA was extracted from archival, paraffin-embedded, cerebellar tissue from 8 cats and from 2 canine littermates with cerebellar hypoplasia, 2 canine littermates with cerebellar cortical abiotrophy, 6 dogs with congenital cerebellar vermal defects, 1 dog with congenital hydranencephaly, and 15 dogs and cats with various encephalitdes. The DNA extracted from each cerebellum was subject to polymerase chain reaction (PCR) amplification by 3 primer pairs specific for parvovirus DNA. Sequence analysis of PCR products from each of the 8 cats and 2 dogs with cerebellar hypoplasia confirmed their identity with parvoviral DNA. The 6 dogs with cerebellar vermal defects, 2 dogs with cortical abiotrophy, 1 dog with congenital hydranencephaly, and all control samples were PCR negative for parvovirus. Parvoviral structural proteins were not identified by immunohistochemistry in either dog with cerebellar hypoplasia. This study shows that parvoviral DNA can be amplified from feline and canine archival brain tissue and that cerebellar hypoplasia in dogs might be associated with in utero parvovirus infection.

Relationship among basilar artery resistance index, degree of ventriculomegaly, and clinical signs in hydrocephalic dogs.

Forty-four transcranial Doppler ultrasound studies were performed in 36 dogs. The ratio of the height of the ventricle to the height of the brain (VB ratio) was calculated to determine the severity of ventriculomegaly. Resistance index (RI) was calculated from Doppler measurements of the blood flow velocity in the basilar artery and neurologic signs were scored on a scale of 0 to 3. Based on clinical and ultrasonographic findings, dogs were divided into four groups (normal controls, asymptomatic hydrocephalus, symptomatic hydrocephalus, and other intracranial disease). RI and VB ratio were compared between the groups of dogs and compared with neurologic signs in hydrocephalic dogs. RI ranged from 0.50 to 0.81 (mean, 0.68). Resistance index was significantly higher in dogs with symptomatic hydrocephalus and other intracranial disease when compared with the other two groups. The degree of ventriculomegaly was significantly higher in dogs with symptomatic hydrocephalus than the other groups, but there was substantial overlap between asymptomatic and symptomatic hydrocephalus groups. Combining measurements of VB ratio and RI allowed detection of symptomatic hydrocephalus with a sensitivity of 77% and a specificity of 94%. The severity of neurological signs was significantly correlated with RI and with VB ratio in hydrocephalic dogs, and in dogs evaluated on more than one occasion, changes in neurologic status were accompanied by changes in RI but not in VB ratio. All asymptomatic hydrocephalic dogs with a VB ratio of greater than 60% eventually developed neurologic signs. Our results suggest that ultrasonographic measurement of VB ratio and basilar artery RI may allow identification of dogs with symptomatic hydrocephalus or dogs that are at risk of developing symptomatic hydrocephalus. Repeated RI measurements are a useful means of monitoring dogs with a variety of intracranial diseases.

Use of vagal nerve stimulation as a treatment for refractory epilepsy in dogs.

OBJECTIVE: To evaluate safety and efficacy of vagal nerve stimulation in dogs with refractory epilepsy. DESIGN: Placebo-controlled, double-masked, crossover study. ANIMALS: 10 dogs with poorly controlled seizures. PROCEDURE: A programmable pacemaker-like device designed to deliver intermittent stimulation to the left cervical trunk of the vagus was surgically implanted in each dog. Dogs were assigned randomly to two 13-week test periods, 1 with nerve stimulation and 1 without nerve stimulation. Owners recorded data on seizure frequency, duration, and intensity, as well as adverse effects. RESULTS: No significant difference in seizure frequency, duration, or severity was detected between overall 13-week treatment and control periods. During the final 4 weeks of the treatment period, a significant decrease in mean seizure frequency (34.4%) was detected, compared with the control period. Complications included transient bradycardia, asystole, and apnea during intraoperative device testing, and seroma formation, subcutaneous migration of the generator, and transient Horner's syndrome during the 14-day period between surgery and suture removal. No adverse effects of stimulation were detected, and most owners were satisfied with the treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Vagal nerve stimulation is a potentially safe approach to seizure control that appears to be efficacious in certain dogs and should be considered a possible treatment option when antiepileptic medications are ineffective.

Dorsal laminectomy for caudal cervical spondylomyelopathy: postoperative recovery and long-term follow-up in 20 dogs.

OBJECTIVE: To evaluate the postoperative morbidity and long-term outcome of dogs after dorsal laminectomy for caudal cervical spondylomyelopathy (CCSM). STUDY DESIGN: Retrospective study. SAMPLE POPULATION: Twenty dogs with CCSM. METHODS: Medical records of dogs treated by dorsal laminectomy for CCSM at North Carolina State University and Colorado State University between 1989 and 1999 were reviewed. Information on signalment, onset, progression and duration of clinical signs, diagnostic testing, sites of dorsal laminectomy, postoperative complications, length of hospitalization, and the ambulatory status on discharge was recorded. A minimum follow-up of 7 months was required for inclusion in the study. Neurologic status was graded (0 to 5) preoperatively, 2 days after surgery, and at the time of the study (final score). Improvement or worsening of the neurologic status was assessed by comparison of different scores for each dog. Additional follow-up information was obtained by means of a detailed telephone questionnaire directed at both the owner and referring veterinarian. RESULTS: Mean duration of clinical signs before surgery was 4.9 months. At admission, 15 dogs were ambulatory and 5 were nonambulatory. Neurologic status worsened in 70% of dogs 2 days after surgery but improved in all but 1 dog over the long term. Mean time to optimal recovery was 3.6 months. Long-term follow-up ranged from 7 months to 9 years (mean +/- SD, 3.2 +/- 2.4 years). Four dogs had confirmed recurrence; 2 other dogs may have had recurrence. CONCLUSIONS: Dorsal cervical laminectomy is an effective treatment for CCSM in those dogs with dorsal compression or multiple sites of involvement. CLINICAL RELEVANCE: Although most dogs' neurologic status transiently worsened after surgery, long-term outcome and recurrence rates were comparable to those seen with other surgical techniques for CCSM.

Magnetic resonance imaging features of lissencephaly in 2 Lhasa Apsos.

Two Lhasa Apsos were diagnosed with lissencephaly based on MR imaging and clinical findings. Histologic confirmation of the diagnosis was obtained in one dog. The MR imaging appearance of the brain in 2 Lhasa Apsos with lissencephaly was of a smooth cerebral surface and a thick neocortex with an absence of the corona radiata. This correlated very well with the histopathologic findings in the dog. Our findings, together with the histopathologic features reported previously, are most consistent with Lhasa Apsos having the canine equivalent of human classical lissencephaly. MR is the imaging modality of choice for antemortem diagnosis of canine lissencephaly.

CT findings of intracranial blastomycosis in a dog.

Computed tomography (CT) findings in a dog with intracranial blastomycosis were marked periventricular contrast enhancement of the lateral ventricles, the 3rd ventricle, and the mesencephalic aqueduct. The CT appearance correlated with the histopathologic findings, where severe ependymitis was present throughout the ventricular system and there was stenosis of the mesencephalic aqueduct due to an inflammatory infiltrate. CT is therefore recommended as a screening test for intracranial blastomycosis in dogs and also as an imaging modality for follow-up evaluation after treatment. This is particularly true in dogs with systemic or ocular blastomycosis, which appear to be at higher risk of developing CNS involvement.