Foramen magnum decompression with cranioplasty for treatment of caudal occipital malformation syndrome in dogs.

OBJECTIVES: To describe a cranioplasty procedure used in conjunction with foramen magnum decompression (FMD) for the treatment of canine caudal occipital malformation syndrome (COMS), and to evaluate the clinical outcome. STUDY DESIGN: Prospective clinical study. ANIMALS: Dogs (n=21) with COMS diagnosed by magnetic resonance imaging (MRI). METHODS: After FMD, titanium screws were placed around the perimeter of the foramen magnum defect and a skull plate fashioned from titanium mesh and polymethylmethacrylate was attached to the back of the skull, using the titanium screws as anchor posts. Follow-up was obtained by direct examination by the authors, telephone interviews with owners and referring veterinarians, and a questionnaire sent to owners of surviving dogs designed to assign objective measures of response to surgical intervention. Surgical success was defined as improvement in >or=1 aspects of clinical dysfunction (e.g. scratching, pain) postoperatively. Owner-assigned pre- and postoperative quality-of-life (QOL) scores (1-5) for surviving dogs were compared using a Wilcoxon's signed rank test for paired data (P

Procarbazine as adjunctive therapy for treatment of dogs with presumptive antemortem diagnosis of granulomatous meningoencephalomyelitis: 21 cases (1998-2004).

BACKGROUND: Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory disease of the central nervous system. Remission often is short-lived in dogs treated with glucocorticoids. Procarbazine is T cell-specific and crosses the blood-brain barrier. HYPOTHESIS: Dogs with presumptive antemortem diagnosis of GME given procarbazine as adjunctive therapy to prednisone will have improved long-term outcome compared with dogs given no treatment or glucocorticoids alone. ANIMALS: Two groups were studied: (1) Dogs with presumptive antemortem diagnosis of GME treated with procarbazine and prednisone (n = 21); (2) Dogs that had a histologic diagnosis of GME at postmortem examination and received no treatment (n = 11). METHODS: Dogs with presumptive GME treated with procarbazine were identified retrospectively from medical records of 2 veterinary referral hospitals. Selection criteria required all dogs have a neurologic examination, blood work, cerebrospinal fluid analysis, and brain imaging (MRI or CT). RESULTS: Median survival time for all dogs studied was 5.0 months. Median survival time for dogs treated with procarbazine was 14.0 months and for untreated dogs, 0.73 months. Treatment with procarbazine was significantly correlated with survival time (P < .001). Procarbazine was the only independent predictor of survival. Prednisone was reduced in dosage or discontinued in 17 dogs. Adverse reactions to procarbazine therapy included myelosuppression in 7 dogs and hemorrhagic gastroenteritis in 3 dogs. CONCLUSION: These data suggest that procarbazine treatment of presumptive GME may result in greater improved long-term outcome than has been previously reported for glucocorticoid treatment alone and may complement other immunomodulatory therapies. Procarbazine-treated dogs must be monitored for adverse reactions.

Foramen magnum decompression for treatment of caudal occipital malformation syndrome in dogs.

A method for foramen magnum decompression (FMD) in dogs with caudal occipital malformation syndrome (COMS) and results for 16 dogs are described. In brief, a dorsal approach to the caudal portion of the occiput and arch of the atlas was made, and a high-speed drill was used to remove a portion of the occiput in the region of the foramen magnum and the dorsal aspect of C1. The meninges that were exposed were removed or marsupialized to surrounding tissues. Foramen magnum decompression was performed in 16 dogs. No intraoperative complications occurred, and postoperative complications occurred in only 2 dogs after initial surgery and in 1 of these dogs after follow-up surgery. In both dogs, postoperative complications after the initial surgery resolved without additional treatment. One dog was nonambulatory tetraparetic after follow-up surgery and died of a suspected ruptured viscus 9 days after surgery. Four dogs developed evidence of scar formation at the surgery site and required additional surgery. Overall, 14 dogs survived, 1 died, and 1 was euthanatized. Clinical signs resolved in 7 of the 14 dogs that survived, improved in 6, and did not change in 1. Results suggest that FMD may be an effective treatment for dogs with COMS, especially if performed early in the course of the disease.

Risk factors associated with development of seizures after use of iohexol for myelography in dogs: 182 cases (1998).

OBJECTIVE: To determine prevalence of seizures after use of iohexol for myelography and identify associated risk factors in dogs. DESIGN: Retrospective study. ANIMALS: 182 dogs that received iohexol for myelography in 1998. PROCEDURE: Medical records were reviewed for age, breed, sex, weight, dose and total volume of iohexol, injection site, number of injections, lesion type and location, total duration of anesthesia, duration from time of iohexol injection to recovery, presence and number of seizures, and whether surgery followed the myelogram. RESULTS: 39 (21.4%) dogs had at least 1 generalized seizure during or after myelography. Injection site was strongly associated with prevalence of seizures, and risk of seizure was significantly higher after cerebellomedullary injections, compared with lumbar injections. Mean total volume of iohexol administered to dogs that had seizures was significantly higher, compared with that administered to dogs that did not have seizures, although dosage did not differ between groups. Weight was significantly correlated with risk of seizure, and dogs that weighed > 20 kg (44 lb) had higher prevalence of seizures than dogs that weighed < 20 kg. CONCLUSIONS AND CLINICAL RELEVANCE: It is preferential to administer iohexol via the L5-6 intervertebral space to minimize the risk of seizures. Higher prevalence of seizures in large dogs, compared with smaller dogs, may be caused by administration of larger total volumes of contrast agent per volume of CSF.