Spinal cord dysfunction secondary to spinal arachnoid cysts (SACs) has been reported previously in dogs. This retrospective study reviews the clinical signs, radiographic findings, and outcome after surgical resection of SACs in 14 dogs. Plain vertebral column radiographs and myelography were done in all dogs. Computed tomography (CT) was done in 7 dogs and magnetic resonance (MR) imaging in 3 dogs. Affected dogs were between 1 and 12 years of age, and 8 of 14 were Rottweilers. Abnormalities detected on neurological examination depended on the location of the SAC. Five dogs had bilobed or multiple SACs. SACs were located in the cervical vertebral column in 11 dogs and in the thoracic vertebral column in 4 dogs. All dogs had dorsally or dorsolaterally located SACs. Two dogs also had additional ventrally located SACs. Spinal cord compression secondary to intervertebral disc extrusion or protrusion was demonstrated at the site of the SACs in 2 dogs. Surgical resection of the SACs was completed in all dogs. Eleven dogs were available for follow-up. Five weeks postoperatively, 7 dogs improved in neurological function, with some residual ataxia and paresis in 6 of these dogs. Neurological function had deteriorated in 4 dogs. It was concluded from this study that Rottweilers have a higher incidence of SACs than other breeds of dog. Furthermore, bilobed or multiple SACs can occur commonly, and myelography effectively localized SACs in dogs. Surgical resection of SACs resulted in improvement in neurological function in the majority of treated dogs.Key words: Canine; Myelogram; Neuroimaging; Rottweiler; Subarachnoid cyst. Spinal arachnoid cysts (SACs) have been reported previously as a cause of neurological dysfunction in dogs and cats. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Although most cysts are thought to be congenital, SACs have been reported in association with spinal cord trauma and intervertebral disc disease.1-10 Thirty-nine cases of SACs have been reported previously. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] In the majority of these reports, there was no age, breed, or gender predilection for cyst occurrence. In 1 report, 6 of 11 dogs were Rottweilers. 16 In most dogs, SACs were located dorsal or dorsolateral to the spinal cord, and in 4 dogs, multiple cysts were reported. In 3 dogs, multiple cysts were present at the same location and in another dog the cysts were located at 2 different anatomic sites. 9,16 Two of the dogs with multiple SACs at the same location also had a ventrally located SAC. 16 Of the 39 dogs previously reported, SACs were located only in the cervical vertebral column in 23 dogs, only in the thoracic vertebral column in 15 dogs, and in both the cervical and thoracic vertebral column in 1 dog. Myelography was used to diagnose SACs in all reports. In 9 dogs, computed tomography (CT) was done, and in 4 dogs, magnetic resonance (MR) imaging was done in addition to myelography to further evaluate the location of SACs. Surgical removal of the SAC was performed in 3...

Forty-six dogs with either cervical (C1-C5 or C6-T2) or thoracolumbar (T3-L3) acute myelopathy underwent prospective conventional computed tomography (CT), angiographic CT, myelography, and CT myelography. Findings were confirmed at either surgery or necropsy. Seventy-eight percent of lesions were extradural, 11% were extradural with an intramedullary abnormality, 7% were intramedullary, 2% were intradural-extra-medullary, and 2% had nerve root compression without spinal cord compression. Intervertebral disc herniation was the most frequent abnormality regardless of signalment or neurolocalization. Twenty-one of 23 Hansen type I disc extrusions but none of the Hansen type II disc protrusions were mineralized. Two chondrodystrophic dogs had acute myelopathy attributable to extradural hemorrhage and subarachnoid cyst. CT myelography had the highest interobserver agreement, was the most sensitive technique for identification of compression, demonstrating lesions in 8% of dogs interpreted as normal from myelography and enabling localization and lateralization in 8% of lesions incompletely localized on myelography due to concurrent spinal cord swelling. None of the imaging techniques evaluated permitted definitive diagnosis of spinal cord infarction or meningo-myelitis but myelography and CT myelography did rule out a surgical lesion in those cases. While conventional CT was adequate for the diagnosis and localization of mineralized Hansen type I disc extrusions in chondro-dystrophic breeds, if no lesion was identified, plegia was present due to concurrent extradural compression and spinal cord swelling, or the dog was nonchondrodystrophic, CT myelography was often necessary for correct diagnosis. r

Seizure control was achieved in most cats with a serum PB concentration between 15 and 45 μg/mL, regardless of the cause of the seizures. A modified 2011 ILAE classification was applied to cats with seizures and enabled classification of cats without specific genetic testing and without identified structural or inflammatory disease. This classification system should be incorporated into veterinary neurology nomenclature to standardize communication between veterinarians and improve comparisons among species.

Spinal cord dysfunction secondary to spinal arachnoid cysts (SACs) has been reported previously in dogs. This retrospective study reviews the clinical signs, radiographic findings, and outcome after surgical resection of SACs in 14 dogs. Plain vertebral column radiographs and myelography were done in all dogs. Computed tomography (CT) was done in 7 dogs and magnetic resonance (MR) imaging in 3 dogs. Affected dogs were between 1 and 12 years of age, and 8 of 14 were Rottweilers. Abnormalities detected on neurological examination depended on the location of the SAC. Five dogs had bilobed or multiple SACs. SACs were located in the cervical vertebral column in 11 dogs and in the thoracic vertebral column in 4 dogs. All dogs had dorsally or dorsolaterally located SACs. Two dogs also had additional ventrally located SACs. Spinal cord compression secondary to intervertebral disc extrusion or protrusion was demonstrated at the site of the SACs in 2 dogs. Surgical resection of the SACs was completed in all dogs. Eleven dogs were available for follow-up. Five weeks postoperatively, 7 dogs improved in neurological function, with some residual ataxia and paresis in 6 of these dogs. Neurological function had deteriorated in 4 dogs. It was concluded from this study that Rottweilers have a higher incidence of SACs than other breeds of dog. Furthermore, bilobed or multiple SACs can occur commonly, and myelography effectively localized SACs in dogs. Surgical resection of SACs resulted in improvement in neurological function in the majority of treated dogs.

A 6-year-old Labrador retriever-cross was evaluated for an abnormal gait and head carriage 6 weeks after suffering trauma. The dog was presented with an ambulatory tetraparesis and was reluctant to move his head. Myelography and computed tomography demonstrated a subluxation of the atlanto-occipital joint with compression of the spinomedullary junction and the brain stem by the occipital bone. Removal of the compressive part of the occipital bone resulted in improvement of the clinical signs within 6 weeks, and resolution of clinical signs occurred 8 months after surgery.

Abstract.A 2-year-old Great Dane dog with a 2.5-week history of progressive paraparesis was presented to the Veterinary Medical Teaching Hospital at the University of Wisconsin-Madison. Neurologic examination revealed nonambulatory paraparesis with reduced to absent withdrawal hind-limb reflexes and lumbar pain. Magnetic resonance imaging and gross pathology confirmed a larger regional lumbar mass and a second smaller extradural mass within the spinal canal. The left lumbar mass was associated with extensive hemorrhage; dissection showed a dark-red, soft, well-circumscribed mass measuring 2 cm 3 1.5 cm 3 0.5 cm within the left fourth lumbar spinal nerve. Histopathological evaluation with immunohistochemistry revealed sheets of round to polygonal cells with diffuse granular cytoplasm demonstrating diastase-resistant periodic acid-Schiff reactivity and positive immunoexpression of S100 and neuron-specific enolase. The smaller extradural mass within the spinal canal exhibited similar morphology. Based on gross, histological, and immunohistochemical evidence, the masses were diagnosed as granular cell tumor.

Brain magnetic resonance images from 42 dogs imaged between 2002 and 2007 were reviewed retrospectively to establish the incidence of trigeminal nerve contrast enhancement. These dogs had otherwise normal MR images and no clinical evidence of trigeminal nerve disease. Contrast enhancement of the entire trigeminal nerve was seen in 39 dogs and in the region of the trigeminal ganglion in all 42 dogs. When contrast enhancement of the trigeminal nerve was observed, the intensity was subjectively less than or equal to that of the pituitary gland. Contrast enhancement of the trigeminal nerve was seen in 42 dogs with no clinical evidence of trigeminal nerve pathology.

Five cats presented with acute-onset neurological signs. Magnetic resonance imaging in four cats showed a T2-weighted hyperintense spinal cord lesion that was mildly contrast-enhancing in three cats. Owing to inflammatory cerebrospinal fluid changes three cats were treated with immunosuppression. One cat was treated with antibiotics. All cats improved initially, but were eventually euthanased owing to the recurrence of neurological signs. Histopathology in all cats showed hyaline degeneration of the ventral spinal artery, basilar artery or associated branches with aneurysmal dilation, thrombosis and ischemic degeneration and necrosis of the spinal cord and brain. Two cats also had similar vascular changes in meningeal vessels. Vascular hyaline degeneration resulting in vascular aneurysmal dilation and thrombosis should be a differential diagnosis in cats presenting with acute central nervous system signs.