OBJECTIVE:To report thoracolumbar caudal articular process malformations with secondary constrictive fibrosis of the spinal cord in Pugs.DESIGN:Retrospective case series.ANIMALS:11 Pugs with neurologic dysfunction resulting from constriction of fibrous tissue secondary to thoracolumbar caudal articular process malformation and 5 Pugs with no neurologic dysfunction.PROCEDURES:Medical records of dogs with myelopathy presumably caused by constriction of fibrous tissue secondary to thoracolumbar caudal articular process malformation at 2 referral institutions between 1993 and 2009 were reviewed. Dogs were included in the study if hypoplastic or aplastic thoracolumbar caudal articular processes were present on radiographs, CT images, or MRI images.RESULTS:The most common neurologic examination findings were paraparesis with ataxia or paraplegia but no evidence of hyperpathia along the vertebral column. All dogs' neurologic lesion localization was to the T3-L3 spinal cord segments. Median age at examination was 7. 7 years (range, 2 to 11 years). Five of 11 dogs had a history of unrelated trauma. Four of 11 dogs had urinary or fecal incontinence. Eight of 11 dogs underwent surgical exploration. Despite surgical intervention, all dogs that survived surgery continued to have neurologic deficits.CONCLUSIONS AND CLINICAL RELEVANCE:In the present study, presence of aplastic or hypoplastic articular processes in the thoracolumbar region did not always produce neurologic signs. However, fibrous constrictive myelopathy should be considered in Pugs with pelvic limb gait and postural reaction deficits and lack of hyperpathia upon palpation of the vertebral column. Additional studies are warranted to further characterize the disease process and determine the most effective means of treatment.

A 5.5-year-old castrated male miniature Dachshund was evaluated for an acute onset of reluctance to move its tail. The dog had a 1-week history of difficulty defecating and signs of pain when its tail was manipulated. The dog’s medical history included an episode of signs of neck pain 4 months previously and detection of intervertebral disk extrusion at C2-3, which was successfully treated with a ventral slot decompression procedure. Physical examination at the time of admission revealed a body condition score of 7 out of 9. Otherwise, findings were normal with the exception of signs of pain detected on neurologic examination. The neurologic examination revealed normal mentation, cranial nerve function, gait, and posture. Postural reactions and spinal reflexes were normal; perineal reflexes and anal tone were preserved. Signs of severe discomfort were elicited upon manipulation of the dog’s tail; signs of pain could not be elicited elsewhere in the paravertebral region. On the basis of the results of neurologic examination, the lesion was localized to the sacrum and caudal vertebrae. Radiographs of the lumbosacral portion of the vertebral column were obtained while the dog was under general anesthesia (Figure 1).

A 3-year-old, spayed female rat terrier was evaluated for acute onset of stupor, disorientation, and tetraparesis. Clinical signs progressed over 3 weeks to eventual right-sided hemiparesis and circling to the left. A Cuterebra spp. larva was discovered in the vomitus of the dog 2 weeks after the onset of clinical signs. Cerebrospinal fluid analysis showed chronic inflammation, and magnetic resonance imaging supported a diagnosis of a parasitic tract through the left cerebral hemisphere. Medical management included a tapering anti-inflammatory dose of prednisone. Clinical signs improved slowly over time. This is the first description of a presumptive antemortem diagnosis of canine cuterebrosis in the central nervous system.

OBJECTIVE:To evaluate the degree of pituitary exposure, completeness of hypophysectomy, and perioperative morbidity associated with an alternative paramedian surgical approach and excisional technique for the canine pituitary gland.STUDY DESIGN:Experimental imaging, surgical, and endocrinologic study.ANIMAL POPULATION:Nine healthy, purpose-bred Beagle dogs.METHODS:Surgical landmarks for the pituitary were determined by computed tomography (CT), and then using a ventral paramedian approach medial to the rami of the mandible, the pituitary was exposed and removed en bloc by manipulation and ultrasonic aspiration. Efficacy of the procedure was evaluated using endocrinologic and pathologic observation.RESULTS:CT images allowed the precise location of surgical landmarks for hypophysectomy. Statistically significant decreases in secretion of all measured pituitary hormones except adrenocorticotropic hormone (ACTH) occurred after hypophysectomy. Despite the absence of gross evidence of residual pituitary tissue, immunohistochemical staining revealed residual pituitary cells in the sella turcica of most dogs.CONCLUSION:CT imaging and a paramedian approach facilitated surgical access to the pituitary gland by a transoral technique; however, use of an ultrasonic aspirator removed all visible pituitary glands but left cellular remnants capable of ACTH secretion in the sella turcica.CLINICAL RELEVANCE:Although this technique did not result in complete hypophysectomy, clinical use in dogs with pituitary-dependent hyperadrenocorticism is warranted because the goal is not complete hypophysectomy but removal of a pituitary tumor.

Objective— To develop a safe neurosurgical procedure that accessed the ventral pons and medulla of the dog primarily for the removal of brain stem neoplasms. Study Design— In vivo study. Methods— A cadaver study was performed on mesocephalic dog heads to develop a neurosurgical approach to the ventral brain stem. Based on this study, an approach to the ventral brain stem was developed by basioccipital craniectomy. This procedure was performed on 4 young neurologically normal Beagle dogs to assess morbidity and mortality associated with the procedure. Morbidity was evaluated by subjective criteria, daily complete neurologic examinations, comparison of preoperative and postoperative brain stem auditory evoked response (BAER) tests, and postmortem examinations. Results— Three dogs developed a transient cough but were neurologically normal after surgery. One dog was euthanatized within 12 hours of surgery because of severe postoperative morbidity associated with basilar artery disruption due to improper development of the craniectomy. Prolongations of postoperative BAER latencies were observed in 2 dogs but did not appear to be associated with clinical deficits or histopathologic changes in the brain stem. Minimal histopathologic changes were observed except in the dog with basilar artery disruption. Results of this study indicate that, although technically challenging, this procedure can be performed with minimal morbidity. Clinical Implications— The main indication for this procedure is surgical reduction or biopsy of ventrally located brain stem neoplasms in dogs. The major disadvantage is anatomic restrictions that prevent access to laterally oriented ventral brain stem masses.

Doppler ultrasonography was performed on the cerebral arteries of 19 neonatal dogs. Vascular structures were identified using anatomic preparations of brains pre-injected with a radiopaque silicone rubber product and cleared using a modified tissue clearing technique. Brain sections were subsequently radiographed or examined under a stereomicroscope. Color flow Doppler imaging was used to facilitate positioning of the Doppler calipers for measurement of peak systolic velocity, minimum diastolic velocity, and resistance index. Blood flow velocities in the internal carotid and middle cerebral arteries were lower when measured in transverse images than in sagittal images. The rostral cerebral arteries could be measured using either plane but values obtained from different locations or using different methods of measurement were statistically different. Blood flow velocities generally increased during the first month after birth. Arterial signals were diphasic with flow throughout diastole. Resistance indices most often were between 0.6 and 0.7 and did not exceed 0.86.

In a three‐year prospective study, computed tomographic (CT) and surgical findings were compared for nine large breed dogs with lumbosacral stenosis. Surgically‐excised tissue was examined histologically in seven dogs and additional necropsy evaluation was performed in one dog. The CT abnormalities observed at sites of confirmed cauda equina compression were: loss of epidural fat, increased soft tissue opacity, bulging of the intervertebral disc margin, spondylosis, thecal sac displacement, narrowed intervertebral foramen, narrowed vertebral canal, thickened articular process, articular process subluxation, articular process osteophyte, and telescoped sacral lamina. The CT characteristics of lumbosacral degenerative disease and discospondylitis were similar to those described in humans. In three dogs, CT findings at the site of cauda equina compression were consistent with congenital or developmental spinal stenosis, but the method of surgical exposure precluded confirmation. Epidural fibrosis (eight dogs) and multi‐level CT abnormalities (six dogs) were identified but the cause(s) and significance were unknown.

A case of type IV glycogen storage disease was identified in a Norwegian Forest Cat. Clinical signs reflected multifocal disease predominating in the nervous and musculoskeletal systems. The clinical signs progressed to generalized tonic-clonic seizures and hypoglycemia which differed from a previous report. Prominent lesions showed glycogen inclusions in multiple organ systems. The presence of type IV glycogen storage disease was demonstrated by the lack of any detectable hepatic glycogen branching enzyme activity.

A model simulating acute-compressive spinal cord trauma at the second lumbar spinal cord segment (100 g, 300 seconds) was used to evaluate the efficacy of a vehicle control, methylprednisolone sodium succinate (MPSS), and a 21-aminosteroid compound (U74389G). Dogs were allocated into one of five treatment groups (A to E) using ultrasonographic determination of spinal cord diameters to ensure even distribution of spinal cord diameters among the treatment groups. Initial dosages of the vehicle control (A), methylprednisolone (30 mg/kg of body weight) (B), or U74389G (30 mg/kg, 3 mg/kg, or 10 mg/kg of body weight) (C, D, or E, respectively) were administered intravenously 30 minutes after trauma. Dosages were reduced by one-half for 2 and 6 hour treatments. Then every 4 hours for 42 hours, dosages were reduced one-third and one-sixth from the original dose of methylprednisolone and U74389G, respectively. Neurological examinations were performed daily for 21 days. Histopathological examination of the traumatized spinal cord showed malacic and degenerative lesions. Although significant differences in some portions of the neurological and histopathologic examinations were observed, clinical efficacy for MPSS and U74389G could not be established in this model.

Doppler ultrasonography of the spinal cord was performed in 34 normal, anesthetized dogs following hemilaminectomy. This study was part of an investigation to evaluate the efficacy of a 21‐aminosteroid compound and high dose methylprednisolone for the treatment of spinal cord trauma. Grey‐scale images of the canine spinal cord were similar to those described for the spinal cord of people. Doppler waveforms of intraparenchymal spinal arteries exhibited high end diastolic blood flow velocities, indicating low resistance to flow. Doppler values (mean ± SD) for arteries immediately ventrolateral to the central canal were: Peak Systolic Velocity = 5.78 ± 2.5 cm/sec, Minimum Diastolic Velocity = 3.5 ± 1.62 cm/sec, Mean Velocity = 4.45 ± 1.96 cm/sec, Minimum Diastolic Velocity = 3.5 ± 1.62 cm/sec, Mean Velocity = 4.45 ± 1.96 cm/sec, Systolic/Diastolic ratio = 169 ± 0.19, Pulsatility Index = 0.53 ± 0.09, and Resistance Index = 0.4 ± 0.06.

Prior to trauma, intraoperative ultrasound of the spinal canal in 31 normal dogs was performed through a hemilaminectomy in the left pedicle of L2. A ventral compressive model of spinal cord injury was performed as part of a clinical drug trial. Maximum ultrasonographic spinal cord diameter ranged from 4.9–7.2 mm (5.7 × 0.6). Significant positive correlation (p = 0.023, r = 0.49) was found between age and spinal cord diameter. The dura mater was a separate, well‐defined, echogenic horizontal line in 28 (90%) dogs, dorsally, and in 29 (94%) dogs, ventrally. Cerebrospinal fluid was anechoic. Eighteen (58%) dogs had a well‐defined anechoic dorsal subarachnoid space, whereas 22 (71%) had a well‐defined ventral space. Pia mater was thin but strongly echogenic and covered spinal cord. Central canal was a double hyperechoic line in 17 (55%) dogs and a single‐line in 14 (45%) dogs. A difference in the ultrasonographic appearance between gray and white matter was not seen. Epidural fat and connective tissue was a lobular echogenic material in the ventral epidural space. The periosteal‐vertebral body interface was seen as a bright curvilinear echo with distal acoustic shadowing. Spinal cord parenchyma could be classified subjectively into four groups based upon ultrasonographic appearance. Spinal cord parenchyma had a uniform hypoechogenicity in 8 (27%) dogs (Group 1), subtle low level echoes in 7 (23%) dogs (Group 2), multiple clusters of defined echogenic foci in 12 (37%) dogs (Group 3), and multiple sharply‐defined linear echoes in 4 (13%) dogs (Group 4). There was a significant relationship between pre‐trauma ultrasonographic appearance of the spinal cord and histopathology 21 days after trauma. One (13%) dog in Group 1, 4 (57%) dogs in Group 2,10 (91%) dogs in Group 3, and 3 (75%) dogs in Group 4 had malacia on histological evaluation. Therefore, dogs with echogenic spinal cords or linear echoes within cord parenchyma were significantly more likely to develop malacia rather than Wallerian degeneration after induced spinal cord trauma (p = 0.002). Spinal cord echogenicity may indicate vascularity in a segment of spinal cord and might be prognostic following spinal cord trauma. No complications were found related to intraoperative ultrasound. Hematoma or fibrous tissue formation appeared to impede percutaneous ultrasound of the spinal cord in dogs re‐evaluated forty‐eight hours and one week after surgery.

Journal of Veterinary Internal MedicineVolume 9, Issue 5 p. 370-370 Open Access Idiopathic Neuromyopathy in a Young American Cocker Spaniel Kyle G. Braund, Kyle G. Braund Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorStephen T. Simpson, Stephen T. Simpson Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorJan E. Steiss, Jan E. Steiss Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorNancy R. Cox, Nancy R. Cox Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorHenry J. Baker, Henry J. Baker Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorBruce F. Smith, Bruce F. Smith Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorLisa S. Klopp, Lisa S. Klopp Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorCharlie D. Knecht, Charlie D. Knecht Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorDon C. Sorjonen, Don C. Sorjonen Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this author Kyle G. Braund, Kyle G. Braund Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorStephen T. Simpson, Stephen T. Simpson Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorJan E. Steiss, Jan E. Steiss Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorNancy R. Cox, Nancy R. Cox Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorHenry J. Baker, Henry J. Baker Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorBruce F. Smith, Bruce F. Smith Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorLisa S. Klopp, Lisa S. Klopp Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorCharlie D. Knecht, Charlie D. Knecht Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this authorDon C. Sorjonen, Don C. Sorjonen Spontaneous Neuromuscular Disease Program Scott-Ritchey Research Center College of Veterinary Medicine Auburn University Auburn, ALSearch for more papers by this author First published: September 1995 https://doi.org/10.1111/j.1939-1676.1995.tb01102.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume9, Issue5September 1995Pages 370-370 RelatedInformation

This article describes the functional anatomy of intervertebral discs and their relationship to the vertebrae and spinal cord. The pathologic events and clinical complications of intervertebral disc disease are described. A discussion of proper staging of disc disease and appropriate conservative management of degenerative disc disease is included.