An 11-year-old 9-kg (19.8-lb) sexually intact female English Cocker Spaniel was referred for evaluation because of gait abnormalities that had developed several weeks previously and had since progressed. The dog had no history of previous illness, and findings of physical examination, CBC, and serum biochemical analysis were unremarkable.
Results of neurologic examination indicated the dog was ambulatory with severe ataxia of the hind limbs. Proprioception was decreased in the right and left hind limbs (right more affected than left), and spinal reflexes were bilaterally unremarkable. Moderate signs of pain were detected during palpation of the lumbar portion of the vertebral column. No history of urinary incontinence was reported by the owner, and abdominal palpation revealed that the urinary bladder was moderately filled. The cutaneous trunci reflex was unremarkable on both sides. Findings suggested a lesion in the T3-L3 spinal cord segment. The degree of neurologic impairment was graded as 3/5 (nonambulatory paraparesis) on the basis of a published grading scheme.1
To further characterize the lesion, the decision was made to perform MRI of the thoracolumbar and lumbar portion of the spinal cord. In preparation for imaging, the dog received a fentanyl bolus administered IV and was anesthetized with propofol. Endotracheal intubation was performed, and anesthesia was maintained with isoflurane in oxygen.
Magnetic resonance imaginga was performed with a 1.5-T magnet. T2-weighted sagittal and transverse scans, T1-weighted precontrast dorsal scans, and T1-weighted sagittal and transverse postcontrast scans with fat saturation were acquired, revealing a labulated mass originating from the right pedicle of L4 (Figure 1). The lesion was extradural in nature, causing considerable compression of the spinal cord (50% stenosis of the vertebral canal). The mass was well demarcated with sharp margins and was generally hypointense relative to healthy myelon on T2-weighted images but had isolated hyperintense areas. The mass was 11.4 mm long, 7.8 mm high, and 6.5 mm wide. In the T1-weighted precontrast dorsal images, the lesion was markedly hypointense relative to CSF, was slightly inhomogeneous, and had sharp margins. T1-weighted postcontrasat transverse images with fat saturation revealed heterogeneous enhancement with infiltration of the L4 lamina on the right side as well as bilateral contrast enhancement in the angle between the L4 processus spinosus and lamina.
On the basis of these findings, an extradural compressive lesion infiltrating or originating from the vertebral arch and reactive soft tissue changes adjacent to the lesion were suspected. Differential diagnoses included a primary or secondary bone tumor or an inflammatory or infectious process, such as a bacterial or fungal granuloma.
The decision was made to perform decompressive surgery. The dog was premedicated and anesthetized as described for the MRI examination. A right lateral approach was chosen to expose the lateral aspects of the vertebral bodies at L4–5. The integrity of the right L4 pedicle was disturbed by a white space-occupying structure that protruded slightly just cranial to the origin of the dorsal articular facet of L4. The lesion was of fibrous consistency and had a cystic center containing a small amount of mucoid, white fluid (approx 0.5 mL), which flowed out when the structure was penetrated with a dental scraper. The vertebral canal was opened with the aid of a pneumatic drill by removal of the intact bone cranial and ventral to the lesion and removal of abnormal tissue with rongeurs. The articular processes caudal to the lesion were removed during the hemilaminectomy. Abnormal tissue was excised in pieces from the vertebral canal. Adhesions of the mass to the dura were identified that could be relieved with gentle blunt dissection. The dura remained intact.
After complete removal of the mass, an imprint was visible on the lateral aspect of the myelon. The surgical site was rigorously flushed with sterile saline (0.9% NaCl) solution, and the wound was closed in layers in a routine fashion. The fascia and subcutaneous tissues were apposed in a simple interrupted pattern with 3–0 polydioxanone synthetic absorbable suture, and the skin was closed in a simple interrupted pattern with 4–0 polyamide synthetic nonabsorbable suture.
The dog recovered from surgery without complication, and neurologic function improved completely within 14 days after surgery. Excised tissue fragments were fixed in neutral-buffered 4% formalin solution, processed, embedded in paraffin, sectioned at 5 μm, and stained with H&E stain. Histologic examination revealed a cyst and several fragments of collagenous fibrous tissue with large foci of mineralization. The cyst was similar in histologic appearance to intestinal tissue (Figure 2). It was delineated by smooth muscle, collagenous fibrous tissue, and epithelium. The smooth muscle was arranged in 2 layers of varying thickness, with the inner layer concentrically arranged and the outer layer longitudinally arranged. These 2 layers were separated in several places by a plexus containing nerve fibers and rare small ganglion cells, resembling the myenteric plexus (Auerbach plexus) found in intestinal tissue. The muscle layer was covered by collagenous tissue, which was covered by a layer of monolayered to pseudostratified columnar epithelium without cilia. Single goblet cells filled with mucus were identified. Multifocal nodular infiltrations of lymphocytes were identified, resembling rudimentary follicles of a gut-associated lymphoid tissue. The epithelium was multifocally ulcerated over large areas. Beneath the ulcerations, the collagenous fibrous tissue was thickened and infiltrated with macrophages. The lumen of the cyst was filled with basophilic, amorphous, mineralized material containing cholesterol clefts.
One year after surgery, the owner reported complete resolution of previously observed clinical signs, and findings of neurologic examination were unremarkable. Two years after surgery, the dog was euthanized for an unrelated reason (end-stage heart disease), and no neurologic deficits were evident before that point. The owner declined necropsy.
MAGNETOM Espree, Siemens, Berlin, Germany.
1. Sharp JHN, Wheeler SJ. Patient examination. In: Sharp JHN, Wheeler SJ, eds. Small animal spinal disorders, diagnosis and surgery. 2nd ed. Edinburgh: Elsevier Mosby, 2005;19–33.
2. Rossi A, Gandolfo C, Morana G, et al. Current classification and imaging of congenital spinal abnormalities. Semin Roentgenol 2006; 41: 250–273.
3. Gauden AJ, Khurana VG, Tsui AE, et al. Intracranial neuroenteric cysts: a concise review including an illustrative patient. J Clin Neurosci 2012; 19: 352–359.
4. Savage JJ, Casey JN, McNeill IT, et al. Neurenteric cysts of the spine. J. Craniovertebr Junction Spine 2010; 1: 58–63.
5. Lippman CR, Arginteanu M, Purohit D, et al. Intramedullary neurenteric cysts of the spine case report and review of the literature. J Neurosurg 2001; 94: 305–309.
6. Doige CE. Congenital cleft vertebral centrum and intra- and extraspinal cyst in a foal. Vet Pathol 1996; 33: 87–89.
7. Rendle DI, Durham AE, Bestbier M, et al. Neurenteric cyst with associated butterfly vertebrae in a seven-month-old colt. Vet Rec 2008; 162: 558–561.
8. Wilkins RH, Odom GL. Spinal intradural cysts. In: Vinken PJ, Bruyn GW, eds. Tumours of the spine and spinal cord, part II. Handbook of clinical neurology. Vol 20. Amsterdam: North Holland Publishing Co, 1976;55–102.
9. Dunham CP, Curry B, Hamilton M. Malignant transformation of an intraaxial-supratentorial neurenteric cyst—case report and review of the literature. Clin Neuropathol 2009; 28: 460–466.
10. Rauzzino MJ, Tubbs RS, Alexander E, et al. Spinal neurenteric cysts and their relation to more common aspects of occult spinal dysraphism. Neurosurg Focus 2001; 10: 1–10.
11. Tubbs RS, Salter EG, Oakes WJ. Neurenteric cyst: case report and a review of the potential dysembryology. Clin Anat 2006; 19: 669–672.
12. Bentley JF, Smith JR. Developmental posterior enteric remnants and spinal malformations: the split notochord syndrome. Arch Dis Child 1960; 35: 76–86.
13. Emura T, Hashizume K, Asashima M. Experimental study of the embryogenesis of gastrointestinal duplication and enteric cyst. Pediatr Surg Int 2003; 19: 147–151.
14. Paleologos TS, Thom M, Thomas DG. Spinal neurenteric cysts without associated malformations. Are they the same as those presenting in spinal dysraphism? Br J Neurosurg 2000; 14: 185–194.
15. Sharma RR, Ravi RR, Gurusinghe NT, et al. Cranio-spinal enterogenous cysts: clinico-radiological analysis in a series of ten cases. J Clin Neurosci 2001; 8: 133–139.
16. Devkota UP, Lam JM, Ng H, et al. An anterior intradural neurenteric cyst of the cervical spine: complete excision through central corpectomy approach. Case report. Neurosurgery 1994; 35: 1150–1154.
17. de Oliveira RS, Cinalli G, Roujeau T, et al. Neurenteric cysts in children: 16 consecutive cases and review of the literature. J Neurosurg 2005; 103: 512–523.
19. Menezes AH, Traynelis VC. Spinal neurenteric cysts in the magnetic resonance imaging era. Neurosurgery 2006; 58: 97–105.
20. Tortori-Donati P, Rossi A, Biancheri R, et al. Magnetic resonance imaging of spinal dysraphism. Top Magn Reson Imaging 2001; 12: 375–409.
21. Sasani M, Ozer AF, Oktenoglu BT, et al. Excision of an asymptomatic cervical intradural neurenteric cyst through the anterior approach: a study of two cases and a review of the literature. Spine J 2007; 7: 720–727
22. Savardekar A, Salunke P, Rane S, et al. Dorsally placed extradural infected neurenteric cyst in a two-year old with paraspinal extension. Neurol India 2012; 60: 129–131.
23. Surash S, Ismail A, Loughrey C, et al. Malignant transformation of a neurenteric cyst in the posterior fossa following complete excision. Br J Neurosurg 2009; 23: 458–461.