Myelographic findings in dogs with vertebral column fractures: A study of 6 clinical cases

Introduction

Myelography is a specialized contrast radiographic technique used to evaluate the spinal cord by injecting a positive contrast medium into the subarachnoid space (Wheeler, 1989) [11] . In dogs with spinal trauma, prompt and accurate diagnosis is essential for appropriate therapeutic intervention. Although conventional radiography is useful for detecting vertebral fractures and luxations, it frequently fails to demonstrate spinal cord compression or associated soft tissue lesions. Consequently, myelography is routinely employed following survey radiography to accurately localize spinal cord lesions and to determine the severity and extent of injury. Since its introduction in canine practice during the early 1950s (Hoerlein, 1953) [4] , myelography has become one of the most commonly used contrast techniques in veterinary neuroradiology. The availability of safer, non-ionic contrast agents and the reduced cost of the procedure have made it a practical diagnostic tool in modern veterinary practice. Myelography is particularly indicated when survey radiographs do not permit precise localization or assessment of spinal cord abnormalities, or when neurological deficits are inconsistent with radiographic findings (Brawner Jr. and Hathcock, 2003) [2] . By outlining the subarachnoid space, the procedure provides indirect evidence of spinal cord compression through alterations in the normal flow of contrast medium and aids in identifying the site and nature of compressive lesions. Therefore, myelography remains an invaluable investigation for establishing a definitive diagnosis, planning surgical intervention, and formulating an accurate prognosis in dogs with spinal disorders.

Materials and Methods

A total of 6 dogs presenting with clinical signs of spinal disorders were included in the study. All cases were subjected to a comprehensive neurological examination and conventional survey radiography of the vertebral column. Further evaluation of spinal cord involvement and damage was carried out using myelography. All 6 dogs were premedicated with Atropine (0.045 mg/kg, S/C) and xylazine (0.5 mg/kg, I/V) 5 minutes before the induction of general anaesthesia. All the dogs were anaesthetized with Propofol (3 mg/kg, I/V) and maintained with Ketofol additional dose as and when required. Cisternal puncture was performed after surgical preparation of the area between the external occipital protuberance and the first cervical vertebra. The dog was positioned in lateral recumbency at the edge of the examination table, with the head maintained in dorsiflexion at approximately 90° to the neck by an assistant. The ear adjacent to the table was tucked beneath the head. Following standard aseptic procedures, anatomical landmarks were identified using the left hand: the external occipital protuberance with the middle finger, the wing of the atlas with the thumb, and the atlanto-occipital space with the index finger. The puncture site was located at the intersection of two imaginary lines: one extending along the midline from the external occipital protuberance to the dorsal spinous process of the axis, and the other drawn perpendicular to it across the cranial borders of the atlas wings. The spinal needle was inserted at the identified site through a slight depression and advanced perpendicularly through the skin and underlying musculature toward the atlanto-occipital space. Advancement continued until a distinct loss of resistance or "pop" was perceived, indicating penetration of the atlanto-occipital joint capsule and ligamentum flavum, and entry into the subarachnoid space. In lightly anesthetized dogs, puncture of the dura mater occasionally elicited a brief cutaneous reflex response. Successful entry into the subarachnoid space was confirmed by the appearance of cerebrospinal fluid (CSF) at the needle hub. Adequate placement of the needle bevel within the subarachnoid space was ensured by observing a steady flow of CSF. Iohexol was then administered at a dosage of 0.3-0.5 mL/kg. All dogs were evaluated by survey radiography and myelography.

Result and Discussion

Myelographic evaluation of the six clinical cases demonstrated a range of alterations in the contrast columns corresponding to the severity and location of spinal cord injury. In Case No. 1, dorsal displacement of the ventral contrast column was observed at the L3-L4 intervertebral disc space, suggesting a traumatic intervertebral disc protrusion with associated extradural spinal cord compression (Plate 1). In Case No. 2, the ventral contrast column was absent between the T 3 and T 12 vertebral segments, which was likely attributable to spinal cord swelling and concussion. Additionally, opacification of the central canal was evident, probably due to inadvertent placement of the spinal needle within the central canal, a finding similar to that reported by Kirberger and Wrigley (1993) [5] (Plate 2). In Case No. 3, attenuation of both the dorsal and ventral contrast columns, together with complete absence of contrast medium over the T 11 -T 13 vertebrae, was recorded (Plate 3). Comparable findings have been described by Tartarelli et al. (2005) [10] in dogs with thoracolumbar disc extrusion. According to Widmer and Thrall (2007) [12] , severe intramedullary swelling may completely obliterate the contrast column over affected spinal segments, thereby masking the extradural component of the lesion. Likewise, Sharp and Wheeler (2005a) [9] reported poor filling of the subarachnoid space in animals with spinal cord swelling, while Olby et al. (1994) [8] and Morgan and Bailey (2000) [7] documented similar myelographic features in dogs with disc protrusion. Although these findings were suggestive of extradural compression, interpretation of the myelogram was difficult because the contrast medium was absent over several spinal segments. In addition, dorsal elevation of the ventral contrast column at the T 10 -T 11 and T 13 -L1 intervertebral spaces indicated mild intervertebral disc protrusion at these levels. In Cases No. 4 and 5, the progression of the contrast medium was interrupted before reaching the lesions identified on survey radiographs. In Case 4, the contrast column terminated at T 12 , despite the lesion being localized at L1 (Plate 4), while in Case 5, contrast flow ceased at L2, although the radiographic abnormalities involved the L3 and L4 vertebrae (Plate 5). This premature cessation of contrast flow was most likely caused by spinal cord oedema, which obliterated the subarachnoid space and prevented normal distribution of the contrast agent, thereby obscuring the exact origin of the lesion. Similar observations were reported by Lamb (1994) [6] . Hoerlein (1971) [3] also noted that contrast medium frequently stops flowing approximately 1/2 to 1 vertebral segment cranial to the lesion due to spinal cord oedema. Comparable findings were documented by Lamb (1994) [6] , who observed that the contrast agent failed to progress to the site of injury, indicating severe spinal cord compression. Furthermore, the absence of contrast medium caudal to the lesion was probably due to marked cord swelling or compression preventing its caudal passage, in agreement with the findings of Adamo (2010) [1] . Consequently, myelography in these cases allowed only approximate localization of the lesion, while accurate assessment of its full extent remained difficult. In Case No. 6, the contrast medium traversed the compressive lesion and outlined the spinal cord up to the L2 vertebral level, with attenuation of both the dorsal and ventral contrast columns extending caudally towards the cauda equina (Plate 6). This appearance was most likely the result of diffuse narrowing of the subarachnoid space caused by spinal cord oedema and haemorrhage. Similar survey radiographic and myelographic findings have previously been reported by Lamb (1994) [6] .

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