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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.

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.