## 1 Introduction  
The vertebral venous plexus (VVP) is a thin-walled, valeveless venous network that surrounds the entire length of the vertebral column, terminating at the cephalad end in the cerebral venous sinuses [1, 2]. According to its position inside or outside of the vertebral canal, the vertebral venous plexus can be divided into three intercommunicating divisions:the internal vertebral venous plexus, external vertebral venous plexus, and basivertebral veins [1]. The internal vertebral venous plexus (_plexus vertebral interrus ventralis_) (IVVP) is also known as the longitudinal venous sinus, vertebral venous sinuses, epidural venous plexus, paravertebral veins, and meningorachidean plexus [3]. The IVVP lies within the vertebral canal, inside the epidural space, and along the dorsal surface of the vertebral bodies and intervertebral disks [1,2] (Figure 1). Cranially, the IVVP communicates with the basilar sinuses at the level of the foramen magnum, and caudally, it extends to the fourth or sixth caudal verteba [1]. The VVP drains blood from the vertebral column, the paravertebral musculature, the spinal cord, the meninges, and the nerve roots of the spinal nerves [3]. In addition to its normal drainage function, this vascular network can also be a collateral pathway for blood return towards the heart in cases of occlusion or ligation of the caval venous system [4]. Clinically, in humans and animals, rupture of the IVVP has been associated with the etiology of spontaneous spinal epidural hematomas [5,6]. Doberman pinchers with a deficiency of von Willebrand factor (VIII-related antigen) can develop significant spinal epidural hemorrhage due to laceration of the IVVP, which results in progressive neurological deficits [7]. Following Hansen type I intervertebral disk herniation, the extruded nucleus pulposus can be expelled laterally and rupture the IVVP. This can result in bleeding, hematoma formation, and subsequent extradural spinal cord compression [8]. The continuity of the valveless IVVP throughout the length of the neuroaxis enables bacteria and tumor cells to travel from the thorax, abdomen, and pelvis to the head and vertebral column when intrathoracic or intra-abdominal pressure is increased [9]. This phenomenon has been termed paradoxical embolism, retrograde venous invasion, and Batson's phenomenon [9]. In dogs, metastasis of osteosarcoma and pheochromocytomas into the central nervous system is hypothesized to occur by retrograde venous spread through the VVP. Diskospondylitis, vertebral osteomyelitisitis, and infectious diskitis in dogs with primary sites of infection elsewhere in the body have been explained by this mechanism [10]. The IVVP may participate in the etiology of fibrocafilaginous embolism of the spinal cord vasculature (also known as embolic myelopathy) in dogs [11]. In humans, the IVVP also participates in the pathophysiology of other spinal cord vascular lesions, such as arteriovenous fistula and venous malformations [12]. Recently, venous aneurism of the IVVP in a Scottish Deerhound was reported concurrently with severe dilatation of the venous sinuses [13]. Additionally, case reports in dogs have described abnormal enlargement of the IVVP in sighthounds by magnetic resonance imaging (MRI) with clinical signs of radiolopathies and myelopathy [14].  
Understanding anatomical vertebral morphometry is an important factor when interpreting the pathological changes associated with several structural spinal diseases. The aims of the present study were to provide an in vivo morphometric description of the normal lumbar IVVP and surrounding vertebral structures using contrast-enhanced computed tomography (CT) in dogs.