Degenerative lumbosacral stenosis

Introduction

Degenerative lumbosacral stenosis (DLSS) is a dynamic disease in many aspects. The controversies surrounding this disease syndrome are numerous and different views how to diagnose and treat DLSS make the discussion of this disease among veterinary colleagues a dynamic event!

DLSS is a term currently used to describe a disorder in dogs associated with degeneration of the structures of the lumbosacral junction leading to signs of low back pain and/or neurologic signs associated with compression of the cauda equina. DLSS has a multifactorial origin in which intervertebral disc (IVD) degeneration plays a major role. The term degenerative lumbosacral stenosis is used to define an acquired narrowing of the vertebral canal, intervertebral foramina, or both, which results in compressive radiculopathy of one or more nerve roots of the cauda equina. Degeneration of the LS junction of large-breed dogs is analogous to L5-S1 intervertebral disc degeneration in humans. Loss of hydration of the nucleus pulposus and chondroid degeneration leads to bulging of the annulus fibrosus of the L7-S1 intervertebral disc (a type II protrusion) and loss of intervertebral spacing. One or more nerve roots of the cauda equina may become compressed by a combination of disc prolapse and hypertrophy/fibrosis/osteophytosis of the supporting tissues associated with the L7-S1 articulations.

DLSS can present in a number of different ways and because of this, patients suffering from DLSS can sometimes be misdiagnosed. DLSS patients are typically neuro-orthopedic patients; the disorder is per definition a spinal disease but the presentation is more that of an orthopedic disorder. As DLSS mainly affects middleaged and older dogs they can often have other concurrent degenerative orthopedic or neurologic disorders such as, respectively, osteoarthritis or degenerative myelopathy. Hence it is helpful if these patients are subjected to both orthopedic and neurologic examinations.

Findings during orthopedic examination are directly related to the compression of the cauda equina, and the most consistent finding is lumbosacral pain on palpation. LS pain can be evoked by the lordosis test and hyperextension of the tail base with simultaneous pressure at the LS region. Hyperextension of the hip joints (one at a time) with the dog standing or in lateral recumbence should not cause pain unless the dog has pain derived from the hip. However, many dogs with DLLS and hip dysplasia allow gradual extension of the hip joints but start to show a pain reaction when hyperextending the lumbosacral junction. Especially in these cases the experienced clinician will note the difference between a mild response to extension of the dysplastic hip joint and the overt pain response due to added compression to the cauda equina. This is proof of the dynamic nature of the compression and stenosis: motions of extension will cause downward deflection of the sacral lamina and worsens compression on the cauda equina (Figure 1). Other common findings are unior bilateral hind limb lameness, atrophy of the hind limb musculature (innervated by the sciatic nerve) and a weight shift from hind limbs to the fore limbs. Unilateral entrapment of the L7 and/or S1 nerves (Figure 1C) causes radiating nerve root pain (the so-called nerve root signature, radiculopathy) and unilateral lameness.

Overt neurological deficits are extremely rare in DLSS patients. Textbooks often state that urinary incontinence is part of the clinical syndrome but it is more likely to be a separate concurrent problem than the direct result of cauda equina compression. The reason for this is that the spinal nerves comprising the cauda equina are much more resilient to compression then the spinal cord itself, and experimental studies have shown that the cauda equina in dogs can withstand considerable compression without suffering nerve fiber damage. Hence it is important that dogs with DLSS showing spinal ataxia and/or proprioceptive deficits are thoroughly investigated to exclude other conditions, such as degenerative myelopathy, thoracolumbar IVD herniation, discospondylitis, or neoplasia.

Imaging of the dog with DLSS

The usefulness of myelography in DLSS is debated since it depends on the extension of the dural sac (containing subarachnoid space) over the lumbosacral junction. Myelography has been reported as a diagnostic method of DLSS but as a normal myelogram cannot exclude DLSS, therefore myelography is not advocated as a reliable diagnostic technique for DLSS. Epidurography is technically easier and diagnostically superior to myelography and it is also associated with less side-effects. Contrast medium is injected into the epidural space at the lumbosacral or sacrococcygeal junction. An epidurogram in dogs with DLSS may show narrowing, elevation, deviation or obstruction of the epidural contrast-medium lines. Dynamic radiographic studies such as flexion/extension studies may increase the diagnostic sensitivity and specificity. Epidurography can nicely demonstrate the dynamic nature of the disc protrusion. Discography (intradiscal injection of contrast medium) is controversial because experimental disc puncture with needle sizes <27G causes degeneration in healthy IVDs.