New Developments in Nonsurgical Treatment of Low Back Pain

Key Points

• The origins of lumbosacral pain are complex and may be discogenic, inflammation- or compression-induced.
• Lumbosacral imaging should also include studies to evaluate the dynamic nature of the disease.
• The first episode of low back can be treated effectively by medication and/or physical therapy.

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.¹

DLSS can present in a number of different ways and patients suffering from DLSS are commonly misdiagnosed or underdiagnosed. DLSS patients are typically neuroorthopedic patients, the disorder is per definition a spinal disorder but the clinical 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.²

Findings during orthopedic examination are directly related to the compression of the cauda equina and the disc disease, and the most consistent finding is lumbosacral pain on palpation.³ LS pain can be evoked by the lordosis test and hyperextension of the low back (standing of in lateral recumbence) with simultaneous pressure at the LS region. Careful hyperextension of the hip joints (one at a time) with the dog standing or in lateral recumbence usually does 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 low back. This is proof of the dynamic nature of the compression and stenosis which worsens in motions of extension (Fig. 1). Other common findings are uni- or 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 (Fig. 1C) causes radiating nerve root pain (the so-called nerve root signature) and can easily be mistaken for the clinical presentation of a dog with a cranial cruciate ligament rupture with medial meniscal disease.

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 disc herniation, discospondylitis, or neoplasia.

Lumbosacral pain can originate from the disc (discogenic pain), from compression of dural structures (meningeal pain), or from compression of spinal nerves (neuritis, radix/root pain).¹ Besides the disc (NP and AF) and neural components (dural sac and spinal nerves), pain may also originate from other innervated structures in the LS region, namely the ligaments (dorsal longitudinal ligament and ligamentum flavum), the endplates, and the articular facets, and little is known about the contribution of each in the total composition of the painful low back patient. As the focus of imaging studies is usually on the component of compression, it is underestimated that degeneration and inflammation are significant components of the pathological cascade in DLSS. Only limited studies have studied the cytokine and chemokine profiles in intervertebral disc (IVD) degeneration in dogs, and mainly focused on gene expression. A better understanding is needed in order to develop biological therapies that address both pain and degeneration in IVD disease.⁴ Willems et al. (2016) studied the levels of prostaglandin E2 (PGE2), a mediator of (osteoarthritic) pain, in IVDs from chondrodystrophic (CD) and non-chondrodystrophic (NCD) dogs with and without clinical signs of IVD disease, and correlated these to degeneration grade (according to Pfirrmann), or herniation type (according to Hansen). In addition, cyclooxygenase 2 (COX-2) expression and signs of inflammation were investigated in histological IVD samples of CD and NCD dogs. PGE2 levels were significantly higher in the nucleus pulposus (NP) of degenerated IVDs compared with non-degenerated IVDs, and in herniated IVDs from NCD dogs compared with non-herniated IVDs of NCD dogs. Future studies are needed to investigate if inhibition of PGE2 levels in degenerated IVDs provides effective analgesia and exerts a protective role in the process of IVD degeneration and the development of IVD disease.⁵

^[...]