Degenerative lumbosacral syndrome (DLSS) poses diagnostic and treatment dilemmas for the veterinary practitioner. Aspects
of these dilemmas were presented at the 2006 Annual ACVIM Forum (Bagley, Carpenter, Shores – 2006). Diagnosis of DLSS is difficult
in distinguishing between significance of clinical signs and associated imaging abnormalities especially while predicting
development of DLSS and detecting instability. Treatment protocols need to take into account the dog's activity level and
lifestyle. Likewise, the appropriate surgical procedure selected may differ for the pet-owned versus the working dog.
Lumbosacral stenosis (cauda equina syndrome, lumbosacral malarticulation and malformation, lumbosacral instability, lumbosacral
spondylopathy) is common in middle- to old-aged, large breed dogs and represents a plethora of orthopaedic abnormalities associated
with the lumbosacral anatomy (De Risio 2000). Neurologic abnormalities occur coincident with tissue (joint capsule, interarcuate
ligament, disc, bone, fibrous adhesions) impingement onto the cauda equina, nerve roots at the level of the foramina, or its
vascular supply. The pathologic process begins with Hansen type II disc degeneration followed by osteophyte formation of the
L 7-S 1 end plates and articular processes (Chambers 1989). The syndrome is characterized by stenosis of the spinal canal
from vertebral subluxation and/or stenotic intervertebral foramen. Attention also has been focused on higher prevalence of
DLSS and disk degeneration in German Shepherd Dogs with relation to differences in motion patterns. Shape and orientation
of articular facets have been found to be different in GSDs than in other breeds (Seiler 2003). However, the complex studies
using of 3-D conformation and motion did not reveal an association between facet joint tropism and disk degeneration and further
in vivo studies will be necessary to assess the role of biomechanical factors (Benninger 2006).
Neuroanatomic localization to the lumbosacral region is determined by the neurologic examination based on signs related to
sensory, motor and autonomic dysfunction. Nonspecific observations include reluctance to rise and pelvic limb lameness. Neurologic
signs commonly include pain and motor dysfunction as a result of lower motor neuron weakness (sciatic, pudendal, coccygeal
nn.). Pain is the most consistent clinical sign and is reflective of compressive or inflammatory processes to pain sensitive
structures (nerve root, meninges, periosteum and joints). It is the opinion of the author that the pain primarily originates
from nerve root (radicular pain) compression (especially L7). The affected patient often stands with the pelvic limbs tucked
under the caudal abdomen to flex the spine and lessen nerve root compression. Pain is manifested by hyperesthesia and/or paresthesia.
Hyperesthesia is elicited upon palpation of the lumbosacral joint or by hyperextension of the pelvic limbs causing the spinal
region to have lordosis. This accentuates canal stenosis and nerve root compression causing pain. Paresthesia is caused by
irritation of the nerve roots without an external stimulus. Clinical signs include biting at the tail, rump and feet. Pain
of lumbosacral origin also is exacerbated with exercise as an asymmetric lameness and may reflect neurogenic intermittent
claudication. Motor dysfunction varies with severity of neural tissue compression. The patient may have mild to severe gait
and postural reaction deficits. The gait is often short-strided. Postural reaction deficits often are asymmetric depending
upon the degree of cauda equina compression.
Reflex dysfunction of the limbs commonly involves those muscles innervated by the sciatic nerve (L6-S1 nerve roots, but L7
and S1 provide major contribution), especially flexor and extensor muscles of the hock. The patellar reflex may be hyperreflexic
due to loss of antagonism from the flexor muscles (pseudo-hyperreflexia). The cranial tibial and gastrocnemius reflexes may
be hyporeflexic. The flexor withdrawal reflexes often are reduced in the stifle and hock joints. Less commonly, the pudendal
and coccygeal nerves may be involved. The pudendal nerve (S1-2 and S3) innervates the perineal region including the external
anal and urethral sphincters. The coccygeal nerves innervate the tail. Decreased tail tone is assessed upon palpation and
inability to wag.
Other clinical signs more common with chronic disease include fecal and urinary incontinence. If micturition dysfunction is
suspected, it is important to closely evaluate sensory perception of the perineal region and the anal reflex. A digital rectal
examination will assess for decreased rectal tone and further assess the urethra and prostate.