Clinical signs of cauda equina dysfunction

The variety of terms used to describe this area of the spine can lead to confusion. In this text, the cauda equina is defined as the leash of nerve roots derived from the terminal spinal cord segments from L7 caudally (Cd1–Cd5) that travels through the vertebral canal in the lumbosacral area (i.e. there are only nerves, the peripheral nervous system in this region, Fig. 14.1). The lumbosacral area, or lumbosacral junction, is defined as the bone (e.g. L7 vertebra, sacrum) and connective tissue (e.g. L7–S1 articular facet joint capsules, interarcuate ligament, disc) enclosing the cauda equina. The end of the spinal cord in cats and small-breed dogs is more caudal and can extend to the lumbosacral area. As with myelopathies, clinical signs associated with cauda equina dysfunction depend upon the location (“sided-ness”) and extent of the lesion. Typical signs of dysfunction associated with cauda equina disorders are listed below. The clinician should bear in mind that lesions of the spinal cord segments which give rise to the cauda equina can result in identical clinical signs of dysfunction, as will lesions of their respective nerve roots. In general, though, diseases affecting the spinal cord cause a more severe presentation than those affecting only the nerve roots or spinal nerves.

1. Hyperesthesia, paresthesia/dysesthesia
   
   
   
   1. Hyperesthesia (pain) may arise from compression and/or inflammation of meninges and nerve roots of the cauda equina, from the bony components of the lumbosacral area, from the L7–S1 disc, and from L7–S1 articular facet joint capsules. Hyperesthesia may be manifested in a number of ways. Some patients exhibit obvious discomfort when rising or sitting down. Others may be reluctant to jump or to climb stairs. A unilateral or bilateral pelvic limb lameness, which may be exacerbated by increased activity, may also indicate hyperesthesia in the area of the lumbosacral joint and cauda equina. With some conditions, the patient may appear to be in constant pain (e.g. discospondylitis, vertebral tumor), whereas in others, careful palpation of the lumbosacral area is required to elicit a painful response from the patient.
      
   2. Paresthesia and dysesthesia are two similar terms that describe abnormal sensations caused by irritation or trauma to sensory nerves or nerve roots. Human patients describe such sensations as pricking, burning, and tingling. These occur without any known external sensory stimulus. It cannot be proven whether such sensations occur in dogs and cats with cauda equina disorders, but historical complaints and clinical signs often suggest the existence of this phenomenon. Dogs and cats with cauda equina disorders will sometimes stare or bite at areas around the rump and pelvic limbs.
   
   
2. Proprioceptive deficits—interference with afferent proprioceptive fibers at the level of the cauda equina can produce various degrees of proprioceptive deficits to the pelvic limbs. This can be as mild as delayed proprioceptive positioning reactions or as severe as pelvic limb weakness with dragging the dorsal aspect of the toes (“knuckling”). The deficits may or may not be symmetric.
   
3. Voluntary motor deficits—motor deficits to the muscles innervated by the sciatic nerve and caudal (coccygeal, or tail, innervation) nerves may be clinically detectable, as the cord segments and nerve roots of the cauda equina give rise to these nerves. Pelvic limb weakness may be apparent with damage to sciatic nerve contributions, and decreased to absent tail tone and movement may occur with damage to caudal segments and/or nerve roots. In some cases, the patient may be observed to exhibit an abnormally low tail carriage or a tail deviated to one of the sides, which are often noticed by the owner. Importantly, paraplegia (complete loss of motor function) is not seen with compressive lesions affecting only the nerves in the lumbosacral region.
   
4. Abnormal reflex activity—decreased to absent withdrawal (flexor) and gastrocnemius reflexes may be appreciated. The patellar reflex is typically normal or may appear hyperreflexive. Caudal thigh muscles normally inhibit the action of the quadriceps muscle group when the patellar reflex is elicited. Removal of this tonic antagonistic influence by disrupting the nerve supply to the caudal thigh muscles may result in an apparently hyperactive patellar reflex (i.e. patellar pseudohyperreflexia). A decreased to absent perineal reflex may result from cauda equina lesions.
   
5. Urinary and fecal abnormalities—varying degrees of urinary and fecal incontinence may occur with damage to sacral segments and/or roots. Bladder dysfunction is classically lower motor neuron in nature (see Chapter 16). These signs are typically seen with more severe presentations and are less reversible.
   
6. Nociceptive (deep pain perception) deficits in areas of the pelvic limbs (see Chapter 17 for autonomous zones), perineum, and tail may occur with severe lesions of the cauda equina.

Disorders affecting the cauda equina in dogs and cats (Table 14.1)

1. Degenerative
   
   
   
   1. Degenerative lumbosacral stenosis^{1–3, 6–10, 12–15, 17–20, 22, 25, 26, 28, 32, 35–37, 42–47, 54, 56, 60–64, 66, 67, 70, 71, 73, 74, 77–79, 81–84, 86, 87, 89, 92, 93, 97, 100} (Video 31)
      
      
      
      1. This is a common disease syndrome that typically affects adult (usually middle-aged to older) large-breed dogs. According to some reports, there is a male predilection for this disease. The German Shepherd dog appears to be particularly predisposed to degenerative lumbosacral stenosis. The pathophysiology involves the following:
         
         
         
         1. 
            

            type II degeneration and subsequent protrusion of the L7–S1 intervertebral disc into the vertebral canal (Fig. 14.2, Fig. 14.3)

            

            

            
            
         2. ventral subluxation of S1 (lumbosacral instability) and misalignment of the articular processes
            
         3. congenital vertebral anomalies (e.g. symmetric or asymmetric transitional vertebrae)
            
         4. proliferation of the soft tissues surrounding the cauda equine (e.g. hypertrophy of the interarcuate ligament [ligamentum flavum], the joint capsule, and epidural fibrosis)
            
         5. sacral osteochondrosis
            
         6. 
            

            vascular compromise of the blood supply to the spinal nerves.

            
            

            Ventral spondylosis is often appreciated at the lumbosacral junction in these patients, but by itself, this radiographic finding has little clinical significance.

            
            

            Reasons for this chronic degenerative process are unknown. In German Shepherd dogs as well as other large-breed dogs, the presence of transitional vertebrae at the lumbosacral junction has been associated with the development of degenerative lumbosacral stenosis. In one study, dogs with transitional lumbosacral vertebrae were eight times more likely to develop degenerative lumbosacral stenosis than dogs without such anomalous vertebrae; in this same study, dogs with transitional lumbosacral vertebrae also developed clinical signs of degenerative lumbosacral stenosis 1–2 yrs earlier than dogs with lumbosacral stenosis that did not have these abnormal vertebrae. The German Shepherd breed was also found to be eight times more likely to develop degenerative lumbosacral stenosis than other large breeds in this investigation. In addition, German Shepherd dogs have been shown to have different orientation of vertebral articular processes (facets) in the caudal lumbar and lumbosacral regions of the spinal column and a greater degree of facet joint tropism in this region, compared with other large-breed dogs. Facet joint tropism means an asymmetry in the angle of orientation between left and right facets at a given level of articulation. A morphologic and morphometric study compared the anatomy of the lumbosacral region of 733 German Shepherds with 334 large-breed dogs of other breeds. The authors found that German Shepherds had a significantly smaller vertebral canal (i.e. stenosis) and a higher step between L7 and S1. All these anatomic differences as well as the propensity for German Shepherd dogs to have transitional lumbosacral vertebrae and sacral osteochondrosis may partly explain the breed prevalence for degenerative lumbosacral stenosis. A possible genetic etiology has also been recently proposed in German Shepherds.

         
         
      2. Clinical signs are variable, but lumbosacral pain is an early and consistent finding. Pain may be manifested in a number of ways (e.g. reluctance to rise or sit) and pelvic limb lameness can be unilateral or bilateral. Pain and lameness may be acute or chronic and may be persistent or episodic. These clinical signs may be misinterpreted as being due to orthopedic disease, most notably hip dysplasia. Many of these dogs have radiographic evidence of hip dysplasia, making this a particularly easy trap to fall into when the only obvious clinical sign of an abnormality is pain and/or pelvic limb lameness. If untreated, clinical signs of dysfunction may progress to proprioceptive loss in the pelvic limbs, voluntary motor weakness (in the distribution area of the sciatic nerve), and urinary/fecal incontinence, usually in that order. In the authors’ experience, deficient pelvic limb withdrawal reflexes are most apparent at the hock level in cases of degenerative lumbosacral stenosis; flexion at the hip and stifle regions often appears normal. Although typically indicative of progressively severe cauda equina compression, urinary and/or fecal incontinence occasionally comprise the initial primary clinical complaint in cases of degenerative lumbosacral stenosis. Careful palpation of the lumbosacral area, including lordosing the caudal spine while pressing on the lumbosacral area, will usually elicit a pain response in affected patients (Fig. 14.4). Elevation of the tail is a good way to isolate the lumbosacral region from the pelvis. It causes stenosis of the lumbosacral foramen and distension of the nerve roots, consistently eliciting pain. Most dogs afflicted with this disease also have obvious deficits on proprioceptive positioning tests of the pelvic limbs. Importantly, all dogs with lumbosacral disease should have a rectal exam performed as neoplasms in the pelvic canal can invade the lumbosacral region and cause signs of cauda equina dysfunction.

         

         
         
      3. 
         

         Diagnosis of degenerative lumbosacral stenosis is based upon signalment, historical and clinical findings, and results of diagnostic imaging of the lumbosacral region. The definitive diagnosis of degenerative lumbosacral stenosis is made by imaging the lumbosacral area and demonstrating compression of the cauda equina. Although degenerative changes at the lumbosacral junction (e.g. spondylosis, misalignment of the sacrum with the L7 vertebra) may often be appreciated on plain radiographs of the region, additional imaging is necessary to demonstrate cauda equina compression. A number of procedures have been advocated, including myelography, epidurography, vertebral sinus venography, discography, computed tomography (CT), and magnetic resonance imaging (MRI). Since the terminal thecal sac (subarachnoid space) of the spinal cord in large-breed dogs often ends cranial to the lumbosacral junction, myelography (Fig. 14.5) may not consistently provide useful information. Vertebral sinus venography is considered both a technically difficult and an unreliable imaging procedure. Discography (Fig. 14.6) is an accurate imaging method for degenerative lumbosacral stenosis but provides information primarily limited to the intervertebral disc. Epidurography is also considered a relatively accurate contrast procedure to identify cauda equina compression. Combination discography/epidurography (Fig. 14.7) has also been demonstrated to be a useful diagnostic imaging method for degenerative lumbosacral stenosis. Currently it is clear that CT (Fig. 14.8) and MRI (Fig. 14.9, Fig. 14.10, Fig. 14.11) provide the most detailed structural information regarding the cauda equina, including information concerning the L7–S1 intervertebral foramina and L7 nerve roots. In one study, there was a high degree of agreement between CT and MRI findings in dogs with degenerative lumbosacral stenosis; however, the findings of neither of these modalities correlated well with what was found at surgery. Although this discrepancy may be partially explainable by differences in patient positioning during imaging vs. surgery, there are other important discrepancies between imaging findings and clinical disease that must be kept in mind. Most importantly, there is evidence that dogs without clinical signs of disease may have imaging findings consistent with a diagnosis of degenerative lumbosacral stenosis and that the degree of cauda equina compression evident on imaging does not correlate with disease presence or severity. In one study of neurologically normal dogs imaged via CT, all dogs had some level of disc protrusion at the L7/S1 disc space; the percentage of the vertebral canal height occupied by these discs varied from approximately 21 to 43%. It is apparent that evidence on imaging studies consistent with a diagnosis of degenerative lumbosacral stenosis may be an incidental finding in some dogs. It is also apparent that the extent of cauda equina compression appreciated on such imaging studies is not necessarily indicative of disease severity in patients that exhibit clinical signs of degenerative lumbosacral stenosis. In the authors’ experience, middle-aged to older large-breed dogs often demonstrate hyperesthesia on palpation of the lumbosacral junction during a neurologic examination that has nothing to do with the presenting complaint or ultimate diagnosis. In other words, some dogs with degenerative lumbosacral stenosis may have subtle or inapparent clinical signs that are only elicitable on palpation. It is imperative to realize that focusing on the lumbosacral junction in some patients may lead to overlooking another spinal disorder which is primarily responsible for the clinical deficits. In patients with subtle deficits (e.g. pelvic limb proprioceptive deficits and spinal hyperesthesia), it may be worthwhile to have survey images of the thoracolumbar region (e.g. T2-sagittal MR survey) to ensure that the lumbosacral lesion is not an incidental finding. Concurrent EMG performed on the epaxial, tail, and pelvic limb musculature may improve the accuracy of diagnosis with the various imaging modalities. Tibial nerve somatosensory evoked potentials (SSEP) have also been shown to be abnormal in dogs with clinical evidence of degenerative lumbosacral stenosis. The challenges associated with the diagnosis and treatment of lumbosacral stenosis were recently highlighted in a review article.

         

         

         

         

         

         

         

         
         
      4. 
         

         The treatment of a patient with degenerative lumbosacral stenosis may be nonsurgical or surgical, similar to other disc-associated diseases. Treatment decisions are based primarily on severity of clinical signs, age of the patient, and concurrent diseases; as mentioned previously, there appears to be no clear correlation between extent of cauda equina compression evident on imaging and disease severity or postoperative outcome. Nonsurgical therapy consists of enforced rest initially for a few weeks, followed by a period of regular short walks to maintain muscle mass. Additionally, anti-inflammatory medication (either nonsteroidal drugs or prednisone, not both), analgesics (such as gabapentin), and body weight reduction are recommended. Nonsurgical or conservative treatment is a reasonable initial option, primarily in older patients with multiple orthopedic or systemic conditions. Reported success rate is 55%. Epidural steroids are a popular therapeutic approach in people with lumbar and lumbosacral disc herniations. It is often used when oral therapy with anti-inflammatories and rest is not successful before considering surgery. A retrospective study evaluated the use of fluoroscopically guided epidural steroid injections in 38 dogs and found an improved outcome in 79% of dogs. The authors used methylprednisolone acetate (40 mg/mL, dose of 1 mg/kg) and three injections (day 1, day 14 and day 45). Aseptic technique is paramount for epidural infiltration due to the risk of infections. In people, nonsurgical treatment consisting of analgesics and physical therapy is the initial standard of care for patients with lumbar disc herniations and the long-term results are comparable to surgical treatment, primarily for patients with mild to moderate signs. In patients with neurologic deficits, or patients for whom pain is refractory to nonsurgical management, surgery is chosen as the preferred mode of therapy. Surgery in dogs usually consists of a dorsal laminectomy over the L7–S1 interspace (Fig. 14.12), often combined with the removal of hypertrophied soft tissue (e.g. annular disc material; Fig. 14.12C

         Only gold members can continue reading. Log In or Register to continue

         Share this:

         • Click to share on Twitter (Opens in new window)
         • Click to share on Facebook (Opens in new window)

         Related

         Related posts:

         1. Signalment and History: The First Considerations
         2. Seizures and Narcolepsy
         3. Head-Trauma Management
         4. Neurodiagnostics
         

         Stay updated, free articles. Join our Telegram channel

         Join