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Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

German Shepherd Dog (Alsatian)

German Shepherd Dog (Alsatian)

Degenerative Lumbosacral Stenosis

Related terms: lumbosacral instability, lumbosacral malformation, lumbosacral malarticulation, lumbar spinal stenosis, lumbosacral spondylolisthesis, lumbosacral nerve root compression, cauda equina syndrome

VeNom term: cauda equina syndrome (VeNom code: 528)

Related conditions: lumbosacral transitional vertebrae

Outline: Degenerative lumbosacral stenosis is a narrowing of the posterior spinal canal, which in turn affects the nerves controlling the tail, pelvic organs, perineum, and hind limbs. It is a complex condition, with multiple factors involved in its development, but it usually involves degeneration of the intervertebral discs of the lumbar region, including disc displacement and bony proliferations resulting in narrowing of the spinal canal and compression of the nerves. This causes pain and weakness in the lower back, hind limbs and tail, stiffness and difficulty rising, jumping, climbing, or sitting, and faecal and/or urinary incontinence. These clinical signs may persist over months or even years. Affected dogs may recover after an extended period of rest, or may require surgery. In both cases, a long period of confinement and exercise restriction may be required, and the condition may re-occur.

German shepherd dogs are over-represented for incidence of degenerative lumbosacral stenosis compared with other breeds, and they have congenital abnormalities in their lumbosacral vertebrae, which make them more prone to developing the condition. Abnormalities in the lumbosacral vertebrae can be identified through screening programmes, and dogs with these abnormalities should not be bred from to try to reduce the prevalence of the condition in the breed. Further work is required to fully understand all of the genetic and environmental risk factors in the development of degenerative lumbosacral stenosis.


Summary of Information

(for more information click on the links below)

1. Brief description

The spine of dogs is made up of many bones, called vertebrae, divided into 5 different regions including those of the lower back (or lumbar) region and the hip or sacrum. There is a hollow in the upper side of each vertebra. These adjacent hollows of bone together form a bony tube called the vertebral or spinal canal, through which the spinal cord - made up of delicate nerve tissue which transmits the messages between the brain and other parts of the body - passes and is protected. Between these vertebrae are specialised discs of tissue, called intervertebral discs that act as shock absorbers and stop the vertebrae rubbing against each other.  

The cauda equina is found near the sacrum at the end the spinal cord and is a bundle of spinal nerves and spinal nerve roots which control the sensory and motor functions of the tail, pelvic organs (eg bladder, rectum), perineum, and hind limbs. Degenerative lumbosacral stenosis, or cauda equina syndrome, is a condition in which there is damage to one or more of these nerve roots at the caudal (tail) end of the spinal cord. This is caused by abnormalities of the spine, and predominantly by degeneration of the intervertebral discs, causing them to become inflamed and painful and to impinge into the spinal canal and to compress the lumbosacral spinal nerves causing problems with normal nerve transmission.

Compression of the nerves leads to abnormal carriage of the tail, faecal and/or urinary incontinence and lameness or elevation of the limbs. The intervertebral disc becomes inflamed and pain occurs.

The clinical signs of lumbosacral stenosis include weakness in the hind limbs, abnormal carriage of the tail, faecal and/or urinary incontinence, pain or stiffness when extending the lumbosacral joint (walking, rising from a lying position), and muscle atrophy

Degenerative lumbosacral stenosis occurs commonly in active, larger breeds of dog. The German shepherd dog breed has a predisposition for degenerative changes in the lumbosacral intervertebral disc and are prone to abnormal development, before birth, of vertebrae in the lumbosacral region, which contributes to the development of this condition.

2. Intensity of welfare impact             

Dogs with degenerative lumbosacral stenosis suffer from pain in the lower back, in one or both hind legs and/or the tail. They may appear stiff, show lameness in their hind legs and have difficulties rising from a lying position, jumping, climbing, or sitting, and may be unable to move their tail. Affected dogs may also have urinary and/or faecal incontinence and reduced muscle tone and deep tendon reflexes in their hind legs.

3. Duration of welfare impact

Degenerative lumbosacral stenosis is generally diagnosed in mature dogs, of around 6 years of age. The clinical signs can persist from 1 week to 2 years, with an average of 3.3 months.

The clinical condition may improve with pain relief and exercise restriction, but otherwise surgery may be required. In both nonsurgical and surgical treatment, affected dogs will need to be confined for long periods of time, of up to 10 weeks, and this may negatively impact on the dog’s mental wellbeing and physical health.

4. Number of animals affected

In several studies of dogs with degenerative lumbosacral stenosis, German shepherd dogs have been more prevalent than dogs of other breeds. Degenerative lumbosacral stenosis appears to be more common in males than females.

5. Diagnosis

Lumbosacral stenosis can be diagnosed by radiography but definitive diagnosis requires magnetic resonance imaging (MRI) or computerised tomography (CT) scanning.

6. Genetics

Degenerative lumbosacral stenosis is a complex condition and there are many factors, both genetic and environmental, which play a role in its development for any one individual. Several morphological traits (eg lumbosacral vertebral canal height and the shape of the vertebrae at the transition from the lumbar to sacrum region of the spine) which are associated with the development of degenerative lumbosacral stenosis, have been shown to be inherited to some degree in German shepherd dogs.

7. How do you know if an animal is a carrier or likely to become affected?

Screening for abnormally shaped lumbosacral transitional vertebrae in addition to hip dysplasia is possible. However, not all dogs with lumbosacral transitional vertebrae will go on to show clinical signs of degenerative lumbosacral stenosis.

8. Methods and prospects for elimination of the problem

Potential breeding dogs should be screened for lumbosacral transitional vertebrae, and those with these abnormalities should be excluded from breeding stock. However, degenerative lumbosacral stenosis is a complex disorder, and further research is required to identify environmental and genetic effects.


For further details about this condition, please click on the following:
(these link to items down this page)


1. Clinical and pathological effects

The spine of dogs is made up of many bones, called vertebrae and it is divided into 5 different regions. There are 7 bones in the neck (cervical) region, 13 in the chest (thoracic) region, 7 in the lower back (lumbar) region and 3 fused together to form the sacrum (at the hips). Lastly, there are the tail (coccygeal) bones (Figure 1).

Figiure 1

http://digital.library.wisc.edu/1711.dl/Science.VetAnatImgs (image published before 1926)

Vertebrae are numbered according to the region of the spine they reside in and starting from the head, working towards the tail; the first cervical vertebra is called C1, the second C2, etc and the first thoracic vertebra is T1 etc. There is a hollow in the upper side of each vertebra. These adjacent hollows of bone together form a bony tube called the vertebral or spinal canal, through which the spinal cord - made up of delicate nerve tissue which transmits the messages between the brain and other parts of the body - passes and is protected. Most of the vertebrae are separated by fibrous discs of tissue called intervertebral discs.

The spinal cord extends from the brain stem and terminates at the anterior lumbar vertebrae. In the lumbosacral region, the nerve roots come together in a bundle that descend along the spinal column in and form the cauda equina. Within the cauda equina are nerves that control the sensory and motor functions of the tail, the pelvic organs (eg bladder, rectum), perineum, and the hind limbs. Degenerative lumbosacral stenosis, or cauda equina syndrome, is a complex condition that involves damage to one or more of these nerve roots at the caudal (tail) end of the cord. Degeneration of the intervertebral discs of the lumbar region is found in many affected dogs.

The specialised discs of tissue, called intervertebral discs, found between most adjacent vertebrae act as shock absorbers and stop the vertebrae rubbing against each other, allowing the joints and the spine to move easily. These fibrocartilaginous discs start between the second and third cervical vertebrae (C2-3) and extend to the transition point between the last lumbar vertebrae (L7) and first sacral vertebrae (S1) (The 3 sacral vertebrae are fused and therefore do not have discs).

Each intervertebral disc is a highly specialised structure and consists of two parts: a central gelatinous area called the nucleus pulposus (NP) and an outer fibrous layer called the annulus fibrosus (AF). The jelly-like nucleus pulposus is virtually incompressible and helps dissipate and spread forces acting on the spine while the surrounding annulus fibrosus gives structure to the disc, securely connecting the vertebrae in front and behind the disc, and adds to the shock absorbing effect whilst containing the NP.

It is common for intervertebral discs to degenerate with age in dogs and the NP gel is replaced by more mature fibrocartilage as part of the normal ageing process. This occurs gradually in most breeds of dog so that by 7 to 8 years of age the whole NP has changed (Braund 1993). As the dogs continue to age, further degeneration sometimes occurs in the discs,

Degeneration of the intervertebral disc in the lumbar region is initiated by degradation of proteoglycans, which is part of the collagen matrix that forms the annulus fibrosus. As a result, the annulus fibrosus is weakened and the inner nucleus pulposus can leak out, resulting in extrusion of the NP into the vertebral canal. Less nutrients and water are drawn into the disc leading to dehydration, which reduces its ability to absorb shocks and further degeneration and loss of disc width.

Extrusion of the vertebral disc creates an unstable spinal segment, and the load is redistributed from the central axis of the intervertebral disc to the peripheral parts of the spine (facet joints and ventral aspect of vertebral bodies). To compensate for the increasing instability, there is proliferation of the surrounding soft-tissue structures, causing thickening and growth of the spinal ligament, scar tissue and thickening of the joint capsules. The cartilaginous end plates of the vertebrae, which are in contact with the intervertebral discs, thicken and bony proliferations develop such as bone spurs (osteophytes) and osteoarthritis of the spinal joints (ventral spondylosis). These processes further impair the nutritional supply to the disc, triggering a negative spiral leading to structural failure of the disc (Meij & Bergknut 2010). The intervertebral disc space is narrowed as the disc extrudes dorsally (Figure 2), and impinges on the nerve roots. Compression of the caudal and sacral nerves causes abnormal carriage of the tail, and faecal and/or urinary incontinence whereas compression of the lateral (foraminal) nerves causes lameness or elevation of the limbs ((Worth et al 2009). Cell-mediated inflammatory responses lead to an ingrowth of blood vessels and nerves into the damaged disc, which contributes to lumbosacral pain. (Meij & Bergknut 2010).

Figure 2 – A radiograph of the lumbosacral region of a dog showing a LS step (where the sacrum has shifted down in comparison to L7), elongation of the sacrum relative to L7, bony spurs (spondylosis deformans) and a narrowed intervertebral disc. Image reproduced with permission from Schattauer GmbH and B.P. Meij, from Suwankong et al (2008).

The clinical signs of lumbosacral stenosis include weakness in the hind limbs and tail, incontinence, pain or stiffness when extending the lumbosacral joint (walking, rising from a lying position), muscle atrophy and weak flexor reflex in the pelvic limbs. 

The German shepherd dog breed has a number of traits that make them more predisposed to develop degenerative lumbosacral stenosis than other breeds (Breit & Künzel 2001, Ondreka et al 2013). They may have greater and more rapid degeneration in the lumbosacral intervertebral discs than other breeds (Amort et al 2012), leading to a more severe form of the condition. German shepherd dogs also exhibit breed-specific morphological traits of the lumbosacral junction (eg reduced vertebral canal height) and this is thought to promote primary lumbosacral disease in this breed (Breit & Künzel 2001, Ondreka et al 2013). German shepherd dogs are more prone to abnormally formed vertebra in the lumbosacral region, between the last normal lumbar vertebra (L7) and the first normal sacral vertebra (S1 - lumbosacral transitional vertebrae; (Damur-Djuric et al 2006). This is a congenital abnormality, which dogs are born with, and is a predisposing factor in the development of the condition in this breed (Morgan et al 1993).

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2. Intensity of welfare impact

Lumbar (or posterior lumbar) pain is common in dogs affected by degenerative lumbosacral stenosis (Watt 1991); this can be episodic or chronic pain and may occur in the lower back, in one or both hind legs or the tail area. There may also be stiffness in the lumbar spine or hind legs, with lameness. Affected dogs may have difficulties rising from a lying position, jumping, climbing, or sitting, and may be unable to move their tail. Dogs may also have urinary and/or faecal incontinence and reduced muscle tone and deep tendon reflexes in the hind legs.

In one study of 30 dogs with degenerative lumbosacral stenosis, all dogs showed symptoms of pain, 18 dogs (60%) showed lameness, and 17 dogs (57%) showed stiffness/abnormal gait (Ness 1994).

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3. Duration of welfare impact

The clinical signs of degenerative lumbosacral stenosis usually occur when dogs are adult, between 2 and 13 years of age, with an average (mean) age of 6 years 10 months (De Risio et al 2001). The duration of clinical signs can range from 1 week to 2 years, with an average of 3.3 months (De Risio et al 2001). Recurrence may be seen in some dogs (Linn et al 2003).

Mild cases of the condition may be managed with pain relief and exercise restriction. Surgery is required where this conservative management is not successful, or where there are more severe clinical signs. Both nonsurgical and surgical management of the condition requires the dogs to be confined for long periods of time (up to 4-10 weeks), and this may negatively impact on the dog’s mental wellbeing and physical health. In one study, the average time taken to achieve the best improvement via exercise restriction was 14.5 weeks (Ness 1994).

With surgical intervention, there is generally a good outcome, and this particularly the case if they are young dogs with mild clinical signs at the time of diagnosis (De Risio et al 2001, Linn et al 2003). Dogs with more severe clinical signs, such as long-term urinary incontinence have a poorer outcome, where clinical signs persist after surgery (De Risio et al 2001). In one study of outcomes following dorsal decompressive laminectomy surgery, ‘excellent’ or ‘good’ outcomes were reported for 54 of 69 dogs (80%), but 15 dogs (22%) were considered to have ‘poor’ outcome due to persistence of clinical signs, 2 of which were euthanized (De Risio et al 2001).

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4. Number of animals affected

In Sweden, German shepherd dogs had an incidence rate of degenerative lumbosacral disease of 33.7 cases per 10,000 dog years at risk (Meij & Bergknut 2010). 

In a screening programme of 4000 large-breed dogs, abnormally formed lumbosacral vertebrae (lumbosacral transitional vertebrae) was noted in 138 dogs (3.5%). Of these dogs, 684 German shepherd dogs were examined, and 39 had lumbosacral transitional vertebrae (5.7%), and this was a significantly higher prevalence than in other breeds (Damur-Djuric et al 2006).

In several studies of dogs with degenerative lumbosacral stenosis, German shepherd dogs have been more prevalent than dogs of other breeds (Watt 1991, Ness 1994, De Risio et al 2001).

Degenerative lumbosacral stenosis appears to be more common in males than females (Watt 1991, Ness 1994, De Risio et al 2001). In one study, with a ratio of about 2.6 males to 1 female (De Risio et al 2001).

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5. Diagnosis

Early detection of lumbosacral stenosis is difficult, since high-drive stoic dogs – such as the German shepherd dog - often do not exhibit or mask clinical signs of stiffness and pain. The clinical signs of degenerative lumbosacral stenosis may be attributed to other neurological or orthopaedic conditions, resulting in delayed or mis-diagnosis (Worth et al 2009).

Lumbosacral stenosis can be diagnosed by radiography but definitive diagnosis requires magnetic resonance imaging (MRI), computerised tomography (CT) scanning. A procedure known as myelography may also be useful in which a dye is injected into the affected area and re-radiographed to determine bone abnormalities.

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6. Genetics

Morphological traits of the German shepherd dog breed are thought to be responsible for increasing the risk of lumbosacral stenosis (Damur-Djuric et al 2006). Several traits (eg lumbosacral vertebral canal height and the shape of the vertebrae at the transition from the lumbar to sacrum region of the spine) have been shown to be inherited to some degree, and therefore dogs with these morphological traits should not be bred from (Ondreka et al 2013). However, it is recognised that degenerative lumbosacral stenosis is a complex condition, of which there are many factors both genetic and environmental, that play a role in its development for any one individual (Krontveit & Sævik 2013).

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7. How do you know if an animal is a carrier or likely to become affected?

Screening for lumbosacral transitional vertebrae in addition to hip dysplasia is possible, since the lumbosacral junction is visible in hip-screening radiographs (Lappalainen et al 2012). However, not all dogs with lumbosacral transitional vertebrae will go on to show clinical signs of degenerative lumbosacral stenosis.

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8. Methods and prospects for elimination of the problem

It has been recommended that potential breeding dogs should be screened for abnormally shaped lumbosacral transitional vertebrae, and that those with these abnormalities be excluded from breeding stock (Morgan et al 1993). However, degenerative lumbosacral stenosis is a complex disorder, and is multi-factorial in origin. Further research is required to identify environmental and genetic effects and the interactions between them (Krontveit & Sævik 2013).

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9. Acknowledgements

UFAW thanks Dr Emma Buckland (BSc PhD), Dr David Brodbelt (MA VetMB PhD DVA DipECVAA MRCVS) and Dr Dan O’Neill (MVB BSc MSc PhD MRCVS) for their work in compiling this section.

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10. References

Amort KH, Ondreka N, Rudorf H, Stock KF, Distl O, Tellhelm B, Kramer M and Wigger A (2012) Mr-imaging of lumbosacral intervertebral disc degeneration in clinically sound german shepherd dogs compared to other breeds. Veterinary Radiology and Ultrasound 53: 289–295

Breit S and Künzel W (2001) Breed specific osteological features of the canine lumbosacral junction.. Annals of Anatomy 183: 151–7

Braund K (1993) Intervertebral Disc Disease in Bojrab, M. Disease mechanism in Small Animal Surgery. 2nd Ed. London: Lippincott, Williams and Wilkins

Damur-Djuric N, Steffen F, Hassig M, Morgan JP and Fluckiger MA (2006) LUMBOSACRAL TRANSITIONAL VERTEBRAE IN DOGS: CLASSIFICATION, PREVALENCE, AND ASSOCIATION WITH SACROILIAC MORPHOLOGY. Veterinary Radiology Ultrasound 47: 32–38

Krontveit RI and Sævik BK (2013) Challenges in tackling inherited skeletal disorders in the dog.. Veterinary Journal 196: 8–9

Lappalainen AK, Salomaa R, Junnila J, Snellman M and Laitinen-Vapaavuori O (2012) Alternative classification and screening protocol for transitional lumbosacral vertebra in German shepherd dogs. Acta veterinaria Scandinavica 54: 27

Linn LL, Bartels KE, Rochat MC, Payton ME and Moore GE (2003) Lumbosacral stenosis in 29 military working dogs: Epidemiologic findings and outcome after surgical intervention (1990-1999). Veterinary Surgery 32: ajvet0320021

Meij BP and Bergknut N (2010) Degenerative lumbosacral stenosis in dogs. The Veterinary Clinics Of North America: Small Animal Practice 40: 983–1009

Morgan JP, Bahr A, Franti CE and Bailey CS (1993) Lumbosacral transitional vertebrae as a predisposing cause of cauda equina syndrome in German shepherd dogs: 161 cases (1987-1990). Journal of the American Veterinary Medical Association 202: 1877–82

Ness MG (1994) Degenerative lumbosacral stenosis in the dog: A review of 30 cases. Journal of Small Animal Practice 35: 185–190

Ondreka N, Amort KH, Stock KF, Tellhelm B, Klumpp SW, Kramer M and Schmidt MJ (2013) Skeletal morphology and morphometry of the lumbosacral junction in German shepherd dogs and an evaluation of the possible genetic basis for radiographic findings. Veterinary Journal 196: 64–70

De Risio L, Sharp NJH, Olby NJ, Munana KR and Thomas WB (2001) Predictors of outcome after dorsal decompressive laminectomy for degenerative lumbosacral stenosis in dogs: 69 cases (1987-1997). Journal of the American Veterinary Medical Association 219: 624–628

Suwankong N, Meij BP, Voorhout G, de Boer AH and Hazewinkel, HAW (2008) Review and retrospective analysis of degenerative lumbosacral stenosis in 156 dogs treated by dorsal laminectomy. Veterinary and Comparative Orthopaedics and Traumatology 21:  285–93

Watt PR (1991) Degenerative lumbosacral stenosis in 18 dogs. Journal of Small Animal Practice 32: 125–134

Worth A, Thompson D and Hartman A (2009) Degenerative lumbosacral stenosis in working dogs: Current concepts and review. New Zealand Veterinary Journal 57: 319–330

© UFAW 2016