Lower Back Pain, Clinical Reasoning, Contextualised Care & Learning From Complications

Colin Driver and Robyn Lowe

In conjunction with Vet Voices On Air Podcast, due for release Sunday 26th July 2026

Introduction

Recent research by Malkani et al. (2024) found that all psychological, environmental, and procedural factors were significantly different between healthy dogs and dogs with chronic pain, evidencing how chronic pain impacts all domains of a dog’s life. Thus, physiological signs of musculoskeletal disorders such as gait changes, stiffness, lameness might manifest after or alongside behavioral changes such as increased fearfulness, prolonged recovery from a stressful event, a reduced interest in social interactions, toys or play. Indeed, behavioural changes may be seen even in the absence of overt physiological signs!

all psychological, environmental, and procedural factors were significantly different between healthy dogs and dogs with chronic pain, evidencing how chronic pain impacts all domains of a dog’s life.

Due to the wide impact chronic pain has on the physical, behavioural and emotional needs of the animal, we must strive to empower both animal caregivers and veterinary professionals in the detection and diagnosis of chronic pain, aiding in effective treatment and interventions.

An area commonly overlooked, because of the complexity of the condition and the signs that ‘mimic’ other pathophysiological processes is canine chronic lower back pain (CLBP); a less common diagnosis.

The aim of the article is to ensure that CLBP is added to possible differentials when managing chronic pain cases looking at identification, clinical signs, history taking, physical assessment, diagnosis and treatment. 

‘Pain is what the patient says it is’

Pain can be defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage; or an aversive sensory and emotional experience typically caused by, or resembling that caused by, actual or potential tissue injury.

Pain may be classified in a range of ways according to its duration; acute, chronic, or intermittent. Broadly speaking, the International Association For The Study Of Pain  (IASP) define acute pain as ‘Acute pain happens suddenly, starts out sharp or intense, and serves as a warning sign of disease or threat to the body’, and chronic pains as ‘Pain is often called chronic when it persists for months or even years, continuing beyond the usual recovery time from an injury or illness. Unlike acute pain, which is temporary, chronic pain can be constant or come and go, often interfering with daily life and affecting your physical and emotional well-being.’

Assessment for chronic pain

Osteoarthritis (OA) is a good example of the challenges owners and veterinary professionals face. Prevalence data showing generally high numbers, although with some with conflicting values; in literature (Anderson 2018), the estimates have ranged from 6.6% based on primary-care data (O’Neill) to 20% based on referral data in the UK dog population (Pettitt) and age-specific prevalence values ranging from the aforementioned 20% in dogs older than one year up to 80% in dogs older than eight years (Johnston, 1997). Despite this high prevalence, owner awareness and recognition is still challenging, as is the diagnosis of chronic pain in the confines of a consultation, where the pet is likely to be hyper-aroused and not displaying typical signs. Furthermore, chronic pain is notoriously difficult to assess and quantify; the pain that a patient with osteoarthritis might exhibit may bear no resemblance to the radiographic features of the disease. 

The complex nature of chronic pain, alongside the possibility of multiple pathologies seen concurrently is particularly noteworthy in CLBP; a key clinical challenge in the early assessment of caudal lumbar and lumbosacral pain in dogs is differentiating between the pain originating from the lumbosacral spine and pain associated with hip pathology.

a key clinical challenge in the early assessment of caudal lumbar and lumbosacral pain in dogs is differentiating between the pain originating from the lumbosacral spine and pain associated with hip pathology.

Chronic Lower Back Pain - Anatomic Basis 

In human medicine, low back pain (LBP) is a term used to describe the pain affecting the lumbar and lumbosacral regions, which on occasions radiates into the gluteal region and pelvic limbs. LBP is multifactorial, involving a complex interplay of nociceptive, neuropathic, and nociplastic pain, as well as the central nervous system’s processing and modulation of pain, which is heavily influenced by behavioural, cognitive, and emotional factors.

There are multiple potential non-neural (nociceptive) spinal pain generators, including the intervertebral discs, the posterior longitudinal ligament, the vertebral end-plates and subchondral bone, facet joints, and interarcuate ligaments. A radiating effect resulting from the nociceptors of these structures is described as ‘mechanical nociceptive pain’, or ‘somatically referred leg pain’ (Bogduk, 2009). Sacro-iliac pain may also cause similar signs. 

The neural (neuropathic) structures mediating LBP include the spinal nerve roots. In humans, the spinal cord terminates in the region of the 1st lumbar vertebra and the spinal nerve roots continue within the dural sac to their respective intervertebral foramina. These spinal nerve roots are long and have the appearance of a horse's tail, hence the term ‘cauda equina’. Neuropathic pain may be perceived from the region that the dorsal branch of the spinal nerve root receives its sensory innervation, which is termed ‘radicular pain’. If compression results in dysfunction of the spinal nerve root, there will be sensory and motor deficits including muscle paresis (particularly a dropped ankle), abnormal segmental spinal reflexes and abnormal sensation; this syndrome is termed ‘radiculopathy’.    

In dogs, the spinal cord descends to the level of the L5 vertebra and so degenerative pathology affecting the L1-5 region will normally cause spinal cord dysfunction (myelopathy) rather than radicular pain or radiculopathy. The L5, 6 and 7 spinal nerve roots have a longer course within the vertebral canal and so degenerative changes in the regions of the L5-6, L6-7 and L7-S1 neuroforamina may cause clinical signs compatible with radicular pain and/or radiculopathy.

Risk Factors for Developing Clinical Signs

In human medicine, risk factors associated with higher odds for spinal pathology and LBP include those who are older, larger, with a sedentary lifestyle, increased body mass and obese. This is primarily due to increased mechanical loading and stress on the spinal joints and intervertebral discs as well as obesity promoting a systemic state that facilitates pain.

Although not extensively studied, the prevalence of spinal disease is greater in dogs of both large breed size and advancing age. Other known pre-disposing factors to Degenerative Lumbosacral stenosis (DLSS) include variability in shape and orientation of the facet joints and a small intervertebral disc area to height ratio (Benniger et al., 2006). 

Clinical Signs

Clinical signs of CLBP can be continuous, intermittent or episodic.

Episodes can be paroxysmal in onset or can have predictable triggers, such as jumping out of cars (which results in extension of the lumbar and lumbosacral spine). Pain can manifest as noticeably distinct changes in personality/demeanour with, for example, distressing vocalisation and change in gait or posture. However, signs of pain can also be more vague and difficult to interpret, reserved to behavioral changes (such as increased fear, anxiety and/or aggression), reduced tolerance of exercise and reluctance to climb stairs or attempt to jump low walls. As causes of CLBP directly involve components of the somatosensory nervous system, neuropathic pain syndromes such as dysaesthesia, parasthesia and allodynia are common. This can manifest as exaggerated, hyperaesthetic behavioural responses to normal tactile stimuli (such as stroking over the lower back), over-grooming, or sudden (sometimes compulsive) attention being given to the tail base or lateral thighs. 

Compression or inflammation of the caudal lumbar and sacral spinal nerve roots can result in radiating radicular pain and/or radiculopathy. Radicular pain potentially manifests as ‘neurogenic’ lameness, which is often a standing (not seen during limb protraction) and severe (toe-touching) form of lameness. This lameness can be transient after jumping, or when standing from recumbency, and can also be associated with painful vocalisation. In milder cases, a bilateral proximal pelvic limb lameness is seen, causing an appreciably stiff or stilted stride pattern and a tendency to maintain a degree of hip flexion with the limbs tucked under the body. Unfortunately, considerable overlap with causes of hip (and potentially iliopsoas muscle) pain exists (see further discussion, below). 

Radiculopathy (disease of the nerve roots) leads to lower motor neuron paresis, ataxia, postural deficits, abnormal segmental spinal reflexes and neurogenic muscle atrophy. Loss of the patellar reflex indicates involvement of the L4-L6 spinal nerve roots or spinal cord segments; loss of the flexor-withdrawal reflex indicates involvement of L6 to S1. Other signs of cauda equina dysfunction include urinary and faecal incontinence, paresis and flaccidity of the tail, poor anal tone, loss of perineal reflexes and potentially analgesia of the tail and perianal regions. 

Most dogs with LBP will demonstrate hyperaesthetic behaviour on firm dorsal palpation of the lumbosacrum. Care must be taken to discriminate LBP from musculoskeletal pain particularly in relation to bilateral orthopaedic disease (such as hip pain or bilateral stifle pain such as that caused by cranial cruciate ligament insufficiency). Clinical examination tests suggested as specific to DLSS include the ‘tail-jack’ (dorsoflexion of the tail base), the ‘lordosis test’ (extension of the lumbosacrum with concurrent dorsal pressure) and pressure applied to the region of the sciatic nerve in the caudal thigh/hamstring recess. All are frustratingly prone to false positive results. The latter test may be broadly analogous to tests of sciatic nerve pain in man, called the ‘straight leg raise’ (SLR) and ‘slump’ test. Both the Slump and the SLR tests elicit pain in the presence of traction of spinal nerve roots that are compressed or unable to ‘glide’ easily within the intervertebral foramen. Further research is required to understand the role of these tests in confirming LBP in dogs. 

Most dogs with LBP will demonstrate hyperaesthetic behaviour on firm dorsal palpation of the lumbosacrum. Care must be taken to discriminate LBP from musculoskeletal pain particularly in relation to bilateral orthopaedic disease (such as hip pain or bilateral stifle pain such as that caused by cranial cruciate ligament insufficiency).

Differential diagnosis for CLBP in dogs 

Degenerative lumbosacral stenosis (DLSS)

DLSS is a disorder of spinal nerve root and cauda equina compression at the L7-S1 level, caused by the chronic proliferation of surrounding bony and/or soft-tissue structures. Compression is often caused by combinations of intervertebral disc protrusion, facet joint hypertrophy, ligamentous hypertrophy and spondylotic bone forming from the caudal L7 vertebral endplate and/or the sacral alar. The biomechanics of the L7-S1 segment are significantly different to other lumbar segments, with a greater degree of movement in flexion/extension (Braund 1977) which is related to the transfer of forces from the pelvis into the spine and the relative stiffness of the adjacent sacro-iliac joints. 

Although DLSS can affect any dog breed of any age, DLSS typically affects older, large-breed dogs, with a predilection for males, working dogs and certain breeds such as the German Shepherd. The aetiology can also potentially involve congenital bony abnormalities that alter joint biomechanics and disc health (such as transitional vertebrae or vertebral end-plate osteochondrosis), dietary factors and previous infection.

Lumbar intervertebral disc disease (IVDD)

Lateralised extrusion or protrusion of the L5-6 or L6-7 disc will cause existing spinal nerve root compression at the respective intervertebral foramina which might lead to neurogenic lameness or lower motor neuron paresis. Cocker spaniels appear over-represented (Cardy et al., 2016). 

IVD extrusion should otherwise be a cause of acute clinical signs, however, sub-acute to chronic presentations are possible if the initial signs are masked or mis-interpreted. IVDD can cause LBP when occurring cranial to the L5 vertebra, however, as the spinal cord occupies the vertebral canal we would expect to see herniations result in myelopathy (pelvic limb ataxia and paraparesis) as more prominent signs over LBP. 

An exception to this is where degeneration and failure of the IVD occurs slowly, leading to partial absorption into the vertebral end-plates which eventually inter-digitate with significant sub-chondral bone inflammation. In such cases there is often palpable crepitus from the spine on clinical examination. 

Discospondylitis (DS)

DS represents infection, typically bacterial, of the intervertebral disc and cartilaginous vertebral end-plates. Haematogenous infection of already degenerate discs are most common, although infection can be associated with migrating foreign bodies or from penetrating injuries. The disorder is more common in large, middle-aged dogs. Male dogs and hunting dogs are over-represented. Clinical signs are normally expected to be acute but can be sub-acute to chronic (Ruoff et al., 2018). In the lower back, the L7-S1 intervertebral disc is the most commonly affected, possibly relating to the proximity of the urinary tract and localised venous blood flow. Ideally, the choice of antibiotic is based on a representative tissue sample for culture and sensitivity testing (blood, urine and/or disc aspirates). Serological testing for Brucella Canis should be considered given its zoonotic potential.

Tethered cord and occult tethered cord syndromes

Tethered cord syndrome (TCS) is a rare congenital or acquired disorder caused by a short or inelastic filum terminale (a connective tissue ‘stalk’ that normally attached the end of the spinal cord, the conus medullaris, to the lamina of the sacrum), with caudal descent of the conus medullaris and traction of the spinal cord and spinal nerve roots. TCS in man causes variable signs of cauda equina syndrome such as an ‘unstable’ bladder and may cause LBP. TCS often occurs in association with other spinal malformations, particularly varying grades of spina bifida, but occasionally without other structural abnormalities. Where compatible clinical signs are present in an individual with a normally positioned conus, the term ‘occult’ tethered cord syndrome (OTCS) is used (Nazar et al., 1995). In dogs, both TCS and OTCS have been described, but remain poorly charachterised syndromes. Clinical signs are predominantly expected to develop in young dogs (younger than might be expected to develop DLSS) and often involve abnormal urinary behaviour.  A recent study has provided additional clinical, diagnostic and therapeutic information (Espinsoa Romero et al, 2025). Alongside LBP, deficits on detailed neurologic examination were present in 90% of dogs. Behavioural changes were also common.

Iliopsoas muscle injury (IMI)

The iliopsoas muscle group serves as a flexor of the hip joint, but also as an important stabiliser of the vertebral column acting to balance the epaxial muscle extensors. It originates from the transverse processes of the lumbar spine and ilium and inserts into the lesser trochanter of the femur. Muscle strains occur when external forces overload its contractile force during eccentric contraction. This most often occurs at the muscle-tendon interface. LBP ensues, as can pelvic limb lameness. Such injuries are most common in agility dogs; Border Collies are over-represented. However, concurrent musculoskeletal and spinal conditions (particularly DLSS) are common findings in dogs with strains confirmed by ultrasound (Sack et al., 2023). 

Other causes of CLBP 

Other potential causes for CLBP include facet joint hypertrophy and osteoarthritis, juxtafacet cysts, spondylosis deformans, diffuse idiopathic skeletal hyperostosis (DISH), multiple cartilaginous exostosis, and spinal dural ossification. These disorders cause proliferation of bone or soft-tissue to potentially compress the exiting spinal nerve roots. However, these conditions are less likely to cause clinical signs in isolation. For example, spondylosis deformans is a common radiologic finding of the ageing canine spine and is a common epiphenomenon of both IVDD and DLSS; its presence at high motion segments (i.e., L7-S1) serves as an indicator that cross-sectional imaging may be beneficial. 

Tumours originating from the vertebrae, neural structures or para-spinal tissues can cause LBP; but the clinical course is normally measured in days to weeks (rather than months) prior to the onset of neurologic abnormalities. Nevertheless, this possibility should always be considered when constructing a list of differential diagnoses particularly where concurrent systemic signs are evident. 

Adding to the complexity of chronic pain identification, lumbar and lumbosacral pain in dogs is often linked to multiple concurrent spinal pathologies, making it difficult to identify the primary source of pain, deciding which pathology is clinically relevant, and prioritising interventions. For example, in a 2025 study by Medina-Serra et al. more than a third of patients (37.3%) presented with three or more concurrent spinal abnormalities.

Differentiating LBP from hip pain

We have previously described considerable overlap in the gait and postural changes seen in dogs with hip and lumbosacral pain. As the underlying cause for hip pain is often osteoarthritis secondary to developmental joint disease, hip pain in dogs is often symmetric in presentation and can be made worse after exercise; in contrast, DLSS can more often cause asymmetric lameness, standing lameness and spontaneous painful vocalisation. 

A common clinical examination indicator for hip pain is resentment of joint extension. However, during extension of the hip joints the lumbosacrum also extends, which tends to reduce the volume of the intervertebral foramen due to cranioventral translation of the sacral lamina and cranial articular processes. Therefore, extension of the hips is expected to elicit discomfort in dogs with LBP, particularly those with DLSS. This highlights the need for radiographic assessment of such cases to include both anatomic regions and for scrutiny when assigning the significance of clinical versus radiologic changes. In dogs without hip pathology, the previous finding of pain on hip extension should prompt the clinician to make a critical review of the changes in lumbosacral region associated with DLSS. 

Always remember that patients with chronic pain can experience central sensitisation, which could prove challenging to the exam, eliciting unexpected reactions and resulting in a fearful or aggressive response. Developing a swift but effective orthopaedic and neurological exam can allow lots of information to be gathered, while minimising patient contact that could prove aggravating to them. 

Diagnostic Imaging

Radiographic changes associated with IVDD and DLSS include narrowing of the affected disc, spondylosis deformans, vertebral end-plate sclerosis (increased radiopacity) and erosive or proliferative changes associated with the facet joints and/or vertebral end-plates. With DLSS, there may be telescoping of the sacral and articular processes lamina cranioventrally such that foraminal stenosis is evident. In extreme cases this cranioventral translation of the vertebra is associated with partial failure of the intervertebral disc, consistent with spondylolisthesis. With IVDD, extruded mineralised disc material may be evident within an intervertebral foramen, but sometimes changes are not apparent. In the case of DS, subtle irregularity of the vertebral end-plates progressing to more fulminant osteolysis of the vertebral bodies can be seen. However, radiologic changes can lag 2-6 weeks after the initial infection. Survey radiography is also beneficial to screen for vertebral or para-spinal tumours which can cause osteo-proliferative or lytic lesions. 

In all cases, cross-sectional imaging studies are beneficial to completely assess foraminal and vertebral canal stenosis, with MRI considered superior for soft-tissue detail. All advanced imaging studies must be correlated with the clinical assessment. A recent study by Medina-Serra et al. (2025) demonstrated that advanced imaging alone was not always sufficient to determine pain sources, as some dogs with spinal abnormalities did not exhibit pain, while others experiencing and exhibiting pain showed no clear MRI pathology. This broadly aligns with previous findings in human medicine, which indicate that not all patients with lumbar and lumbosacral spinal pathology will necessarily show signs of pain. However, patients with MRI pathology were significantly more likely to experience pain compared to those without MRI pathology; spinal nerve root compression (termed radiculopathy in the study) was the most common feature recorded as causing pain. 

It is well recognised that L7-S1 foraminal and vertebral canal volumes can significantly vary between extension (worsened) and flexion (improved) of the lumbosacrum in normal dogs (Lampe et al., 2020) and in dogs with DLSS (Jones et al., 2008). In certain cases, performing such ‘dynamic’ imaging studies can be beneficial for diagnostic purposes, to either confirm a suspicion that episodic clinical signs may be related to exercise-induced foraminal stenosis (with images acquired in extension) or to confirm that foraminal or vertebral canal stenosis can be alleviated by patient positioning during surgical intervention (with images acquired in flexion). In a practical sense, there is a degree of subjectivity to such assessments and controversy exists as to the validity of this approach in confirming an association between clinical signs and imaging findings.  

In summary, radiography is a beneficial initial tool in cases with CLBP to assess for the presence of predisposing anatomical variances (such as transitional anomalies), to identify degenerative changes, to exclude major concerning osteolytic or productive lesions compatible with infection or neoplasia, and to determine the presence and severity of coxofemoral osteoarthritis. MRI is then beneficial in confirming which spinal nerve roots are compressed or inflamed, whether there is foraminal or canal stenosis (or both) and in determining whether such changes are mild, moderate or severe. This determination can assist with the choice of therapy and potentially quantify the risk of radiculopathy and cauda equina syndrome. MRI is also necessary to diagnose certain specific differential diagnoses (such as OTCS, for example). Dynamic MRI sequences can be of benefit in DLSS and OTCS on a case-by-case basis, as previously described. Experience in the clinical assessment, diagnosis and management of CLBP is beneficial - particularly as decision making during image acquisition is conducted under general anaesthesia.  

In summary, radiography is a beneficial initial tool in cases with CLBP to assess for the presence of predisposing anatomical variances (such as transitional anomalies), to identify degenerative changes, to exclude major concerning osteolytic or productive lesions compatible with infection or neoplasia, and to determine the presence and severity of coxofemoral osteoarthritis. MRI is then beneficial in confirming which spinal nerve roots are compressed or inflamed, whether there is foraminal or canal stenosis (or both) and in determining whether such changes are mild, moderate or severe.

Other diagnostic tests

The benefit of other diagnostic tests is dependent on a prioritised differential diagnosis list. Where DS or neoplasia is suspected, there is significant benefit in obtaining additional clinicopathologic data. Electrodiagnostic evaluation (cord dorsum potentials and f-wave latencies) may support sciatic nerve dysfunction but these techniques require significant technical expertise. 

Treatment

A range of management and treatment options exist for CLBP in dogs, some of which will be targeted based on the specific diagnosis suspected to be clinically significant, and other more broad management options. 

It should first be noted that this is a heterogenous patient population and there is a lack of controlled clinical trials to form a strong evidence base for specific recommendations. In addition, much like the field of osteoarthritis study in dogs, there is a need for the adoption of validated outcome measures to determine the relative success of specific therapies.  

Also much like osteoarthritis related pain, the proposed management options for CLBP can be analogised as a tool-box; with multiple accessible options at any one time. The options can be accessed in the event of incomplete responses to initial therapies, on consideration of individual circumstances (including the confirmed diagnosis), or on the severity of the initial clinical syndrome (such as the presence of neurologic deficits). Access and implementation of these options is not linear, as interventions may be returned to after others, at which stage they may prove useful; a good example is rehabilitation after surgical intervention including the use of physical therapies. Some animals can benefit significantly from ‘prehabiliation’, yet others are not clinically able to engage due to severity of the disease, but that is not to say they will not significantly benefit afterwards. 

Options include:

• Lifestyle adaptations; including temporary or permanent exercise modification, rest periods or retirement from agility, behavioural management including provision of environmental enrichment and engagement activities 

• Physical and non-medical therapies; including improving muscle strength and coordination, acupuncture, extra-corporeal shock wave therapy, cryotherapy, laser therapy, myotherapy 

• Multi-model medical therapy, by mouth. 

• Targeted or imaging-guided interventions; including steroid injections (perineural and epidural) and local analgesic injections 

• Surgery; including decompressive vs instrumented and open vs minimally invasive techniques 

A multi-disciplinary approach is likely to be beneficial; with optimised management representing cooperation between pet carer, primary care clinicians, (neuro)surgeons, pain management specialists and allied professionals (including rehabilitation practitioners, physiotherapists and behavourists).    

the proposed management options for CLBP can be analogised as a tool-box; with multiple accessible options at any one time. The options can be accessed in the event of incomplete responses to initial therapies, on consideration of individual circumstances (including the confirmed diagnosis), or on the severity of the initial clinical syndrome (such as the presence of neurologic deficits). Access and implementation of these options is not linear

Multi-modal medical therapy 

Medical management options have been described for DLSS, IVDD, TCS/OTCS, IMI and DS. Amongst these diseases, medical options are shared (with the exception of DS, where appropriate and targeted antibiosis is additionally required). For DLSS, medical therapy was successful in 55% of 49 dogs in one study, with 32% subsequently undergoing surgery and 10% being euthanized due to progression in clinical signs (De Decker et al., 2014). 

Typical first-line options include paracetamol, non-steroidal anti-inflammatory drugs or short courses of low-dose corticosteroids. In simple cases these medications may be sufficient to manage acute flare-ups. A gabapentinoid medication (such as gabapentin, or pregabalin) can be a reasonable addition, particularly where para- or dysaesthesia is suspected. Some dogs may benefit from the addition of an NMDA antagonist such as amantadine (3-5 mg/kg once daily) or memantine (smaller formulations available). Amantadine has been studied for long-term use in dogs with osteoarthritis. Intermittent subcutaneous injection of ketamine is proposed for managing central sensitisation leading to hyper-algesia in chronic cases where other interventions are not possible. In man, there is a proposed role for serotonin re-uptake inhibitors (such as fluoxetine) and tri-cyclic antidepressants (such as amitriptyline) in managing spinal pain, as increasing the availability of serotonin, an important inhibitor of spinal pain pathways, may also improve compulsive behaviours triggered by pain. Amitriptyline is expected to have a less favourable side effect profile. 

It should be noted that the use of several of these medications is off-license and should only be prescribed by veterinary surgeons according to the Veterinary Medicine Directorate cascade system. 

Targeted or imaging-guided interventions 

The epidural injection of the corticosteroid methylprednisolone acetate has been described for the management of pain associated within DLSS, although the author (CD) has also used it in dogs with IVDD and OTCS.

Injected into the dorsal epidural space at L7-S1 via an interlaminar approach, the medication should diffuse around the cauda equina and their spinal nerve roots, the dorsal longitudinal and interarcuate ligaments, the intervertebral disc and the paired facet joint synovium. In one study (Jannssens et al., 2009), a cohort of 38 dogs with DLSS (excluding dogs with severe clinical or radiologic syndromes) were managed with one (7 dogs), two (7 dogs, second injection around 15 days later) or three (24 dogs, third injection around six weeks later) epidural injections; 79% of dogs improved and 53% were considered by their owners to be pain-free over a median of 46 months. In another study (Gomes et al., 2020) 27 of 32 dogs improved after a single injection and 5 remained improved at mean follow up of 9.4 months; the remaining 17 dogs relapsed at a mean of 2.4 months. 

Ultrasound or fluoroscopic guided perineural injections of methylprednisolone have also been described in the case of cervical foraminal IVDD (Wolf et al., 2021) and the author (CD) has used these in cases of far-lateral lumbar IVDD. 

The addition of a local anaesthetic agent to the injections can aid in both diagnostic and therapeutic terms.

In man, other image-guided techniques include facet joint injections, pulsed radiofrequency and radiofrequency ablation of the dorsal (sensory) branches of the spinal nerve roots. These techniques appear safe to perform in dogs despite operator exposure to radiation (Medina-Serra et al., 2025(2) and can be combined in dogs with DLSS with beneficial clinic effects (Medina-Serra et al., 2026).

Surgery 

Surgical options for managing CLBP are specific to the underlying cause, in some instances multiple options exist. Surgical treatment should rarely be considered a definitive solution to CLBP, but can be a very effective option in improving clinical signs and limiting the need for complex medical management. 

Surgical intervention for OTCS (de-tethering of the spinal cord by transection of the external or internal filum terminale) has been significantly associated with a full recovery and discontinuation of medical treatment at a median follow up of 9 months (Espinosa Romera et al., 2025). 

DS can cause failure of an IVD with subsequent instability, an issue more common at high motion segments such as the lumbosacrum. In such cases (and where medical therapy proves unsuccessful), surgical distraction and stabilisation to obtain intervertebral fusion is effective (Auger et al., 2000). This approach also allows for the direct application of antibiotic-impregnated sponges into the infected IVD (Renwick et al., 2010). 

The objective of surgical management of DLSS is decompression of the L7 (in the intervertebral foramina) and/or sacrocaudal (in the vertebral canal) spinal nerve roots. Two contrasting strategies have been described:

1. Direct decompression of the respective spinal nerve roots by: 

• Dorsal flavectomy and laminectomy L7-S1, often combined with dorsal annulectomy; however, this approach provides limited access for decompression of the more lateral L7 spinal nerve roots and may (where the laminectomy is too wide) contribute to IVD degeneration which could exacerbate foraminal stenosis (Worth et al., 2017). The technique is most effective where there is sudden IVD extrusion or significant asymmetric IVD protrusion, in order to relieve cauda equina compression and to resect any acquired epidural adhesions. The author (CD) prefers to perform these procedures in a minimally invasive fashion via a microscopic approach using muscle sparing tubular retractors. 

• Lateral foraminotomy i.e., approaching from a dorsolateral angle to the vertebral pedicle, with bone removed to enlarge the L7-S1 foramen and decompress the L7 nerve root within the lateral recess of the vertebral canal. Long-term carer-reported clinical outcomes suggested resolution of clinical signs in 33/34 dogs at a mean follow-up of 22.9 months (Gomes et al., 2018). As the sacrocaudal nerve roots are not approached, case selection is important. This procedure can be performed using a keyhole technique utilising a spine-specific endoscope, using a technique developed by the author (Driver et al., 2026). The technique is expected to reduce blood loss, opioid usage, length of hospital stay and risk of infection. As there is only an 8mm skin incision with a single suture, dogs can be discharged the same day and resume moderate exercise within a few days. Similar techniques can be used to treat IVDD (Driver et al., 2026B).   

2. Indirect decompression of the respective spinal nerve roots by vertebral distraction with subsequent fixation. 

Distraction of the vertebrae is normally achieved by positioning the patient such that the lumbosacrum is flexed (with the benefits for intervertebral foraminal and vertebral canal volumes previously described). Direct distraction with laminectomy spreaders has also been described (Slocum and Devine, 1986). Various fixation techniques have been described, including trans-articular facet screws, multiple vertebral body or pedicle implants (threaded pins or screws) with bone cement, and trans-ilial bars (Beam et al,, 2014, Golini et al., 2014, Müller et al., 2017). These are described in small case series suggesting good clinical outcomes. The use of polyaxial locking plate systems or ‘pedicle’ screws with interconnecting rods is increasingly common (Smolders et al., 2012) and can be utilised alongside an intervertebral disc spacer or ‘cage’ for interbody fusion (Reints Bok et al, 2020, van den Brink et al, 2026). Similar to work previously published on ‘wobbler syndrome’ (Driver et al., 2023), the author prefers an anatomically accurate microporous titanium cage that can be anchored to the adjacent vertebra.  

In summary, there are a range of surgical options suitable on a case-by-case basis and experience with all available techniques is beneficial in recommending specific interventions. 

Conclusion

CLBP is an important and increasingly recognised cause of behavioural, gait and postural changes in dogs.

A suspicion for CLBP can be raised following careful physical examination and following the exclusion of other metabolic and musculoskeletal disorders.

There are challenges in interpreting the clinical examination and there is risk of both under- and over-diagnosis; particularly as routine and advanced diagnostic imaging may identify both clinically relevant and incidental changes. There are behavioural medicine, physical therapy, medical and surgical management options. With a carefully considered multi-disciplinary approach, successful long-term outcomes can be achieved. 

References

1. Anderson, K.L., O'Neill, D.G., Brodbelt, D.C., Church, D.B., Meeson, R.L., Sargan, D. et al. (2018) 'Prevalence, duration and risk factors for appendicular osteoarthritis in a UK dog population under primary veterinary care', Scientific Reports, 8(1), p. 5641. https://doi.org/10.1038/s41598-018-23940-z

2. Auger, J., Dupuis, J., Quesnel, A. and Beauregard, G. (2000) 'Surgical treatment of lumbosacral instability caused by discospondylitis in four dogs', Veterinary Surgery, 29(1), pp. 70–80.

3. Beam, R., Powers, D., Hauptman, J. and Sanders, S. (2014) 'Dynamic lumbosacral instability: clinical evaluation and owner-perceived outcome of a novel distraction-stabilisation technique for L7–S1 in 51 dogs (2008–2013)', Journal of Veterinary Internal Medicine, 28, p. 1016.

4. Cardy, T.J., Tzounos, C.E., Volk, H.A. and De Decker, S. (2016) 'Clinical characterization of thoracolumbar and lumbar intervertebral disk extrusions in English Cocker Spaniels', Journal of the American Veterinary Medical Association, 248, pp. 405–412.

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