Also see Diseases of the Spinal Column and Cord.
Inherited Spinal Cord Disorders in Dogs
Spinal Muscular Atrophy in Dogs
Spinal muscular atrophy is an inherited lower motor neuron (LMN) disorder in Brittany spaniels that can have an early (by 1 month), intermediate (by 4–6 months), or delayed (> 1 year old) onset. Rottweilers can also develop an early form of spinal muscular atrophy that is referred to as a motor neuron disease.
Swedish Lapland puppies are affected at the age of 5–7 weeks, Stockard paralysis (which occurs in Great Danes crossed with either Bloodhounds or Saint Bernards) has an onset at 11–14 weeks, and English Pointers are affected at approximately 5 months old. LMN disease also occurs in puppies of other breeds, including Doberman Pinschers and Briquet Griffon Vendeens; a focal form involving the thoracic limbs occurs in German Shepherd Dogs.
Paraparesis or tetraparesis with neurogenic muscle atrophy is the main clinical sign of spinal muscular atrophy in dogs. The severe, generalized LMN disease in spinal muscular atrophy closely resembles the signs of peripheral neuropathy. Loss of motor neurons in the spinal cord is the most striking feature on necropsy.
There is no treatment.
Demyelination of Miniature Poodles
Demyelination of Miniature Poodles is presumed to be an inherited disorder involving primarily the spinal cord. This rare condition causes paraparesis at the age of 2–4 months that rapidly progresses to tetraplegia.
There is no treatment.
Hereditary Ataxia in Dogs
Hereditary ataxia has been reported in several dog breeds, including Parson Russell, Jack Russell, and Smooth Fox Terriers. Several forms of disease exist. In general, the diseases affecting these breeds are spinocerebellar ataxia.
In one form of ataxia in Parson Russell, Jack Russell, and Smooth Fox Terriers, an autosomal recessive mutation in the KCNJ10 gene has been identified. A mutation in the CAPN1 gene has also been identified in some dogs; however, this might be a rare variant.
The predominant clinical signs of ataxia are cerebellar (cerebellar ataxia, intention tremor, hypermetria).
Some forms of ataxia include myokymia (in which the muscles appear to show verminous movement), seizures, or both.
Clinical signs begin to appear at approximately 2–6 months of age, but some forms of the disease have a later onset, at approximately 6–12 months of age.
Histological evaluation at necropsy shows spinal cord demyelination.
Ataxia is progressive; in some cases, however, clinical signs stabilize but do not regress, and some affected animals are able to live a relatively normal life, despite the abnormal movements.
Afghan Hound Myelopathy
Afghan Hound myelopathy is an inherited disorder that causes both demyelination and necrosis of the spinal cord. Paraparesis develops during the first year of life and progresses to paraplegia within 1 week. The thoracic limbs become involved over the next 1–2 weeks.
A similar condition occurs in young Kooikerhondje dogs (decoy dogs of the Netherlands) of either sex, with signs beginning at the age of 3–12 months.
The prognosis is poor in both breeds.
Leukoencephalomyelopathy of Rottweilers
Leukoencephalomyelopathy of Rottweilers has a later onset than neuraxonal dystrophy, usually at approximately 2–3 years of age. A similar basis is suggested for the two disorders because animals occasionally show histopathological features of both conditions (co-occurrence has been reported in both Rottweilers and Chihuahuas). A genetic test is available through UC Davis's Veterinary Genetics Laboratory.
In leukoencephalomyelopathy, there is no head tremor, and proprioception is delayed. Bilaterally symmetrical areas of spinal cord demyelination are the predominant findings on necropsy.
Calcium Phosphate Deposition in Great Danes
Calcium phosphate deposition in Great Danes causes mineralization of soft tissues and bone deformity, with dorsal displacement of C7. The resultant compressive myelopathy occurs in puppies 1–2 months old.
This condition is distinct from caudal cervical spondylomyelopathy.
Degenerative Myelopathy in Dogs
Degenerative myelopathy is a painless, slowly progressive myelopathy that occurs commonly in dogs.
A mutation (SOD1) has been identified that is associated with increased risk of developing degenerative myelopathy, and a genetic test is available to identify dogs at higher risk of developing the disease. Increased concentrations of a microRNA (miR26b) that regulates genes associated with SOD1 have been associated with progression of the disease.
Clinical signs are typically consistent with a thoracolumbar spinal cord localization with pelvic limb paresis and ataxia; however, radiculopathy can cause LMN signs in the pelvic limbs, and progression can eventually lead to involvement of the thoracic limbs.
Histopathological changes with degenerative myelopathy include noninflammatory axonopathy and myelinopathy.
German Shepherd Dogs, Pembroke Welsh Corgis, Boxers, Rhodesian Ridgebacks, and Chesapeake Bay Retrievers are predisposed; many other breeds can also be affected.
There is no treatment for degenerative myelopathy. Physical therapy slows the progression of clinical signs.
Progressive Axonopathy of Boxer Dogs
Progressive axonopathy of Boxers is an autosomal recessive disorder that causes patellar hyporeflexia, severe dysmetria, loss of proprioception, and spastic paresis at the age of 1–7 months. Axonal spheroids are widespread in both the central and the peripheral nervous systems on necropsy.
Although this condition causes loss of the patellar reflex, in general the clinical signs are more suggestive of spinal cord disease than of peripheral neuropathy.
There is no treatment; however, affected dogs can live relatively comfortably for a considerable amount of time.
Breed-Associated Aseptic Meningitis in Dogs
Breed-associated aseptic meningitis (steroid-responsive meningitis-arteritis) has been reported in Beagles, Bernese Mountain Dogs, Boxers, and German Shorthaired Pointers, and sporadically in other dog breeds.
The main clinical signs are neck pain, fever, and dramatic pleocytosis in the CSF in young dogs.
The prognosis for dogs with aseptic meningitis is guarded to favorable, especially for dogs with acute disease that are treated promptly with immunosuppressive doses of corticosteroids, tapered slowly over 6–8 months. Rapid tapering can result in relapse.
Infectious causes of meningitis should be ruled out.
Caudal Cervical Spondylomyelopathy in Dogs
Caudal cervical spondylomyelopathy (wobbler syndrome) might have a heritable basis in Borzois (with onset at the age of 5–8 years) and Basset Hounds (< 8 months), as well as probably Doberman Pinschers (≥ 2 years) and Great Danes (< 2 years). Many breeds might be affected.
Neurological deficits in this disorder range from mild ataxia of the pelvic limbs to tetraplegia. Affected dogs often keep their neck flexed ventrally, and there might be caudal cervical pain.
Two forms of caudal cervical spondylomyelopathy have been recognized: a disk-associated form (older age of onset) and a facet-associated form (younger age of onset, often in giant breeds).
Spinal radiographs might show malalignment or remodeling of the vertebrae, narrowing of one or more disk spaces, or spondylosis deformans. CT, myelography, or MRI usually reveals marked stenosis at the cranial orifice or at the level of the facets of the midcervical or caudal cervical vertebrae (see ).
Courtesy of Dr. Ronald Green.
Several surgical techniques, including stabilization, decompression, and disk replacement, have been developed to treat caudal cervical spondylomyelopathy in dogs.
This condition is distinct from calcium phosphate deposition in Great Danes.
Arachnoid Diverticuli in Dogs
Arachnoid diverticuli (arachnoid cysts, arachnoid pseudocysts, meningeal cysts, leptomeningeal cysts, subarachnoid cysts) cause accumulations of CSF and focal myelopathy in young dogs. The cause is unknown, but some diverticuli might have a congenital origin.
Clinical signs consist of progressive ataxia and weakness.
Diagnosis is based on myelography and/or MRI.
The prognosis for dogs with arachnoid diverticuli might be favorable after surgical excision; however, recurrence is possible.
Congenital Spinal Cord Disorders in Dogs and Cats
Congenital Vertebral Malformations in Dogs
Congenital vertebral malformations in dogs include hemivertebrae (shortened or misshapen vertebrae), block (fused) vertebrae, and butterfly vertebrae (having a sagittal cleft). Hemivertebrae (see ) are most common in screw-tailed dog breeds and are inherited in German Shorthaired Pointers.
Courtesy of Dr. Rebecca Packer.
Studies suggest that approximately 80% of neurologically normal Pugs, French Bulldogs, and English Bulldogs have vertebral malformations (1). The likelihood that these malformations will be clinically important is greater in Pugs than in French Bulldogs.
Decompressive surgery can be successful for treating vertebral malformations; often, however, surgery needs to be combined with spinal stabilization.
Caudal Articular Hypoplasia in Dogs
Caudal articular hypoplasia is reported in Pugs, French Bulldogs, and English Bulldogs and can cause spinal instability.
Surgical stabilization might be beneficial; however, often multiple vertebrae are affected.
Multiple Cartilaginous Exostosis in Dogs
Multiple cartilaginous exostosis, which occurs most commonly in German Shepherd Dogs, is a benign proliferation of cartilage or bone that can affect the ribs, long bones, or vertebrae. It might have a familial basis.
Treatment consists of surgical removal; however, recurrence or occurrence at additional sites is common.
Transitional vertebrae are often clinically associated with lumbosacral stenosis. Myelography or specialized imaging techniques (eg, CT, MRI) are usually required to confirm spinal cord compression in these congenital conditions (see ).
Courtesy of Dr. Rebecca Packer.
Atlantoaxial Subluxation in Dogs
Atlantoaxial subluxation (instability or increased mobility between the atlas, or first cervical vertebra [C1] and the axis, or second cervical vertebra [C2]) occurs most commonly as a congenital disorder in young toy or miniature dog breeds and occasionally as a congenital disorder in several large breeds, including Rottweilers and Doberman Pinschers.
Clinical signs usually develop within the first few years of life and consist of an acute or slowly progressive onset of neck pain or gait dysfunction, ranging from ataxia to tetraplegia.
Radiographic confirmation of atlantoaxial subluxation (see ) should be followed by stabilization using ventral fixation.
The prognosis is guarded.
Courtesy of Dr. Genesis Lopez Bonilla.
Syringomyelia in Dogs
Syringomyelia is the development of one or more fluid-filled cavities within the spinal cord. Hydromyelia is accumulation of fluid within an enlarged central canal of the spinal cord. It can be difficult to differentiate between syringomyelia and hydromyelia, so the term syringohydromyelia is often used.
Syringohydromyelia causes progressive ataxia and paresis; scoliosis and spinal pain are possible.
Causes of syringohydromyelia include trauma, neoplasia, inflammatory conditions, and developmental malformations (eg, spina bifida). The most common cause in dogs is caudal occipital malformation syndrome.
Spinal Dysraphism in Dogs
Spinal dysraphism (also known as myelodysplasia) includes anomalies of the skin, vertebrae, and spinal cord that are secondary to faulty closure of the neural tube. Generally, this term is used for neural tissues rather than for vertebrae. Where vertebral malformations occur, the condition is generally referred to as spina bifida. Spinal dysraphism is inherited in Weimaraners; similar malformations occur in other dog breeds as well.
Neurological deficits of spinal dysraphism are evident by the age of 4–6 weeks and include paraparesis and a symmetrical bunny-hopping gait in the pelvic limbs. There is a bilateral flexor reflex: pinching one paw elicits flexion of both pelvic limbs. There can be scoliosis or abnormal hair streams on the dorsal aspect of the neck.
Diagnosis of spinal dysraphism is based on clinical signs and imaging techniques such as myelography or MRI.
There is no treatment; however, neurological deficits usually do not progress.
Spina Bifida in Dogs and Cats
Spina bifida is a failure of the vertebral arch to fuse; it affects both dogs and cats. Sometimes only the bones are involved, causing no clinical signs(called spina bifida occulta); if the spinal cord is also involved, it is called spina bifida manifesta. Meningomyeloceles can occur with spina bifida, as can tethered cord syndrome.
The most likely clinical signs of spina bifida in dogs are LMN signs in the pelvic limbs and urinary or fecal incontinence.
The prognosis for animals with substantial neurological deficits is poor.
Screw-tail dog breeds are the most commonly affected.
Spina bifida can accompany sacrocaudal dysgenesis (see ). In Manx cats, sacrocaudal dysgenesis is inherited as an autosomal dominant trait.
Courtesy of Dr. Rebecca Packer.
Tethered Cord Syndrome in Dogs
Tethered cord syndrome in the absence of another congenital malformation, such as spina bifida, has been identified in dogs. It occurs because a tight filum terminale (a fibrous band of connective tissue that extends from the caudal end of the spinal cord to the coccyx) forms, preventing normal movement of the spinal cord.
Diagnosis is based on dynamic MRI.
Tethered cord syndrome is currently underrecognized and previously poorly described in the literature. The median age at diagnosis is 13 months; however, some patients begin showing clinical signs as early as 8 weeks old.
The most common clinical signs of occult tethered syndrome include low back pain, gait abnormalities such as intermittent lameness or skipping gait, behavioral problems such as anxiety, and urinary incontinence.
Treatment involves detethering the spinal cord by transecting the intradural or extradural filum terminale. Long-term success after detethering is reported to be 64% (2).
Pilonidal Sinus in Dogs and Cats
Pilonidal sinus (dermoid sinus, dermoid cyst) is a disorder that appears to result from faulty neurulation seems to be inherited (autosomal recessive) in Rhodesian Ridgebacks. It can occur in other dog breeds as well.
In this disorder, the sinus is lined by skin and can communicate with the subarachnoid space, causing possible meningitis or myelitis.
Treatment consists of surgical excision of the sinus to the level of the dura, along with, in dogs with bacterial meningitis, long-term administration of antimicrobials (minimum of 3 months).
The type of antimicrobial should be based on culture and susceptibility testing, when possible; however, CSF cultures often fail to yield positive cultures even in the presence of bacteria. Any empirically selected antimicrobial should penetrate the blood-brain barrier, with a preference for bacteriocidal drugs.
For young puppies and kittens, trimethoprim-sulfadiazine (15–30 mg/kg, PO, every 12 hours) can be effective; for older animals, a combination of enrofloxacin (in dogs only: 10 mg/kg, PO, every 24 hours) and amoxicillin-clavulanic acid (11–20 mg/kg, PO, every 12 hours) (3, 4). Antimicrobial treatment for bacterial meningitis is typically continued for 4–8 weeks, or until the infection resolves.
Key Points
Congenital and inherited disorders of the spinal cord in dogs and cats can be present at birth or develop later in life.
Even if present at birth, as with atlantoaxial instability, clinical signs typically do not arise until at least several months of age.
Most spinal cord congenital malformations are breed specific, highlighting the importance of signalment when considering congenital malformations as a differential in patients presenting with appropriate clinical signs.
Plain radiography or CT can be helpful in diagnosing congenital malformations involving the vertebrae.
Diagnosis of other malformations requires the use of advanced imaging such as CT with myelography or MRI.
Genetic testing or CSF analysis might also be necessary for accurate diagnosis.
For More Information
Slanina MC. Atlantoaxial instability, Vet Clin North Am Small Anim Pract. 2016;46(2):265-275.
Dewey CW, Davies E, Bouma JL. Kyphosis and kyphoscoliosis associated with congenital malformations of the thoracic vertebral bodies in dogs. Vet Clin North Am Small Anim Pract. 2016;46(2):295-306.
Espinosa Romero JE, de Decker S, Santifort K, et al. Occult tethered cord syndrome: insights into clinical and MRI features, prognostic factors, and treatment outcomes in 30 dogs with confirmed or presumptive diagnosis. Front Vet Sci. 2025;12:1588538.
Also see pet owner content regarding brain, spinal cord, and nerve disorders of dogs and cats.
References
De Decker S, Rohdin C, Gutierrez-Quintana R. Vertebral and spinal malformations in small brachycephalic dog breeds: current knowledge and remaining questions. Vet J. 204;304:106094. doi:10.1016/j.tvjl.2024.106095
Espinosa Romero J, de Decker S, Santifort K, et al. Occult tethered cord syndrome: insights into clinical and MRI features, prognostic factors, and treatment outcomes in 30 dogs with confirmed or presumptive diagnosis. Front Vet Sci. 2025;12:1588538. doi:10.3389/fvets.2025.1588538
Hertzsch R, Richter A. Systematic review of the pharmacological evidence for the selection of antimicrobials in bacterial infections of the central nervous system in dogs and cats. Front Vet Sci. 2022;8:769588. doi:10.3389/fvets.2021.769588
Kiviranta A-M, Lappalainen AK, Hagner K, Jokinen T. Dermoid sinus and spina bifida in three dogs and a cat. J Small Anim Pract. 2011;52(6):319-324. doi:10.1111/j.1748-5827.2011.01062.x
