Maigan Espinili Maruquin


The Degenerative Myelopathy (DM) in dogs was initially described in German Shepherd Dogs in 1973 [1]. However, the disease has been reported to affect at least 56 breeds [2] with around 0.19 % prevalence [3]. Some of the breeds of high risk include German shepherds; Pembroke Welsh Corgi, Boxer, Cavalier King Charles Spaniel, Chesapeake Bay Retriever, and Rhodesian Ridgeback [4]. Typically, dogs of 8 years old and above gets the disease [5], with no sex preference [1].


The Canine DM affects the spinal cord, with most cases presenting homozygous A allele of a superoxide dismutase 1 (SOD1) missense mutation, SOD1:c.118 G > A, predicting the E40 K amino acid substitution in the SOD1 protein [2, 5, 6].


Clinical Signs

Following insidious onset, non-painful neurodegeneration is progressive in the spinal cord of the affected dogs [4]. Among the symptoms of DM, early indications show ataxia of the hind limbs, with mild spastic paresis (often asymmetrical signs) including: knuckling, stumbling and uneven wear of the nails of the hind paws [7, 8]. The dorsal roots of the femoral nerve may play a role in inhibiting the sensory impulses from stretch receptors located in the quadriceps muscle [9].


When left to progress without euthanasia, upper motor neuron disease develops to lower motor neuron disease, which eventually leads to the absence of spinal reflexes and will eventually result to flaccid tetraplegia [9]. Incontinence on both urine and fecal are also most likely, while difficulties with eating and swallowing may be observed as a result of brain stem disease [7, 10]. After which, failure of respiratory muscles may cause eventual death due to hypoxemia  [11].



Differential Diagnosis

Existing orthopedic and neurologic diseases can often confuse the interpretation of the neurologic examination results [12], while many acquired spinal cord diseases can be presented clinically [9]. Other disorders shall be suspected and considered on ageing dogs including: (a) Chronic Hansen type II intervertebral disc disease; (b) Spine/spinal cord neoplasm; (c) Sub-arachnoid diverticuli; (d) Discospondylitis and spinal empyema; (e) Meningo-myelitis [4]. Different spinal cord disorders have different anatomical distribution, clinical signs and age of onset, which often suggests breed predisposition and usually diagnosed by histopathology of the central nervous system (CNS) and peripheral nervous system [9]. The post- mortem histopathological examination of the spinal cord however is used as a definitive diagnosis, wherein segmental degeneration of the axon and associated myelin can be reported [9].


On the other hand, identifying disease-related genes can be done by gene sequencing, linkage mapping, and genome-wide association [9]. Despite the detection of SOD1 gene mutation, it is still possible that the dog will not develop the DM [10], and other distinct genetic mechanisms or aetiology may be the source of the DM onset in dogs without the SOD-1 mutation [4].

Fig. 01. Histopathology of the thoracic spinal cord. Comparison of Luxol fast blue with a periodic acid-Schiff couterstain (LFB/PAS) staining (A–C) and immunohistochemistry detecting glial fibrillary acidic protein (D–F) from a normal unaffected 14.5-year-old Pembroke Welsh Corgi (PWC) (A, D), a 10-year-old PWC with clinical signs of DM for 6 months and mild paraparesis and pelvic limb ataxia (B, E), and a 14-year-old PWC with clinical signs of DM for 48 months and flaccid tetraplegia (C, F). Myelin loss in the white matter is depicted by loss of blue color with LFB (B, C). Note the severity of pallor in the white matter and increased areas of astrogliosis in the PWC with longer disease duration. (Courtesy of Gayle C. Johnson, DVM, PhD, Columbia, MO.) [9]


Diagnostic Approach

The antemortem diagnosis is based on the patient history, wherein the onset and progression of the clinical signs are considered, and after excluding all the other disorders [4, 9, 12, 13]. The DM is presumptively diagnosed thru myelography or magnetic resonance imaging (MRI), while cerebrospinal fluid (CSF) analysis, electrodiagnostic testing, and spinal cord imaging procedures are usually conducted to evaluate spinal cord disease, and, SOD1 mutation can be tested with commercially available DNA based tests [9].

Treatment and Management

Despite the lack of specific therapy over the past 40 years, genetic advances show promising future in understanding more of the complex disease [4, 7]. Pain management was attempted by using corticosteroids or non-steroidal anti-inflammatory drugs (NSAIDs) [7]. Intensive physical therapies, however, increased survival times and the period for which the dog was ambulatory, as observed in a study, and may be the best supportive approach [8].


The disease may be inevitable from progressing, however, quality of life can be sustained thru appropriate supportive treatment; and the affected animals’ survival depends on different factors including breed, and the time of diagnosis [4].



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