Thoracolumbar Type I Disc Disease

Clinical signs: Onset of neurological signs may be peracute (<1 hour), acute (<24 hours) or gradual (>24 hours). Dogs presented with peracute or acute thoracolumbar disc extrusions may manifest clinical signs of spinal shock or Schiff-Sherrington postures. These indicate acute and severe spinal cord injury but do not determine prognosis. The degree of neurological dysfunction is variable and affects prognosis. Clinical signs vary from spinal hyperaesthesia only to paraplegia with or without pain perception. Dogs with back pain only are usually reluctant to walk and may show kyphosis. Dogs with back pain alone and no neurological deficits often have myelographic evidence of substantial spinal cord compression. Neuroanatomic localization for thoracolumbar lesions is determined by intact (T3-L3) or hyporeflexive (L4-S3) spinal reflexes and by site of paraspinal hyperaesthesia. Asymmetric neurological deficits maybe less reliable for determining the side of disc extrusion.

Conservative management - Indications for non-surgical treatment of thoracolumbar IVDD include a first time incident of spinal pain only, mild to moderate paraparesis and the financial constraints of the client. The latter is the only reason for non-surgical treatment of a recumbent patient, which should always be considered a surgical candidate if possible. Dogs can be managed with strict cage rest for 4–6 weeks combined with pain relief using anti-inflammatory drugs, opioids and muscle relaxants. Gastrointestinal protectants also may be necessary with use of anti-inflammatory therapies. Dogs should be monitored closely for deterioration of neurological status. If pain persists or the neurological status worsens, surgical management is recommended. Success rates for conservative management of ambulatory dogs with pain only or mild paresis ranges from 82% to 100%. Studies have shown that recovery rates in non­ambulatory dogs are lower and recurrence rates are higher following conservative treatment.

Overall success rates after decompressive surgery range from 58.8% to 95%. However, the success of a surgical approach may depend on what criteria are used to define it, how long after the surgery the patient is assessed, as well as the outcome which the owners are willing to accept. Surgical success may be improvement of the patient's pre-surgery neurological grade but may not mean that the patient is functionally normal, and residual signs (e.g., incontinence) can be unacceptable to many owners. Differences in recovery rates of non-ambulatory dogs vary according to the severity of neurological dysfunction (neurological grade), time interval from initial clinical signs to surgery, and speed of onset of signs.

Neurological grade - Deep pain perception is considered the most important prognostic indicator for a functional recovery. In general, the majority of dogs with intact deep pain perception, whether paraplegic or simply paraparetic, have an excellent prognosis, particularly if treated surgically. Dogs with loss of deep pain perception for more than 24–48 hours prior to surgery have a poorer prognosis for return of function. Without surgery, or with delayed surgery, dogs with absence of deep pain perception have an extremely guarded prognosis, although duration of absence of deep pain perception prior to surgery as a prognostic indicator is controversial. Recovery rates for dogs with thoracolumbar IVDD and absent deep pain perception range from 0–76%. A recent study of 87 dogs with loss of deep pain perception reported 58% of the animals regained deep pain perception and the ability to walk. In summary, dogs with absence of deep pain perception that have surgery within 12–36 hours have a better chance of more rapid and complete recovery than those with delayed surgery. Dogs with more severe neurological dysfunction have a longer period of recovery. The mean time from post­surgery to walking varied from 10 days for pain only or paraparetic dogs to 51.5 days for paraplegic dogs. More recent long-term studies reported recovery times of 2–14 days for dogs that were either ambulatory or non­ambulatory with voluntary motor movement, and up to 4 weeks for paraplegic dogs.

Vertebral Body Tumors

Tumors affecting the spinal cord are described based on their location as extradural, intradural (extramedullary and intramedullary). Extramedullary tumors are the most frequent and most commonly are primary vertebral tumors. Clinical signs may be focal or multifocal depending upon the extension of the tumor. Signs include pain and paraparesis or paralysis. Pathological fractures of the vertebral body result in an acute onset of neurological deficits. Vertebral body tumors are primary or metastatic tumors most frequently reported in large- and giant-breed dogs. Commonly described tumors in dogs include osteosarcoma, fibrosarcoma, chondrosarcoma, hemangiosarcoma, plasma cell tumor, carcinoma, lymphoma, and liposarcoma. Small-breed dogs have a higher rate of vertebral metastasis than large-breed dogs. In cats, the most commonly described vertebral body tumor is osteosarcoma. Primary vertebral body tumors will cause a secondary myelopathy by compression or direct spinal cord invasion. The diagnosis is often based on survey radiographic findings, such as lysis, and pathological fractures secondary to tumor destruction of the bone. Other supportive diagnostic techniques, such as CT, MRI and myelography, are used to determine lesion extent. MRI and scintigraphy can be used to detect multiple metastases. Fluoroscopic-guided needle aspiration or surgical biopsy can be used to obtain a definitive diagnosis. Palliative treatment options include surgery, radiation therapy, chemotherapy or various combinations of the three. A vertebrectomy with a bone allograft fusion has been used for the treatment of a primary vertebral neoplasm in a dog. Decompression or stabilization techniques are used in patients that are rapidly deteriorating. The overall prognosis is considered guarded for dogs and cats with vertebral neoplasia. Survival is not impacted greatly by various treatments but is often determined by the neurological deficits at the time of diagnosis.

Discospondylitis/Osteomyelitis

Discospondylitis is due to infection of the intervertebral disc and adjacent vertebral endplates; if the infection is confined to the vertebral body, it is called vertebral osteomyelitis or spondylitis. The sites most commonly affected are L7-S1, caudal cervical, midthoracic, and thoracolumbar spine. The infection is usually slowly progressive but can result in acute signs due to secondary pathological vertebral fractures and intervertebral disc disease. Its most common clinical sign is that of spinal pain but neurologic signs are seen and relate to the localization. An association with empyema has been documented in several dogs, which may represent an extension of the disease and should be considered when considering diagnostic tests and or when dealing with a refractory case. Coagulase-positive Staphylococcus spp. (S. intermedius or S. aureus) is the most common etiological agent associated with canine discospondylitis; other less commonly identified organisms include Streptococcus spp., Escherichia coli, Actinomyces spp. and Brucella canis, as well as Aspergillus spp. Young German shepherd bitches seem to be predisposed to aspergillosis, whereas young basset hounds contract discospondylitis due to systemic tuberculosis. Spinal pain is the most common initial clinical sign in this disease, which is most frequently seen in large intact male young to middle-aged dogs. With proliferation of inflammatory tissue, compression of neural tissue can lead to ataxia, paresis and, occasionally, paralysis dependent on where the lesion is located. Although it can occur in any animal, the condition is less common in toy and chondrodystrophoid breeds of dog, and rare in cats. Purebred dogs seem more commonly affected than mixed-breeds.

Once imaging-based radiographic evidence of discospondylitis is present, treatment for the common potential pathogen Staphylococcus intermedius infection may be started. The initial treatment of discospondylitis consists of antibiotics (potentiated amoxicillin or cephalexin), cage rest and analgesics. Results of cultures may require alteration of this choice.

Intravenous antibiotics should be considered if severe neurological compromise or signs of sepsis are present; otherwise, oral antibiotics are acceptable. However quickly the patient improves, continuation of the antibiotics for 8–16 weeks is recommended. Resolution of clinical signs, such as pain and fever, should be expected within 5 days of initiating therapy; however, complete neurological resolution may take 2–3 months. Residual deficits may remain, but persistent pain indicates an active disease, and these patients should be treated with an additional antibiotic and considered for further diagnostics as they may have a potential fungal infection or surgical lesion. Discospondylitis associated with Aspergillus spp. has been treated with itraconazole (5 mg/kg of body weight, PO, q 24 h) although long-term reports of success are lacking with the belief being that chronic recurrence and progression is likely.

The prognosis for this disease is generally very good unless the aetiology is fungal, there are multiple lesions, vertebral fracture or subluxation occurs or there is endocarditis; the potential for recurrence should be considered, especially if brucellosis has been diagnosed or an underlying immunosuppressive condition is present. Residual neurological deficits are possible, and in those cases that have severe neurological deficits associated with the infection the prognosis should initially be guarded.