Acute paraplegia is a very common neurological presentation. The main diseases that must be considered in the differential diagnosis of acute paraplegia in dogs are acute intervertebral disk herniation, spinal trauma and fibrocartilaginous embolic myelopathy. Their presentation, diagnosis and treatment will be briefly described in the following discussion.
Acute Intervertebral Disk Herniation (Extrusion)
Intervertebral disk herniation or extrusion is a very common disease in small breed dogs, mostly chondrodystrophic dogs (e.g., Dachshund, Pekingese), but it also occurs in large breed dogs. It is mostly a disease of dogs older than 2 years of age. The presentation is usually acute or subacute. Spinal pain is a consistent finding. Paraparesis is often associated with proprioceptive ataxia. The neurological examination will allow the clinician to objectively localize the lesion in the spinal cord, and this is a fundamental step in the diagnostic process. Paraplegia or paraparesis indicates a lesion caudal to T2. Normal to increased spinal reflexes and muscle tone in the pelvic limbs (signs of upper motor neuron dysfunction--UMN) indicate a T3-L3 lesion, usually located in the T12-L2 area. Specific lesion localization within the segment T3-L3 can be achieved using the cutaneous trunci reflex and spinal palpation. Decreased tone and reflexes in the pelvic limbs (signs of lower motor neuron dysfunction) indicate a L4-S3 lesion. If the patient is paralyzed, nociception (deep pain perception) should be always evaluated.
A tentative diagnosis of acute disk extrusion can be obtained by combining the signalment, history, and neurological findings. Ancillary diagnostic tests are mainly imaging. Survey radiographs can be used to rule out major osseous abnormalities and can demonstrate features suggestive of disk herniation, but they cannot definitively establish the diagnosis. Further imaging tests are needed for diagnostic confirmation. Myelography, computed tomography (CT) myelography, and magnetic resonance imaging (MRI) can definitively establish a diagnosis of disk herniation.
Treatment of acute disk extrusion can be done surgically and non-surgically. If the patient is paralyzed, surgical removal of the extruded disk offers the best chance for a rapid and complete recovery and resolution of the spinal pain. The surgical technique should allow removal of the disk material preserving as much as possible the vertebral anatomy. The author uses a pediculectomy (mini-hemilaminectomy) combined with fenestration of the affected disk. In patients with paraparesis, medical treatment improves the status of the majority of patients. The most important aspect of medical management is strict confinement. Short term corticosteroids (prednisone 1 mg/kg q24h for 3 days, then 0.5 mg/kg q24h for 3-5 days) can be used to decrease spinal pain, and decrease the vasogenic edema of the spinal cord. The use of corticosteroids without strict confinement is highly contraindicated because of the risk of increased activity and deterioration of the neurological status.
Spinal traumas are caused by external causes (e.g., road traffic accidents) or internal causes (acute disk extrusion). A clear history of trauma of sufficient intensity to damage the spinal cord is essential to diagnose spinal trauma. The presentation of trauma cases is almost always acute non-progressive. The signs may progress for a few hours in cases of unstable fractures and luxations. A history of progressive neurological signs for days or weeks essentially rules out trauma as a differential diagnosis.
The diagnosis of spinal trauma can be achieved by a history suggestive of trauma, physical and neurological examinations and imaging. Care should be exercised when performing the neurological examination in a patient paralyzed with a possible spinal trauma. It is better to delay the evaluation of postural reactions until knowing that the area of trauma is not unstable. The evaluation of tone and spinal reflexes allows the clinician to localize the lesion and it can be performed with the patient in lateral recumbency. If the patient is paralyzed, evaluation of nociception (deep pain perception) is critical. Absence of nociception in cases of external spinal trauma does indicate a poor prognosis for functional recovery.
The diagnosis and extension of the lesion can be confirmed with imaging. Survey radiographs cannot reliably exclude spinal fractures or luxations. Approximately 25% of fractures or luxations cannot be seen with radiographs. Therefore, whenever possible, CT or MRI is recommended. Severe parenchymal spinal cord changes can be seen on MRI in the absence of radiographic abnormalities. Treatment of acute spinal cord injury can be made with steroids if the patient is presented less than 8 hours after injury. Methylprednisolone sodium succinate--MPSS (first dose of 30 mg/kg/IV) can be used for 24 or 48 hours. The real efficacy of the MPSS has been questioned in recent years in both human and veterinary neurology but no consensus has yet been reached. In cases of unstable fractures or luxations, surgical fixation is recommended.
Physical therapy can hasten the recovery of all spinal disorders and is highly recommended.
Fibrocartilaginous Embolic Myelopathy (FCEM)
FCEM is one of the commonest spinal diseases of large breed dogs. It is caused by fragments of the nucleosis pulposus that enter the spinal vascular system, embolize, and cause spinal cord infarct. As it would be expected with an infarct, the signs are acute or superacute and usually not progressive beyond the initial 6-12 hours post-infarct. FCEM is commonly seen in large and giant breed dogs. It is less common in medium and small canine breeds, with the exception of the miniature schnauzers that have a high incidence of FCEM. Approximately 50% of cases of FCEM have a history of intense activity or exercise before the onset of clinical signs. Neurological deficits tend to strongly asymmetric, although in a few cases the asymmetry can only be perceived with a careful neurological examination. Even though FCEM can affect any spinal cord region, the segment L4-S3 is the most commonly affected. Because FCEM is a parenchymal spinal cord disease, the only way to confirm the diagnosis is by MRI. Clinically, a presumptive diagnosis of FCEM can be established if a dog (usually large breed) presents with an acute onset of non-progressive, non-painful, asymmetric neurological deficits. The absence of spinal pain differentiates FCEM from acute disk herniation and spinal trauma. Blood work should always be performed to rule out infectious diseases or coagulopathies. Usually patients start to show clinical improvement within 3 to 7 days, with or without the use of corticosteroids. It is unclear the role of corticosteroids in the treatment of FCEM. In very severe cases it is possible that they are beneficial. The vast majority of dogs with FCEM will recover very well. Dogs with LMN signs tend to have a more protracted functional recovery but still usually recover. FCEMs affecting the C6-T2 spinal cord segment have a more guarded prognosis. Physical therapy is essential to hasten the recovery of dogs with FCEM.