Fibrocartilaginous embolic myelopathy
Clinical signs: Neuroanatomical localization often is associated with the spinal cord intumescences but other spinal cord regions can be involved (). Thoracolumbar signs are more common than cervicothoracic. Clinical signs usually are associated with trauma or exercise. Asymmetrical lesion distribution () is a clinical feature due to the distribution of the blood vessels to the spinal cord parenchyma (); however, the lesion can be symmetrical. Symmetrical lesions more often are associated with loss of nociception. Spinal hyper-aesthesia can be present initially but is absent afterthe onset of ischaemia. Maximal neurological deficits usually occur within the first 24 hours. Dogs with lumbosacral intumescent involvement more often have loss of deep pain perception.
Pathogenesis: FCE is characterized by acute spinal cord infarction caused by embolism of fibrocartilage identical to that of the nucleus pulposus of the intervertebral disc (). Many theories exist as to the pathophysiology for embolization (). Entry of disc material into the vascular system and embolization from the point of entry to the arteries and veins of the spinal cord has yet to be elucidated. Non-chohdrodystrophoid breeds are predisposed, which may relate to the disc being more gelatinous and prone to cause microextrusion. FCE is frequently recognized in large and giant breed dogs but also affects small- to medium-sized dogs (). Certain pure-bred dogs that have been documented with FCE include Miniature Schnauzers (), German Shepherd Dogs and Irish Wolfhounds (). FCE is rare in cats ().
Diagnosis: The diagnosis is based on history, signalment and clinical signs. Early myelographic evidence of FCE is intramedullary spinal cord swelling (). MRI may be a more sensitive technique for detection of intramedullary lesions and rule out possible associations with intervertebral disc extrusions. CSF analysis may reveal abnormalities in severe cases. Diagnosis of FCE is confirmed by histopathology and documentation of nucleus pulposus in the spinal cord vasculature ().
Treatment and prognosis: Treatment is with medical and supportive care. Early in onset of FCE (<8 hours) administration of methylprednisolone sodium succinate has been recommended (). As for all spinal cord injuries, physical therapy is important in the process of recovery ().
Recovery is dependent upon the extent of spinal cord damage. A poor prognosis has been correlated with involvement of the intumescences, symmetry of signs and decreased deep pain sensation (). Dog size and severity of clinical signs contribute to owners electing for euthanasia (). Animals with functional recovery within two weeks have a better prognosis; however, recovery may not be complete ().
Clinical signs: Clinical signs consist of acute onset of an asymmetrical pelvic limb paresis and/or paralysis. Abyssinian, Birman, Ragdoll and male cats were overrepresented in one study (). The femoral pulse is weak or absent. The limbs are cold and nail beds are cyanotic and fail to bleed when cut. The pelvic limbs are stiff and the muscles are hard and painful upon palpation. Typically there is loss of pelvic limb nociception distally. Tachypnoea and hypothermia were seen in 91 % and 66% of 127 cats, respectively (). Congestive heart failure and arrhythmias were each seen in over 40% of cats in this study.
Pathogenesis: Obstruction of the aortic or iliac arteries commonly occurs in cats with thromboembolic disease (). Aortic thromboembolism is also known as saddle thrombi. The most frequent underlying disease in cats with thromboembolism is hypertrophic cardiomyopathy (). Both restriction of blood flow by the embolus and release of vasoactive substances cause ischaemia to the sciatic nerve and muscles of the pelvic limbs.
Diagnosis: Aortic thromboembolism is suspected upon clinical signs. Common biochemical abnormalities in these cats include hyperglycaemia, azotaemia and a markedly elevated creatine kinase concentration soon afterthe embolic episode. Evidence of cardiac disease is further supported by physical examination findings, thoracic radiographs and echocardiography. Doppler ultrasonography of the aorta and its trifurcation can sometimes identify thrombotic disease.
Treatment and prognosis: Initially therapy involves management of the cardiac disease and supportive care. Cats benefit from administration of acepromazine maleate (ACP), heparin and analgesia. Use of ACP is controversial; although it may improve collateral blood flow and decrease anxiety, it may cause hypotension and current advice is to avoid its use. Specific therapies for the clot include surgical removal and thrombolytic agents; but risks versus benefits need to be considered. No significant difference has been found with survival or recurrence rate between cats receiving high-dose aspirin (>40 mg/cat q72h) and cats receiving low-dose aspirin (5 mg/kg q72h) (). Given time the clot will undergo spontaneous thrombolysis.
Long-term prognosis for cats with aortic thomoboembolism is poor. A review of 100 cases reported that of the 37% of cases to survive the initial episode, the average long-term survival was 11 months (). A more recent review of 127 cases found that 45% survived to be discharged, and median survival for discharged cats was 117 days (), although cats with congestive heart failure had a significantly shorter survival time than cats without this problem.
Bleeding disorders can cause focal signs of myelopathy.