Ischemic Neuromyopathy in Animals
Ischemic neuromyopathy is most common in cats with arterial thromboembolism secondary to myocardial disease. It also is seen in dogs with a variety of underlying disorders, including hyperadrenocorticism, hypothyroidism, renal disease, cancer, and heart disease. Occlusion occurs most commonly at the distal aortic trifurcation, resulting in ischemia of muscles and nerves in the pelvic limbs. There is acute, painful paraparesis and an inability to flex or extend the hock (tarsus). The flexor reflex and, in some cases, the patellar reflex are lost. Sensation distal to the hock is decreased. The gastrocnemius and cranial tibial muscles are often firm and painful. The nails may be cyanotic, and the femoral pulses are weak or absent.
Diagnosis can usually be made based on clinical features. Serum creatine concentration is often increased. Doppler ultrasonography helps evaluate blood flow in the distal aorta and femoral arteries. Histopathologic changes are present distal to the level of the middle to lower thigh and are characterized as focal muscle necrosis and degeneration of the central portions of the sciatic nerve and its branches.
Management consists of analgesics, nursing care, and treatment of any underlying disease (eg, cardiomyopathy). Thrombolytic therapy such as administration of streptokinase or tissue plasminogen activator does not improve survival. Anticoagulants, such as unfractionated heparin or low-molecular-weight heparin, are used to reduce continued thrombus formation. Neurologic deficits may improve within 2–3 weeks, but 6 months may be required for complete recovery. Permanent deficits are possible. Approximately 60% of affected cats die or are euthanized during the initial episode. In the cats that survive, the longterm prognosis is guarded (median 12 months) because of the underlying heart disease and high risk of recurrence of thromboembolism.