Suprascapular Neuropathy in Horses
This syndrome describes the physical appearance of the horse’s shoulder. It is not a diagnosis in itself, because there are a number of potential causes. The most common cause is injury to the suprascapular nerve.
All cases have atrophy of the supraspinatus and infraspinatus muscles that cover the scapula. This results in the scapular spine becoming prominent; in severe cases, the muscles virtually disappear. The atrophy is unusual in that it is often profound and very localized, which are hallmarks of an injury to a single lower motor nerve. The nerve involved is the suprascapular. Although the site of damage is rarely documented clinically, most cases involve trauma to the cranial shoulder at the point where the nerve is exposed to potential compression as it courses over the cranial aspect of the scapula. The severity of damage determines the degree of atrophy and the chances of recovery. If nerve function is severely compromised, the shoulder joint becomes unstable (it is a synarthrosis with no true collateral ligaments, relying on the surrounding muscles to support it) and the joint “pops out” sideways as the horse bears weight. This subluxation does not appear overtly painful to the horse, but if the joint cannot be stabilized, it may have significant implications for the longterm health of the joint and the horse’s athletic career.
Therapy is aimed at maintaining muscle health during the period of nerve recovery and maximizing neurogenesis. Horses should be restricted to stable rest or a very small paddock. Complete immobilization may negatively impact the nerve and muscles, but activity probably hastens joint degeneration. A surgical procedure to remove part of the scapula over which the nerve courses has been described, aiming to provide optimal conditions for nerve recovery. This should be considered, but its usefulness is open to debate. Muscle stimulation, under the guidance of a trained physiotherapist, will help to limit muscle fibrosis and may encourage nerve regeneration. The vast majority of cases seem to be a result of neuropraxia or axonotmesis (based on clinical observations and rates of recovery), and function is recovered with time. However, this process can take many months, and frequently some loss of muscle bulk will remain. The prognosis seems most affected by duration of injury before diagnosis, degree of atrophy at diagnosis, and willingness of the owner to perform time-consuming physical treatments for many months.
Other causes of sweeney include disuse atrophy (which does not appear focal and is rarely severe), brachial plexus injury (which usually disrupts a number of nerves; atrophy is not focal but observable in a number of muscle groups), and caudal cervical disease resulting in spinal nerve radiculopathy (in which a number of motor nerves are also affected so that other muscles atrophy). Careful assessment of the muscles involved and radiography of the neck and shoulder will aid differentiation. Scintigraphy is useful for rapid screening of the proximal limb and cervical and thoracic vertebra for damage that may have an adverse effect on prognosis.