The term ‘sweeny-syndrome‘ (also spelled ‘sweeney‘) was introduced more than a century ago to describe a syndrome of muscle atrophy over the shoulder caused by the harnesses used by horses to pull heavy objects. The harness would put pressure on the suprascapular nerve leading to atrophy of the muscles innervated by that nerve.
The suprascular and subscapular nerves originate in the cranial aspect of the brachial plexus (the ventral branches of spinal nerves C6, C7, C8, T1 and T2). The suprascapular nerve originates in C6 and C7 spinal nerves and innervates the supraspinatus and infraspinatus muscles. The subscapular nerve also arises from the C6 and C7 ventral nerve roots and innervates the subscapularis muscles.
The nerve is commonly damaged as it runs over the cranial border of the neck of the scapula, known as the collum scapulae. This can occur when horses run front on into stationary objects or when galloping horses collide. The nerve can also be stretched if horse stumbles forward with forelimb stretched back. When these injuries occur they damage more than the suprascapular nerve, with other nerves that arise from the cranial section of the brachial plexus. Therefore the injury often includes damage to the suprascapular, subscapular, and branches of the axillary, ulnar, median and radial nerves. However it is denervation of the supraspinatus, infraspinatus, and subscapularis muscles that are chiefly responsible for the classic sweeny gait. Interestingly, if the suprascular nerve is transected then atrophy of the infra- and supraspinatus muscles occur but the classical gait does not.
There is subsequent instability of the shoulder joint, which allows the shoulder to subluxate or “pop” laterally as the affected limb bears weight. Some horses circumduct the affected limb during forward movement to avoid dragging the toe (see video 3).
An EMG will reveal signs of muscle denervation, including positive sharp waves, fibrillations and prolonged insertional activity.
Most of these cases are caused by closed trauma, exacerbated by local swelling. It is therefore recommended to treat with anti-inflammatories during the initial period after the trauma. This includes drugs like dexamethasone and flunixin, as well applying ice packs to the area. The horse should be confined.
If the nerve has been ‘concussed’ (neuropraxia) then function should return in days to weeks. For these cases the prognosis for recovery is good.
If nerve axons have been severed (axonotmesis) or whole nerves severed (neuronotmesis) the nerve fibres downstream will undergo Wallerian degeneration. This is a complex series of events that initially leads to axon death similar to programmed cell death, followed by an influx of white blood cells that release cytokines impacting both the neurons and neighbouring non-neuronal cells. The end result in the induction of a positive environment for cell regrowth from the injured axon terminus. This axon regrowth occurs at a rate of 1 inch per month to reinnervate the affected muscles. The problem is that denervated muscle will undergo atrophy and then irreversible fibrosis.
There are surgical procedures described to decompress damaged nerves, however it should be performed within 4-8 weeks of the injury. The two most common procedures are to dissect the nerve free of compressive tissue bands at the front of the scapular, or to create a notch in the scapular where the nerve passes by removing a 2 x 0.5 cm piece of bone from the cranial edge of scapula. The latter procedure can induce a serious weakness in the scapular where the notch is performed.
Tags: Neurology