South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
Neuromuscular causes of gait deficits
Piercy RJ*
MA VetMB MD PhD DipACVIM MRCVS
Professor of Comparative Neuromuscular Disease
Royal Veterinary College
Introduction
Gait abnormalities are commonly encountered in equine veterinary work and reaching a diagnosis
to enable provision of appropriate prognosis and treatment is important for both patient and client.
It can be difficult to distinguish between the relative contributions of weakness, lameness and
central or peripheral nervous system involvement. Mixed deficits also occur which can
complicate the clinical picture. In contrast to small animal veterinary work, the long legs of horses
and their athletic use, often means that subtle abnormalities are encountered, or considered
problematic for owners of trainers. The contribution of such deficits to problems of poor
performance is frequently a consideration.
Lameness
The term „lameness‟ is generally reserved for a gait abnormality associated with pain; in most
cases the deficit is consistent between strides (either at the walk or trot). Localising the site of the
painful focus is a key component of the lameness examination, and involves flexion tests,
palpation and application of hoof testers. Confirmation is usually made by a variety of local
analgesic techniques. Furthermore, most musculoskeletal lameness will improve with systemic
non-steroidal anti-inflammatory medication.
In some horses however, extensive and repeated lameness investigations fail to identify any cause
for the gait deficit. In these cases, and particularly in those that have not shown any response to a
“phenylbutazone trial”, other potential causes of the abnormality should be considered.
Mechanical deficits for example, may be a non-painful manifestation of an old musculoskeletal
injury. Some mechanical deficits are readily recognised by their characteristic presentations (for
example fibrotic myopathy and upward fixation of the patella).
A commonly overlooked, but important sub-category of lameness cases have compression of
caudal cervical spinal nerve roots. Similarly, radiculopathy is a common feature of cervical disc
prolapse in humans with localised cervical and shoulder pain and parasthesia of the arm and hand.
In horses, cervical radiculopathy may be static or dynamic in nature. In the latter cases gait
abnormalities might only be seen with the head and neck flexed (or collected) or may be
exacerbated by turning. Horses with radiculopathy usually have articular process degenerative
joint disease, or synovial cysts and occasionally cervical fractures. Some equine cervical
radiculopathy cases that present as lameness are associated with localised shoulder or thoracic
limb muscle atrophy. EMG and / or muscle biopsy is useful in determining whether the atrophy is
associated with a neurogenic cause (damage to the lower motor neurone) or whether it is
associated with disuse. Some, though not all horses with cervical radiculopathy have concomitant
cervical pain and/or signs of spinal cord compression, such as ataxia and upper motor neurone
weakness.
In humans, radiculopathy of lumbar spinal nerves may manifest as sciatica and lumbar back pain.
Similarly, thoracolumbar spinal nerve root compression may be a source of chronic back pain in
horses, although definitive diagnosis is difficult. Vertebral spondylosis and discospondylitis
affecting the lumbar vertebrae, diagnosed by radiography, ultrasound and scintigraphy has been
described in horses. Lumbar vertebral trauma may affect spinal nerve roots that contribute to the
lumbar-sacral plexus, causing pelvic limb lameness, and if severe, weakness (see below) and
muscle atrophy.
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