Median / ulnar nerve: paralysis
Introduction
- Cause: singular or combined paralysis is uncommon. Brachial plexus injuries and spinal cord lesions involving the brachial intumescence may affect these nerves along with other nerves. External trauma directly or indirectly (via upper forelimb fractures) to these nerves individually or together is a very uncommon cause.
- Signs: goose-stepping gait, hyperextension of the carpus, the fetlock and the pastern, dragging of the toe.
- Diagnosis: clinical signs, neurological examination and electrodiagnostics.
- Treatment: DMSO, corticosteroids, physiotherapy, rest.
- Prognosis: fair to good depending which nerve(s) are affected.
- Resulting syndromes are not well documented.
Presenting signs
- Usually a unilateral stiff goose-stepping gait may occur with hyperextension of the carpus, fetlock, and pastern joints.
- Toe-dragging is associated with decreased carpal and fetlock flexion.
- Atrophy of the digital flexor muscles may be found in severe and long-term cases, especially where the ulnar nerve is involved.
- Hypoalgesia of the medial pastern (median nerve) and lateral aspect of cannon and caudal forearm (ulnar nerve).
- Other abnormalities may be present if other peripheral nerves are involved Brachial plexus: trauma Musculocutaneous nerve: paralysis or there is other pathology, such as fractures, involved.
Acute presentation
- Sudden onset unilateral gait deficits, inability to flex carpus and digits, and hypoalgesia.
- Signs of trauma or injury in upper forelimb.
Geographic incidence
- Worldwide.
Cost considerations
- Costs of diagnosis and treatment.
- Permanent loss of function and use.
Pathogenesis
Etiology
- An isolated paralysis of the median ulnar and/or ulnar nerves is a rare condition and it is slightly more common alongside other nerve dysfunction, including the musculocutaneous.
- Brachial plexus injuries and spinal cord lesions involving the gray matter of the brachial intumescence may affect these nerves.
- External trauma directly or indirectly (via upper forelimb fractures, especially of the elbow) to these nerves individually or collectively does occur, but is not common.
Pathophysiology
- The nerves are well protected under the shoulder girdle and not often involved in long-bone fractures, though elbow fractures may affect the ulnar and median nerves.
- Paralysis of these nerves rarely occurs individually and usually they are affected together. Paralysis of these nerves can be associated with dysfunction of other peripheral nerves such as the musculocutaneous.
- The median and ulnar nerves supply the muscles flexing the carpus and digits. Section of the proximal part of the median nerve experimentally resulted in decreased carpal and fetlock flexion and subsequent toe-dragging. Partial sensory loss occurred in the skin over the medial pastern region. Transection of the ulnar nerve proximally lead to similar gait changes as in the median nerve, but to a slightly more obvious degree. There was decreased sensation in the lateral aspect of the cannon and caudal forearm.
Timecourse
- Experimental studies showed that the gait deficits may disappear within 2 or 3 months due to compensation and adaptation, although if the ulnar nerve is involved, they may continue for longer with persistent stumbling on the leg and decreased fetlock flexion.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Hahn C (2008) Common peripheral nerve disorders in the horse. In Pract 30 (6), 322-326 VetMedResource.
- Alexander K & Dobson H (2003) Ultrasonography of peripheral nerves in the normal adult horse. Vet Radiol Ultrasound 44 (4), 456-464 PubMed.
- Blythe L L & Kitchell R L (1982) Electrophysiologic studies of the thoracic limb of the horse. Am J Vet Res 43 (9), 1511-1524 PubMed.
Other sources of information
- Mayhew I G (2009) Large Animal Neurology. 2nd edn. Wiley-Blackwell, UK. pp 309.
- Blythe L L (1997) Peripheral neuropathy. In: Current Therapy in Equine Medicine. 4th edn. Ed: Robinson N E. Saunders, USA. pp 314-318.