Compressive Damage to the Deep Branch of the Lateral Plantar Nerve Associated with Lameness Caused by Proximal Suspensory Desmitis

Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Veterinary Surgery (Impact Factor: 1.04). 06/2008; 37(4):328-35. DOI: 10.1111/j.1532-950X.2008.00385.x
Source: PubMed


To describe pathologic changes in the deep branch of the lateral plantar nerve (DBLPN) of horses determined to be lame because of proximal suspensory desmitis (PSD), and to report the outcome after treatment by excision of a segment of the horses' DBLPN.
Retrospective case series.
Adult horses (n=16).
Horses determined to be lame on one or both pelvic limbs because of PSD were treated by excision of a segment of the DBLPN, and 30 nerves were examined histologically. Owners were contacted to obtain information about the horses >or=6 months after surgery.
Histologic changes suggestive of chronic nerve compression were identified in both nerves of 11 bilaterally lame horses and in the lame limb of 5 unilaterally lame horses. The nerve of the sound limb of 2 of 3 unilaterally lame horses that had bilateral nerve resection also had histologic changes compatible with nerve compression. Ten of 16 horses (62.5%) with follow-up information returned to soundness after excision of the DBLPN.
Pathologic changes of the DBLPN associated with compression may complicate PSD of the pelvic limbs. Excision of the nerve may resolve lameness caused by PSD.
Horses lame because of PSD of the pelvic limb may remain lame after desmitis has resolved because of compression of the DBLPN. Excising a portion of this nerve may resolve lameness.

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    • "As a result, when a horse is presented because of hindlimb proximal suspensory desmitis, the lesions at the origin of the ligament may be chronic and more pronounced than in a horse with similar forelimb lameness. Furthermore lameness attributable to the proximal suspensory ligament in hindlimbs may be exacerbated by pressure damage to the deep branch of the lateral plantar nerve, which runs in close proximity to the proximal suspensory ligament (Toth et al. 2008). "
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    ABSTRACT: Medical records of horses examined from 1994 to 2011 at the Equine Hospital, Vetsuisse Faculty, University of Zurich, because of proximal suspensory desmitis (PSD) were reviewed. Radiographic changes visible on dorsopalmar and dorsoplantar projections of the proximal third metacarpal/metatarsal bone (MCIII/MTIII) were analysed with respect to localisation, degree of increased radiopacity, length, width and pattern of radiopacity in relation to sex, age, breed, duration and degree of lameness and affected limb of the horses. Results were compared with those from sound control horses. Horses with PSD had increased radiopacity, which was significantly more prevalent medially than laterally in the forelimbs (p < 0.05) and more prevalent laterally than medially in the hindlimbs (p < 0.05). The width of the area of increased radiopacity was significantly greater in the forelimbs than in the hindlimbs (p < 0.05). The pattern of increased radiopacity was diffuse in 102 (85.7%) horses and multifocal in the remaining 17 (14.3%). 35.3% (n = 6) of multifocal changes were detected on one of the front limbs, whereas 74.7% (n = 11) were diagnosed on the hind limbs. Mildly increased diffuse radiopacity, with a distribution pattern comparable to cases with PSD was detected in 15 of 60 control horses. In comparison to control cases, the degree of increased diffuse radiopacity was significant more pronounced in horses with PSD (p< 0.001). The multifocal pattern of increased radiopacity could not be detected in any of the control horses. The results aid in the interpretation of radiographic changes seen in horses with PSD. Whereas a diffuse increased radiopacity of the proximal MCIII/MTIII needs to be interpreted with caution, as a mild degree may be seen in sound horses, the multifocal distribution pattern seems to be unique feature of horses with PSD.
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    • "Neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy was first described by Bathe (2006a,b) and has subsequently been reported by Bathe (2008), Kelly (2007) and Toth et al. (2008), with success ranging from 62 to 91%. However, there are limited long-term studies documenting the outcome of horses with PSD treated by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy. "
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    ABSTRACT: Neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy have become accepted as methods of treatment of proximal suspensory desmopathy (PSD), but there are limited long-term studies documenting the outcome. To describe long-term follow-up in horses with PSD alone or with other injuries contributing to lameness and poor performance, including complications, following neurectomy and fasciotomy. Follow-up information was acquired for 155 horses that had undergone neurectomy and fasciotomy for treatment of PSD between 2003 and 2008. Success was classified as a horse having been in full work for >1 year post operatively. Horses were divided into 3 groups on the basis of the results of clinical assessment and diagnostic analgesia. Horses in Group 1 had primary PSD and no other musculoskeletal problem. Horses in Group 2 had primary PSD in association with straight hock conformation and/or hyperextension of the metatarsophalangeal joint. Horses in Group 3 had PSD and other problems contributing to lameness or poor performance. In Group 1, 70 of 90 horses (77.8%) had a successful outcome, whereas in Group 3, 23 of 52 horses (44.2%) returned to full function for >1 year. Complications included iatrogenic damage to the plantar aspect of the suspensory ligament, seroma formation, residual curb-like swellings and the development of white hairs. All horses in Group 2 remained lame. There is a role for neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy for long-term management of hindlimb PSD, but a prerequisite for successful management requires recognition of risk factors for poor outcome including conformation features of straight hock or fetlock hyperextension.
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