Neuroaxonal dystrophy in a rottweiler pup

An 8-month-old Rottweiler pup was evaluated for neurologic disorder. Clinical signs included ataxia, hypermetria of all 4 limbs, intention tremors of the head, lack of a menace reflex bilaterally, and mild proprioceptive deficits. The pup was euthanatized because of the progressive nature of the disease. Histopathologic findings consisted of decreased numbers of Purkinje cells in the cerebellum and moderate numbers of axonal spheroids in the nucleus cuneatus. This latter finding confirmed the diagnosis of neuroaxonal dystrophy.     

Neuroaxonal dystrophy in a litter of papillon pups

A litter of five 14-week-old papillon puppies was referred for investigation of pelvic limb ataxia. Clinical examination revealed signs of ataxia, hypermetria and depressed postural reflexes affecting all four limbs. The severity of these signs varied between members of the litter. The condition became progressively worse and by 19 weeks of age all but the least severely affected pup (the single male of the litter) had deteriorated to the point that euthanasia was indicated on humane grounds. Pathological examination revealed widespread changes in both white and grey matter of the neuraxis caudal to the fore-brain, particularly involving the dorsolateral white matter of the spinal cord, which were characterised by axonal swellings typical of neuroaxonal dystrophy.     

Neurological diseases of rottweilers: Neuroaxonal dystrophy and leukoenceph- alomalacia

Neuroaxonal dystrophy (NAD) and leukoencephalomalacia (LEM) are two neurological disorders of the rottweiler that initially present as ataxia of all four limbs. Disorders to be included in the differential diagnosis are caudal cervical spondylomyelopathy, canine distemper virus meningoencephalomyelitis, other nervous system infections or inflammations and spinal cord neoplasia. All diagnostic tests including myelography, cerebrospinal fluid analysis, electrodiagnos-tic testing and serum and cerebrospinal fluid titres for canine distemper virus are normal in NAD and LEM. There is no treatment for either disease and neurological signs progressively deteriorate. Eventually neurological deficits develop besides ataxia and these help differentiate NAD from LEM. Dogs with NAD develop head tremors and nystagmus while dogs with LEM develop conscious proprioceptive deficits and quadriparesis; the short term prognosis for NAD is better than LEM. Most dogs with LEM are euthanased because of non-ambulatory tetraparesis within one year. The histopathological lesions associated with NAD include axonal spheroids in many spinal cord and caudal brainstem nuclei and reduced numbers of Purkinje cells in the cerebellum, while in LEM, multifocal areas of demyelination and malacia of the spinal cord and brainstem are the primary histopathological lesions. Both NAD and LEM are suspected to have an autosomal recessive genetic transmission.     

Neuroaxonal dystrophy in raccoons (Procyon lotor) from Iowa.

During a 12-month period (1998-1999), microscopic evidence of neuroaxonal dystrophy (NAD) in medullae oblongata of raccoons (Procyon lotor) was observed in 17/39 (47% prevalence in adults) from Iowa, USA. Three of the animals were kits (<3 months), 26 were between 1 and 2 years, and 10 were over 7 years. Lesions were not seen in the medullae of the 3 kits. In young adults, the lesions were mild and were seen in 7 animals. More severe lesions were present in the 10 older raccoons. Grossly, the brains were unremarkable. Microscopically, NAD was confined to the dorsal caudal medulla, where certain nuclei (predominantly gracilis and cuneate) were bilaterally affected. Severely affected animals had vacuolar degeneration of neurons or neuronal loss and extensive areas of spongiosis. Tests for the presence of PrP(res) in the brain were negative. Spongiotic areas often contained axonal spheroids. Degenerate neurons and axons occasionally contained amphophilic periodic acid-Schiff-positive granular material. There was a paucity of inflammatory cells in the affected areas. Since lesions were not present in kits, were either absent or mild in young adults, and were severe in older raccoons, the findings may be related to advancing age. Neuroaxonal dystrophy has not been previously reported in raccoons. Retrospective examination of raccoon brains from the eastern and northwestern areas of the country revealed very low prevalence of NAD. Because of the apparently high prevalence of this condition at this geographic location, factors other than age (genetic, nutritional, and/or environmental) may influence this degenerative process in the brains of raccoons in Iowa.     

Coronary band dystrophy in two horses

Two mature large-breed horses with coronary band dystrophy and chorioptic mange are described. They both had clinical signs of coronary band scaling and crusting but were not lame. Coronary band dystrophy can be differentiated from similar clinical conditions on the basis of the histological appearance of skin biopsy specimens, and by the exclusion of other possible disease processes. Its aetiology is uncertain, but probably involves a localised defect of keratinisation affecting the specialised epithelium of the coronary band.     

Cerebello-olivary and lateral (accessory) cuneate degeneration in a juvenile American Miniature horse

A 12-month-old American Miniature horse colt was presented to the Virginia Tech Veterinary Teaching Hospital with a 7-month history of progressive ataxia. Physical examination revealed a head intention tremor, base-wide stance, and ataxia. Necropsy findings were confined to the brain. There were bilateral areas of liquefactive necrosis and cavitation corresponding to the dorsal accessory olivary and lateral (accessory) cuneate nuclei. Cerebellar folia of the dorsal vermis were thin. Microscopically, the cerebellar cortex was characterized by patchy areas of Purkinje cell loss with associated variable thinning of the molecular and granule cell layers and astrogliosis. Dorsal accessory olivary and lateral cuneate nuclei were cavitated and had mild glial response around their periphery. Additionally, a focus of necrosis and neuropil vacuolization was found in the right putamen. These findings indicate the presence of a neurodegenerative disorder centered, but not confined to, the cerebellum and its connections in this American Miniature horse colt.     

Minimally invasive desmotomy of the accessory ligament of the deep digital flexor tendon in horses

This retrospective study describes ultrasound guided desmotomy of the accessory ligament of the deep digital flexor tendon in 35 cases, and a modification of this procedure using an adapted surgical instrument. The procedure was successful in 97% of cases. Wound healing was excellent in all except 4 cases. Corrective shoeing prior to surgery contributes to success. The procedure can be performed on the standing horse and offers the advantages of minimally invasive surgery which include: reduced incision length, reduced morbidity and improved cosmetic outcome. The adapted surgical instrument can be an alternative to isolate the ligament under ultrasound guidance.     

Ultrasonographic anatomy of the accessory ligament of the superficial digital flexor tendon in horses.

The ultrasonographic anatomy of the accessory ligament of the superficial digital flexor tendon (AL-SDFT) in the horse is presented. Comparison between anatomical sections of isolated limbs and ultrasound scans of the distal antebrachium in sound horses enabled the authors to establish the normal reference ultrasonographic images of this structure. The AL-SDFT inserts 7-14 cm above the antebrachiocarpal joint on the palmaromedial aspect of the radius. Ultrasonographically it appears as an uniformly echogenic structure located deep to the median artery. The knowledge of ultrasonographic anatomy is essential for identification of abnormal images and assessment of AL-SDFT damage.     

Evaluation of a tenoscopic approach for desmotomy of the accessory ligament of the deep digital flexor tendon in horses

Objective: To develop a tenoscopic approach for desmotomy of the accessory ligament of the deep digital flexor tendon (AL‐DDFT) in horses. Study Design: Experimental. Animals: Cadaveric forelimbs (n=10) and 4 forelimbs from 2 horses anesthetized for terminal teaching procedures, and 12 forelimbs of 6 experimental horses. Methods: Saline distention of the carpal flexor sheath facilitated insertion of an arthroscope into the distal medial aspect of the sheath between the AL‐DDFT and deep digital flexor tendon (DDFT). Location of an instrument portal on the lateral aspect of the metacarpus was identified with a needle. The lateral aspect of the AL‐DDFT was transected and the arthroscope and instrument were switched to transect the remaining fibers on the medial aspect. Cadaveric specimens were dissected for evaluation. Experimental horses were monitored for 30 days postoperatively. Results: Minor complications including incomplete division of the AL‐DDFT and shallow incision into the suspensory ligament were observed in some cadaver specimens. The AL‐DDFT was completely transected in all experimental horses with no suspensory ligament damage. Mean±SD surgical time (incision to skin closure) was 28.3±11.8 minutes. On ultrasonographic examination, transection of the AL‐DDFT was complete in all experimental horses. Minor DDFT fiber disruption was noted in 1 limb during ultrasound examination at day 30. Conclusions: A tenoscopic approach through the carpal flexor sheath provided adequate access for desmotomy of the AL‐DDFT.     

Two clinical manifestations of desmopathy of the accessory ligament of the deep digital flexor tendon in the hindlimb of 23 horses

REASONS FOR PERFORMING STUDY: Desmopathy of the accessory ligament of the deep digital flexor tendon (ALDDFT) in the hindlimb is an unusual cause of lameness in horses, and reports of the condition are sparse. OBJECTIVES: To describe the clinical and ultrasonographic findings, therapy and outcome of 23 horses treated for desmopathy of the ALDDFT in the hindlimb. METHODS: Records of 23 horses with ultrasonographic evidence of desmopathy of the ALDDFT in one or both hindlimbs from 3 referral centres were reviewed retrospectively. Age, breed, sex, duration and nature of clinical signs, results of clinical and lameness examinations, treatment and outcome were recorded. RESULTS: In 13 horses (Group A), there was an acute onset of unilateral lameness. Ten horses (Group B) had an insidious or sudden onset of postural abnormality. There were 10 cobs, 5 British native-breed ponies and 8 horses of various larger breeds. Twenty horses were used for general purposes, and mean age was 12 years. Enlargement of the ALDDFT in the affected hindlimb(s) was identified in all horses. In 44% of horses, ultrasonographic abnormalities were localised to part of the ALDDFT. Treatment included box-rest and controlled exercise, and 10 horses were subjected to desmotomy or desmectomy of the ALDDFT. Seventy-three percent of horses in Group A returned to full function, while 90% of those in Group B remained lame. CONCLUSIONS: Two distinct clinical conditions are associated with the ALDDFT of the hindlimb. Traumatically induced injury resulting in acute onset lameness appears to have a favourable prognosis, with most horses returning to previous work. However, postural changes, once present, are irreversible and indicate a poor prognosis. POTENTIAL RELEVANCE: Desmopathy of the ALDDFT should be recognised as a potential cause of hindlimb lameness and this study provides clinical and prognostic information. Knuckling and/or semiflexion of the metatarsophalangeal joint may accompany the condition; therefore, if a horse is presented with a flexural deformity of this joint, desmopathy of the ALDDFT should be considered as a primary differential diagnosis.     

Desmotomy of the accessory ligament of the deep digital flexor tendon in the forelimb of 24 horses 2 years and older

Objective: To report outcome after desmotomy of the accessory ligament of the deep digital flexor tendon (ALDDFT) in adult horses (≥2 years) for treatment of desmitis of the ALDDFT or flexural deformity of the distal interphalangeal joint (FDDIJ). Study Design: Case series. Animals: Horses with desmitis of the ALDDFT (n=9) and FDDIJ (n=15). Methods: Records (April 1996–July 2008) of 24 adult horses (mean age, 6.7 years) that had ALDDFT desmotomy were reviewed. Follow‐up data was obtained 12–120 months after desmotomy. Results: Outcome was available for 22 horses; 18 (82%; 6 of 8 horses with desmitis of the ALDDFT and 12 of 14 with FDDIJ) returned to their intended use within 6–24 months (mean, 12 months). Conclusion: In mature horses, ALDDFT desmotomy resulted in successful return to intended use in most horses with ALDDFT desmitis (75%) or FDDIJ (86%).     

Electrosurgical tenoscopic desmotomy of the accessory ligament of the superficial digital flexor muscle (proximal check ligament) in horses

Objective: To report a tenoscopic technique using monopolar electrosurgery to transect the accessory ligament of superficial digital flexor muscle (AL‐SDFM) and outcome in 33 horses. Study Design: Case series. Animals: Horses (n=33). Methods: Medical files and surgery video recordings of horses that had AL‐SDFM desmotomy performed by tenoscopy with monopolar electrosurgical electrodes were reviewed. Results: Of 33 horses, 24 were Standardbred racehorses with surgery performed bilaterally for superficial digital flexor tendonitis and 9 horses had flexural deformity. Severe (n=6) and mild (6) intrathecal hemorrhage was the most common intraoperative complication. Large intrathecal vessels including the nutrient artery were successfully electrocoagulated and AL‐SDFM transection was completed. Clear/serosanguinous drainage from skin incisions was observed for 4.3±3.3 days (mean, SD). Protracted wound drainage for >4 days occurred in 10 horses, principally in the group treated for flexural deformities (P=.01). Conclusions: Sixty‐four AL‐SDFM were transected under tenoscopic observation using monopolar electrodes. Electrocoagulation of large intrathecal vessels, including the nutrient artery, was possible in all cases and allowed completion of desmotomy. Postoperative wound care was similar to routine tenoscopy in most (70%) horses. Aseptic protracted wound drainage was observed in 30% of horses (principally those with flexural deformity), and led to a prolonged hospitalization.     

Hindlimb lameness associated with proximal suspensory desmopathy and injury of the accessory ligament of the suspensory ligament in five horses

The accessory ligament of the hindlimb suspensory ligament arises from the plantar aspect of the calcaneus and fourth tarsal bones and blends with the suspensory ligament in the proximal aspect of the metatarsus. The accessory ligament of the suspensory ligament of both hindlimbs of 12 mature horses, with no history of hindlimb lameness, was assessed ultrasonographically. The ligament comprised linear parallel echoes which were consistently shorter than those of the lateral digital flexor tendon; the dorsal and plantar borders were parallel. Lameness associated with injury of the accessory ligament of the suspensory ligament was identified in 6 of 8 lame hindlimbs of 5 horses, unilaterally in 4 horses and bilaterally in one horse. In all horses there was concurrent proximal suspensory desmopathy. There was localised oedematous swelling on the distal medial aspect of the chestnut extending distally in 2 horses. Lameness was best identified when the horses were ridden. Perineural analgesia of the deep branch of the lateral plantar nerve abolished lameness in 3 horses but perineural analgesia of the tibial nerve was required to abolish lameness in the hindlimb with injury of the accessory ligament of the suspensory ligament in 2 horses. Injury of the accessory ligament of the suspensory ligament was characterised by marked decrease in echogenicity of the ligament and loss of parallel alignment of the linear echoes, which were shorter than normal in longitudinal images.