Interpretation of laryngeal function tests in the horse

Idiopathic left-sided laryngeal paralysis was present in 14 of 169 horses on a thoroughbred horse farm (8.3 per cent). In nine animals, it was evident only after exercise and arytenoid abduction and adduction were normal at rest. Asynchronous movement of the arytenoid cartilages was observed in 94 horses at rest (55.6 per cent), 86 of which were considered to be normal after exercise. Conversely, synchronous movement of the arytenoids was noted when at rest in six of the 14 animals diagnosed as having laryngeal hemiplegia after exercise. An abnormal inspiratory noise during exercise was detectable in 11 of these 14 horses, but not in the remainder. An abnormal noise on inspiration was also produced by nine horses in which laryngeal hemiplegia was not diagnosed.     

Ceratohyoidectomy for treatment of equine temporohyoid osteoarthopathy (15 cases)

This study investigated 15 horses diagnosed with temporohyoid osteoarthopathy (THO) and treated by ceratohyoidectomy between 2004 and 2012. The presenting complaint, duration and nature of the clinical signs, additional diagnostic procedures, and complications were reviewed retrospectively. Long-term follow-up on horses was used to determine prognosis. All horses were diagnosed by guttural pouch endoscopy. Follow-up was available for 14 horses that survived to discharge. Eight of 10 horses that were used athletically prior to surgery returned to previous levels of use. Persisting clinical signs included mild facial nerve paralysis (3/14; 21.4%) or head tilt (6/14; 42.8%) but these were not functionally limiting. It was concluded that equine THO affects a wide range of breeds, disciplines, and ages of horses, and has a variety of presenting clinical signs most commonly associated with vestibular and facial nerves. Prognosis following ceratohyoidectomy is good for resolution of ataxia but some cranial nerve deficits may persist.     

Paraphimosis in seven debilitated horses

This paper reports seven cases of penile paraphimosis which occurred in both entire and castrated horses in association with general debility. Two cases were discharged after treatment while still suffering from partial paralysis; one was discharged at the owner's request with complete paralysis; three were destroyed and one died during treatment. Identified causes of debility were malnutrition, severe parasitism, glucose malabsorption and salmonellosis.     

Familial incidence of hyperkalemic periodic paralysis in quarter horses.

The pedigrees of 17 horses with hyperkalemic paralysis were studied. All were first-, second-, or third-generation offspring of a common sire, 16 were registered Quarter Horses. Analysis indicated that it was unlikely that the concentration of hyperkalemic periodic paralysis in the offspring of this sire was attributable to chance. The familial nature of this condition should help veterinarians diagnostically. It also suggests that it is possible to reduce the incidence of this condition by breeding from non-affected lines of horses and reinforces the need for studies to determine whether the disease is genetic in origin. Although more affected horses were second-generation offspring, the proportion of horses affected was largest in the first generation and decreased progressively with each generation. This is probably because horses in the earlier generations have been observed for longer periods and thus clinical signs are more likely to have been noticed in these horses.     

Hyperkalaemic periodic paralysis in Australian Quarter Horses

SUMMARY Three Quarter Horse stallions and 5 of their 11 tested progeny were diagnosed as affected with the inherited autosomal dominant defect hyperkalaemic periodic paralysis in Victoria in 1992. The diagnoses were based on the appearance of clinical signs and associated increased plasma potassium concentrations in response to oral potassium loading. All affected horses were descendants of the American Quarter Horse Impressive. Indirect evidence indicates that at least 3 other affected Quarter Horse stallions have stood or are standing at stud in Australia. The clinical details of the affected horses are described and the size of the affected population in Australia is discussed.     

A survey of neurological diseases in horses

SUMMARY: Case records of 450 horses with signs of neurological disease are reviewed. One hundred and nineteen horses with neurological disease due to trauma were examined, of which 60 were due to spinal cord trauma, 47 to brain or cranial nerve trauma and 12 to peripheral nerve trauma. Cervical vertebral fractures/trauma were the most common injury. Basisphenold/basloccipital bone fractures were the most common form of cranial trauma and facial nerve paralysis the most common cranial nerve injury. Eighty-nine horses with neurological disease due to malformation were examined. Cervical vertebral malformation occurred in 83 horses and congenital defects in 6 foals. Neurological disease due to inflammation or infection occurred in 30 horses. The most common disease of this type was meningitis, which occurred in 11 horses and foals. Neoplasms in the CNS caused neurological disease in 8 horses. The final category was miscellaneous neurological disease, which was diagnosed in 204 horses. Diseases in this category included neonatal (28 cases), toxic/metabolic (27 cases), idiopathic (133 cases), degenerative (3 cases) and other neurological diseases (13 cases). The most common condition was idiopathic laryngeal hemiplegia (116 cases).
Where possible, diagnosis relied on a thorough neurological examination with use of ancillary tests in selected cases including rhinolaryngoscopy, radiography, myelography, ophthalmoscopy and cerebrospinal fluid analysis when indicated. In many cases necropsy and histopathological confirmation or diagnosis was necessary.     

STRESS FRACTURES OF THE HUMERUS, RADIUS, AND TIBIA IN HORSES

The medical records, radiographic and nuclear scintigraphic findings of 26 racing horses with 27 stress fracture episodes of the humerus, radius, or tibia were reviewed. The purposes of this study were to describe the radiographic and/or scintigraphic features of stress fractures of the humerus, radius, or tibia, and to evaluate the signalment and history of horses in which stress fracture occurred. Stress fractures of the three long bones examined were primarily seen in 2-and 3-year-old male Thoroughbred horses; commonly, the onset of lameness was immediately following training gallops or racing. There were 13 humeral stress fracture episodes in 12 horses. Ten were in the proximal caudolateral cortex, and three were in the distal craniomedial cortex. Radial stress fractures were seen in three horses, all in the midshaft radius. Tibial stress fractures were diagnosed in 11 horses. They were located in the proximal lateral tibia in six horses, the distal caudolateral tibia in three horses, and the midshaft tibia in three horses. Fifteen stress fractures were diagnosed with radiographs alone, one was diagnosed with scintigraphy alone, nine were diagnosed with radiographs and scintigraphy, and, in two horses, radiographs were negative, but the scintigraphic findings were consistent with stress fracture.     

Inheritance of myotonic discharges in American quarter horses and the relationship to hyperkalemic periodic paralysis.

Electromyography (EMG) was used to detect myotonic discharges in Quarter Horse breeding stock and to follow the results of mating horses with hyperkalemic periodic paralysis (HPP). The studies were performed on two brood mare farms. A total of six breeding stock showed myotonic discharges and 15 were nonmyotonic. Myotonic discharges were seen in five of six horses belonging to the blood line previously implicated as being predisposed to HPP. Two of these horses had shown clinical signs of HPP. Only one of 15 breeding horses unrelated to the HPP predisposed blood line showed myotonic discharges. When both parents were non-myotonic on EMG than the F1 generation (n = 6) were also nonmyotonic. When a stallion with HPP and myotonic discharges was mated to eight nonmyotonic mares over a six year period half the animals of the F1 generation (n = 25) showed myotonic discharges. When both parents showed myotonic discharges four F1 offspring were myotonic and two were nonmyotonic on EMG testing. There was no evidence of sex linkage. The results are consistent with an autosomal dominant mode of inheritance. Hyperkalemic periodic paralysis and myotonic discharges on EMG may be different manifestations of the same underlying defect.     

Laryngeal paralysis: a study of 375 cases in a mixed-breed population of horses

Referred cases (n = 375) of laryngeal paralysis (1985-1998) from a mixed-breed equine population included 351 (94%) cases of recurrent laryngeal neuropathy (RLN) (idiopathic laryngeal hemiplegia) and 24 cases (6%) of laryngeal paralysis from causes other than RLN. Laryngeal movements were classified endoscopically into one of 6 grades, in contrast to the usual 4 grades. The RLN cases had a median grade 4 laryngeal paralysis, of which 96% were left-sided, 2% right-sided and 2% bilaterally affected. RLN cases included 204 (58%) Thoroughbred, 96 (27%) Thoroughbred-cross, 23 (7%) draught, 16 (5%) Warmbloods and 10 (3%) other breeds, including only 4 (1%) ponies. The median age of RLN cases at referral was 6 years (range 2-12) and their median height was 170.2 cm. The work of RLN horses included National Hunt racing (42%), flat racing (1%), hunting (19%), eventing (16%) and miscellaneous work (22%). Reported presenting signs in RLN-affected horses included abnormal exercise-related respiratory sounds in 90% and reduced exercise tolerance in only 64%. However, many horses were referred before their exercise tolerance could be fully assessed. Forty percent of the RLN cases had intercurrent disorders, including 10% with additional upper respiratory and 7% with lower respiratory tract diseases. The 24 nonidiopathic RLN cases included 12 with bilateral laryngeal paralysis, 11 (92%) of which were ponies. Bilateral laryngeal paralysis occurred with hepatic encephalopathy in 7 cases and following general anaesthesia in 2 cases. The 12 cases of acquired unilateral laryngeal paralysis included 7 caused by guttural pouch mycosis.     

Delayed onset vagus nerve paralysis after occipital condyle fracture in a horse

Occipital condylar fractures (OCFs) causing delayed onset lower cranial nerve paralysis (LCNPs) are rare. We present a 7‐year‐old Friesian horse with delayed onset dysphagia caused by vagus nerve (CNX) paralysis and suspicion of glossopharyngeal nerve (CNIX) paralysis developed several days after a minor head injury. Endoscopic examination revealed right laryngeal hemiplegia and intermittent dorsal displacement of the soft palate. An area of submucosal hemorrhage and bulging was appreciated over the dorsal aspect of the medial compartment of the right guttural pouch. Radiological examination of the proximal cervical region showed rotation of the atlas and the presence of a large bone fragment dorsal to the guttural pouches. Occipital condyle fracture with delayed onset cranial nerve paralysis was diagnosed. Delayed onset cranial nerve paralysis causing dysphagia might be a distinguishable sign of OCF in horses. Delayed onset dysphagia after head injury should prompt equine clinicians to evaluate the condition of the atlanto‐occipital articulation and skull base.     

Clinical findings in 10 horses diagnosed with monorchidism following exploratory laparotomy or standing laparoscopic surgery

Monorchidism describes the complete absence of one testis and is rare in horses. This study reports the clinical findings in 10 horses diagnosed as monorchids by standing laparoscopy or exploratory laparotomy. Hospital records for all horses undergoing cryptorchidectomy (2000–2016) in four centres were reviewed from which horses diagnosed with monorchidism were identified. Surgery was by either standing flank laparoscopy or an inguinal exploration and subsequent exploratory laparotomy under general anaesthesia. Ten horses were diagnosed as monorchids, five by laparoscopy (one bilateral laparoscopy) and five by laparotomy. Nine horses had a normally descended scrotal testicle, which was also removed at surgery. The right testicle was absent in three horses, and the left testicle was absent in seven horses. Anatomical findings were recorded in each case; the vaginal process was present in all horses, ductus deferens and epididymis were present in 80% of horses and the ligament of the tail of the epididymis and testicular vessels were present in 50% of horses. Laparoscopy allowed easy identification of spermatic structures enabling a prompt diagnosis of monorchidism. In conclusion, when monorchidism occurs, most other associated spermatic structures are likely to be present. A diagnosis of true monorchidism is reliant on hormonal testing and absence of testicular tissue on histopathology and so some of these horses may strictly be somewhere on the spectrum of testicular degeneration. This information is particularly useful in the surgical situation when it is not clear whether the testicle is present or not.     

Metallic foreign bodies in the tongues of 16 horses

The history, clinical signs, results of diagnostic imaging, treatment methods and outcome of 16 adult horses with a metallic foreign body in the tongue are reviewed. All the horses had a swollen tongue, they salivated excessively and were partially to completely anorexic. Less common clinical signs were fever, an enlarged and painful intermandibular space, dysphagia, unilateral tongue paralysis and halitosis. Most of the horses had shown clinical signs for less than 24 hours. The foreign bodies were diagnosed by oral examination, radiography and ultrasonography; they were removed from the tongue of four of the horses during the initial oral examination, and were removed surgically from nine others; the other three horses were treated medically without attempts being made to extract the foreign bodies. Twelve of the bodies were small pieces of wire and one was a hypodermic needle. All the horses received a combination of antimicrobial and non-steroidal anti-inflammatory drugs and they all made an uneventful recovery. Feeding hay and the use of cable-framed tractor tyres as feeders were commonly associated with the cases.     

Bilateral laryngeal paralysis in the horse

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.     

Idiopathic perforating ulceration of the small intestine in five adult horses

Perforating ulceration of the small intestine was diagnosed in 5 adult horses. Affected horses presented with signs of low‐grade colic, depression and inappetance. Abdominal paracentesis yielded abnormal peritoneal fluid in all cases. Perforating ulcers were located at the mesenteric border in 4 horses and the ileum in one horse. All horses had diffuse septic peritonitis. The aetiology of the condition is unknown.     

Determination of sensitivity to metocurine in exercised horses.

On the basis of results in dogs, conditioning exercise may increase sensitivity to nondepolarizing muscle relaxants. Five Thoroughbreds were exercised/conditioned 3 times weekly on a treadmill for 8 months. Increasing maximal rate of O2 consumption verified that the horses were responding to exercise conditioning. Six nonexercised Thoroughbreds served as the control group. Studies were done with horses under general anesthesia by use of halothane during partial paralysis by a brief constant-rate infusion with the muscle relaxant, metocurine iodide. Quantification of degree of paralysis of the hoof twitch (eg, digital extensor) occurred with simultaneous quantification of blood values of metocurine. Pharmacokinetic and pharmacodynamic analyses of the data were done by a nonlinear regression program, using the Hill equation. There were no differences in findings between exercised and nonexercised horses. The mean blood concentration for the 50% paralyzing dose of metocurine was 0.44 +/- 0.11 (SD) microgram/ml in exercised horses, and 0.58 +/- 0.22 microgram/ml in nonexercised horses. Despite evidence for a response to conditioning, a significant change in the sensitivity of the neuromuscular junction to metocurine was not found.     

Urolithiasis in the horse — A review of 13 cases

The presenting signs, treatment and postoperative progress of 13 horses with vesical and urethral calculi are reviewed. Single, discrete stones were present in 10 animals in which the results of treatment were generally good. In three horses with sabulous cystic deposits, urolithiasis was associated with bladder paralysis and the response to treatment was poor.     

Thoracic limb digital extensor denervation in young horses

Low radial neurectomy in the left thoracic limb was performed in 4 mixed-breed weanling horses, with subsequent paralysis of the lateral and common digital extensor muscles. Weight bearing of the denervated and control limbs was discouraged by the use of special shoeing. Clinical signs of flexural deformity were not induced in the horses.     

Fractures of the distal phalanx in horses

Summary. Nineteen cases of fracture of the distal phalanx in horses are reviewed. This represented 1.1% of the total number of horses seen at Murdoch University Veterinary Hospital (MUVH) over a 32-month period. All horses were managed conservatively. Eight horses made a complete recovery. Three are being trained again and are not lame. Four horses made a limited recovery. Two horses are still resting and one horse was killed humanely when it still showed lameness after 2 years. One horse was killed humanely after the fracture was first diagnosed.     

Serum thyroid hormone concentrations in New Zealand horses

Total thyroxine and total tri-iodothyronine concentrations were measured in the sera from 125 horses of mixed age, breed and sex, and varied clinical histories. While low serum thyroxine concentrations were detected in 35 horses, the majority of those horses had serum thyroxine values within the reference range when retested. Only one horse had a mildly decreased serum tri-iodothyronine concentration. Those horses in which the serum thyroxine concentration was low when retested had a normal thyrotropin releasing hormone stimulation test. Hypothyroidism was not diagnosed in any horses in this study. The low serum thyroxine concentrations measured in the present study were attributed to either normal fluctuations in serum concentrations in healthy horses, the effect of drugs, or to the effects of non-thyroidal illness. Because thyroid hormone concentrations are altered by many factors, hypothyroidism should not be diagnosed on the basis of a single low value and further testing, preferably including active stimulation of the thyroid gland, should be carried out.     

Equine hyperkalemic periodic paralysis: review and implications.

The purpose of this review is to present an up-to-date summary of the signs, diagnosis, treatment, and implications of equine hyperkalemic periodic paralysis. The review encompasses all original articles published between 1986 and early 1993. Hyperkalemic periodic paralysis is the result of a genetic mutation in the skeletal muscle sodium channel gene. It is inherited as an autosomal dominant trait; most affected horses are heterozygotes. The classical signs are muscle fasciculation, spasm, and weakness associated with hyperkalemia. However, these signs are only rarely observed in affected horses. Potential sequelae to attacks are abrasions and involuntary recumbency; these problems are not specific for hyperkalemic periodic paralysis, but they occur more frequently in hyperkalemic periodic paralysis-affected horses. It is also likely that hyperkalemic periodic paralysis results in greater muscle mass. There are suggestions that homozygotes may be more severely affected and show signs of upper respiratory obstruction as foals. The practitioner needs to be aware of the tests for hyperkalemic periodic paralysis, and their limitations, so that he can properly diagnose this condition. The industry has the difficult problem of deciding whether or not testing should be mandatory and the fate of positive horses.