B.E. Goulden

Equine laryngeal hemiplegia part I. A light microscopic study of peripheral nerves

This light microscopic investigation of 15 Thoroughbred horses provided substantial evidence for the classification of equine laryngeal hemiplegia as a distal axonopathy. Morphologic and morphometric examinations were performed on resin embedded recurrent laryngeal nerves from control, subclinical and clinical laryngeal hemiplegic animals. In the latter group of animals some distal hindlimb nerves were also examined. A distally graded loss of myelinated fibres selectively affecting those of large diameter was demonstrated in both left and right recurrent laryngeal nerves. Morphologic evidence of similar pathological changes in long hindlimb nerves was also present. An explanation for the early involvement of the cricoarytenoideus lateralis muscle in the course of laryngeal hemiplegia, was offered by the demonstration of more large diameter fibres in the branch of the recurrent laryngeal nerve innervating it, thus making it more susceptible to the disease process.

Equine laryngeal hemiplegia. Part III. Treatment by laryngoplasty

During the years 1971-1979, 127 horses with left laryngeal hemiplegia were studied. The physical characteristics and clinical signs observed in this study were recorded in Part I and Part II of ths series of papers. Of these 127 horses, 81 were treated by the laryngoplasty procedure. Complications of surgery are described and the effects of the operation on respiratory noise and performance are evaluated. In 54.8% of horses the chronic respiratory noise observed during exercise was apparently diminished or eliminated post-operatively. The performance of 44% of horses was apparently improved after surgery. Post-operative racing success occurred in 38% of horses treated. Satisfactory arytenoid adduction as assessed endoscopically within 9 days of surgery was achieved in 77% of cases. Surgical failure appeared to be related to cutting of the laryngeal cartilages by the prosthesis and techniques to minimise this are discussed.

Stringhalt in horses : a distal axonopathy

A detailed investigation of the neuropathology of a horse affected with stringhalt was performed. Qualitative and quantitative light and electron microscopy, and single teased fibre preparations of peripheral nerve demonstrated predominantly axonal degeneration, the stage of which was appropriate for the duration of clinical signs. There was selective involvement of large myelinated nerve fibres. A proximal to distal increase in the severity of pathological changes was present in the peripheral nerves. The long left recurrent laryngeal nerve was the most severely affected, followed in order by its right counterpart, the hindlimb and forelimb nerves. Neurogenic atrophy of muscles innervated by affected peripheral nerves also showed a distally graded increase in severity. No lesions were observed in the central nervous system. It was concluded that this disease should be classified as a distal axonopathy.

A review and some observations on stringhalt

A review of the literature on stringhalt in horses is presented, including the aetiology, clinical signs, pathology and treatment of this disease. Three New Zealand outbreaks of stringhalt are reported and discussed. The occurrence of these (and most previously reported outbreaks) in the late summer and autumn, and the association of the disease with various weeds, indicates a likely toxic aetiology.

The pathogenesis of equine laryngeal hemiplegia — a review

Recent research on the muscular and nervous changes which occur in idiopathic equine laryngeal hemiplegia has indicated that many of the traditional concepts of the aetiology of this disease are erroneous. In light of the new knowledge gained, the various predispositions and possible causes of laryngeal hemiplegia are discussed, and it is suggested that the underlying mechanism of axonal damage in this neuropathy of horses may be related to abnormal energy metabolism in the axon.

Equine laryngeal hemiplegia part IV. muscle pathology

This study confirmed that neurogenic muscle pathology exists in intrinsic laryngeal muscles supplied by the recurrent laryngeal nerves in horses subclinically and clinically affected with laryngeal hemiplegia. An important additional observation was the occurrence in three out of four laryngeal hemiplegic horses of neurogenic muscle changes in a hindlimb muscle, the extensor digitorum longus, a muscle supplied by another long peripheral nerve. This finding suggests that a polynenropathy exists in laryngeal hemiplegic horses, and supports the classification of this disease as a distal axonopathy. Comparison of the degree of pathology in the intrinsic laryngeal muscles and that of the recurrent laryngeal nerves innervating them, demonstrated a strong correlation between the extent of damage in the distal left recurrent laryngeal nerve and the overall degree of muscle pathology. The muscle damage in clinically affected horses is a reflection of the nerve damage present in the most distal portion of the recurrent laryngeal nerve. The more variable pathological changes found in proximal levels of the left and right recurrent laryngeal nerves probably reflects the ongoing nature of the pathological process affecting nerve fibres. The existence of a subclinically affected group of horses, the earliest involvement of an adductor, the left cricoarytenoideus lateralis muscle, and the presence of changes in the right intrinsic laryngeal muscles all confirmed the findings of previous workers.

Equine laryngeal hemiplegia Part II. An electron microscopic study of peripheral nerve

The recurrent laryngeal nerves were examined by electron microscopy in five control, four subclinical and four clinical laryngeal hemiplegic horses. In addition, the peroneal nerve was examined in two horses in the latter group. The distally distributed loss of large myelinated fibres in the left recurrent laryngeal nerve seen by light microscopy was confirmed. In addition, active axonal pathology was found to be more evident than indicated by light microscopic investigations. The onion bulb formations observed indicated the repetitive nature of the damaging influence to nerve fibres. Although the pathological changes were most obvious in the distal left recurrent laryngeal nerve, alterations similar in type and distribution were present in other areas of the left and right nerves, and in the distal hindlimb nerves. The observation of fibres with inappropriately thick myelin sheaths relative to their axonal calibre, was confirmed statistically by determining the regressions of axis cylinder perimeter against the number of myelin lamellae. In conclusion, the peripheral nerve pathology of equine laryngeal hemiplegia was demonstrated to be a distally distributed loss of myelinated fibres, with considerable active axonal damage, in conjunction with axonal atrophy. These features suggest that this disease may be classified as a distal axonopathy.

Endoscopic observations on laryngeal symmetry and movements in young racing horses

An endoscopic survey of young race horses was performed to examine the prevalence and character of laryngeal movements during quiet respiration. The main aim was to determine whether those arytenoid movements which could possibly reflect the efficiency of left dorsal cricoarytenoid muscle function changed over a period of time. Of the 452 horses examined, 439 were Thoroughbreds and 23 were Standardbreds, 250 were less than 2 years of age (6-21 months), and 202 were 2 years old. One hundred and nine of these horses were examined again 16 months later. Arytenoid movements were given one of four grades. Grades 1 and 2 were considered normal and unlikely to be the result of abnormal left dorsal cricoarytenoid muscle function, whilst grades 3 and 4 were considered likely, or almost certainly, the result of abnormal left dorsal cricoarytenoid muscle function. The percutaneous prominence of the muscular process of left and right arytenoid cartilages, endoscopic arytenoid movement on left and right sides, age, sex and breed was recorded. Chi squared analysis was used to determine the association between age, breed, sex and the other recorded variables, and the presence or absence of abnormal laryngeal movements. At the first examination, 48% of the horses had grade 1, 37% grade 2, 15% grade 3 and 0.2% grade 4 left laryngeal movements. Of the horses examined I6 months later, 52% had grade 1, 33% grade 2, 14% grade 3 and 1% grade 4 left laryngeal movements. Fifteen percent of horses with grade 1 and 9% with grade 2 initially were found to be grade 3 at the subsequent examination. Conversely, 53% of horses with grade 3 initially were found to be grade 1 and 21% grade 2 at the subsequent examination. One horse that was grade 3 at the initial examination was grade 4 at the subsequent examination. Overall, 43% of horses were graded the same, 29% were given a better grade and 28% were given a worse grade. Age and sex were not associated with abnormal left laryngeal movements. The presence of abnormal arytenoid movements was significantly less in Standardbreds, but significantly higher in those horses that had a more prominent muscular process of the left arytenoid cartilage. The number of grade 2 and 3 laryngeal movements recorded on the left side was significantly higher than the right. It was concluded that asymmetrical laryngeal movements are common in young race horses; at this age laryngeal movements may interchange between what is considered normal and abnormal; the proportion of young horses with normal or minor variations in their left arytenoid movements that develop more obvious degrees of asynchrony is low (12%); and the proportion of horses considered to have endoscopic evidence of deficient left abductor muscle function that eventually develop laryngeal hemiplegia is also low (5%).

Radiographic changes in the lungs of horses with exercise-induced epistaxis

This paper describes the distinctive radiographic changes detected in the dorso-caudal lungfields of four racing thoroughbreds recently affected by exercise-induced epistaxis. A diffuse but localized increase in density was seen in all four cases, which demonstrated a variation from a predominantly alveolar density to an interstitial pattern and finally to increased bronchial markings. Evolution of the radiographic pattern of the pulmonary densities appeared to be related to the time that had elapsed since the bleeding incident. The implications of the changing pattern and site of the densities are discussed.

Equine laryngeal hemiplegia part III. A teased fibre study of peripheral nerves

Individual nerve fibres were isolated from the recurrent laryngeal and some distal hindlimb nerves, in an investigation of equine laryngeal hemiplegia. One hundred teased fibres were obtained from each of three sampling sites on both left and right recurrent laryngeal nerves, from 15 Thoroughbred horses. These fibres were graded descriptively and internode lengths measured. A distal distribution of pathology was demonstrated in all groups studied, but was most severe in the clinical group of horses. The predominant change was one of short thinly myelinated internodes interspersed amongst normally myelinated internodes, indicating remyelination of previously demyelinated areas of nerve fibre. Such pathological change was also reflected by the decreased mean internode length, and its increased variability associated with disease. However, it was determined statistically that these abnormal internodes were grouped along particular nerve fibres, rather than being randomly distributed between all nerve fibres. This is thought to indicate myelin sheath changes secondary to underlying axonal pathology. Thus it was concluded that the primary pathology was likely to be axonal in nature, while the high incidence of demyelination changes was a reflection of the chronic nature of the disease process. Thus, the distal distribution of pathology, the primary axonal involvement, the presence of changes in left and right recurrent laryngeal and distal limb nerves, all support the classification of equine laryngeal hemiplegia as a distal axonopathy.