The purpose of this study was to determine the age of onset, incidence and severity of neurogenic disease in the intrinsic laryngeal muscles of a single breed of competitive horse, the New Zealand Thoroughbred. Some palatal muscles from these horses were also studied to ascertain whether neurogenic disease occurred in them. The left and right dorsal cricoarytenoid, lateral cricoarytenoid, transverse arytenoid, ventricular, vocal, cricothyroid, hyoepiglottic, palatopharyngeal, palatine levator, palatine, and palatine tensor muscles were collected from some or all of 53 Thoroughbred horses. Forty-six of the horses had no history of upper respiratory tract abnormalities, six had suffered from idiopathic laryngeal hemiplegia and one from laryngo-palatal dislocation. For comparative purposes similar muscles from three ponies were also studied. The muscles were weighed and then frozen sections were prepared from them. Some of these were stained with haematoxylin and eosin and others to demonstrate the activity of myosin adenosine triphosphatase, succinate dehydrogenase and glycogen phosphorylase. These sections were then studied to determine the muscle fibre types present and their proportions. The mean sizes of the groups of myosin adenosine triphosphatase low reacting fibres were measured as were the mean cross sectional areas of the fibres. Abnormal staining characteristics of the fibres were noted along with histological signs of denervation and reinnervation. Where possible this information was analysed to determine the significance of the differences observed between the measured mean values. A difference in weight between some of the left and right laryngeal muscles was found to be very common in Thoroughbred horses with no history of upper respiratory tract abnormalities. The left lateral cricoarytenoid muscle was lighter than the right in approximately half of these horses. This difference was significant between the muscles of these horses over three years of age and was most obvious in the muscles of the geldings. The left and right dorsal crico-arytenoid muscles showed similar but not such marked differences. These differences were more obvious in the laryngeal hemiplegic horses. The fibres of the intrinsic laryngeal muscles were predominantly highly reactive for the enzyme myosin adenosine triphosphatase with the ventricular and vocal muscles having the highest proportions of these fibres and the cricothyroid and hyoepiglottic muscles the lowest. Glycogen phosphorylase reactivity in these muscles was again predominantly high, and the fibres were almost exclusively, highly reactive for succinate dehydrogenase. Neurogenic disease appeared to have an influence on the proportions of fibre types present in affected muscles. The incidence of larger groups of myosin adenosine triphosphatase low reacting fibres in some of the left than right intrinsic laryngeal muscles was also very common in Thoroughbred horses with no history of upper respiratory tract abnormalities. Eighty percent of these horses over three years of age had larger groups in their left than right lateral cricoarytenoid muscles and the youngest horse where this difference was noted was six weeks Old. The adductor muscles showed more evidence of this side difference in group size than the abductor muscles. The mean cross sectional area of the fibres of the intrinsic laryngeal muscles studied increased till approximately the end of the third year of a horse's life. Neurogenic disease eventually reduced the cross sectional area of the fibres of affected muscles but early in its course it may have produced an increase in the mean cross sectional area of fibres. This increase occurred in mildly affected and also in some unaffected muscles. The latter may have been required to increase their activity to compensate for inefficient function in atrophied muscles. The histological signs of denervation and reinnervation were also very common in the intrinsic laryngeal muscles supplied by the left recurrent laryngeal nerve. These signs were noted in almost 70% of the left lateral cricoarytenoid muscles from horses over one year of age, with no history of upper respiratory tract abnormalities. The incidence of these signs in the dorsal cricoarytenoid muscle was lower but they appeared suddenly and severely in the left muscles of horses during adolescence and early adult life. In the cricothyroid muscle which is not supplied by the recurrent laryngeal nerve, the only histological signs of this nature appeared in the muscles of a few of the aged horses. In the palatal muscles examined there was no evidence of a difference in weight between the left and right muscles and most of their fibres were highly reactive for the three enzymes studied. There was no evidence of fibre type grouping resulting from denervation and reinnervation and none of the other histological signs resulting from severe neurogenic disease were noted.