Spastic paresis was diagnosed in 3 male Pygmy goats of which 2 were related (sire and offspring). Signs began an under 1 year of age in 1 of the goats and at 2 years in the other, characterized by an arching of the back and marked extension of the tibial-tarsal joints. On rising, weight was shifted to the front limbs for short periods. The gastrocnemius muscle of both hindlimbs were constantly contracted. Results of hematologic and serum chemistry studies were unremarkable. All goats were seronegative to CAE virus. Radiographs of the tibial-tarsal joints revealed varying degrees of arthritis. EMG studies were conducted in one of the goats and no abnormalities were detected. Epidural injection of 0.38% procaine (0.2ml/kg) to 2 of the goats briefly attenuated these signs. Bilateral tibial nerve neurectomy in 1 of the goats reduced the spasticity. In another goat, bilateral surgical desafferentation of the gastrocnemius muscle by resection of the spinal dorsal (afferent) roots resulted in diminished signs. No lesions were observed in the tibial and peroneal nerves, spinal cord and gastrocnemius muscle at necropsy.

Spastic paresis is reported for the first time in goats from North America. It was concluded that spastic paresis in goats shares many similarities with the disease in cattle. The possibility of inheritance is suggested by 2 of the goats being related. Results of surgical desafferentation indicate that the defect is in the myotatic reflex (stretch reflex). Results from the epidural block using dilute procaine indicate that spastic paralysis in goats is caused by a relative over-stimulation (or lack of inhibition) of the gamma efferent motor neurons.

From: Goat Medicine (1994, P. 170)
Mary C. Smith and David M. Sherman

This condition is well known in cattle and is considered to be inherited in that species. Spastic paresis is characterized by intermittent, unilateral or bilateral spastic contracture of the gastrocnemius muscle leading to hyperextension of one or both hind limbs. The hyperextension may be so extreme that the animal is unable to place the foot on the ground and the leg is carried straight behind. The hock is straight and the gastrocnemius muscle is palpably firm or knotted. It has been demonstrated that selective depression of gamma efferent neurons in the spinal cord by epidural administration of dilute procaine will alleviate the condition, indicating that the disorder occurs from overstimulation of the myotatic (stretch) reflex.

Reports of the condition in goats are infrequent. The condition was first reported in Czechoslovakia in 1973 and involved a 3-year-old male Saanen. The goat was reluctant to stand and when forced to do so remained on its carpi with rump in the air, hindlimbs overextended with the hocks straight, and with the gastrocnemius tendons palpably taut. Though the diagnosis could not be confirmed, tibial neurectomy, as frequently applied in cattle, corrected the condition.

More recently, the condition was reported in two familial related Pygmy goats in the United States. In these cases, the diagnosis was supported by application of a dilute procaine epidural with subsequent alleviation of the signs.

Despite this evidence of spastic paresis in goats, the diagnosis must be made with caution because of the hereditary implications of the disease, which are not well defined in the caprine species. The author has observed at least two goats with classically described signs of spastic paresis that turned out to be cases of the arthritic form of CAE. The occurrence of joint pain without joint swelling is not uncommon in CAE and can lead to abnormalities of gait and posture that can mimic spastic paresis.

From Unknown Source

Species of Animals Affected: Has been reported in many breed of dairy and beef cattle and in a variety of goat breeds.

 Description of Clinical Signs: The disease can occur suddenly at any age but typically less than 2 years old. The condition may affect one or both hind limbs. Classically, the affected limb is in rigid extension, often thrust out behind the animal. If the limb is palpated, one can appreciate excessive tone in the muscles that extend the hock joint and their associated tendon (the gastrocnemius) is taut. These muscles lie on the caudal aspect of the limb below the level of the stifle. Some affected goats appear to stand on the tips of their toes as if there was pain in the soles of their feet. Lameness becomes progressively worse. In the goats seen with the disease, some will adopt a dog sitting position. Due to the excessive uncontrolled extension of the hind limbs, severely affected animals may have difficulty getting up onto their front legs.

Nature of the Disease: Not clearly established. It is thought that for some reason the nerves that supply the particular group of muscles involved are "over active" and bring about persistent contraction.

Cause of the Disease: In cattle there is evidence that the disease is inherited, but the rate of occurrence is very low and perhaps inheritance involves only a susceptibility to it. Seven cases in Pygmy goats have been diagnosed at Michigan State University, of which 2 were related (sire and son).

Treatment: There are surgical options available which involve cutting the nerve that supplies the affected muscles. Current recommendations are that it would be unwise to breed affected individuals. In cattle, sires that have produced affected offspring continue to be used as there are insufficient grounds to withdraw them.

From Unknown Source

This condition is characterized by spastic contracture of muscles and extension of the stifle and tarsal joints of one or both hindlimbs. It has been referred to as contraction of the Achilles tendon, spastic paresis and Elso heel. The spasticity characteristically affects the gastrocnemius and superficial flexor muscles and tendons. In some cases the biceps femoris, semitendinosus, semimembranosus, quadriceps and abductor muscles are affected. Bilateral involvement is not common. This progressive disease varies in severity and time of onset from 3 to 6 months of age to as late as 2 years.

Radiographic findings in affected hock joints are fairly consistent and are characterized by an increased angle of the joint, osteoporosis and exostosis around the distal epiphysis of the tibia, curvature and exostosis of the dorsal side of the calcaneus, and widening of the epiphyseal line of the calcaneous. All of these lesions are considered secondary to muscular tension, which may prevent or delay union of the epiphysis of the tuber calcis. Central nervous system lesions have not been found. Although spastic paresis was thought to be inherited as a simple recessive, recent breeding experiments refute this. Genetic influences as well as environmental factors interact to cause spastic paresis.

From: The Merck Veterinary Manual, 7th Edition

Spastic Paresis (Elso Heel), P. 503 - A hereditary spastic condition seen in many breeds, most commonly Holstein and Angus. It appears first in one or both hindlimbs at 3 months to 2 years. Eventually, both hindlimbs become affected, even though only one initially exhibited signs. The cause is not known. Recent findings provide good evidence that the disease is not transmitted as a simple recessive. CSF contains a reduced amount of phosphorus, calcium, and homovanillic acid, the major metabolite of the neurotransmitter dopamine. AST (SGOT) is lowered and alkaline phosphatase is raised.

Taut gastrocnemius and superficial flexor muscles are characteristic. The hock and stifle are maintained in full extension, and the calcaneus is pulled into close apposition to the distal tibia. This anatomical relationship results in an excessively straight lower limb and a small, weak-appearing hock. Tremulous muscle contractions are evident in the affected limb when the animal is forced to move. The affected limb appears to be shorter and may not touch the ground; it swings as a pendulum when the animal walks or runs. An arched back and elevated tailhead are also often noted. Differential diagnoses [in cattle] include spastic syndrome, gonitis, dorsal luxation of the patella, and progressive posterior paralysis. The age at which first signs appear, the initial unilateral involvement, and the dorsal displacement of the tuber calcaneus are aids in the diagnosis.

Muscle relaxants may give slight temporary relief. Tenotomy of the gastrocnemius tendon and partial or complete tenotomy of the superficial flexor tendon 3" to 4.5" (8 to12 cm) dorsal to the tuber calcaneous may be beneficial. [Note: these measurements are for cattle!]  Tibial neurectomy has produced better results, but there is no real justification for any treatment of breeding animals, since this condition is apparently inherited. Treatment of non-breeding animals may be justified for humane reasons, while they are being finished for market.

Congenital and Inherited Diseases of the CNS, P. 581 - Spastic paresis occurs in many breeds of cattle, and is characterized by spastic contracture of the muscles and extension of the stifle and tarsus of one or both hindlegs. It has been referred to as "contraction of the Achilles tendon," "straight hock," and "Elso heel. Spasticity affects the gastrocnemius and superficial flexor muscles and tendons and, in some cases, also the biceps femoris, semitendinosus, semimembranosus, quadriceps, and abductor muscles. It is a progressive disease and varies in severity and time of onset; it is usually noted first in 3- to 6-month-old calves.

Radiographs of affected hocks are characterized by increased joint angle, osteoporosis, exostosis of the distal epiphyseal line of the tibia, curvature and exostosis of the dorsal aspect of the calcaneus, and widening of the epiphyseal line of the calcaneus. Genetic influences as well as environmental factors interact to express spastic paresis. Affected bulls should not be used for breeding.

Diseases of the Spinal Column and Cord, P. 593 - Spastic paresis is common in young dairy and beef calves (1-9 months old), especially among those nursing. The cause is not clear; however, a neurotransmitter imbalance is suspected. Signs are characterized by progressive, tremulous spasms of the gastrocnemius and digital flexor muscles. Signs are usually asymmetric, initially with the affected limb swinging as a pendulum when the animal moves. Tenotomy of the gastrocnemius tendon and tibial neurectomy have proved beneficial in some cases.

Source: Current Therapy in Theriogenology 2

Spastic Paresis, P. 105 - This disease has some clinical signs  and part of its name in common with spastic syndrome. Therefore, it seems appropriate to consider spastic paresis briefly from a standpoint of differential diagnosis. Spastic paresis is most common in European Friesian cattle. It is uncommon in the United States but has been reported in Holstein, Ayrshire, Angus and Beef Shorthorn breeds. Clinical signs are most frequently unilateral. Onset is rare after 1 year of age, but it may occur within a few weeks of birth. The disease is characterized and explainable by chronic contraction of gastrocnemius and superficial digital flexor muscles. As a result, hock and stifle joints are typically maintained in near full extension, holding the fibular tarsal bone and its os calcis in close apposition to the distal tibia. Partial separation of the os calcis from the fibular tarsal bone gives an increased area of reduced radiopacity at its epiphyseal plate.

Tremulous muscle contractions are present in the affected limb, especially on arising. The limb appears shorter, may not touch the ground, often swings in a pendulous manner and usually points anterolaterally. Symptomatic surgery, in which either the Achilles tendon or branches from the tibial nerve to the gastrocnemius muscle are interrupted, usually gives marked relief. 

Relief has also resulted through surgical transection of dorsal roots of spinal nerves supplying gastrocnemius muscle (desafferentation). This suggests that the primary neurophysiologic defect in spastic paresis is, as suggested herein for spastic syndrome, an exaggerated efferent response in the myotatic (stretch) reflex.

Sire-daughter matings provide firm evidence that spastic paresis is not transmitted by a simple recessive mechanism.

It has been determined that calves with spastic paresis display deviations from normal of some components of cerebrospinal fluid. The most significant deviation may be a substantial reduction of homovanillic acid, the main metabolite of the neurotransmitter dopamine.

Serving Disability Due to Abnormalities of Feet and Legs, P. 140 - Joint lesions are increasingly being detected in young bulls. Genetic, nutritional and conformational factors have been implicated. A degenerative arthropathy of the hip has been reported in young Hereford bulls, affecting approximately 1/4 of the male progeny of one sire. This condition, which primarily affects the stifle joint, can have variable effects on  the stifle joint, can have variable effects on breeding ability. Evidence implicating both heredity and nutrition in the pathogenesis of this condition is strong.

In one report all of 223 fattened young European bulls examined showed joint lesions of varying severity in the forelimbs. The most severe lesions occurred in those bulls fed most intensively and that grew the fastest. Overweight, straight-hocked bulls were also predisposed to stifle lameness.

Conformational defects such as straight [rear] legs, "sickle hocks' and "pigeon toes" can not only lead to mating disabilities but can also contribute to associated problems such as penile hematomas. In addition, it has been shown that conformational defects of the feet ad legs of young bulls can be highly heritable.

A progressive spastic syndrome affecting one or both hind legs in young calves (and occasionally older animals) has been reported. This disease is manifested by a straightening and backward extension of the affected hindlimb with certain breeds and conformations (e.g., "post legs") being predisposed. The disease is inherited and has been referred to as spastic paresis, spastic syndrome and "Elso heel."

Another condition has been reported in older animals. This is characterized by clonic-tonic muscular spasms, generally first evident in the hind quarters. It has been termed "crampy," "stretches" and progressive hindlimb paralysis. The condition is incurable, inherited and probably sex linked. Its development has been associated with arthritis, straight hindlimbs, and weak hocks and with lumbar spondylosis and lumbosacral disc protrusions.

Foot problems such as overgrown hooves, interdigital necrobacillosis, bruised sole, pododermatitis, interdigital fibromas and laminitis can interfere with breeding ability. For a complete review of these and other foot and limb conditions that may affect breeding ability in bulls, readers are referred to the work of Greenough and colleagues.

Veterinary Clinics of North America, Food Animal Practice (1993, P. 84)
Congenital Abnormalities, Spastic and Paralytic Diseases

This group of diseases includes those with clinical evidence of CNS involvement and genetic studies indicating a hereditary basis. They may be primarily functional disorders.

Bovine spastic paresis is characterized by spastic contracture of muscles and extension of the stifle and tarsal joints of affected hind limb(s). The clinical signs usually indicate a unilateral condition, with the right hind limb being frequently involved; bilateral involvement is rare (Fig. 4). Although the disease is assumed to be genetic, the evidence is inconclusive; genetic influence(s) as well as environmental factors, play an important part in its incidence,  ^{58, 61, 77, 78} and the role of trace elements such as lithium recently was discussed. ¹

1. Arnault GA: Bovine spastic paresis. An epidemiologic, clinical and therapeutic study in a Charolais practice in France. Efficacy of lithium therapy. World Association of Buiatrics. In Proceedings of the 12th World Congress on Diseases of Cattle, vol II. Amsterdam, The Netherlands, 1982, pp 853-858

58. Leipold HW, Dennis SM: Congenital defects of the bovine central nervous system. Vet Clin North Am 3:159-177, 1987

61. Leipold HW, Huston K, Dennis SM: Bovine congenital defects. Adv Vet Sci Comp Med 27:197-271, 1983

77. Roberts SJ, Hereditary spastic diseases affecting cattle in New York State, Cornell Vet 55:639-644, 1965

78. Roberts SJ, Veterinary obstetrics and genital diseases, ed 2. Ithaca, New York, published by the author, 1971