A 16-year-old 4.2-kg (9.2-lb) neutered male domestic shorthair cat was evaluated because of sudden onset, nonprogressive pelvic limb weakness of 1 week's duration. The cat was ambulatory but reportedly had difficulty climbing onto furniture and appeared unable to generate a normal thrust from its pelvic limbs. There was no history suggestive of systemic disease. Results of a general physical examination were largely unremarkable, with no cardiac abnormalities and apparently normal femoral pulses. Neurologic evaluation revealed a bilateral, plantigrade stance at rest, although the cat was able to walk without support. Hopping responses were normal in the thoracic limbs and although impaired in the pelvic limbs, conscious proprioceptive placing appeared normal. The patellar and cranial tibial reflexes were intact, but the gastrocnemius reflex was absent; withdrawal reflexes were considered normal in all 4 limbs, and all other aspects of the neurologic examination were unremarkable.
Neurologic examination
What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.
Assessment
Anatomic diagnosis
| Problem | Rule out location |
|---|---|
| Bilateral partial plantigrade stance of pelvic limbs | Lower motor neuron lesion to the pelvic limb |
Likely location of one lesion
| The mild postural deficits in the absence of other notable neurologic deficits were considered indicative of an orthopedic problem; damage to the calcaneal tendon or associated structures was the most likely cause. |
Etiologic diagnosis—Differential disease processes for a cat with a plantigrade stance included a neuropathy (eg, demyelinating neuropathy as a result of diabetes mellitus), neurologic lesions affecting the spinal cord or nerve roots of the caudal lumbosacral intumescence, systemic causes of generalized weakness (eg, myositis or hypokalemia), or a localized lesion affecting the musculoskeletal structures of the tarsus. The diagnostic plan included serum biochemical analysis (to rule out metabolic abnormalities) and diagnostic imaging of the hind limbs (to assess for musculoskeletal problems).
Diagnostic test findings—Serum biochemical analysis revealed no important metabolic abnormalities, thereby excluding the possibility of hypokalemia-associated weakness and diabetes mellitus. In addition, serum creatinine kinase concentration was within the reference interval, making focal myositis unlikely and excluding the possibility of ischemic damage to the muscles.
Physical examination in the cat of the present report indicated an inability to extend the tarsus (hock joint) normally. Although the neurologic examination revealed impaired hopping responses in the pelvic limbs, conscious proprioception was intact and hopping responses were good when the cat's weight was fully supported, suggesting that proprioceptive awareness was normal and that a spinal cord or sensory abnormality was unlikely. Spinal reflexes were intact, with normal withdrawal reflexes and normal sensation of the digits; any neurologic lesion would therefore have to be restricted to the motor innervation of the hock extensors, the tibial nerve, or the muscles themselves.
Although diabetes mellitus can cause demyelinating neuropathy with weakness preferentially affecting the pelvic limbs, the neurologic findings indicated no clear evidence of weakness, with intact spinal reflexes and normal withdrawal reflexes. Moreover, there was no history suggestive of diabetes mellitus. Sacral segment dysfunction would be expected to impair urinary continence and cause an abnormal perineal reflex and diminished anal tone, which was not present in the case described in the present report. A lesion affecting only the L7 nerve roots or the sciatic nerve was also plausible but would have resulted in diminished withdrawal reflexes. A discrete lesion affecting only the tibial nerves would also be theoretically possible, but such a lesion, causing only restricted motor neuropathy with no sensory abnormalities, would be very unusual. Given the findings of the neurologic examination, the most likely diagnosis was considered to be a musculoskeletal problem affecting the extensors of the hock joint or their tendinous insertions.
The cat was sedated, and the hind limbs were evaluated; flexion of the digits occurred when the hock was flexed (Figure 1), suggesting partial rupture of the calcaneal tendon with preservation of superficial digital flexor tendon. Ultrasonographic examinationa of the calcaneal tendon revealed bilateral disruption of the gastrocnemius muscle and combined tendons of the biceps femoris, gracilis, and semitendinosus muscles; however, the superficial digital flexor tendon remained intact. This confirmed a partial rupture of the calcaneal tendon.
Photograph of the left hind limb (A) and longitudinal ultrasonographic images of the right (B) and left (C) calcaneal tendons of a cat that was evaluated because of sudden-onset, nonprogressive pelvic limb weakness of 1 week's duration. The cat had a bilateral plantigrade stance. The photograph illustrates that hyperflexion of the hock joint results in flexion of the digits, indicative of preservation of the superficial digital flexor tendon. There is a small, focal region of swelling just proximal to the tuber calcaneus, likely the site of the rupture. In the ultrasonographic images of the right and left calcaneal tendons, the proximal part of each limb is to the left of the images. The superficial flexor tendon is slightly thickened but the fiber pattern remains intact (asterisk). In contrast, the deeper structures of the calcaneal tendon are poorly delineated, are hypoechoic, and lack a normal fiber pattern (arrow). CT = Tuber calcaneus.
Citation: Journal of the American Veterinary Medical Association 246, 1; 10.2460/javma.246.1.59
Comments
Common calcaneal tendon injury is rare in cats. The tendon comprises 3 components: the tendon of the gastrocnemius muscle; the combined tendons of the biceps femoris, semitendinosus, and gracilis muscles; and the tendon of the superficial digital flexor muscle.1 All components contribute to extension of the hock joint, and damage to any or all of these structures will result in hyperflexion of the hock joint with a plantigrade stance.
Rupture of the calcaneal tendon can be partial or complete, depending on the tendons involved. The former typically involves rupture of the gastrocnemius muscle tendon alone, resulting in partial hyperflexion of the hock joint with preserved function of the superficial digital flexor muscle that prevents complete collapse of the hock joint and preserves digital flexion. This can be identified clinically as flexion of the digits during weight bearing or during passive hyperflexion of the hock joint; the absence of gastrocnemius muscle tendon support for the hock joint permits hyperflexion, which stretches the superficial digital flexor tendon and passively flexes the digits (Figure 1). In complete rupture, tendinous support for the tarsus is obliterated and the tarsus is hyperflexed during weight bearing.
In dogs and cats, unilateral injury to the calcaneal tendon is often traumatic in origin, although predisposing factors are known.2–5 Bilateral rupture occasionally occurs in dogs, particularly in middle-aged, active, large breeds,2,3,5 but is very rare in cats, with 2 cases reported3,6 in the veterinary medical literature.
The cat of the present report was referred for suspected neurologic dysfunction. Neurologic examination findings were fairly normal, which suggested that a musculoskeletal condition—however unusual—was the more likely diagnosis. Many of the differential diagnoses were ruled out on the basis of the results of physical examination and simple laboratory tests, and a definitive diagnosis was achieved by means of ultrasonographic examination of the hind limbs.
Surgical correction is the treatment of choice in cases of complete calcanean tendon disruption. In cats and dogs with partial rupture, surgery is also preferred over conservative management because more predictable results are attained and the likelihood of return to normal function is greater.2,4,7 The aim of surgery is to provide close apposition of the damaged ends of the calcanean tendon, or between the tendon and calcaneus, thereby preventing or minimizing development of disorganized fibrosis and delayed healing. The prognosis for return to normal function following surgical repair of unilateral common calcaneal tendon rupture, whether partial or complete, in cats is good and owner-perceived long-term success of surgery is reportedly excellent.3,7
In the cat of this report, the owners declined surgery. Physiotherapy was used to improve strength in the intact flexor muscles but was not well tolerated by the cat. Follow-up examination performed 2 months after diagnosis revealed that the cat was able to ambulate without support and to climb onto furniture and over low fences, although its stance remained partially plantigrade.
Esaote Mylab Twice system with a 6- to 18-MHz transducer, Cambridge, England.
References
1. Hermanson JW. The muscular system. In: Evans HE, de Lahunta A, eds. Miller's anatomy of the dog. 4th ed. St Louis: Elsevier Saunders, 2013; 259–260.
2. Corr SA, Draffan D, Kulendra E. Retrospective study of Achilles mechanism disruption in 45 dogs. Vet Rec 2010; 167: 407–411.
3. Cervi M, Brebner N, Liptak J. Short- and long-term outcomes of primary Achilles tendon repair in cats: 21 cases. Vet Comp Orthop Traumatol 2010; 23: 348–353.
4. Harasen G. Ruptures of the common calcaneal tendon. Can Vet J 2006; 47: 1219–1220.
5. Lamb CR, Duvernois A. Ultrasonographic anatomy of the normal canine calcaneal tendon. Vet Radiol Ultrasound 2005; 46: 326–330.
6. Mughannam A, Reinke JR. Avulsion of the gastrocnemius tendon in three cats. J Am Anim Hosp Assoc 1994; 30: 550–556.
7. Schulz K. Management of muscle and tendon injury or disease. In: Fossum TW, ed. Small animal surgery. 3rd ed. St Louis: Mosby Elsevier, 2007; 1316–1324.
