In the pelvic limb, the clinically important nerves are the femoral and sciatic nerves.1 The L6, L7, and S1 spinal cord segments; spinal nerves; and lumbosacral plexus give rise to the lumbosacral trunk, which is continued caudally through the pelvis as the sciatic nerve. The sciatic nerve divides into the tibial and common fibular nerves.1 Disease affecting the common fibular nerve results in an inability to flex the tarsus, assessed via the withdrawal reflex, and atrophy of the craniolateral crural muscles.1 Disease affecting the tibial nerve results in a plantigrade stance and atrophy of the caudal crural muscles.1
In the present case, a presumptive diagnosis of NSN was made on the basis of MRI findings. Nerve sheath neoplasms typically occur in older dogs and more commonly affect the brachial plexus or thoracic limb nerves than the lumbosacral plexus or pelvic limb nerves.2,3 Signs reflect chronic, progressive lameness in a single limb that progresses to varying degrees of paresis or paralysis, postural reaction deficits, decreased reflexes, decreased muscle tone, and atrophy. Nerve sheath neoplasms are often painful. With NSN involving the brachial plexus, a palpable mass may be appreciated.2 Presumptive diagnosis is made on the basis of MRI. Definitive diagnosis requires histopathology. Definitive treatment involves surgical resection combined with limb amputation. Depending on the proximal extent of the neoplasm, laminectomy and rhizotomy may be warranted. Radiation alone or following surgical excision may also be utilized. Survival times with surgery alone or combined with radiation therapy vary.2,3 Proximal involvement results in shorter survival times (median, 7.5 months) as compared with involvement distally in the plexus (median, 12 months).2 More recently, a median survival time of approximately 19 months was observed with surgery alone or combined with radiation therapy regardless of the tumor location.3 Radiation alone may provide a median survival time of approximately 12 months.4
In the present case, dysfunction of the main branches of the sciatic nerve and common fibular and tibial nerves was recognized by an inability to flex the tarsus and a plantigrade posture, respectively.1 Exaggerated flexion of the hip during the swing phase likely represented a compensatory means of advancing the limb.1 Hip flexion was preserved by the actions of the rectus femoris (quadriceps muscle innervated by L4-L6 spinal cord segments and femoral nerve) and the iliopsoas muscles (innervated by multiple lumbar spinal nerves).5
An unusual feature of the dog’s gait was the external rotation of the hip during the stance phase of the gait. Antagonism between the muscles that provide for internal and external hip rotation maintains normal hip orientation. Internal rotation of the hip occurs via the lateral pelvic muscles (gluteal muscles and piriformis muscle), which are innervated by the cranial and caudal gluteal nerves, which branch from the lumbosacral trunk prior to becoming the sciatic nerve.5 External rotation of the hip occurs via the medial pelvic muscles (obturator internus, obturator externus, quadratus femoris, and gemelli muscles) and the iliopsoas muscle.5 The psoas major originates along the transverse processes and bodies of the lumbar vertebrae and combines with the iliacus muscle to insert on the lesser trochanter (caudal medial aspect of the femur).5 Consequently, the iliopsoas muscle contraction flexes and externally rotates the hip. We postulate that the exaggerated flexion of the hip involves the action of the iliopsoas muscle, which concurrently externally rotates the hip. The external hip rotation is normally opposed by the gluteal muscles; however, the gluteal muscles were denervated and therefore unable to counteract external rotation. Denervation was supported by gluteal muscle atrophy and the location of the lesion involving the lumbosacral trunk.
