Page 416 - Canine Lameness

388 21 ­Neurorogico giNciN rAectNe Nolgi gim

21.3.2.4 Femoral Nerve Injury
Femoral nerve injuries are less common than those of the sciatic nerve, largely because of better
protection afforded by the sublumbar and quadriceps musculature. Unilateral lesions restricted to
the ventral gray matter of the L4–L6 segments can result in femoral neuropathy. Injury can be
associated with trauma, iliopsoas myopathies (Stepnik et al. 2006), retroperitoneal abscess, hema-
toma, neoplasia, and positioning in ventral recumbency during surgery (i.e. extreme extension of
the hips).
Clinical features with femoral nerve injury are distinct. They include severe monoparesis, with a
loss of the ability to extend the stifle to allow for weight‐bearing. The limb may be carried or may
collapse when weight is placed on it and the patellar reflex will be reduced or absent. However, the
flexor withdrawal reflex is almost normal, except there may be decreased flexion of the hip. With
complete support, proprioceptive placement will be normal, although the hopping postural reac-
tion will be greatly diminished because the dog will be unable to support weight on the affected
limb. Rapid neurogenic atrophy becomes apparent in the quadriceps muscles and cutaneous sen-
sation may be lost to the medical aspect of the limb and medial digits, regions of sensory innerva-
tion by the saphenous branch of the femoral nerve.
Generally speaking, lesions closer to the muscle innervated carry a more favorable prognosis
than those more proximal. Treatment recommendations and prognosis are as described in
Section 21.3.2.1. If there is no improvement seen in three months, recovery is unlikely; amputation
may need to be considered.

21.3.3 Myopathies and Junctionopathies

Myopathies and junctionopathies can begin as shifting leg lameness or stiff gait, sometimes affect-
ing the pelvic limbs before the thoracic. Idiopathic polymyositis is the most common example;
others include endocrine and infectious myopathies. Junctionopathies refer to conditions altering
the neuromuscular junction, with myasthenia gravis being the most reported and investigated. In
most cases, these conditions are characterized by pain, generalized weakness/paresis, exercise
intolerance, and/or stiff and stilted gait. Clinical signs are typically bilaterally symmetric but can
occasionally demonstrate a shifting or unilateral leg lameness, particularly in the early stages.
Many times, spinal reflexes are normal, discerning these from spinal cord diseases. Distinguishing
features that point towards these PNS disorders rather than orthopedic disease include gait abnor-
malities that worsen with activity, neurogenic muscle atrophy, and elevated muscle enzyme levels,
and electrodiagnostic abnormalities.
Serum muscle enzyme levels, including creatine kinase (CK), lactate dehydrogenase, and aspar-
tate aminotransferase, may be significantly elevated in inflammatory conditions like myositis.
Myoglobinuria may be detected with inflammatory myopathies (e.g. idiopathic polymyositis). In
cases of endocrine myopathies, such as hyperadrenocorticoid (Cushing’s) myopathy, for example,
other supportive evidence is usually seen on serum chemistry analysis (e.g. elevated alkaline phos-
phatase). Total serum protein can be elevated in infectious myositis due to the presence of increased
β‐ and γ‐globulins. Electrodiagnostic tests can be used to confirm that PNS disease is present, but
they will usually not diagnose the specific condition. However, in most cases, muscle and nerve
biopsy samples are required to establish a final diagnosis; these techniques are described in detail
elsewhere (Dickinson and Lecouteur 2002; Lecouteur and Williams 2012). Definitive diagnosis of
myasthenia gravis relies on detecting serum antibodies to the acetylcholine receptors. If signs of
megaesophagus are present, thoracic radiographs are also warranted. Some clinical features aid in
deriving a list of differentials. For example, neurogenic, generalized muscle atrophy is a classic