Page 285 - Canine Lameness
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16.3  ­Neurorogico  giNciNi  AANicgio ctNe trucigi  gim  257

             a pre- or post-fixed plexus, respectively. Nevertheless, two or three spinal nerve branches combine
             to form the major named nerves of the brachial plexus, specifically the suprascapular, subscapular,
             axillary, musculocutaneous, radial, median, ulnar, and lateral thoracic nerves. Table 16.2 provides
             a summary of each nerve and the spinal cord segments from which they arise. Wide variations
             exist among individuals but as a general guideline, nerves exiting cranially in a plexus will inner-
             vate more cranial and proximal muscle groups of the limb, while more caudally exiting nerves will
             innervate caudal and distal muscle groups of the limb.
               The flexors of the shoulder joint (infraspinatus, teres major, deltoideus, and teres minor) are
             innervated by the suprascapular and axillary nerves with small contributions from the radial nerve
             (Hermanson 2013). Elbow flexion is facilitated through activation of the biceps brachii and bra-
             chialis muscles innervated by the musculocutaneous nerve. Lastly, carpal and digit flexion are
             mediated by median and ulnar nerve innervation to the palmar antebrachial muscles (flexor carpi
             radialis and flexor carpi ulnaris muscles, and superficial digital flexor and interosseous muscles).
               Muscles and their respective nerves responsible for extension of the thoracic limb include the
             shoulder extensors (supraspinatus, biceps brachii, and coracobrachialis) supplied by suprascapu-
             lar, axillary, and musculocutaneous nerves; the elbow extensors in the caudal brachial muscle
             group (triceps brachii, anconeus, tensor fasciae antebrachia, and extensor carpi radialis) all inner-
             vated by the radial nerve; and the carpal and digital extensors belonging to the craniolateral ante-
             brachial muscles (extensor carpi radialis, ulnaris lateralis, common digital extensor, lateral digital
             extensor,  extensor  digiti,  and  pollicis  longus)  supplied  by  the  radial  nerve  (Hermanson  2013).
             Compromise to these muscles and/or nerves, particularly the radial nerve responsible for elbow
             extension, will affect the weight-bearing abilities of the limb. Injury to the other nerves may cause
             gait abnormalities but the animal will be able to support its own weight.



             16.3   Neurological Diseases Affecting the Thoracic Limb


             Signalment and clinical progression are key factors in considering likely causes of monoparesis or
             lameness affecting the thoracic limb. Commonly encountered conditions include Type I interver-
             tebral disc (IVD) extrusion, neoplasia, fibrocartilaginous embolism (FCE), myelitis/meningomy-
             elitis, and brachial plexus injury (Table 16.1).



             16.3.1  Myelopathies and Radiculopathies
             Unilateral injury or damage to the C6–T2 spinal cord segments forming the cervical intumescence
             (i.e. a myelopathy) or to the associated nerve roots (i.e. a radiculopathy) can cause gait abnormali-
             ties that are either restricted to only one thoracic limb, such as a lameness or monoparesis, or that
             are more pronounced in both thoracic limbs (e.g. short-strided gait).
               Damage to the motor neuron cell bodies in the ventral gray matter of the cervical intumescence
             causes a lower motor neuron (LMN) paresis in the thoracic limbs characterized by a stiff, short-
             strided gait with symmetric lesions, or a monoparesis if the lesion is unilateral. Cervical myelopa-
             thies often also involve the white matter, containing the caudally directed general proprioceptive/
             upper motor neuron (GP/UMN) pathways to the ipsilateral pelvic limb causing a hemiparesis, or
             to both pelvic limbs causing a paraparesis (Figure 4.1); a GP ataxia may also be noted in either
             scenario. Deficits to GP/UMN tracts manifest as a long-strided gait in the pelvic limbs and, when
             present with a short choppy LMN thoracic limb stride, this combination is referred to as a
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