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nerve problems are rarely, if ever, encountered alone, and after some initial stumbling any permanent gait abnormality may be difficult to detect.

      Immediately after an episode of shoulder injury, signs of damage to the motor suprascapular nerve often include a degree of lameness, presumably associated with adjacent soft tissue and periosteal damage. Suprascapular muscle atrophy will ensue in a week or two. Shoulder abduction that occurs on weight‐bearing, or so‐called shoulder slip, that is seen with thoracic limb trauma is presumed to be lateral laxity to the shoulder joint. This sign likely results from loss of lateral support of the shoulder, but although it can occur when local anesthetic solution is deposited in the region of the suprascapular nerve it may well not be due to suprascapular nerve paralysis alone.³⁷ Other signs, such as sensory deficits over the caudal neck and shoulder and ensuing muscle atrophy elsewhere in the limb, must make the clinician suspicious of more than suprascapular nerve involvement such as additional damage to neural components from the brachial plexus.

      The femoral nerve is incredibly well protected from external injury although damage to it will ultimately result in quadriceps atrophy. Even with moderate muscle atrophy and posturing with the pelvis flexed and back arched, horses with partial unilateral femoral nerve lesions can have a remarkably normal gait at the gallop although athletic performance probably is curtailed. Femoral nerve lesions must be quite proximal in the limb before medial thigh hypalgesia resulting from saphenous nerve branch involvement can be detected.

      Cauda equina involvement most frequently results from a fractured sacrum or from polyneuritis equi. Such signs may begin acutely or may be delayed following the onset of the disease. A slightly abnormal gait may be detected in the pelvic limbs, but the cause may not be identified until the perineal region is evaluated closely when other signs of cauda equina involvement became apparent.

Other characteristic gait abnormalities do strongly suggest peripheral nerve disease. Stringhalt is one example where there is exaggerated flexion of the limb during protraction with excessive hock flexion and digital extension resulting from inappropriate contraction of the digital extensor muscles or lack of opposition from digital flexor muscles. This syndrome can occur with spinal cord disease but most commonly—in regions where flat weed plants are abundant—due to toxic peripheral axonopathy. A thorough musculoskeletal examination including ultrasound evaluation of the affected limb may reveal abnormalities detected within the lateral digital extensor muscle, tendon or sheath, or in the hock. Any abnormalities detected are often assumed to initiate the abnormal neural reflexes, thus increasing tone in the digital extensor muscles during protraction. Another interesting gait that results from mechanical interference to contraction of caudal thigh muscles, or perhaps sometimes because of reflex hypertonia involving these muscles, is referred to as fibrotic myopathy. In this syndrome, the gait classically results in excessive slapping of the foot to the ground at the end of protraction, thus shortening the stride length. Mild to moderate fibrotic myopathy usually does not appear to interfere with high‐speed performance; however, dressage horses, show horses, and trotters and pacers do show an abnormal gait during their performance.

      Variations in these characteristic gait abnormalities occur. These include repetitive or intermittent mild abduction of the hindlimb during protraction and caudal jerking of the distal hindlimb after the initiation of protraction. It is possible to explain these and other movement disorders by an initiation of abnormal muscle spindle activity, as in Stringhalt, with a result that certain muscles or groups of muscles contract too early or too late, or excessively or poorly, at a particular phase of the stride. Thus, intermittent abduction and caudal jerking in the hindlimb may result from hypertonia and hyperreflexia involving the biceps femoris muscle during the swing phase of the stride.

      Cantering with synchronous movement of the hindlimbs is referred to as bunny hopping and is seen with numerous pelvic limb musculoskeletal, often bilateral, problems. It is rarely the result of acquired neurologic disease but can occur with certain congenital or acquired spinal cord malformations. Overt evidence of peripheral nerve or spinal cord disease, or the identification of bilateral and synchronous hindlimb reflexes determined during recumbency, needs to be present before such neurologic causes for bunny hopping can be confirmed.

      Finally, horses diagnosed with shivers demonstrate a wide variety of signs. These include slightly excessive flexion of the hindlimbs along with thigh muscle and tail trembling at the onset of backing, reluctance to have the hindlimbs picked up with degrees of thigh muscle trembling, inability to back‐up, and spontaneous and induced episodes of muscle trembling with hindlimb and forelimb and neck extension, all of which may wax and wane. Interestingly, an acquired lameness can abruptly exacerbate the syndrome. A few horses demonstrating shivering also suffer from mild spinal cord disease, some from marked lumbar arthropathy, some from destructive lesions of the lumbosacral vertebrae, and others from painful conditions involving the distal hindlimbs. However most do not, and recent evidence points to a degenerative cerebellar nuclear axonal lesion as possibly being related to this enigmatic syndrome.³⁸

Final interpretation: where and what is the lesion?

      Results of the neurologic examination should be documented and not left to memory (Figure 2.1).

      After completion of the neurologic examination, the examiner may be able to decide if and where any possible lesion exists. Sites include the basic areas of the following body components:

      1 Forebrain

      2 Brainstem

      3 Peripheral cranial nerves

      4 Cerebellum

      5 Spinal cord

      6 Peripheral spinal nerves and nerve roots

      7 Neuromuscular junctions

      8 Muscles

      9 Autonomic nervous system

Often the exact location of a lesion or lesions within these divisions will be able to be defined precisely, albeit cautiously (see Figure 2.22). If the location of a lesion is not clear, then it is often worthwhile returning to the patient and performing an even more critical evaluation. Thus, if facial weakness is suspected but not clearly seen, the examiner can return to observe the horse for facial asymmetry while it is standing quietly in its stall without any stimulation. Also, a blindfold may be applied to exaggerate evidence of vestibular disease. Finally, a very fractious or a very excited horse suspected of having a degree of weakness in the limbs may be exercised before a re‐evaluation for evidence of weakness is made.

Figure 2.22 In a case of limb ataxia and weakness and based on absolute, definitive neurologic findings, the thought process at this stage of the workup may be that “All or part of the lesion(s) is between A and D.”

      Any additional information that is not definitive or is ill‐defined can be used to modify the working hypothesis that the lesion is “Probably between B and C.”

      This way, further scrutiny with repeated examinations and ancillary testing can be focused without losing sight of unusual, additional, or partial lesion(s).

      The presence of lameness can undoubtedly interfere with the interpretation of a patient’s gait and posture, and even its behaviour. If this is suspected, then appropriate regional analgesia or the use of short acting synthetic opioid drugs (analgesics) may help to resolve the issue. With more chronic lameness cases, nonsteroidal anti‐inflammatory

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