Large Animal Neurology - Joe Mayhew

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The sensory fibers are contained within the perineal branches of the pudendal nerve from S1–S3. Contraction of the anal sphincter is mediated by the caudal rectal branch of the pudendal nerve, and tail flexion is mediated by the sacral and caudal segments and nerves, S1–Ca. Light tactile rubbing of the anus will usually result in reflex tail extension that in adult cows at least can herald the onset of a micturition reflex. An animal with a flaccid tail and anus due to a final motor neuron lesion will not have an anal or tail reflex. However, it may still have normal sensation from the anus and tail provided that the sensory nerves and spinal cord and brainstem white matter nociceptive pathways are intact. Thus, as with all other reflex testing, the sensory perception of the stimulus must be evaluated separately from segmental reflex action.

      The spinal cord ends at the level of the first or second sacral vertebra in large animals. Therefore, focal lesions of the last lumbar and of the sacral and caudal vertebrae may involve components of the cauda equina, hence the afferent and efferent spinal nerve roots from many sacrocaudal spinal cord segments. Depending on the level, this causes varying degrees of hypalgesia, hyporeflexia, hypotonia, and ultimately muscle atrophy of the tail, anus, perineum, hips, and caudal thighs. A rectal examination may detect a space‐occupying lesion or fracture or luxation of the lumbar, sacral, or caudal vertebrae. In addition, assessment should be made of urinary bladder volume and the tone of the bladder and rectal walls. Adult animals, especially male horses, that are recumbent for any reason, often do not urinate. Thus, they usually have a distended bladder that eventually results in urine dribbling. Manipulating such an animal to help it stand, or violent attempts by the animal itself to stand, can result in rupture of a bladder wall that is already weakened by pressure necrosis.

      Paraplegic large patients frequently contuse the perineum and tail while dog‐sitting and while attempting to stand. Also, tail ropes and various forms of sling support frequently damage these areas. An assessment of the neurologic function must be made as soon as possible because perineal and tail contusion results in edema, quickly followed by hypotonia, hyporeflexia, and hypalgesia.

      By this stage of the examination, the clinician should have a clear idea of the presence and location of lesions in the brain, spinal cord, and the peripheral nerves and muscles of the thoracic and pelvic limbs. The more peripheral the lesion, the better defined the sensory and motor deficits. Syndromes resulting from lesions involving specific limb peripheral nerves involve characteristic abnormalities of gait, paralysis of specific muscles with resulting muscle atrophy, specific reflex loss, and sensory deficits that are discussed further below.

      For an accurate interpretation of signs of peripheral nerve disease, some consideration must be given to the neuropathological classification of damage to peripheral nerves that can result in degrees of loss of function termed neurapraxia, axonotmesis, and neurotmesis.

      With loss of somatic efferent motor innervation due to axonal or whole nerve fiber damage, there is muscle atrophy, which occurs relatively rapidly although in large patients it may take up to 2 weeks to become clinically prominent. Electromyographic changes indicating denervation of muscle may take even longer and may take 3–4 weeks to become prominent in the horse. Surprisingly, disuse atrophy appears to occur quite rapidly in the (fit) horse and therefore distinguishing neurogenic atrophy from disuse atrophy clinically can be blurred. A good example of the significance of this would be an unusual asymmetric hindlimb gait abnormality in a horse with accompanying gluteal muscle asymmetry. Unless marked, such asymmetric muscle atrophy should be taken as evidence for disuse due to lameness until proven otherwise.

      Clinico‐pathologic categories of peripheral nerve damage.

       Neurapraxia is temporary loss of function with no morphological changes.

       Axonotmesis is damage to axons with preservation of myelin sheaths resulting in prolonged loss of function until axonal regrowth re‐establishes innervation of the target organ (muscle).

       Neurotmesis is severance of axons and their myelin sheaths with prolonged to permanent loss of function, sometimes with partial reinnervation depending on both the distance between the proximal and distal nerve stumps and between the lesion and the muscle.

      From a practical point of view, peripheral nerves are very difficult to injure directly or to stretch unless they are fixed in situ, or they overlie a bony structure such as the case for portions of the facial and suprascapular nerves, or there is a sharp penetrating injury.

      Presumed peripheral nerve irritation and vascular compromise can result in unusual syndromes in horses. Perhaps the best example of these is the abrupt onset of distress involving one limb when the horse will kick out and repeatedly stomp the foot on the ground. This is occasionally seen following an intramuscular injection, presumed to have been deposited adjacent to a peripheral sensory or mixed nerve. The other example would be the similar syndrome that can appear upon recovery from general anesthesia wherein there is no overt evidence of a myopathy or a motor neuropathy, the most likely explanation being the onset of paresthesia or, as it is referred to in humans, pins and needles. Such unusual syndromes can occur spontaneously in horses, sometimes with no associated or predisposing incident and sometimes are associated with exertion. Most often these signs dissipate rapidly, with occasional notable and enigmatic exceptions.

      Except for those affecting the cauda equina, peripheral spinal nerve lesions most often result in a gait abnormality involving only one limb. Classically, the further the lesion is away from the central nervous system, the more selective are any motor and sensory deficits. This is less true in the horse compared to small animals for several reasons, perhaps because of peripheral nerve anastomoses and second because incomplete peripheral neuropathies frequently occur.

      The gait abnormalities present after several days following onset of selective median or ulnar neuropathies are minimal. The same can be said of distal tibial and peroneal nerve lesions although sometimes there will be a change in stride with occasional stumbling associated with hock and fetlock flexion with the former and with hock extension with the latter.

      The radial nerve is probably rarely damaged alone due to its protected course. However, the commonly recognized signs of typical proximal radial nerve paralysis, including a lack of carpal and fetlock extension and an inability to bear weight on the limb with a dropped elbow, usually result from partial brachial plexus involvement. Theoretically, this syndrome should be distinguishable from myopathy involving the triceps or the extensor carpi radialis muscles, elbow joint lameness, humeral fracture, and bicipital bursitis. However, in practice, such distinction can be difficult to achieve without a thorough evaluation usually requiring ancillary aids, including ultrasonography, radiography, synovial fluid analysis, and electromyography. Because partial brachial plexus lesions are quite common following proximal thoracic limb impact injury, this problem should be considered foremost when an inability to bear weight on an otherwise pain‐free thoracic limb is being evaluated.

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