LITMIR.BIZ

Figure 2.15 Autonomous zones are areas of desensitivity that can be detected when individual peripheral spinal nerves to the limbs are not functioning.

      Source: Adapted from Blythe³³; Blythe and Engel³⁴; Blythe and Kitchell³⁵.

      If a large, adult animal has significant gait abnormality and it is feasible to cast it to lateral recumbency, then this should be done to assess the spinal reflexes. If the animal is ambulating well, it may be assumed that the flexor and extensor spinal reflexes are at least intact. These reflexes can be studied in all smaller patients.

When evaluating wobblers with evidence of a neurologic abnormality in both thoracic and pelvic limbs and no evidence of brain disease, one should allow for a lesion to be present anywhere from C₁ through T₂. Conversely, when there is evidence of a mild neurologic gait abnormality in the pelvic limbs but not the thoracic limbs, then the possibility of a lesion anywhere from C₁ through S₂ must be considered. If the signs of pelvic limb ataxia and/or paraparesis in a large adult patient are moderate or even marked, then a lesion can be considered anywhere in these segments. The reason to include lesions sites at C₆–T₂ is because such lesions, when intramedullary, can be very selective and spare white matter tracts and gray matter involving the thoracic limbs resulting in no definitive thoracic limb signs. Such has been the case in adult horses suffering from S. neurona myelitis, fibrocartilagenous thromboembolism, granulomatous meningoencephalomyelitis, and migrating helminth parasites affecting C₆–T₂ spinal segments.

       Trunk and hindlimbs

If the examination of the head, gait and posture, and neck and thoracic limbs reveals evidence of a nervous system lesion(s), then an attempt should be made to associate such lesions with any further signs found during examination of the trunk and hindlimbs. If there are only signs in the trunk and hindlimbs (Figure 2.16), then the lesion(s) must be between C₁ and S₂, but most probably between T₃ and S₂, or in the trunk and pelvic limb nerves or muscles. This part of the examination helps localize such lesions more precisely. However, the examiner must remember that with a subtle grade neurologic gait abnormality in the pelvic limbs, the lesion may be anywhere between the rostral brainstem and the mid‐sacral spinal cord.

Figure 2.16 This Holstein calf (A) suffered from vertebral trauma during an assisted delivery that resulted in paraplegia due to an epiphyseal separation at caudal L4 vertebra. With nursing care, the calf recovered quite well to be able to stand and walk but with a tendency to knuckle over on its fetlocks as shown. The residual gross lesion shown below (B), particularly the focal necrosis of dorsal gray and white matter at L_4‐5, explains the clinical syndrome that related mostly to bilateral deficits of the sciatic/peroneal nerve distribution with very poor flexor reflexes present in the pelvic limbs.

The trunk and hindlimbs must be observed and palpated for malformation and asymmetry (Figure 2.17). Lesions affecting thoracolumbar gray matter cause muscle atrophy, which is a helpful localizing finding. With asymmetric myelopathies, scoliosis of the thoracolumbar vertebral column often occurs, initially with the concave side opposite the lesion, but changing with subsequent fibrous contracture setting in. Once again, evidence of muscle atrophy, especially common over the gluteal region (Figure 2.18), should be taken as evidence of an underlying lameness until there is additional evidence that it is neurogenic.

Figure 2.17 Very occasionally, portions of muscles, whole muscles, or muscle groups are found to be absent and often there are no definitive neurologic signs present. Such was the case with this horse in which a large portion of the left medial thigh muscles, at least including the medial quadriceps group, was missing with no evidence of weakness or ataxia in either hind limb. Whether individual cases are congenital or acquired (from say S. neurona) is usually very difficult to determine when present for such a long time.

Figure 2.18 Proximal limb atrophy more often is due to disuse mostly because of orthopedic disease. However, selective middle gluteal muscle atrophy in the absence of lameness and the absence of atrophy of other proximal limb musculature as seen on the left side in this horse is likely to be due to final motor neuron disease such as that caused by S. neurona myelitis at L₆ as was the case here.

      Sweating in the horse over the trunk and hindlimbs, excluding the neck and face, can be a helpful localizing sign. Ipsilateral sweating caudal to the lesion signals involvement of the descending sympathetic tracts in the spinal cord caudal to T₃. Lesions involving specific pre‐ or postganglionic peripheral sympathetic fibers that are second‐ and third‐order neurons cause saddles or patches of sweating at the level of the lesion.

Firm prodding of the skin over the trunk, particularly the mid‐lateral aspects of the thoracic wall, causes a contraction of the cutaneous trunci muscle, seen as a flicking of the skin over the trunk—the cutaneous trunci reflex. The sensory stimulus travels to the spinal cord in thoracolumbar dorsal spinal nerve roots at the level of the site of stimulation. Transmission is then cranial in the spinal cord to C₈–T₁, where the final motor neuron cell bodies of the lateral

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