Large Animal Neurology. Joe Mayhew

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СКАЧАТЬ target="_blank" rel="nofollow" href="#ulink_1504f124-7879-580e-a88b-68cd83a90534">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 thoracic nerve are stimulated resulting in contraction of the cutaneous trunci muscle. Lesions anywhere along this pathway may cause suppression of the response, which is easiest to detect with an asymmetric lesion. In addition to this, an assessment of sensory perception from the trunk and hindlimbs (Figure 2.19) must be made. This appears as a cerebral, behavioral response to a two‐pinch stimulus described above, which includes the assessment of the autonomous zones for the pelvic limbs (Figure 2.15). Degrees of hypalgesia have been detected caudal to the sites of thoracolumbar spinal cord lesions, but only when they are severe.

      The cutaneous trunci reflex should not be referred to as the panniculus reflex as panniculus refers to the subcuticular fat depots over the abdomen.

Stroking firmly with a blunt probe or pinching and pressing down firmly with the fingers over the thoracolumbar paravertebral muscles causes a normal animal to extend into a slightly lordotic stance and fix the thoracolumbar vertebral column. The patient also resists the ventral motion and usually does not flex the thoracic or pelvic limbs. Continuing this stimulus to the dorsal sacral region and caudally along the rump results in a degree of vertebral flexion and a kyphotic stance. A weak animal usually is not able to resist the pressure by fixing the vertebral column, and thus it overextends or overflexes the back and begins to buckle in the pelvic limbs. The onset of buckling can be viewed as the patella pops out of its “stayed” position during these maneuvers. With additional proprioceptive lesions, the patient can sometimes react to this test by sinking but with irregular swaying movements of the pelvic region on sinking and on recovery – truncal ataxia. Prominent back pain can result in poor responses and evidence of pain perception by, say, a grunt from the patient. With lumbosacral and sacroiliac orthopedic lesions, such responses may be more localized to be most evident with downward pressure on each tuber sacrale in turn.

      Lordosis refers to extension, and kyphosis refers to flexion, of the vertebral column. There is no such thing as dorsiflexion.

Figure 2.19 This foal developed sciatic paralysis after being treated for Klebsiella sp. sepsis. This resulted from the development of severe empyema over the caudal hip, entrapping the sciatic nerve onto the pelvis. The knuckled fetlock while standing (A) and walking suggests peroneal branch involvement, and the analgesia from the caudal cannon region (B) is consistent with tibial nerve involvement.

       Recumbent patient

Every effort should be made to help a recumbent patient stand and walk unless there is suspicion of bone fracture. By so doing, one can learn as much or more about voluntary effort and lesion localization than one can from reflex testing (Figure 2.20). Heavy animals should be moved early in the course of recumbency to avoid secondary problems such as decubital sores, decreased blood supply to limbs and dehydration, which makes evaluation difficult.

      A patient that has recently become recumbent but uses the thoracic limbs well to get up likely has a lesion caudal to C₆, most often caudal to T₂. If such an animal cannot attain a dog‐sitting posture, the lesion is likely to be in the cervical spinal cord (Figures 2.13 and 2.20). If only the head, but not the neck, can be raised off the ground, there is probably a severe cranial cervical lesion. With a severe caudal cervical lesion, the head and neck usually can be raised off the ground, although thoracic limb effort decreases, and the animal usually is unable to maintain sternal recumbency. Assessments of limb function cannot be relied on while a heavy animal is lying on the limb being tested. Muscular tone can be determined by manipulating each limb. A flaccid limb, with no motor activity, is typical of a final motor neuron lesion to that limb, but in heavy recumbent animals there can be poor tone and little observable voluntary effort in a limb that has suffered pressure damage from been lain upon. A severe central motor pathway lesion to the thoracic limbs at C₁–C₆ causes poor or absent voluntary effort, but there will be normal or sometimes increased muscle tone in the limbs. This is because there is a release of the final motor neuron that is reflexly maintaining normal muscle tone under the calming influences of the descending central motor pathways. Interestingly, such a spastic (hypertonic) paralysis only in the pelvic limbs can also be seen with lesions between C₆ and T₂ if little or no thoracic limb gray matter is affected. A Schiff–Sherrington phenomenon of short duration (hours to a few days), with excessive extensor tone in the thoracic limbs in the presence of good voluntary activity and normal reflexes, has been seen rarely in horses and usually follows a cranial thoracic vertebral fracture.³⁶

Finally, spinal reflexes are tested in the thoracic limbs. The flexor reflex in the thoracic limb involves stimulation of the skin of the distal limb with needle holders and observing for flexion of the fetlock, knee, elbow, and shoulder (Figure 2.21). This reflex arc involves sensory fibers in the median and ulnar nerves, spinal cord segments C₆ to T₂, and motor fibers in the axillary, musculocutaneous, median, and ulnar nerves. Lesions cranial to C₆ may release this reflex from the calming effect of the central motor pathways and cause an exaggerated reflex with rapid flexion of the limb. The limb may remain flexed for some time and even show repetitive movements or clonus. Such lesions may also result in a crossed extensor reflex, with synchronous extension of the untested limb. This usually occurs only with severe and chronic central motor pathway lesions. Thus, an animal affected by such a lesion may demonstrate considerable reflex movement following stimuli, but usually will have little coordinated voluntary motor activity in the limbs being tested. A spinal reflex can be intact without the animal perceiving the stimulus, and the latter must be observed independent of the local reflex movement. Cerebral responses associated with the perception of the skin pinch include changes in facial expression, head movement, and phonation. Conscious perception of the stimulus will be intact only if the afferent fibers in the median and ulnar nerves, the dorsal gray columns at C₆–T₂, and the central sensory pathways in the cervical spinal cord and brainstem are intact.

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