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Localizing findings in spinal cord disease Neck and forelimbs

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If a gait alteration was detected in the thoracic limbs and there were no signs of brain involvement, then this part of the examination can confirm involvement of the C1–T2 spinal cord or thoracic limb peripheral nerves or muscles; it should also help localize the lesion within these regions.

Results of the thoracolaryngeal adductor response or the slap test can be a useful part of the complete neurologic evaluation of horses suspected to be suffering from lesions of the vagal or recurrent laryngeal nerves, caudal medulla oblongata, or cervical and cranial thoracic spinal cord. As most emphasis is placed on its utility in diagnosing cervical spinal cord disease in wobbler horses, some aspects of testing will be reiterated here. The test can be performed in cooperative horses by palpating the dorsal and lateral laryngeal musculature while simultaneously slapping the contralateral dorsolateral thoracic region from the cranial withers to near the last rib, while the horse is exhaling. If there is difficulty in interpretation of this test, observing the larynx via an endoscope while performing the test may be necessary. It should be emphasized that the thoracolaryngeal response is not consistently absent in horses with cervical spinal cord disease or caudal brainstem disease and can be absent in horses with no evidence of CNS disease.27,28 However, a reduced or absent slap reflex on the left side of the larynx must be taken as strong evidence for the presence of idiopathic recurrent laryngeal neuropathy or prior laryngeal surgery, although exercise and endoscopic examination of the horse will be necessary to confirm any clinical problem of reduced laryngeal function and of roaring. Bilateral absence of the response without other signs of severe laryngeal or cervicomedullary disease must be interpreted cautiously, particularly in an excitable horse. A normal response on the left side of the larynx and absent response on the right side will indicate a neurologic disease, most likely right‐sided brainstem or spinal cord C1 to cranial‐thoracic, other than classical idiopathic recurrent laryngeal neuropathy. Thus to repeat, the only useful result from the right to left test is a positive test, whereas both unequivocal positive and negative test results from left to right have utility.

The commonest cause of acute, acquired, severe bilateral laryngeal paralysis is hepatoencephalopathy.

Observation and palpation of the neck and forelimbs will detect gross skeletal defects, asymmetry in the neck and muscle atrophy. These signs may be associated with neurologic disease and thus be localizing findings. The neck should be manipulated to assess a normal range of movement. Interpretation of what appears to be reluctance to move the neck passively or actively in any direction as indicating neck pain is fraught with difficulties. On the other hand, if a horse will not lower or bend its head to eat, drink, or reach for a treat, or the head and neck gets “locked” in an abnormal position/posture, this usually indicates a mechanical or painful disruption to movement of the cervical vertebrae, particularly involving intervertebral disk damage in the caudal neck and cranial thoracic region.29 Cervical vertebral arthrosis, involvement of cervical nerve roots, and marked cervical spinal cord disease can cause scoliosis and even torticollis.

Importantly, as musculoskeletal diseases are far more common than neurologic disease and as disuse atrophy can occur within at least weeks of the onset of lameness, muscle atrophy, especially common over the scapula, should be taken as evidence of an underlying lameness until there is additional evidence that it is neurologic in origin.

Clearly delineated regions of cervical and thoracic sweating can be useful indicators of localized spinal cord or peripheral nerve disease in that they can represent sympathetic denervation or decentralization of the vasculature in the skin, resulting in increased circulating adrenalin stimulating sweat glands to secrete. Care must be taken in interpreting patchy sweating that is not well delineated. Very asymmetric patchy sweating can occur in horses that are excited or distressed, particularly when in a draughty area, without a specific sympathetic lesion being present. Involvement of the peripheral pre‐ and postganglionic sympathetic neurons in the horse results in localized sweating; this can be an extremely helpful localizing sign. Horner syndrome will result if the cervical sympathetic trunk is damaged. In the horse, dermatomal patterns of sweating on the neck and cranial shoulder occur with involvement of the C3–C8 branches of the sympathetic fibers. These arise segmentally from the vertebral nerve that follows the vertebral artery up the neck after the vertebral nerve has left the stellate ganglion near the thoracic inlet (see Figure 2.10).

When the skin of the lateral neck of a horse just above the jugular groove from the level of the atlas to the shoulder is prodded firmly with a blunt probe, the cutaneous coli muscle contracts, which causes skin flicking. With stronger stimuli, the sternocephalicus and brachiocephalicus muscles often contract, causing the shoulder to be pulled cranially and even the head to be flexed laterally. This response tends to be less obvious in other species. In horses, there is also flicking of the ear rostrally, blinking of the eyelids, and lip retraction when the test is performed. Originally introduced by Rooney,30 these are termed the local cervical and cervicofacial responses, respectively. The precise anatomic pathways are not entirely clear, although they must involve several cervical segments and the facial nucleus in the medulla. At least in the cranial cervical region, even the local cervical reflex may well be a cervical/trigeminal–facial reflex associated with the anastomoses between the cervical branch of the facial nerve with cutaneous branches of the C2–C6 segmental nerves.31 Cervical lesions that involve gray and white matter can cause depressed or absent cervical responses; however interpretation of abnormal responses may need to be expressed as imprecisely as for example “consistent with a right‐side caudal cervical lesion” or “consistent with a cranial cervical lesion.” In contrast, the segmental absence of the cutaneous trunci reflex can be very useful in delineating the precise cranial extent of a thoracic spinal cord lesion particularly when such a lesion is asymmetrical.

Sensory perception from the neck and forelimbs must be assessed. This can be difficult to evaluate accurately in stoic and in excited animals. Perception of a noxious stimulus is noted by observing the animal’s behavioral response while observing the local cervical responses and continuing the skin prodding over the shoulders and down the limbs to include testing the autonomous zones for the thoracic limbs (Figure 2.15). As with any cutaneous sensory test, a two‐step technique is recommended.32 This is accomplished by initially tenting and grasping a fold of skin between the jaws of heavy duty hemostats or needle holders. After pausing to allow the patient to settle, a second, sharp skin pinch is applied to determine superficial sensation. There may be reflex withdrawal of the part, with or without a cerebral response such as vocalization or moving the whole body away from the stimulus; the latter events being taken as representing the conscious perception of the noxious stimulus.


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.

Large Animal Neurology

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