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of the pelvis, trunk, neck, and sometimes the whole body. These may also appear as a weaving of the affected limb during the swing phase. Such abnormalities can be well evident while an assistant maneuvers the patient and also while the horse is walked with the head elevated and the examiner is pulling on the tail. The examiner should also walk backward on a serpentine course with the patient’s head raised while watching the pattern of stride and placement of limbs. The aim of these maneuvers is to change the direction of limb flight during mid‐stride to promote errors due to proprioceptive abnormalities. Any irregular, abnormal foot placement in abducted or adducted positions, irregular crossing of the limbs, and intermittent stepping on the opposite foot especially while the animal is circling or turning tightly all can be seen as possible evidence for ataxia. Any animal that is substantially ataxic for any reason tends to pace when walking with both feet on the same side off the ground at the same time. Circumduction of the outside limbs when turning and circling is also considered a proprioceptive abnormality. Walking an animal up and down a slope with the head elevated often exaggerates ataxia, particularly in the pelvic limbs. This maneuver also frequently allows the expression of a hypermetric or a hypometric component of ataxia in the thoracic limbs. When a weak and ataxic animal is turned sharply in circles, it leaves the affected limb in one place while pivoting around it, particularly so for the pelvic limb. This may also occur when backing up.

      Ataxia can also be classified into three syndromes by the quality of the signs seen and the system or pathway involved in the nervous system. These are subconscious proprioceptive or spinal ataxia, cerebellar ataxia, and vestibular ataxia; and after observing characteristics of a gait abnormality in a patient, it is reasonable to attempt to define which of one or more of these syndromes are present.

      Subconscious proprioceptive (spinal) ataxia results from involvement of afferent proprioceptive pathways in sensory nerves and more commonly in spinal cord and brainstem tracts. These proprioceptive deficits are caused by lesions affecting the general proprioception pathways relaying information on limb and body position to the cerebellum for subconscious proprioception. In contrast, general proprioceptive conscious pathways pass to the thalamus and cerebral cortex for conscious proprioception and are more involved in position sense at rest, i.e., posture. With subconscious proprioceptive ataxia, the gait is irregularly irregular and prominently unpredictable. There is a delay in onset and a swaying or floating swing phase and subsequent variable foot placement exaggerated by maneuvering the patient. This movement and placement may include adduction and abduction. Hyperflexion in hindlimbs and hypoflexion or hypometria in forelimbs are common. Subconscious proprioceptive deficits likely contribute to scuffing toes and stumbling, especially on thoracic limbs. Obviously, some of these signs are also associated with motor pathway weakness, but because general proprioception and central motor tracts are adjacent in large parts of the central and peripheral nervous system, and involved in disease processes together, it usually is not necessary to distinguish which gait characteristics is due to dysfunction of one or the other.

Cerebellar ataxia can have characteristics of spinal ataxia, but changes in limb placement and movement tend to be more abrupt in onset and to be excessive; the best definition of cerebellar ataxia being alterations in the rate, range, and force of movement.¹⁵ Thus, jerky onsets of movement and hypermetria are often seen, becoming more pronounced with more complex maneuvers such as hurriedly regaining an upright posture from recumbency, abruptly turning to flee from being frightened, or changing direction while running. There is no central motor pathway or final motor neuron paresis accompanying cerebellar disease, but other signs of cerebellar involvement including head tremor and defective menace responses are often present. Less commonly, signs of vestibular involvement can also be present with pan‐cerebellar disease.

      Concerning vestibular ataxia, although the limb movement and foot placement accompanying mild to moderate vestibular disease are irregular, and therefore can be called ataxic, they are somewhat less unpredictable. For example, if thoracic limb movement is forced to change in direction while the patient is lead with its head raised, the resulting correction will be predictably abducted. Also, on turning a patient with mild vestibular disease, the wide movement and placement of an outside hindlimb will not usually be accompanied by hypermetria, and any hurried movements to maintain a balanced posture will be strong and multiple, thus again being somewhat predictable.

      Normal animals react in different ways to blindfolding, from extremes of excitement or distress to acting imobile. Subsequent movements they make while blindfolded then often depend on this variable behavioral response. Vestibular ataxia and loss of balance will often be markedly exacerbated when a blindfold is applied to a patient suffering from vestibular, diffuse spinocerebellar, or cranial cervical spinal cord disease. On the other hand, blindfolding a horse suspected of suffering from typical mid to caudal cervical spinal cord compression usually does not add anything substantial to the neurologic evaluation. Damage to the sensory, C_1–3 dorsal nerve roots can produce vestibular ataxia, and this may be expected to exacerbate with blindfolding the horse.²⁴

Regarding the assessment of posture and postural abnormalities, flexing the foot to attempt to make the animal stand on the dorsum of the pastern and determine how long the animal leaves the foot in this state before returning it to a normal position is said to be a test for conscious proprioception in dogs and cats. Almost certainly, this involves somatic afferent (tactile) pathways as well, and a very weak patient may not be able to move the foot from many abnormal positions. This test can be attempted in large animals, but in our hands has not been helpful in adding accurate information to lesion location. Inactive and somnolent patients, especially calves, often allow the foot to rest on the dorsum for prolonged periods. Horses need to have almost total paralysis of the limb or to have a nociceptive sensory deficit in the limb before they allow such postural anomalies to be maintained. Other tests, such as manually crossing the limbs or placing one limb on a sack and slowly sliding the sack to the side, have been tried to test conscious proprioception, but again in our hands have proven to be noncontributory to the examination process. Rather than manually placing limbs in abnormal positions, it appears more reliable to maneuver the horse rapidly, say in a circle, and stop the maneuver abruptly (Figure 2.14). This often results in an initial awkward placement of the limbs, and then the examiner can determine how long the horse leaves the limbs in such an abnormal posture to determine the presence or not of conscious proprioceptive deficits. This procedure probably does test for deficiencies in conscious proprioception. Examination of horses walking across kerbs has not proven to be a useful test of proprioceptive dysfunction. Normal horses, particularly if distracted, will often trip and those that are moving cautiously, even if quite weak and ataxic, can often maneuver such obstacles.

Figure 2.14 Stopping a patient abruptly after maneuvering it may result in abnormal limb postures being adopted and maintained. This is evident here in a pony (A) and a young ram (B), both of which have cervical spinal cord compression, and this may be taken as evidence for abnormal conscious proprioceptive input from the limbs to the forebrain. On the other hand, an obtunded patient or one with prominent weakness may not correct such abnormal limb positioning without having any specific conscious proprioceptive pathway lesion.

      Gait alterations can occur in all four limbs with lesions affecting the white matter in the caudal brainstem when head signs such as cranial nerve deficits are used to help define the site of the lesion. Subacute to chronic lesions affecting the forebrain usually cause no substantial change in gait. However, postural reactions, such as hopping, are abnormal and sometimes the gait is slowly initiated on the thoracic limb contralateral to the side of a forebrain lesion.

      In smaller patients, other postural reactions can be performed. These primarily help detect signs of subtle proprioceptive and motor system lesions when the straight‐line gait is normal. Wheelbarrowing the patient to make it walk on just the thoracic limbs, hopping it laterally on each individual thoracic and each individual pelvic

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