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performed far too vigorously; it is not a contest between examiner and patient! For this assessment, it is best to apply constant lateral tension to the tail and determine what voluntary pull the patient exerts against that tension while it is weight‐bearing on the nearest limb during the stance phase.

      Interpretation of results of tail pull test

       Abnormal standing test: Suggestive of ipsilateral final motor neuron lesion, L3 to S2 gray matter or nerves.

       Normal standing and abnormal walking tests: Lateralizing only, ipsilateral brainstem to S2 central motor and/or general proprioceptive pathways.

      The tail and halter pull test is performed by pulling on a lead rope and on the tail while circling the horse around the examiner who is testing a postural reaction and also evaluating voluntary strength. In addition, it can exaggerate a patient’s tendency to pivot on a hindlimb demonstrating either flexor weakness or hypometria and to exacerbate maneuvering limbs in an ataxic fashion. Again, ease in pulling the patient to the side during circling occurs usuall because of weakness resulting from central motor pathway involvement, from a lesion that involves final motor neurons in either ventral horn gray matter level with the limb or the peripheral nerves, from a lesion involving muscle, or as a result of a painful process. With final motor neuron, muscle, and painful conditions, extensor weakness is often profound, and it is easy to pull such a patient to the side while it is standing still and while circling. In contrast, a weak animal with a lesion of the central motor pathways can usually reflexly fix the limb in extension when pulled to one side by the halter and tail, whereas while circling, the patient does not have the voluntary motor strength necessary to forcibly resist against the examiner’s pull.

      Hopping a patient laterally on one thoracic limb while the pelvic limbs are free to move may reveal that a horse is weak by a tendency for it to tremble on a thoracic limb when the opposite thoracic limb is held up to initiate the hopping test. Such a patient will also have difficulty in hopping to the side and may stumble when pushed away with the examiner’s shoulder; this test being best performed on soft ground.

Flexor paresis is often evident when an animal drags its toes, has worn hooves, and has a low arc and long swing phase to the stride. When an animal bears weight on a limb demonstrating extensor weakness, the limb often trembles and the animal may even collapse on that limb because of the lack of support. While circling, walking on a slope, and walking with the head elevated, such an animal frequently will stumble on a limb having extensor weakness and will knuckle over at the fetlock. This compares nicely with the patient having central motor pathway weakness, and ataxia, that walks stiff legged with the thoracic limbs but usually without knuckling over at the fetlock.

      With severe weakness in all four limbs, but with no ataxia, neuromuscular disease must be considered. Profound weakness in only one limb is suggestive of a peripheral nerve or muscle lesion in that limb. Weakness occurs with central motor pathway lesions in the brainstem and spinal cord, and it is present in the limb(s) on the same side and caudal to the lesion. A patient with a peracute peripheral vestibular syndrome may appear weak in the limbs on the same side as the lesion because of the decreased extensor tone and tendency to fall in that direction and the increased extensor tone in the contralateral limbs. It can be difficult to be sure that a patient with prominent ataxia but no pathologic evidence of motor pathway problems such as with cerebellar abiotrophy or perennial ryegrass toxicity is not clinically weak. Such patients can be readily made to move laterally with constant tail pulling but will pull forcibly against such lateral pull when standing and when the lateral force is applied firmly only when the limb is in the propulsive phase of stride.

      Markedly asymmetric weakness and/or pain can result in the sidewinder syndrome with the patient “crab walking” or moving “on two tracks”¹⁴ (see Chapter 25).

      Ataxia is a term that, by its Greek derivative, means a lack of order or an inconsistency. In this context, ataxia is a proprioceptive dysfunction causing abnormal rate, range and force of movement, and placement of the limbs and other body parts, including head, neck, trunk, and even at times the eyes. Ataxia thus essentially reflects changes in function of the subconscious proprioceptive mechanisms. What the examiner must see to interpret as ataxia is irregular and mostly unpredictable movement and placement of the limbs, head, neck, or trunk.

      The patient is observed while standing still, walking, trotting, turning tightly, and backing up, and while the patient moves in a serpentine path with the head held elevated and while moving on a slope. The best way of accomplishing the latter maneuvers is to walk backward in a zigzag manner while holding the lead rope high to extend the patient’s head and neck. The aim is to alter the intended direction of the patient’s limbs while they are in protraction by turning the lead abruptly such that there must be a change in direction of each foot to be placed in the site the examiner intends for it to be placed. Some horses will not obligingly turn in tight or even large circles for examination. With practice, circling can be best accompanied by walking the horse forward and then starting to turn in one direction slowly making the turn slightly tighter as the examiner moves from in front of the horse to level with the shoulder, then to level with the middle of the trunk, while coaxing the horse by flicking the rump with the free end of the lead rope. This way the patient turns around the examiner, not the examiner around the horse. Essentially, these maneuvers comprise the postural reaction tests for large animals. These tests alter input to the central motor pathways through changes in many modalities, including the visual horizon, vestibular stimulation, and neck and limb proprioception, that is synthesized with cerebellar input into refined motor system signals. Subtle neurologic abnormalities, which may be compensated for under conditions of normal gait, are exaggerated during these maneuvers. Ataxic movements can be seen as irregular and mostly unpredictable foot flight and placement. To detect subtle asymmetry in limb protraction and the length of stride, it can be useful to walk parallel to, or behind the animal, matching step‐for‐stride. An ataxic gait is sometimes most pronounced when an animal is moving freely in a paddock especially when attempting to stop abruptly from a trot or canter when the limbs may be wildly adducted or abducted.

      It is important for the examiner to observe the patient performing these maneuvers from a distance and also from close‐up by handling the patient oneself while making it perform the same maneuvers.

Three descriptors are often used to characterize the inconsistent movements that comprise ataxia. Hypermetria is used to describe a lack of direction and increased range of movement, and is seen as an overreaching of the limbs with excessive joint flexion. Hypermetria without paresis is characteristic of spinocerebellar and cerebellar disease. Hypometria is seen as a stiff movement of the limbs with little flexion of the joints, particularly the carpal and tarsal joints. This is generally indicative of increased extensor tone, and of a lesion affecting the central motor, or spinocerebellar pathways from that limb. A hypometric gait, particularly in the thoracic limbs, is seen best when the animal is backed up or when it is maneuvered on a slope with the head held elevated. The thoracic limbs may move almost without flexing and resemble a marching tin soldier. The short‐stride, staggering gait seen with vestibular disease may be considered hypometria. Also, movement of a limb with prominent flexor weakness, as with botulism, can result in poor joint flexion and dragging of toes as with hypometria, but the abnormal movement and placement of the weak limb is relatively repetitive and predictable. Finally, dysmetria is a term that incorporates both hypermetria and hypometria (and all others from the Ministry for Funny Walks). Animals with severe cerebellar lesions may have a high stepping ataxic gait, but have limited movement of the distal limb joints, especially in thoracic limbs; this is best termed dysmetria. And in this context, it is worth consideration of the characteristic stringhalt gait with marked flexion of all pelvic limb joints made during onset of a flexor movement. This is not a form of ataxia as it is particularly predictable, even though it may be markedly variable in degree. In all these various situations, we do need to take other abnormalities into consideration in defining the presence and characteristics of ataxia.

      Ataxic movements are thus seen as a swaying from

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