Читать книгу Large Animal Neurology - Joe Mayhew - Страница 45

 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 side to side 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 limb, and hemistanding and hemiwalking the animal by making it stand and then walk sideways on both left and then both right limbs are three useful postural reactions to perform. Even in large, adult animals, particularly horses, it is possible to perform a modified hopping response test with the thoracic limbs. This is performed by lifting each thoracic limb in turn while using the shoulder to make the horse hop laterally on the other thoracic limb. This test can help the clinician decide if there are subtle neurologic abnormalities involving the control of a thoracic limb. Brainstem and spinal cord lesions appear to result in postural reaction deficits on the same side as the lesion, whereas cerebral lesions produce contralateral abnormalities.

At the conclusion of the examination, a most likely site of any acute nervous system lesion frequently can be defined accurately by determining the precise characteristics and severity of any gait and posture abnormalities present. The degree of weakness, ataxia, hypometria, hypermetria, and conscious postural deficits should be graded for each limb (Table 2.4).

With peracute lesions, particularly those of an inflammatory nature and those with soft tissue compression of the spinal cord such as with caudal cervical arthritis and synovial cyst formation, resulting signs can wax and wane quite dramatically over periods of hours to days. Such signs usually stabilize with subacute to chronic lesions. For example, a horse that has suffered a single insult of cervical spinal cord compression a year prior to the examination may have an unusual, perhaps hypermetric, mild ataxia in the pelvic limbs with no evidence of pelvic limb weakness and no signs in the thoracic limbs other than a questionably poor response to hopping. The anatomic diagnosis in such cases may be a lesion in the thoracolumbar or cervical spinal cord, or diffuse or multifocal spinal cord disease. A moderate or severe abnormality in the pelvic limbs, and none in the thoracic limbs, is however far more consistent with a thoracolumbar spinal cord lesion. With a very mild and a very severe neurologic abnormality in the thoracic and the pelvic limb gaits respectively, one must also consider a severe thoracolumbar lesion plus a mild cervical lesion or a diffuse spinal cord disease. Lesions involving the brachial intumescence at C₆–T₂, with involvement of the gray matter supplying the thoracic limbs, and diffuse spinal cord lesions may both result in a severe gait abnormality in the thoracic limbs and the pelvic limbs. A severely abnormal gait in the thoracic limbs, with normal pelvic limbs, indicates final motor neuron involvement of the thoracic limbs; a lesion is most likely present in the ventral gray columns at C₆–T₂ or involving thoracic limb peripheral nerves or muscle (Chapter 26).