Page 764 - Clinical Small Animal Internal Medicine

732 Section 8 Neurologic Disease

weight is placed on it. Animals with LMN disorders in a loss of balance. Lesions limited to this system cause
VetBooks.ir affecting both pelvic limbs will occasionally use them the patient to lean, drift, or fall to one side. However, the
patient’s strength and awareness of where its limbs are in
simultaneously. This action is described as bunny
hopping. Be aware that bunny hopping can also be seen
This ataxia is usually accompanied by a head tilt and
in orthopedic disorders, as well as spinal cord dyspla- space are normal with lesions confined to this system.
sias. Upper motor neuron (UMN) paresis causes a delay sometimes abnormal nystagmus. We will occasionally
in the onset of protraction, which is the swing phase of blindfold our patients with bandage material which will
the gait. The stride will usually be longer than normal. exacerbate the vestibular ataxia.
Stiffness and spasticity may be apparent in the stride. Cerebellar ataxia most commonly causes hypermetric
Most of the UMN pathways necessary for gait generation ataxia characterized by sudden bursts of motor activity
are anatomically adjacent to the pathways of the general with a marked overflexion of the limbs on protraction.
proprioceptive (GP) sensory system, and lesions usually Vestibular system components exist in the cerebellum
affect both simultaneously. Therefore, the gait that that, if dysfunctional, may cause loss of balance, head tilt,
reflects UMN paresis also reflects ataxia caused by dys- and abnormal nystagmus. As a rule, hypertonia accom-
function in the GP system. It is unnecessary to recognize panies cerebellar ataxia.
the separate clinical signs of dysfunction of these two
systems. Therefore, we recognize a pattern that reflects Postural Reactions
the combined dysfunction of UMN paresis and GP
ataxia. As you observe the gait of a dog with UMN pare- Remember that spinal nerve reflexes require only the
sis and GP ataxia, you have the sense that the patient specific nerves that innervate the area being tested and
does not know where its limbs are located. This is never the spinal cord segments with which they connect.
a concern with LMN paresis. Postural reactions depend on the same components as
Ataxia is a synonym for incoordination, and we recog- the spinal nerve reflexes plus the cranial projecting
nize three qualities of ataxia: (1) GP, (2) vestibular (special pathways in the spinal cord white matter to the brain-
proprioception [SP]), and (3) cerebellar. GP ataxia reflects stem, cerebellum, and frontoparietal portion of the
the lack of information reaching the central nervous sys- cerebral hemisphere and the caudal‐projecting UMN
tem (CNS) that informs the CNS of where the neck, trunk, pathways that return from the cerebrum and brainstem
and limbs are in space and the state of muscle contraction and comprise tracts in the white matter of the spinal
at any time. Without this GP information, the onset of cord that terminate in the cervical and lumbosacral
protraction of a limb may be delayed, and the stride may intumescences. These postural reactions test the integ-
be lengthened. During protraction, the limb may swing to rity of nearly the entire peripheral and central nervous
the side (abduct) or swing under the body (adduct), over- systems. By themselves, the postural reactions are rela-
extend during protraction, scuff or drag one or more dig- tively less reliable for lesion location.
its, and in the support phase, stand on the dorsal aspect of The degree of functional limb deficit will determine
the digits. Remember that these clinical signs overlap with the need for postural reaction testing. In a patient that is
those caused by dysfunction of the UMN. The gait pattern recumbent with tetraplegia or is paraplegic, you need
of a patient with a focal cervical spinal cord lesion between not perform postural reactions in the affected limbs.
the C1 and C5 segments reflects dysfunction of the UMN However, in the paraplegic patient, you must test the
and GP systems and is observed as spastic tetraparesis and thoracic limb postural reactions so as to avoid overlook-
ataxia. This cervical spinal cord pattern is often recog- ing a focal cranial thoracic lesion or a multifocal
nized by the overextension of the thoracic limbs creating disorder.
an overreaching or floating action. This clinical sign can In small animals, we evaluate muscle size and tone just
be augmented by holding the head and neck extended as before our evaluation of the postural reactions. Be sure
the patient is led. This unique form of hypermetria must to talk to your patient continually, and use its name to
not be confused with cerebellar ataxia in which the limb gain its cooperation. Stand over the patient with both of
is overflexed on protraction. At no time do we try to dif- you facing in the same direction. Simultaneously palpate
ferentiate between conscious (cerebral) and unconscious the muscles of the neck and both thoracic limbs from
(cerebellar) GP pathways! No examination will clearly proximal to distal for any evidence of atrophy. Flex and
differentiate these two pathways from each other or from extend each limb for range of motion and to determine
the UMN pathways. No pure conscious proprioceptive the degree of muscle tone. A short stride or stiffness in
deficit exists. This term should be dropped from the clini- the gait may be caused by a joint disorder, limiting
cian’s vocabulary. the range of motion. When you place the limb back on
Vestibular ataxia reflects the loss of orientation of the the ground surface, turn the paw over so that its dorsal
head with the eyes, neck, trunk, and limbs, which results surface bears the weight of the limb to determine how