Page 80 - Canine Lameness

52 4 The Neurologic Examination

Box 4.4 Loss of Voluntary Motor Terminology
Paresis = partial loss of voluntary motor function (i.e. disruption of UMN signal transmission
●
or LMN implementation of movement)
Plegia/paralysis = complete loss of voluntary motor function (i.e. severe paresis)
●
○ Mono‐ = Single limb
○ Hemi‐ = Thoracic limb and pelvic limb of one side
○ Tetra‐ = All limbs
○ Para‐ = Only pelvic limbs

present with LMN dysfunction, it is a key feature localizing to a UMN lesion (Box 4.1). Severe
paresis with complete loss of voluntary movements is termed plegia or paralysis (Box 4.4). The only
difference between paresis and paralysis is the severity of the lesion, and it cannot be used to dif-
ferentiate between UMN and LMN lesions. Further, in a paralyzed patient, ataxia cannot be
assessed.
Paresis, or paralysis, can result from UMN or LMN lesions. UMN lesions disrupt the signal trans-
mission and therefore result in a loss of voluntary movement thus producing a spastic paresis (i.e.
increased muscle tone). LMN lesions disrupt execution of the movement by the muscle due to loss
of muscle power producing a flaccid paresis (i.e. decreased muscle tone). The degree of LMN pare-
sis can range from shortened stride length to partial or complete inability to support weight. If the
animal is ambulatory, the shortened stride length or partial inability to supporting weight can
appear as lameness making the gait in LMN disease similar to that of a patient with orthopedic
disease. Stride length in UMN paresis is typically lengthened due to both delayed initiation and
completion of the protraction (swing) phase. Determining the quality of paresis or paralysis is criti-
cal in differentiating LMN from UMN lesions and is made through evaluating muscle mass, mus-
cle tone, and reflexes.
Gait abnormalities usually result from injury or disease to musculoskeletal components, nerve
roots, or the LMN. As mentioned above, gait abnormalities are more commonly associated with
orthopedic disease and are typically the result of pain or abnormal anatomy. Orthopedic disease is
not usually associated with paresis or paralysis nor should the patient be ataxic. However, gait
abnormalities can occur from neurologic lesions, from pain associated with compression or inflam-
mation of a nerve root, for example from a disc extrusion or a nerve sheath tumor (Video 4.1). This
“neurogenic lameness” is called nerve root signature lameness (i.e. pain from irritation of the nerve
root that is referred down the limb). Signs of nerve root signature vary in severity where some
animals will hold up the limb completely while standing, presumably to minimize stretching of
the irritated nerve, and others show only off‐weighting or a minor weight‐bearing lameness.
Ataxia is a hallmark of UMN disease and does not accompany pure LMN lesions nor orthopedic
diseases. As such, if ataxia is present, the animal has UMN dysfunction. Given the location of the
UMN, ataxia generally affects at least two limbs (unless a severely lateralized lesion is present
which is rare). There are three types of ataxia in veterinary neurology, the name of each indicating
the level of the lesion: cerebellar, vestibular, and GP ataxia. Animals with cerebellar and vestibular
ataxia generally display obvious gait abnormalities in all four limbs (such as hypermetria, base‐
wide gait, or loss of balance), which can be symmetric or asymmetric, respectively. Animals with
GP ataxia can demonstrate various degrees of scuffing and knuckling of the nails or footpads,
limbs crossing midline, stumbling, and a base‐wide or base‐narrow gait (Table 4.1). The swing
phase is prolonged (from loss of inhibition) producing a longer stride than normal and many times,