The Hands-Off Evaluation - Gait

Examination of the gait should be done in a place where the patient can be allowed to move freely.  This is best accomplished by having the owner walk the animal over a non-slippery surface.  If the animal is not making any attempt to walk, body support (such as a sling or harness) should be provided as necessary so that any subtle voluntary movement can be detected. 

Sedation prior to the examination may affect your interpretation. In one study, gabapentin significantly altered gait analyses and postural reactions in this group of healthy cats. The administration of gabapentin could lead to false-positive results and, possibly, an incorrect identification of neurological lesions. In contrast, gabapentin does not impair the assessment of cranial nerves and spinal reflexes, which can be assessed in patients receiving the drug.

A normal gait requires intact function of the brainstem, cerebellum, spinal cord, sensory and motor peripheral nerves, neuromuscular junction, and muscles.  The cerebrum’s contribution to the gait is less important in dogs and cats compared to primates.  

Evaluation of the gait should be done to determine if the animal is ataxic (uncoordinated), paretic (weak), or lame (from either neuromuscular disease or an orthopedic disorder) and which limb(s) are involved.  

Ataxia is defined as an uncoordinated gait and can arise from either a sensory peripheral nerve or a spinal cord lesion (general proprioceptive ataxia), a vestibular lesion (vestibular ataxia), or a cerebellar lesion (cerebellar ataxia). 

Vestibular or cerebellar ataxia are accompanied by other signs of dysfunction of the vestibular apparatus or cerebellum.

The cat in this video exhibits a left-sided head tilt in addition to displaying a falling and leaning ataxia, typical of vestibular ataxia.

Ataxia can be further divided into hypometria (shorter protraction phase of gait), hypermetria (longer protraction phase of gait), and dysmetria (combination of both hypo- and hypermetria). 

Note in this dog that there is a profound incoordination affecting all 4 limbs which exhibit a hypermetric gait - this is an example of a cerebellar ataxia.

General proprioceptive (GP) ataxia reflects the lack of information responsible for the awareness of the movement and position of the neck, trunk, and limbs in space reaching the CNS.  As a consequence, there may be a delay in the onset of protraction of the limb which may cause a longer stride than normal.  The patient may walk on the dorsal part of its foot or may drag its digits.  These signs often overlap with those caused by UMN paresis. 

The cat below exhibits moderate GP ataxia and mild UMN paresis.

As can be seen in this dog, crossing of the legs can indicate moderate incoordination and this would be expected to manifest as ataxia when the dog is walked.

Paresis is defined as a loss of ability to support weight (lower motor neuron disease) or inability to generate a gait (upper motor neuron disease).  The term paresis implies that some voluntary movement is still present as compared to paralysis which refers to a more severe paresis with complete (-plegia) loss of voluntary movement.  Depending which limbs are affected, the terms paresis/paralysis can be further defined as tetraparesis/plegia (all four limbs affected caused by a lesion located cranial to T3 spinal cord segment or from a generalized lower motor neuron disorder), paraparesis/plegia (pelvic limbs affected caused by a lesion caudal to T2), monoparesis/plegia (only one limb affected caused by a lesion of the lower motor neuron innervating the affected limb), hemiparesis/plegia (limbs on one side affected due to ipsilateral lesion located between T2 and the caudal midbrain or contralateral lesion located in the rostral midbrain).

The Dachshund below exhibits a reduced ability to generate gait in the pelvic limbs compatible with paraparesis.

With further deterioration of neurological function, we can see a complete loss of motor function as noted in this dog with paralysis.

Gait generation requires the interaction between two motor systems: upper motor neuron (UMN) and lower motor neuron (LMN) systems.   

The upper motor neuron (UMN) system is the motor system that is confined to the central nervous system (CNS).  It is responsible for the initiation and maintenance of normal movements and for the maintenance of tone in the extensor muscles to support the body against gravity.  Its cell body lies within the cerebral cortex, basal nuclei, brainstem or spinal cord.  It travels through the brain and/or spinal cord white matter and synapses indirectly (via an interneuron) with a LMN to modulate its activity (essentially inhibitory).  

The lower motor neuron (LMN) system is the motor system connecting the central nervous system with the muscle to be innervated.  Its cell body lies within the ventral horn of the spinal cord grey matter or within the cranial nerve nucleus of the brainstem.  Its axon leaves the central nervous system by the ventral nerve roots to join successively a spinal nerve and a peripheral nerve before it synapses with an effector muscle.  The LMN is the last neuron in the chain of neurons that produce muscular contraction necessary to maintain posture, support weight and provide the gait (final common pathway to the effector).

The UMN pathways are responsible for stimulating the appropriate LMN that induces the postural and protraction phases of locomotion.

Two qualities of paresis can be distinguished:  UMN and LMN paresis:  

UMN paresis causes a delay in the onset of protraction (swing phase of the gait) with a resultant stride being longer than normal and a stiff quality of movement.  Lesions of the UMN typically result in the release of the inhibitory effect that the UMN system has on LMNs (disinhibition) located caudal to the level of the injury.  This disinhibition is usually more apparent on the extensor muscles which results clinically in spastic paresis/paralysis.  Lesions at many different levels of the CNS can produce the same set of UMN clinical signs.  Due to their close anatomic relationship within the brainstem and spinal cord, most gait abnormalities involving the UMN pathways necessary for gait generation also cause some degree of general proprioceptive (GP) ataxia.  From a lesion localization point of view, UMN paresis and GP ataxia visible in the gait can occur as a consequence of a lesion affecting the brainstem, or spinal cord.  Aside from lesions caused by acute disease processes (i.e., infarct, haemorrhage, and head trauma), lesions affecting the forebrain cause contralateral paresis that is so mild that it is usually not apparent in the gait.  

LMN paresis reflects degrees of difficulty in supporting weight and varies from a short stride, choppy gait, to complete inability to support weight, causing collapse of the limb whenever weight is placed on it.  When standing, the affected limbs may exhibit a tremor in the muscles.  LMN paresis affects the gait with lesions in the peripheral nerves, neuromuscular junction, and muscles.  Motor deficits observed are ipsilateral to the lesion.  Compared to UMN paresis, a disorder of the LMN does not cause ataxia but only paresis.

The dog below exhibits an LMN gait in the thoracic limbs and a UMN gait in the pelvic limbs. This is sometimes referred to as a 'two-engine' gait and can be indicative of a lesion affecting the C6-T2 spinal cord segments.

Lameness usually presents with a short stride on the affected limb and a long stride on the contralateral limb.  Lameness is usually associated with pain from orthopaedic disease.  Additionally, it can be associated with nervous system dysfunction referred to as nerve root signature (referred pain down a limb, causing lameness or elevation of the limb, resulting from entrapment of the spinal nerve, usually by a lateralized disc extrusion or nerve root tumour).

Loss of motor function in one limb is termed monoplegia as seen in the dog below, or monoparesis if some function remains, and not lameness which does not affect the ability to generate movement.

The dog below exhibits a nerve root signature with a mild right thoracic limb gait abnormality and sigs of pain such as a guarded neck posture.