Neurologic gait deficits should be evaluated with basic systems and physiology in mind. If basic neuroanatomy and function
is kept in mind, true neurological gait deficits can be detected.
The take home message is that subtle gait deficits can be present with musculoskeletal and/or neurological gait deficits.
1. When neurological gait deficits present alone, the gait should be arrhythmic
2. When musculoskeletal gait deficits present the gait deficit should be rhythmic
3. When horses have a subtle component of both, the gait deficits can present as arrhythmic
Diagnosis begins with neuroanatomy
Neuromuscular function can be divided into 3 categories: lower motor neuron (LMN), upper motor neuron (UMN), and proprioception
The anatomy of the LMN places the cell bodies within the spinal cord segment ventral gray matter (Figure 1). This system functions
to directly stimulate contraction of muscle during conscious and unconscious locomotion. Clinical signs of disease associated
with this system depend on the degree of loss relative to each muscle group and include paresis with sub-clinical atrophy
to paralysis with complete muscle atrophy and areflexia. No ascending or descending spinal cord tracts are necessary for the
reflex response, but do affect the quality of the response.
Figure 1: The structure of the lower motor neuron reflex. The presence or absence of this response is independent of the
However, the quality of this function is dependent on higher centers.
Figure 2: Major pathways of upper motor neuron function. This system generates inhibitory control of movement including ocular
Upper motor neuron (Figure 2) and proprioceptive (Figure 3) deficits related to spinal cord lesions often occur in tandem.
This is because within the spinal cord the UMN and Pr tracts course together.
Figure 3. Major tracts of the proprioceptive system
The UMN calms and fine tunes the LMN. It also provides, via the LMN, continual tone and strength of muscle action. There is
a higher likelihood that a gait abnormality is related to spinal cord disease when Pr and UMN deficits are present concurrently.
Proprioceptive information is collected from sensory fibers that are located in joint capsules and muscle fascia via ascending
conscious (cortical) and unconscious (cerebellar) pathways from Pr function that senses limb and trunk position awareness.
Neuroanatomic diagnosis is made by understanding the anatomy of spinal cord reflexes and using these reflexes for localization.
The cutaneous trunci and coli reflexes are useful in this regard. Localization to cervical and/or thoracolumbar spine is made
by association of the physical signs with long tract neuroanatomy. Compressive spinal cord lesions in the cervical area are
associated with deficits in both the front and rear limbs that are more severe in the rear. The pelvic limb UMN and Pr tracts
are peripheral and are more likely to be compressed externally.
Figure 4. Illustration of an atlanto-occipital (left) and lumbo-sacral cerebral spinal fluid centesis.