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Neurology case presentations (Proceedings)
Neurologic gait deficits should be evaluated with basic systems and physiology in mind.
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 arrythmic
Diagnosis begins with neuroanatomy
Neuromuscular function can be divided into 3 categories: lower motor neuron (LMN), upper motor neuron (UMN), and proprioception (Pr).
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 higher centers.
However, the quality of this function is dependent on higher centers.
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 2: Major pathways of upper motor neuron function. This system generates inhibitory control of movement including ocular musculature.
The UMN calms and finetunes 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.
Figure 3: Major tracts of the proprioceptive system
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 cerbral spinal fluid centesis.
Radiography should be the next step when a neuroanatomic diagnosis places the lesion in the cervical area. General radiographic appearance should be evaluated and sagital ratios calculated for each vertebra and its articulations. Cerebral spinal fluid analysis may be useful in some conditions, and can be collected at either the lumbosacral or antlantooccipital spaces.
Figure 5: Sagital ratio measures for evaluating relative spinal canal size (left). The right side indicates a severe spondylosis. The image below indicates a myelogram with a suspect compressive lesion.
Foals at high risk for CVM (i.e., breed predilection, older siblings or relatives with disease, etc.) but not as yet showing clinical signs should be evaluated radiographically. Subtle changes should be seriously considered. These foals should be placed on dietary restriction, and microminerals should be analyzed and balanced.
Figure 6: Myelogram indicating a concerning C6/C7 compression
Surgical intervention may be attempted in middle-aged horses showing clinical signs. The prognosis is dependent on the site of the lesion, but in general, 90% improve by 1 grade and 55% improve 2 or more grades with ventral stabilization.
Figure 7: Cervical radiographs of a fairly normal (left) and a suspect (right) foal. There is moderate ârampingâ of the ventral surface of the vertebral canal.
In older horses with osteoarthitis of the cervical facets, injection of the facets with anti-inflammatory preparations may be useful to reduce pain and increase the animals capability to compensate for the deficit. In addition, this may reduce soft tissue swelling and therefore reduce spinal cord compression.
Mayhew, GJ. The equine spinal cord in health and disease. Proc 45th Ann Conv AAEP. 1999;45-84.
Grisel, GR, et al. Arthrocentesis of the equine cervical facets. Proc 42th Ann AAEP. 1996;197-198.
Knight DA, et al,The effects of copper supplementation on the prevalence of cartilage lesions in foals. Equine Vet J 1990;22:426-32.