Biomechanics in Ataxic Horses
Krista Page
Abstract
Ataxia, a gross loss of limb coordination, is a clinical sign seen in horses with impaired
proprioception resulting from neurologic disease that leads to to gait abnormalities. Ataxia
severity in horses is graded from 0 to 5; 0 denotes a neurologically sound horse free from
abnormalities, while 5 represents a completely recumbent animal unable to stand without
assistance. Correct assessment and grading of ataxia in horses is critical to diagnostics, treatment,
evaluation of response to treatment, and classification of animals for research purposes. The
current grading scale is subject to evaluator bias based on for example experience. The goal for
this study is to quantify ataxia in order to standardize evaluator grading. Objectives: 1) to
simulate ataxia through sedation; and 2) use detailed gait analysis to identify relevant parameters
that could be included in an objective grading scale. This study used four Arabian horses, assessed before (Baseline) and after administration of
xylazine, a commonly used alpha-2 adrenoceptor agonist (Sedation). Horses were instrumented
with 2 accelerometers that recorded spatial movements along the x, y, and z-axes. Gait kinematic
data were collected on the equine high-speed treadmill while horses walked on the flat and 10%
decline. Physiological data were collected until 60 minutes after xylazine administration.
Preliminary data analysis shows appropriate physiological response to xylazine, including
development of ataxia. Treadmill and accelerometer data after sedation show alterations in stride
frequency, stride length, stride duration, and lateral hip movement.
We conclude that we can use this model of ataxia to identify relevant quantifiable parameters to
use for development of an objective scale for assessing equine ataxia.
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Introduction
Ataxia denotes a gross loss of limb coordination usually resulting from neurologic disease
affecting the spinal cord, and can preclude normal activity while being difficult to cure. In these
cases the horse displays uncertain foot placement, trunkal sway, and stumbling or falling. Spinal
ataxia is a serious problem; of horses experiencing central nervous system disorders, 22%
resulted from physical trauma mainly to the cervical spine and spinal cord, and at this point in
time the challenge of describing an objective method of assessment has not been met (Mayhew
et al., 1978, Tyler et al., 1993, Feige et al., 2000, USDA 2001, Keegan et al., 2004a, Van
Biervliet et al., 2004, Strobach et al., 2006, Hahn et al., 2008, Levine et al., 2010). Horses have
four basic, normal gaits: the walk, trot, canter, and gallop (Robilliard et al., 2007). Any change
seen in the pattern of any of these gaits is an indicator that the horse has been compromised
either physically or as a result of some pathological influence. Common factors contributing to
gait deficits are musculoskeletal disease or trauma resulting in pain and subsequent lameness,
neurologic disease, and sedation. Xylazine is a sedative drug commonly used in horses. It is an
alpha-2 adrenoceptor agonist synthetic drug affecting the central nervous system, which causes
sedation and is shown to have physiological side effects such as decreased heart rate and head
height, a lessened response to physical and auditory stimuli, as well as a dose-dependent ataxia
(England et al., 1992). These drugs can be used to induce ataxia in the absence of a population of
clinically neurologic horses. The current grading scale for ataxia is inadequate due to its inherent
subjectivity. It is an ordinal scale, which ranges from 0 (a horse that is neurologically normal) to
5 (a horse that is completely recumbent with the inability to stand without assistance). Grade 4
describes a horse that stumbles and falls during examination, but is able to rise unassisted.
Grades 4 and 5 therefore, are relatively straightforward and easy to judge universally. However,
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it is the lower grades (1, 2, and 3) wherein the subjectivity lies since the signs are not as obvious.
Divergence in the grading of ataxia can derail an accurate diagnosis and plans for treatment.
Objectives
Identification of relevant quantifiable parameters through kinematic gait analysis can standardize
the assessment of the severity of ataxia by improving veterinary evaluations both in clinical and
research settings. The correct assessment of ataxia in horses is critical to diagnostics, treatment,
and evaluation of response to treatment. The objective for this study was to simulate a dosedependent ataxia in horses through drug administration, and use detailed quantifiable gait
analysis to create a new, more objective grading scale for ataxia in horses.
Experimental Design
Horses were assessed at three experimental conditions: baseline (BL), low dose sedation with
xylazine (LD), and high dose sedation with xylazine (HD). Each condition was assessed in two
different environments: on the equine treadmill, flat (TF); and on the equine treadmill at a
decline of -10% (TD). Each horse served as its own control. The schedule of xylazine injection
dosages was randomized for each horse. No horse was sedated more than once within a 24-hour
period. The experimental protocol and study design were approved by the Institutional Animal
Care and Use Committee, California State Polytechnic University, Pomona (protocol #11.018).
Materials & Methods
Table 1. Physiology of experimental animals; measurements at T = 0 and T = 5 min. Range
Age
Mass
Heart
Rate BL
Heart Rate
HD
5-19 years
433-519.7
kg
44-48 bpm
30-42 bpm
Head
height BL
44-57
inches
Head
height HD
5-20 inches
3
Mean ±
S.D.
12.4 ± 5.2
years
476.85 ±
29.4 kg
46.4 ± 2.0
bpm
35 ± 5.0
bpm
49.5 ± 5.6
inches
14 ± 4.3
inches
Eight adult Arabian horses were used for this study, consisting of five mares and three geldings
(Table 1). All horses were sedated using xylazine (xylazine HCl, 100 mg/ml, Fermenta Animal
Health Co., Kansas City, MO) injected intravenously into the left jugular vein. Horses were
weighed each day of data collection on a digital scale (Livestock Scale; Tru-Test LTB,
Auckland, New Zealand) for accurate dose calculations. A dose of 0.2 mg/kg xylazine was used
in the LD group, while the HD group received a dose of 0.7 mg/kg xylazine. All horses were
acclimatized to the high-speed equine treadmill (Säto I, Säto AB, Knivsta, Sweden) in the month
preceding data collection, at a range of speeds and incline levels. Data collection began with a
five-minute warm-up period of walking horses at 1.7-1.8 m/s at the flat. Study data was collected
with horses walking at 1.25 m/s on the treadmill, alternating between flat and a -10% decline
over six trials, for each experimental condition (BL, LD, HD). Each trial included the horse
walking with its head held normally, followed by handlers lifting the horse’s head for the
remainder of the trial time. This was done in simulation of one of the challenges horses are put
through during a routine veterinary neurologic exam. All treadmill trials were video recorded for
further analysis. Video recording for each trial only began once the treadmill reached target
speed at each incline level. Horses were affixed with 15 self-adhesive reflective markers
denoting specific anatomical locations on the right side, including the fore and hind limbs (Fig.
1). Video recording of kinematic parameters on the treadmill was done at 125 Hz with a
HotShot E64 camera. Stride data were calculated from videos through movement of the
reflective markers. Three basic, descriptive kinematic stride parameters calculated were: stride
time, which is the amount of time it took for the horse to complete one full stride, defined as the
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time from toe on to the successive toe on (1 limb); stride frequency, which is the number of
whole strides per minute; and stride length, which is the distance covered during one full stride.
Figure 1. Anatomical locations of 15 reflective markers.
Results
Heart rate was depressed in response to xylazine, from a mean of 46 beats per minute to 35 beats
per minute after sedation (Table 1). Head height also dropped significantly, from a mean of 49
inches above the ground to 14 inches. As the level of sedation with xylazine increased from BL
to LD and from LD to HD, stride time and stride length both increased while stride frequency
decreased (Fig. 2). Stride time and stride length both decreased on the decline, while stride
frequency increased (Fig. 2). With the head held in an elevated position, stride time and stride
length both decreased for all conditions and on both treadmill incline levels; once again, stride
frequency showed the opposite and increased with the head raised (Fig. 2). Overall, these data
show that when asked to walk downhill or walk with their heads raised, horses take shorter faster
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Mean Stride Time
Stride Time (msec)
1600
1400
Head
normal
Head up
1200
1000
800
Mean Stride Frequency
Number of Strides per
Minute
60
55
50
45
40
35
30
Mean Stride Length
Stride Length (m)
2.0
1.8
1.6
1.4
1.2
1.0
Baseline Baseline Low
Flat
Decline Dose
Flat
Low
Dose
Decline
High
Dose
Flat
High
Dose
Decline
Condi'on*Environment Figure 2. Mean stride parameters for all horses. steps, but after sedation horses take increasingly longer, slower steps. These are reflected in the
stride frequency; when taking shorter faster steps, stride frequency increases and when taking
longer slower steps stride frequency decreases. Fig. 3 shows the percentage change for the same
three parameters from baseline flat with the normal head position. When taken as percentage
changes, the two different head positions showed the same pattern with a nearly exact match in
magnitude. Even as the horses were presented with different challenges, their basic stride
patterns remained intact.
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% Change from Baseline 1.20 Head Normal Stride Time (msec) 1.15 1.10 1.05 Stride Frequency (/min) 1.00 0.95 0.90 0.85 0.80 Baseline Baseline Low Dose Low Dose High Dose High Dose Flat Decline Flat Decline Flat Decline Stride length (m) Condi'on*Environment Figure 3. Stride parameters percent change from baseline flat.
Conclusions
Stride time, stride frequency, and stride length are all quantifiable variables that can demonstrate
the presence of gait deviations, and are both easily measurable and applicable to clinicians in the
field. These parameters were altered in response to drug administration, head elevation, and
walking downhill. Changes in head position and incline level are designed to highlight the
instability of ataxic horses and are useful in assessing gait abnormalities. In this study, horses’
altered gait patterns persisted with their heads raised. This could be due to their controlled
forward movement based on the set speed of the treadmill, and may differ in horses tested over
ground. Future goals should include using these results to modify the equine ataxia grading scale
for increased objectivity in order to improve diagnostic and treatment procedures for neurologic
horses, followed by a study verifying these results with clinically ataxic horses.
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