Original ResearchInternational Journal of Current Research and Review
DOI: http://dx.doi.org/10.31782/IJCRR.2021.131220

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Section: Healthcare
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Rest-induced Reduction in Walking Speed
Helps Differentiate Degenerative Compression
Myelopathies from Lumbar Spinal Stenosis
Enoki H1, Tani T2,4, Ishida K3,4, Wang S5, Kimura J6
Department of Physical Therapy Faculty of Health and Welfare, Tokushima Bunri University, 180 Nishihamahoji, Yamashiro-cho, Tokushimacity, Tokushima770-8514, Japan; 2Department of Orthopaedic Surgery, Kubokawa Hospital, 902-1 Mitsuke, Shimanto-cho, Takaoka-gun,
Kochi786-0002, Japan; 3Department of Orthopaedic Surgery, Reihokuchuou Hospital, 620 Motoyama, Motoyama-cho, Nagaoka-gun,
Kochi781-3601, Japan; 4Department of Rehabilitation Center, Kochi Medical School Hospital, 185-1 Kohasu, Oko-cho, Nankoku-city,
Kochi783-8505, Japan; 5Department of Intelligent Mechanical Systems Engineering, Kochi University of Technology, 185 Miyanoguchi,
Tosayamada-cho, Kami-city, Kochi782-8502, Japan; 6Division of Clinical Electrophysiology, Department of Neurology, University of Iowa
Health Care, 200 Hawkins Dr, Iowa City, IA 52242, US.
1

ABSTRACTIntroduction: Patients with degenerative compression myelopathy (DCM) most commonly complain of gait-onset difficulty typically prominent after periods of inactivity. This feature stands in contrast with the post-exercise neurogenic claudication characteristic of lumbar spinal stenosis (LSS).
Aims: To test if DCM patients indeed have a greater difficulty at the beginning of gait than in steady-state conditions as compared with age-, gender-, and height-matched healthy subjects and LSS patients.
Methodology: We studied 49 consecutive, ambulatory DCM patients, 11 controls, and 10 LSS patients. After sitting in a chairfor 10-min, immobilizing the lower-limb muscles, the subject walked 15 m one way and returned the same distance with one
turn at the maximum comfortable speed. A 2.64-m long ground reaction force plate allowed measurement of the step lengths,
cadences, and speeds for the initial and terminal 2.64-m walks.
Results: Unlike the controls or LSS, the DCM had a smaller (p<0.001) step length-to-height ratio for the initial than final 2.64m walk. The initial-to-final walking speed ratios showed smaller values in DCM (85.1±9.4 %,) than in the controls (93.8±6.2 %;p<0.01) and LSS (96.5±7.3 %; p<0.001). Both the step length and walking speed for the initial 2.64-m in DCM significantly correlated with the lower-limb motor scores and the number of taps in the 10-sec foot-tapping test that quantifies the slowness ofvoluntary leg movements.
Conclusions: Reduced walking speed in DCM became more pronounced immediately following 10-min sitting. This phenomenon seems to represent an additional aspect of the same physiologic mechanisms that characterize spastic gait disorders.
Altered descending central drive caused by corticospinal tract involvement may account for this phenomenon, combined with arest-induced hypoexcitability of the pertinent anterior horn cells.
Key Words: Gait initiation, Degenerative compression myelopathy, Spasticity, Rest-induced hypoexcitability, Anterior horn cell

INTRODUCTION
Degenerative compression myelopathies (DCM), the commonest non-traumatic spinal cord disorders in Japan, gives
rise to a variable combination of gait disturbance such as
stiffness, clumsiness and unsteadiness.1 These features reflect spastic limb paresis characterized, in part, by functionally impaired fast movements2 especially in rapid repetition,3
which retard voluntary execution out of proportion to thedegree of weakness.4 Thus, 30-m walking5 and 10-sec foot-tapping speed 6,7 have proven useful as quantifiable measures
for gait impairment in DCM patients with spastic paraparesis. Spastic gait results from inappropriate activation of
rapidly lengthened muscle at a certain point during the gait
cycle, altering its mechanical properties with increased stiffness.8
Although not as well-recognized as slowness of movements, DCM patients tend to show the most noticeable clumsiness of gait after periods of inactivity such as on rising in the

Corresponding Author:
Enoki H., Department of Physical Therapy Faculty of Health and Welfare, Tokushima Bunri University, 180 Nishihamahoji, Yamashiro-cho,
Tokushima-city, Tokushima770-8514, Japan; Tel.: +81-88-602-8539; Fax: +81-88-657-4237; E-mail: enoki@tks.bunri-u.ac.jp
ISSN: 2231-2196 (Print)
Received: 10.02.2021

ISSN: 0975-5241 (Online)
Revised: 19.03.2021

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Accepted: 04.04.2021

Published: 22.06.2021

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Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

morning and after extended sitting.1 This feature of rest-induced gait difficulty seen in upper motor neuron disorders
stands in contrast with post-exercise neurogenic claudication
characteristic of lumbar spinal stenosis (LSS). The opposing
presentations of the two very common entities serve as animportant clue in identifying the primary site of involvement
when cervical and lumbar lesions coexist. Despite the clinically important implication, few previous studies dealt withfurther confirmation of this point. The present study attempts
to verify rest-induced gait disturbances in DCM as comparedto healthy controls and LSS.

MATERIALS AND METHODS
Subjects

We analyzed 49 ambulatory DCM patients (26 men), 62 ±
14 (mean ± SD) years in age and 160 ± 9 cm in height, withspastic paraparesis either by cervical (45) or thoracic myelopathy (4), 11 volunteers (7 men), 70 ± 7 years in age and
158 ± 8 cm in height, with no history of peripheral or central nervous system disease or orthopedic diseases impairing
the gait, and 10 LSS patients (6 men), 67 ± 17 years in age
and 160 ± 10 cm in height, with neurogenic claudication.
Both DCM and LSS patients were selected out of those who
had been consecutively referred to a university hospital for
surgical treatment between October 2016 and March 2017.
They all underwent a gait performance test using a groundreaction force plate, and the DCM patients also had a 10-sec
foot-tapping test6,7 to study the correlations between the twotest results.
The three groups showed no statistical difference (p>0.05)
in age, gender ratio or height. All subjects agreed in writing to participate in the study after reading and signing an
informed consent form approved by the ethics committee of
Kochi Medical School with the approval number of 23-84 on
1 November 2011.

Table 1: Grading system for lower limb motor function by Japanese Orthopaedic Association (1994)10
Walks normally despite signs of spinal cord
compromise

4 points

Able to walk fast unaided but with some difficulty

3 points

Needs support when going downstairs

2.5 points

Needs support when going up and down thestairs2 points

Able to walk unaided but with some difficulty

1.5 points

Required walking aids

1 point

Able to stand up but unable to walk

0.5 points

Chairbound or bedridden

0 points

Gait performance test

A gait analysis system (Gait scan 4000; Nitta Corp, TokyoJapan) consisted of a rectangular-shaped ground reaction
force plate 2.64 m long and 0.54 m wide, an analogue todigital (A-to-D) converter, and an amplifier capable of driving an analogue monitor display. The force plate contained athin sensor sheet with a resolution of 5 mm for detection offoot pressure greater than 0.5 kg. The subject sat on a chairquietly for 10 min and then stood up on bare feet in responseto the verbal signal. The test did not include a measurementof the time taken to rise from sitting, excluding the influenceof lower limb strength and balance deficits. When the subject
was ready, he/she started to walk over a smooth, flat surface in a corridor for a measured distance of 30 m (going 15
m one way and returning the same distance with one turn).
We instructed subjects to walk at the maximum comfortablespeed from the beginning, using personal walking aids, andto go through the finish line without reducing the speed. All
the participants understood these instructions. The 2.64-m
ground reaction force plate covered each end of the 30-m
walkway (Figure 1).

Functional scale

The functional scale developed by the Japanese Orthopedic
Association (JOA) for DCM9 scores motor function from 0
to 4 points for lower limbs (Table 1). Three patients walked
normally despite signs of spinal cord compromise (4 points);
4 could walk fast unaided but with some difficulty (3 points);
3 needed supports when going downstairs (2.5 points); 24
had supports when going up and down the stairs (2 points);
13 walked unaided but with difficulty (1.5 points); and 2 required walking aids (1 point). Stretch reflexes were generally hyperactive although responses were diminished for thequadriceps in 4 patients and the gastrocnemius in 11. A positive Babinski sign was found in 24 patients. We excluded thepatients who were able to stand up but unable to walk (0.5
points), and chair-bound or bedridden patients (0 points).
75

Figure 1: Experimental arrangement for gait performance test.
First, the subject quietly sat on a chair for 10 min, and then,stood up to his/her bare feet and started walking for a measured 30 m distance (15 m there and back with one turn) at
the maximum comfortable speed. We instructed the subject to

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Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

walk through the finish line without reducing the walking speed.
The ground reaction force plate 2.64 m in length recorded the
movement trajectories of the centre of foot pressure from heel
strike to toe-off as a function of time for the initial and final
2.64-m walks.

The gait analysis system allowed recording of the sequential changes of the ground reaction force from heel striketo toe-off as a function of time during the stance phaseof walking (Figure 2). Based on the raw data recorded,
this automated device digitally displayed the measured
temporal and distance values for initial and final 2.64-mwalks, including (1) step length, defined as the average
distance from one heel strike to the other for a few strides,
which was converted into a percentage of the height, (2)step frequency (cadence), the number of steps per unit oftime reported as steps per minute, and (3) walking speed,
defined as the average horizontal speed of the body overthe 2.64-m distance.8 To assess the degree of slowing at
the beginning of gait relative to the steady-state gait, we
calculated the measured values for the initial 2.64-m walkin the percentage of those for the final 2.64-m walk (initial/final).

quantifying the slowness of voluntary leg movements resulting from spasticity. In short, the subject sat on a chairwith its height adjusted to have both soles flat on the floor
and the hip and knee joints flexed at approximately 90°.
We instructed the subjects to keep both heels firmly placedon the ground and repeatedly tap the floor quickly and vigorously for 10 sec unilaterally. Following a few practice
trials, the subjects carried out two test trials once on eachside. The examiner counted the number of taps for eachtrial and obtained the average of the two as the score.

Statistics

Statistical measures, setting the significance level at p <0.05, included: (1) the Chi-square test for comparing categorical data, (2) Paired t-test for evaluating paired continuous data, (3) the one-way ANOVA followed by Tukey post
hoc test (for homoscedasticity data) or Games-Howell test(for heteroscedasticity data) for comparing unpaired continuous data between groups, and (4) the Spearman’s rankcorrelation coefficients for interrelation analyses. We used
SPSS software, version 21.0 (SPSS Inc., Japan) for thesestatistical analyses.
We used G*Power version 3.1.9.2 software (Heinrich-HeineUniversität Düsseldorf, Germany) for power analyses to estimate the statistical power of the results obtained with thecurrent sample sizes.

RESULTS
Step length in gait performance test

Figure 2: Sequential changes of the ground reaction force forthe right leg support (R) and the left leg support (L) recordedwith the force plate during the initial 2.64-m walk (top) and thefinal 2.64-m walk (bottom) in a 78-year-old man with cervicalspondylotic myelopathy. Abscissa, time in seconds after heelstrike of the first swing leg. Ordinate, foot pressure in the percentage of the maximal value of each recording. The measurement showed the step length of 0.35 m and the walking speedof 0.71 m/s for the initial 2.64-m walk and 0.40 m and 0.96 m/s,
respectively, for the final 2.64-m walk.

10-sec foot-tapping test (FTT)

Table 2 summarizes the results (mean ± SD) of the quantitative assessment of the gait performance test. Comparisonof the step length (expressed in percentage of the height)
within each group demonstrated a significantly smaller
value for the initial than final 2.64-m walk in the DCM(34.2±6.5 % vs. 36.1±6.3 %; p<0.001 [power=0.914])
but not in the healthy controls or LSS. Comparison of thestep length between DCM and other two groups showed asmaller value in the DCM than in the controls for the initial(34.2±6.5 % vs. 41.4±2.2 %; p<0.001 [power=0.990]) andfinal 2.64-m walks (36.1±6.3 % vs. 40.6±2.5 %; p=0.005[power=0.771]). The initial-to-final step length ratios (initial/final) showed a significantly smaller value in DCM(94.8±9.9 %) than in LSS (104.5±13.3 %; p=0.018 [power=0.629]) (Figure 3) [Table 2].

We used a previously described method for a 10-sec
foot-tapping test,7 an objective, easy-to-use means of

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76

77

NS

NS

36.7 ± 7.0
p =0.018(0.629)104.5± 3.3

102.0 ± 6.2

NSNS94.8 ± 9.9

p < 0.001(0.914)NS(Mean ± SD)"p-value*(power†)"NS

Final 2.64-m
walk

NS

NS

130.7 ±
12.0

NS

p =0.047(0.482)p < 0.001(1.0)"p-value*(power†)"NS

92.6 ± 6.9

NS94.9 ± 7.4

90.1 ± 8.2(Mean ± SD)

Initial / Final(%)

NS

1.22 ± 0.26

p < 0.005(0.984)1.38 ± 0.16

1.08 ± 0.25

(Mean ± SD)

NS

1.27± .28

NS

1.47 ± 0.17

1.28 ± 0.27

NS, not significant; DCM, degenerative compression myelopathy; LSS, lumbar spinal stenosis.

† Statistical power obtained by using G*Power version 3.1.9.2 software.

***Comparison between DCM patient group and LSS patient group with one-way ANOVA followed by Tukey post hoc test or Games-Howell test.

NS

p <0.01(0.785)p < 0.001(1.0)(Mean ± SD) "p-value*(power†)"Initial 2.64-m Final 2.64-m
walk
walk

Walking speed (m/s)** Comparison between DCM patient group and Healthy subject group with one-way ANOVA followed by Tukey post hoc test or Games-Howell test.

p <0.01(0.537)129.6 ± 21.0

124.9 ± 11.2

124.5 ± 18.9

118.1 ± 17.5

(Mean ± SD) (Mean ±SD)

Initial 2.64m walk

15.2± 8.7

Initial / Final(%)

Cadence (steps/min)* Comparison between Initial 2.64-m walk and Final 2.64-m walk with paired t-test.

p-value***(power†)37.8 ± 5.8

10LSS patientsp <0.005(0.771)41.4 ± 2.2 40.6 ± 2.5p<0.001(0.990)11

Healthysubjects

34.2 ± 6.5 36.1± 6.3(Mean ±SD)

(Mean ±
SD)"p-value**(power†)"49

DCM patiens

Final 2.64m walk

Initial2.64-mwalk

Number Step length/Heightof Sub- (%)
jects

Table 2: Quantitative assessment of the gait performance testp < 0.001(0.961)96.5 ± 7.3

p <0.01(0.882)93.8 ± 6.2

85.1 ± 9.4(Mean ± SD)

Initial / Final(%)

Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

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Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

1.28±0.27 m/s; p<0.001 [power=1.000]) and healthy group(1.38±0.16 m/s vs. 1.47±0.17 m/s; p<0.01 [power=0.785]),
but not in LSS. Comparison of the walking speed between
DCM and other two groups showed smaller values in DCM
than in controls only for the initial 2.64-m walk (1.08±0.25
m/s vs. 1.38±0.16 m/s; p<0.005 [power=0.984]). The initialto-final walking speed ratios (initial/final) showed a significantly smaller value in DCM (85.1±9.9 %) compared to either controls (93.8±6.2 %; p<0.01 [power=0.882]) or LSS(96.5±7.3 %; p<0.001 [power=0.961]) (Figure 5).
Figure 3: Bar graphs illustrating the step length expressed inpercentage of the height for the initial 2.64-m walk (dark graybar) and the final 2.64-m walk (light grey bar), and the initialto-final step length ratio (black bar) in patients with degenerative compression myelopathy (DCM group), healthy subjects(healthy group), and the patients with lumbar spinal stenosis(LSS group). Note that only the DCM group showed a significant difference between the initial and final step length and asignificantly smaller initial-to-final step length ratio than LSSgroups.

Cadence in gait performance test

Comparison of the cadence within each group demonstrated
a significantly smaller value for the initial than final 2.64-mwalk in all three groups (p<0.001 [power=1.000] for DCM;
p=0.047 [power=0.482] for controls; p<0.01 [power=0.537]
for LSS). Comparison of the cadence between DCM and theother two groups revealed no significant differences for the
initial nor final 2.64-m walk, nor the initial-to-final cadence
ratios (initial/final) (Figure 4).

Figure 5: Bar graphs of the same arrangement as in Figs.
3 and 4 to illustrate the changes in walking speed. Note thatboth DCM and the healthy groups showed significant differences between the initial and final walking speeds, and theDCM group had a significantly smaller initial-to-final walking
speed ratio than the other two groups.

Correlation of step length and walking speed
for the initial 2.64-m walk with functional scaleand FTT in DCM patients

The JOA lower-limb motor scores averaged 2.1±0.7 points,
and the number of taps in FTT, 19.2±4.3 times, for DCM.
The step length and the walking speed for the initial 2.64-mwalk showed a significant correlation with the JOA scores(r=0.479; p<0.001 and r=0.364; p<0.01) and the number oftaps in FTT (r=0.349; p=0.014 and r=0.342; p=0.016).

DISCUSSION

Figure 4: Bar graphs of the same arrangement as in Figure 3
illustrate the changes in cadence (i.e., step frequency). Notethat all three groups showed a significant difference between
the initial and final cadence.

Walking speed in gait performance test

Walking speed measured significantly smaller for the initialthan the final 2.64-m walk both in DCM (1.08±0.25 m/s vs.
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Gait initiation constitutes a critical part of mobility function
and presents a challenge for many patients with central nervous system pathology8 such as stroke,10-14 cerebral palsy,15
and Parkinson’s disease.16-21 The complex process of gait initiation involves various anticipatory postural adjustments in
preparation for stepping, including soleus muscle inhibition
followed by tibialis anterior (TA) muscle activation in theswing limb before heel-off.8,22,23Electromyographic (EMG)
studies with surface electrodes combined with kinematic
analysis in patients with poststroke gait disorders revealed78

Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

a delayed onset and reduced amplitude of TA muscle activation when initiating gait with the paretic limb.10,11,13
In one study, spinal cord injury patients with lower limb
spasticity had a prominent interval prolongation from the beginning of the quadriceps EMG activity to the onset of fastknee extension.24 Also, spinal cord injury patients, classified
as ASIA Grade D (Chang et al., 2004),25 demonstrated a prolonged gait initiation period between the auditory cue andheel-strike of the first swing leg and the reduced first step
length. Most previous studies on DCM primarily focused onkinematical gait pattern analyses under steady-state conditions.26-31 Therefore, few dealt with gait-onset difficulty typically prominent after periods of inactivity, which patientsmost commonly complain about.
We thus designed the present study to document if DCM
patients indeed have a greater difficulty at the beginning ofgait than in steady-state conditions as compared with healthy
subjects and LSS patients.
Our data confirm significantly slower speeds in DCM than incontrols for the initial 2.64-m. Although both groups walked
more slowly for the initial than final 2.64-m, the reduced
speed reflected a decline in both step length and cadence for
DCM and a decline in cadence alone for controls. Like thehealthy group, LSS also had an initial decline of cadence
without step length shortening. This finding stands in contrast to a previous report that walking speed initially changes as a function of step length rather than step frequency
or cadence.8 This discrepancy may have resulted from the
instructions given to the participants for baseline walking:maximum comfortable speed from the beginning in the current study; and subjects’ comfortable speed in the previous
study. Accordingly, our healthy subjects and LSS patients
must have managed a longer step length from the beginningto maximize the speed but DCM patients could not keep up
because of spasticity. Furthermore, DCM had significantly
lower initial-to-final ratios in step length than in LSS, andwalking speed than controls and in LSS. All things considered, these findings indicate that DCM characteristically affects gait initiation, reducing both step length and cadence
immediately following a period of leg muscle relaxation
more than during steady-state gait.
In addition, both the initial step length and walking speed in
DCM showed a significant correlation with the JOA functional assessment scores and FTT data that quantify theslowness of voluntary leg movements. This finding indicatesthat the pronounced slowness in gait initiation after sitting
constitutes an additional physiologic mechanism for spastic
gait seen in DCM.
Based on the available data, we can only speculate on thephysiological mechanisms underlying this phenomenon. As
shown by early studies with rectified surface EMG analyses,
79

spastic limbs require a longer duration of EMG activity thannormal to reach the muscular tension for movement initiation.24.32,33 These data suggest that the corticospinal tract lesions reduce the number of functional upper motor neurons,
which then must fire repetitively for temporal summationof the discharges to activate a sufficient amount of anterior
horn cells.32 Because of this compensatory mechanism, gait
initiation takes longer after corticospinal tract lesions thannormal. In addition, as demonstrated in recent studies using F-wave34-38 and H-reflex,39 the anterior horn cell requires
ongoing descending facilitatory influences to maintain its
excitability. Consequently, sustained leg muscle relaxation
while lying or sitting could induce rest-induced hypoexcitability of the pertinent anterior horn cells. This, in turn, may
further reduce walking speed at the beginning of gait immediately after a certain period of inactivity of the leg muscles.
Regardless of the underlying mechanisms, the presence ofrest-induced delay in gait initiation often hints at the diagnosis of DCM. In addition, awareness of this symptom helps
provide appropriate care to prevent a fall-related hip fracture. For DCM patient care and rehabilitation, assistants
must remember “speed-accuracy trade-off”, a well-known
phenomenon in motor behaviour,40 which predicts quicker
the attempt, less accurate the outcome.

STUDY LIMITATIONS
We tested only a relatively small number of healthy subjects
and LSS patients and unfortunately, the manufacturer now
provides only a revised version of the ground reaction force
plate different from that used in this study, which may preclude conducting a larger scaled study to further confirm theresults. According to a post-hoc power analysis, the differences detected in the present study had a power level greaterthan 80% (i.e., 0.8) for the significance level at p<0.001, but
not necessarily so for the lower significance levels.

CONCLUSIONS
We conclude that reduced walking speed in DCM patients
becomes more pronounced immediately following a 10-min
sitting. This phenomenon seems to represent an additional
aspect of the physiologic mechanisms that characterize spastic gait disorders. Altered descending central drive causedby corticospinal tract involvement may account for this phenomenon in combination with rest-induced hypoexcitabilityof the pertinent anterior horn cells.

ACKNOWLEDGEMENTS
The authors acknowledge the immense help received from thescholars whose articles are cited and included in references of
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Enoki et al: Rest-induced reduction in walking speed helps differentiate degenerative compression myelopathies from lumbar spinal stenosis

this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals, and books from
where the literature for this article has been reviewed and discussed.
Conflict of Interest: NIL
Source of Funding: NIL

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Int J Cur Res Rev | Vol 13 • Issue 12 • June 2021