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Modulation of Locomotor Patterns and Spasticity with Clonidine in Spinal Cord Injured Patients

Published online by Cambridge University Press:  18 September 2015

J.E. Stewart ,
H. Barbeau  and
S. Gauthier
J.E. Stewart
Affiliation:
School of Physical and Occupational Therapy, McGill University, Montreal
H. Barbeau*
Affiliation:
School of Physical and Occupational Therapy, McGill University, Montreal
S. Gauthier
Affiliation:
School of Physical and Occupational Therapy, McGill University, Montreal
*
School of Physical and Occupational Therapy, McGill University, 3654 Drummond Street, Montreal, Quebec, Canada H3G 1Y5
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Abstract:

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This double blind cross-over study, involving 9 chronic spinal cord injured (SCI) patients (6 paraplegic and 3 paretic), was a first attempt to investigate the effects of the noradrenergic agonist, clonidine, on the modulation of the locomotor pattern and spasticity in patients with spinal cord lesions. Electromyographic (EMG), footswitch and video recordings were made as the patients walked on a treadmill with the support of an overhead harness if needed. Overground locomotion was also assessed in the paretic patients. All 3 spastic paretic patients had kinematic deviations and abnormal EMG recruitment profiles during the premedication or placebo sessions. With clonidine therapy one patient demonstrated a marked improvement in locomotor function. This patient progressed from non-ambulation to limited independent ambulation as the extent of coactivation in antogonist muscles decreased. The other 2 paretics who presented limited spasticity showed minimal changes while on clonidine. In the paraplegic patients, clonidine did not elicit locomotor activity, although there were marked reductions in stretch reactions and clonus during assisted locomotion. They remained incapable of locomotion, either during the control period or during the clonidine therapy. These results indicate that clonidine may be a potentially useful medication for both locomotion and certain manifestations of spasticity in SCI patients but further investigation is warranted.

Information

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 18 , Issue 3 , August 1991 , pp. 321 - 332
Copyright
Copyright © Canadian Neurological Sciences Federation 1991

References

REFERENCES

1.Knutsson, E. Analysis of gait and isokinetic movements for evaluation of antispastic drugs or physical therapies. In: Desmedt, JE,ed. Motor Control Mechanisms in Health and Disease. New York: Raven Press, 1983.1013–1034.Google Scholar
2.Conrad, B, Beneke, R, Carnehl, J, et al. Pathophysiological aspects of human locomotions. In: Desmedt, JE,ed. Advances in Neurology, New York: Raven Press 1983; 717–726.Google Scholar
3.Conrad, B. Beneke, R, Meinck, HM, Gait disturbances in paraspastic patients. In: Delwaide, PJ, Young, RR, ed. Restorative Neurology, Vol I. Clinical Neurophysiology in Spasticity . Netherlands: Elsevier Science Publishers BV(Biomedical Division) 1985.155–174.Google Scholar
4.Dietz, V. Impaired reflex control of posture and gait in spastic paresis. In: Bles, W, Brandt, TH, eds. Disorders of Posture and Gait . Netherlands: Elsevier Science Publishers BV(Biomedical Division) 1986.243–252.Google Scholar
5.Barbeau, H, Fung, J, Stewart, J, et al. Impairment of spastic paraparetic gait: Implications for new rehabilitation strategies. Proceeding of the fifth biennial conference and human locomotion symposium of the Canadian Society for Biomechanics 1988; 12–16.Google Scholar
6.Chapman, CE, Wiesendanger, M. The physiological and anatomical basis of spasticity: A review. Physiotherapy Canada 1982; 34: 125–135.Google Scholar
7.Knutsson, E, Richards, C. Different types of disturbed motor control in gait of hemiparetic patients. Brain 1979; 102: 405–430.CrossRefGoogle ScholarPubMed
8.Knutsson, E. Studies of gait control in patients with spastic paresis. In: Delwaide, PJ, Young, RR, eds. Clinical Neurophysiology in Spasticity . Netherlands: Elsevier Science Publishers BV(Biomedical Division) 1985.175–182.Google Scholar
9.Tuckman, J, Chu, DS, Petrillo, CR, et al. Clinical trial of an alpha adrenergic receptor stimulating drug (Clonidine) for the treatment of spasticity in spinal cord injured patients. In: Naftchi, NZE, ed. Spinal Cord Injuries; Spectrum Publications 1983.133–137.Google Scholar
10.Maynard, FM. Early clinical experience with clonidine in spinal spasticity. Paraplegia 1986; 24: 175–192.Google ScholarPubMed
11.Nance, PW, Shears, AH, Nance, DM. Clonidine in spinal cord injury. Chest 1985; 133: 41–42.Google ScholarPubMed
12.Rossignol, S, Barbeau, H, Julien, C. Locomotion of the adult chronic spinal cat and its modifications by monoaminergic agonists and antagonists. In: Goldberger, ME, Gorio, A, and Murray, M, eds. Development and Plasticity of the Mammalian Spinal Cord. Fidia Research Series . 3: Padova: Liviana Press 1986; 323–345.Google Scholar
13.Barbeau, H, Julien, C, Rossignol, S. The effects of clonidine and yohimbine on locomotion and cutaneous reflexes in the adult spinal cat. Brain Res 1987; 437: 83–96.CrossRefGoogle Scholar
14.Forssberg, H, Grillner, S, The locomotion of the acute spinal cat injected with Clonidine iv. Brain Res 1973; 50: 184–186.CrossRefGoogle Scholar
15.Barbeau, H, Rossignol, S, Effects of noradrenergic, serotonergic and dopaminergic drugs on the initiation of locomotion in the adult spinal cat. Neurosci Abst 1989; 15: 393.Google Scholar
16.Grillner, S. Control of locomotion in bipeds, tetrapods, and fish. In: Brooks, VB, ed. The Nervous System: Motor Control. Handbook of Physiology, Section 1 Amer Physiol Soc Maryland: Waverly Press 1981; 1179–1236.Google Scholar
17.Stewart, JE, Barbeau, H. Gauthier, S, The effects of clonidine on clinical spasticity and on the modulation of the locomotor pattern in chronic spastic spinal cord patients. Neurosci Abst 1987; 13: 353.Google Scholar
18.Frankel, HL, Hancock, DO, Hyslop, G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia. Paraplegia 1967; 7: 179–192.Google Scholar
19.Arndts, D, Doevendans, J, Kirsten, R, et al. New aspects of the pharmacokinetics and pharmacodynamics of clonidine in man. Eur J Clin Pharmacol 1983; 24: 21–30.CrossRefGoogle ScholarPubMed
20.Anavekar, N, Jarott, B, Toscano, M, et al. Pharmacokinetics and pharmacodynamic studies of oral clonidine in normotensive subjects. Eur J Clin Pharmacol 1982; 23: 1–5.CrossRefGoogle ScholarPubMed
21.Barbeau, H, Wainberg, M, Finch, L. Description and application of a system for locomotor rehabilitation. Med Biol Eng Comp 1987; 25: 341–344.CrossRefGoogle ScholarPubMed
22.McLellan, DL. Co-contraction and stretch reflexes in spasticity during treatment with baclofen. J Neurol Neurosurg Psychiatry 1977; 40: 30–38.CrossRefGoogle Scholar
23.Landau, WM. Spasticity - What is it? What is it not?, In: Feldman, RG, Young, RR, and Koella, WP, eds. Spasticity: Disordered Motor Control, Chicago Yearbook 1980; 17–24.Google Scholar
24.Knutsson, E, Martensson, A. Dynamic motor capacity in spastic paresis and its relation to prime motor dysfunction, spastic reflexes and antagonist coactivation. Scand J Rehab Med 1980; 138: 1–14.Google Scholar
25.Dietz, V, Berger, W. Normal and impaired regulation of muscle stiffness in gait: A new hypothesis about hypertonia. Exp Neurol 1983; 79: 680–687.CrossRefGoogle Scholar
26.Grillner, S, Zangger, P. On the central generation of locomotion in the low spinal cat. Exp Brain Res 1979; 34: 241–261.CrossRefGoogle ScholarPubMed
27.Eidelberg, E. Consequences of spinal cord lesions upon motor function, with special reference to locomotor activity. Prog Neurobiology 1981; 17: 135–202.CrossRefGoogle ScholarPubMed
28.Zomlefer, MR, Gaines, RF, McCleary, LG. Locomotor control in spinal cord injured humans. Neuroscience Abst 1986; 188. (2): 634.Google Scholar
29.Eidelberg, E, Walsen, JG, Nguyen, LH. Locomotor control in macaque monkeys. Brain 1981; 104: 647–663.CrossRefGoogle ScholarPubMed
30.Vilensky, AJ. Locomotor behavior and control in human and nonhuman primates: Comparisons with cats and dogs. Neurosci Biobehav Rev 1987; 11: 263–274.CrossRefGoogle ScholarPubMed
31.Forssberg, H, Stumbling corrective reaction: A phase-dependent compensatory reaction during locomotion. J Neurophysiol 1979; 42: 936–953.CrossRefGoogle ScholarPubMed
32.Forssberg, H. Phasic gating of cutaneous reflexes during locomotion. In: Taylor, A, Young, RR, and Prochazka, A, eds. Muscle receptors and movement. London, (MacMillan) 1981; 403–412.CrossRefGoogle Scholar
33.Tremblay, LE, Bedard, P, Effect of clonidine on motoneuron excitability in spinalized rats. Neuropharmacology 1986; 25: 41–46.CrossRefGoogle ScholarPubMed
34.Andres, K, Takesu, H, Matsushita, AS. Modulation of spinal reflex activities in acute spinal rats with alpha-adrenergic agonists and antagonists. Jap J Pharmacol 1978; 28: 165–168.Google Scholar
35.Kehne, J, Gallager, DW, Davis, M, Spinalization unmasks clonidine's alpha-1 adrenergic mediated excitation of the flexor reflex in rats. J Neurosci 1985; 5: 1583–1590.CrossRefGoogle ScholarPubMed
36.Yaksh, T, Pharmacology of spinal adrenergic systems which modulate spinal nociceptive processing. Pharmacol Biochem Behav 1985; 22: 845–858.CrossRefGoogle ScholarPubMed