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The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is ...
The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is ...
SUMMARY Equinus in hemiplegic children is multifactorial. In some cases it is due to a short muscle, in others to simple foot‐drop, tonic spasticity, rigidity, compensation for a short limb, fixed flexion contracture at the hip, dominantly inherited forefoot deformity, forefoot equinus secondary to chronic toe‐walking, or abnormalities of the visco‐elastic properties of the muscle, with true intramuscular contracture. This neurophysiological study confirms that hemiplegia in children is not a homogeneous condition. Some have tonic spasticity; some, although stiff, show electrical silence on stretching; some appear to have a short muscle, with no hypertonicity; and others have hypertonicity in relation to position (i. e. rigidity). A short muscle is not always associated with tonic spasticity with reciprocal inhibition. Weakness can occur without spasticity. Speed of movement of toes, ankle and hip is also significantly reduced. RÉSUMÉ Neurophysiologie de la fonction du membre infeieur chez l'enfant hémiplégique L'équin de l'enfant hémiplégique est multifactoriel. Dans quelques cas, il est dûà un muscle court, dans d'autres à une chute du pied, une spasticité tonique, une rigidité, une compensation de membre court, une rétraction fixée en flexion de la hanche, une déformation de l'avant‐pied d'origine génétique dominante, un équin de l'avant‐pied par marche chronique sur les orteils, ou à des anomalies dans les propriétés visco‐élastiques du muscle, avec rétraction intra‐musculaire vraie. Cette étude neuro‐physiologique confirme que l'hémiplégie infantile n'est pas une condition homogéne. Quelques unes présentent une spasticité tonique; quelques unes se traduisent par un silence électrique à l'étirement en dépil d'une raideur; quelques unes se traduisent par un muscle court sans hypertonicité; d'autres ont une hypertonicité en rapport avec la position (p. e. la rigidité). Un muscle court n'est pas toujours associéà une spasticité tonique avec inhibition réciproque. La faiblesse peut survenir sans spasticité. La vitesse des mouvements des orteils, de la cheville et de la hanche est également réduite de façon significative. ZUSAMMENFASSUNG Neurophysiologie der Funktion der unteren Extremität bei Kindern mit Hemiplegie Der Spitzfuß bei Kindern mit Hemiplegie ist multifactoriell. In einigen Fällen ist er bedingt durch eine Muskelverkürzung, bei anderen durch einen einfachen Fallfuß, tonische Spastik, Rigidität, Kompensation für ein verkürztes Bein, fixierte Beugekontraktur der Hüfte, dominant vererbte Fußmißbildung, Spitzfuß durch ständiges Laufen auf den Zehen oder Anomalien der viskoelastischen Eigenschaften des Muskels mit intramuskulärer Kontraktur. Diese neurophysiologische Studie zeigt, daß die Hemiplegie bei Kindern keinen einheitlichen Charakter hat. Einige haben eine tonische Spastik; einige, obwohl starr, zeigen beim Strecken keine elektrische Reaktion; einige scheinen eine Muskelverkürzung ohne Tonuserhöhung zu haben; andere haben eine lageabhängige Hypertonic (Rigidität). Eine Muskelverkürrung ist nicht im...
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