ライフサイエンスコーパス: H-reflex

1 timulation of the median nerve generating an H-reflex.

2 a afferent activation of motoneurons via the H-reflex.

3 offman reflex (H-reflex) and (3) conditioned H-reflex.

4 ove M-response threshold elicited the SOL(R) H-reflex.

5 l hip oscillations on the ipsilateral soleus H-reflex.

6 ost-alpha motoneuronal control of the soleus H-reflex.

7 electrophysiologically by the presence of an H-reflex.

8 included cortical electrical stimulation and H-reflexes.

9 ous procedures elicited the QD(R) and SOL(L) H-reflexes.

10 ed the frequency-dependent modulation of the H-reflex, (3) reduced antagonist ankle muscle co-contrac

11 ensory CV, determined via Hoffmann's reflex (H-reflex) (A-fiber), was decreased in diabetic compared

12 We found an overall decrease in average RF H-reflex amplitude among all 7 participants (44% drop, p

13 ain is the slope of the relationship between H-reflex amplitude and EMG amplitude.

14 Agonist H reflex amplitudes were linearly related to, and increa

15 H-reflex amplitudes were higher than running H-reflex amplitudes by a constant amount.

16 At all levels of EMG, walking H-reflex amplitudes were higher than running H-reflex am

17 has emerged based on operant conditioning of H-reflex, an electrical analog of the spinal stretch ref

18 th the transition from silence to firing, so H reflex and other tests of 'excitability' must then be

19 ound between the amplitude of the antagonist H reflexes and the preceding antagonist IEMG.

20 To address this question, the soleus H-reflex and conditioning of the H-reflex by stimulating

21 The plasticity that changes the QD(R) H-reflex and locomotor kinematics may be inevitable (i.e

22 Electrophysiological recordings of the H-reflex and nonnociceptive flexion reflex were obtained

23 trical stimulation, (2) test Hoffman reflex (H-reflex) and (3) conditioned H-reflex.

24 In addition, Hoffman reflex (H-reflex) and motor evoked potentials (MEPs) were record

25 ent increases postsynaptic inhibition of the H-reflex, and it hyperpolarizes the reversal potential f

26 ned increase or decrease in the right soleus H-reflex-and examined an old behavior-locomotion.

27 ributions to reciprocal inhibition of soleus H-reflexes are not static but rather are task-specific a

28 neal nerve, was assessed from changes in the H reflex at long conditioning intervals, in six normal s

29 ed by a paired-pulse TMS, and forearm flexor H reflexes before and after 750 pulses of 5 Hz rTMS over

30 a, the frequency-dependent modulation of the H-reflex, behavioural reflex activity, and neuroanatomic

31 record direct muscle responses (M-waves) and H-reflexes, both of which are comparable to those record

32 nide decreased presynaptic inhibition of the H-reflex, but not postsynaptic inhibition.

33 nide decreases presynaptic inhibition of the H-reflex, but not postsynaptic inhibition.

34 the soleus H-reflex and conditioning of the H-reflex by stimulating homonymous [depression of the so

35 Facilitation of H-reflexes by this conditioning was likely not mediated

36 dy asked whether operant conditioning of the H-reflex can modify locomotion in spinal cord-injured ra

37 normally prevents the plasticity underlying H-reflex change from impairing locomotion.

38 The final H-reflex change was the sum of within-session (i.e., tas

39 ans the development of operantly conditioned H-reflex change, a simple motor skill that develops grad

40 rrelated in direction and magnitude with the H-reflex change.

41 ributions to reciprocal inhibition of soleus H-reflexes changed with increasing levels of TA contract

42 esign that allowed us to assess pathological H-reflex changes and drug intervention effects over time

43 An H reflex conditioning technique was used to monitor the

44 y is associated with and might contribute to H-reflex conditioning adds to evidence that motor learni

45 pinal dorsal ascending tract transection nor H-reflex conditioning alone impaired locomotion.

46 Using two separate methods (H-reflex conditioning and directional effects of TMS), w

47 Although H-reflex conditioning and locomotion did not interfere w

48 ations between AIS plasticity and successful H-reflex conditioning are consistent with those between

49 Thus, the acquisition of H-reflex conditioning consists of two phenomena, task-de

50 ocomotion did not interfere with each other, H-reflex conditioning did affect how locomotion was prod

51 Soleus H-reflex conditioning did not affect the duration, lengt

52 H-reflex conditioning is a model for studying the plasti

53 de promising initial results that operant RF H-reflex conditioning is feasible, encouraging expansion

54 They also suggest that H-reflex conditioning might be used to improve the abnor

55 methods to study in adult rats the impact of H-reflex conditioning on the AIS of the spinal motoneuro

56 ation with other recent data, they show that H-reflex conditioning produces a complex pattern of spin

57 pinal dorsal ascending tract transection and H-reflex conditioning were combined, the rats developed

58 l rats the interactions of this new skill of H-reflex conditioning with the old well established skil

59 The H-reflex decrease was accompanied by improvements in wal

60 s and weaker AnkG-IR correlated with greater H-reflex decrease.

61 ft in motoneuron firing threshold underlying H-reflex decrease; they are consistent with modelling su

62 Over the 30 sessions, the soleus H-reflex decreased in two-thirds of the DC subjects (a s

63 With swing-phase down-conditioning, the H-reflex decreased much faster and farther than did the

64 Further, the soleus H-reflex depression did not vary with the contralateral

65 The lack of an H reflex despite normal motor nerve function in the hind

66 The SOL(L) H-reflex did not change.

67 The H-reflex did not decrease in the other DC subjects or in

68 H-reflex down-conditioning did not affect AIS dimensions

69 n was assessed, subjects completed either 30 H-reflex down-conditioning sessions (DC subjects) or 30

70 Successful, but not unsuccessful, H-reflex down-conditioning was associated with more GABA

71 antagonistic group I afferents on the soleus H-reflex during imposed sinusoidal hip movements.

72 The degree of depression of the second H-reflex during standing ( > 78%) was similar in magnitu

73 Specifically, we down-conditioned the soleus H-reflex during the swing-phase of locomotion in people

74 litation were correlated with changes in the H-reflex during voluntary contraction, suggesting an ass

75 he conditioned H-reflex relative to the test H-reflex) during APAs before step initiation (functional

76 muli which had no effect on the amplitude of H reflexes elicited in active ADM muscle.

77 phase of walking as observed for the soleus H-reflex elicited by tibial nerve stimulation.

78 In rats in which the soleus H-reflex elicited in the conditioning protocol (i.e., th

79 had been decreased by down-conditioning, the H-reflexes elicited during the stance and swing phases o

80 ulating homonymous [depression of the soleus H-reflex evoked by common peroneal nerve (CPN) stimulati

81 [monosynaptic Ia facilitation of the soleus H-reflex evoked by femoral nerve stimulation (FN facilit

82 ut not presynaptic inhibition of the plantar H-reflex evoked by posterior biceps and semitendinosus (

83 d significant restoration of RDD and reduced H-reflex excitability in SCI animals.

84 target cell-specific molecular regulators of H-reflex excitability to manage spasticity after SCI.Sig

85 After transection, the H-reflex exhibited decreased depression at high stimulat

86 produced longer-lasting facilitation of the H-reflex for up to 2 min, consistent with tonic PAD in r

87 To examine soleus H-reflex gain across a range of EMG levels during human

88 us system adjusts H-reflex threshold but not H-reflex gain between walking and running.

89 stretch reflex responses.A common measure of H-reflex gain is the slope of the relationship between H

90 We hypothesised that H-reflex gain would be independent of gravity level.We r

91 Similarly, in rats in which the conditioning H-reflex had been increased by up-conditioning, the loco

92 onditioning protocol (i.e., the conditioning H-reflex) had been decreased by down-conditioning, the H

93 psin treatment after SCI reduced SCI-induced H-reflex hyperexcitability and abnormal alpha-motor neur

94 cally, astrocytic Rac1KO reduced SCI-related H-reflex hyperexcitability, decreased dendritic spine dy

95 s the utility of targeting PAK1 to attenuate H-reflex hyperexcitability, we administered Romidepsin,

96 There was no effect on H reflexes in the flexor carpi radialis muscle, even tho

97 creased much faster and farther than did the H-reflex in all previous animal or human studies with th

98 he conditioned H-reflex relative to the test H-reflex in both the tasks.

99 peripheral nerves it is difficult to elicit H-reflex in leg muscles other than the soleus, especiall

100 rons from animals in which the triceps surae H-reflex in one leg had been increased (HRup mode) or de

101 d the impact of down-conditioning the soleus H-reflex in people with impaired locomotion caused by ch

102 H-reflexes in several leg muscles were facilitated by pr

103 Combined with the larger H-reflexes in TU rats, this anatomical finding supports

104 g the hypothesis that they may contribute to H-reflex increase.

105 soma; greater length correlated with greater H-reflex increase.

106 s as we observed an enhanced Hoffman reflex (H-reflex), indicating a hyperexcitable spinal cord.

107 The Hoffmann (H-) reflex is an electrical analogue of the monosynaptic

108 pendent depression (RDD) of the monosynaptic H-reflex is indicative of hyperreflexia, a physiological

109 Operant conditioning of Hoffmann's reflex (H-reflex) is a non-invasive and targeted therapeutic int

110 Studying H-reflex modulation provides insight into how the nervou

111 e plasticity, rats had near normalization of H-reflex modulation.

112 Results showed that the flexor, but not H-reflex, of Chronic Spinal rats was significantly large

113 d the effect of up-conditioning soleus (SOL) H-reflex on SOL and tibialis anterior (TA) function afte

114 We are studying the mechanisms of H-reflex operant conditioning, a simple form of learning

115 A condition-test (C-T) H-reflex paradigm (conditioned stimulus applied to the c

116 tude combined with no significant changes in H-reflex parameters suggests this increased strength is

117 mptom of hyperexcitability within the spinal H-reflex pathway.

118 ise be disturbed by the change in the SOL(R) H-reflex pathway.

119 stretch reflex or its electrical analog, the H-reflex, produces spinal cord plasticity and can thereb

120 h astrocytic Rac1KO demonstrated near-normal H-reflex RDD similar to pre-injury levels.

121 control Rac1(wt) animals displayed a loss of H-reflex RDD, that is, hyperreflexia.

122 The percent depression of the second H-reflex relative to the first was used as a measure of

123 s quantified by the ratio of the conditioned H-reflex relative to the test H-reflex in both the tasks

124 of PSI (i.e. higher ratio of the conditioned H-reflex relative to the test H-reflex) during APAs befo

125 al and pre-synaptic inhibition of the soleus H-reflex, respectively.

126 We assessed the soleus H-reflex, shear modulus (ultrasound elastography) and va

127 Over the 24 conditioning sessions, H-reflex size gradually increased in six of eight HRup s

128 The soleus H-reflex size increased in both groups during voluntary

129 After a baseline period in which soleus H-reflex size was measured and locomotion was assessed,

130 When the subject was asked to change H-reflex size, immediate visual feedback indicated wheth

131 ion in frequency-dependent depression of the H-reflex, suggesting hyperreflexia.

132 inhibition acting on the ipsilateral soleus H-reflex, supporting cross-leg reflex and heteronymous m

133 Result of the H-reflex test and membrane expression of KCC2 were not s

134 for 50 d to a protocol that rewarded SOL(R) H-reflexes that were above (HRup rats) or below (HRdown

135 nt conditioning of the primate triceps surae H-reflex, the electrical analog of the spinal stretch re

136 and monkeys gradually change the size of the H-reflex, the electrical analog of the spinal stretch re

137 The frequency-related depression of the Sol H reflex, thought to reflect HD, was tested at rest, bef

138 We conclude that the nervous system adjusts H-reflex threshold but not H-reflex gain between walking

139 9 +/- 2% (p < 0.001) and increased the QD(R) H-reflex to 121 +/- 7% (p = 0.02).

140 HRup conditioning increased the SOL(R) H-reflex to 214 +/- 37% (mean +/- SEM) of control (p = 0

141 HRdown conditioning decreased the SOL(R) H-reflex to 69 +/- 2% (p < 0.001) and increased the QD(R

142 f control (p = 0.02) and decreased the QD(R) H-reflex to 71 +/- 26% (p = 0.06).

143 normalised the stimulus M-wave and resulting H-reflex to the maximal M-wave amplitude (Mmax) elicited

144 ued control data collection (TC rats) or SOL H-reflex up-conditioning (TU rats).

145 H-reflex up-conditioning increased the right soleus burs

146 Successful, but not unsuccessful, H-reflex up-conditioning is associated with greater AIS

147 These results suggest that H-reflex up-conditioning may improve functional recovery

148 ere then either exposed or not exposed to an H-reflex up-conditioning protocol that greatly increased

149 cal finding supports the hypothesis that SOL H-reflex up-conditioning strengthened primary afferent r

150 Successful, but not unsuccessful, H-reflex up-conditioning was associated with greater AIS

151 act, 2 post-stroke) to down-condition the RF H-reflex using visual feedback.

152 ised, slopes of linear regressions fitted to H-reflex versus EMG data were independent of gravity for

153 The soleus H-reflex was also conditioned by medial gastrocnemius (M

154 The soleus H-reflex was conditioned by stimulating the common peron

155 hip was higher than the left; when the right H-reflex was decreased by conditioning, the opposite occ

156 The soleus H-reflex was evoked every 4 s during bilateral synchrono

157 When the right H-reflex was increased by conditioning, the right step l

158 time of, or shortly after, symptom onset the H-reflex was lost.

159 In each conditioning session, the soleus H-reflex was measured while the subject was or was not a

160 owever, the conditioned change in the stance H-reflex was positively correlated with change in the am

161 The ipsilateral soleus H-reflex was profoundly depressed in all conditions.

162 than in TC rats, and the final recovered SOL H-reflex was significantly larger in TU than in TC rats.

163 ns (DC subjects) or 30 sessions in which the H-reflex was simply measured [unconditioned (UC) subject

164 The inhibition of H-reflex was sustained up to 4 minutes and 3 minutes on

165 In a separate set of experiments H reflexes were elicited in the wrist flexors instead of

166 Ipsilateral SA H reflexes were evoked at a latency of 9.9 +/- 0.8 ms (p

167 H reflexes were induced in the human quadriceps muscle b

168 Similar suppression of MEP and H-reflex were also seen.

169 increased by up-conditioning, the locomotor H-reflexes were also larger.

170 H-reflexes were also suppressed on these trials, indicat

171 At rest, the second H-reflexes were depressed an average of 73% relative to

172 In the step initiation task, the H-reflexes were evoked on the soleus muscle when the amp

173 Notably, left hand H-reflexes were not modulated on these trials, consisten

174 In the second experiment, paired H-reflexes were obtained from the S and medial (MG) and

175 During a terminal experiment, H-reflexes were recorded from interosseus muscles after

176 transcranial magnetic stimulation (TMS) and H-reflexes were recorded from left hand muscles during c

177 soleus evoked V-waves (cortical drive), and H-reflexes were recorded in 12 chronic stroke patients,

178 ng phases of locomotion (i.e., the locomotor H-reflexes) were also smaller.

179 s inferred from modifications in the size of H reflex, which are often more prominent after skilled m

180 Operant conditioning of the vertebrate H-reflex, which appears to be closely related to learnin

181 The swing-phase H-reflex, which is absent or very small in neurologicall

182 cles was measured by conditioning the soleus H-reflex with stimulation of the common peroneal nerve.

183 single motor units (motoneurons) during the H-reflex without increasing their firing rate at this ti