Low frequency depression of H-reflexes in humans with acute and chronic spinal-cord injury

Abstract

We measured low-frequency depression of soleus H-reflexes in individuals with acute (n=5) and chronic (n=7) spinal-cord injury and in able-bodied controls (n=7). In one acute subject, we monitored longitudinal changes in low-frequency depression of H-reflexes over 44 weeks and examined the relationship between H-reflex depression and soleus-muscle fatigue properties. Soleus H-reflexes were elicited at 0.1, 0.2, 1, 5, and 10 Hz. The mean peak-to-peak amplitude of ten reflexes at each frequency was calculated, and values obtained at each frequency were normalized to 0.1 Hz. H-reflex amplitude decreased with increasing stimulation frequency in all three groups, but H-reflex suppression was significantly larger in the able-bodied and acute groups than in the chronic group. The acute subject who was monitored longitudinally displayed reduced low-frequency depression with increasing time post injury. At 44 weeks post injury, the acute subject's H-reflex depression was similar to that of chronic subjects, and his soleus fatigue index (assessed with a modified Burke fatigue protocol) dropped substantially, consistent with transformation to faster muscle. There was a significant inverse correlation over the 44 weeks between the fatigue index and the mean normalized H-reflex amplitude at 1, 5, and 10 Hz. We conclude that: (1) the chronically paralyzed soleus muscle displays impaired low-frequency depression of H-reflexes, (2) attenuation of rate-sensitive depression in humans with spinal-cord injury occurs gradually, and (3) changes in H-reflex excitability are generally correlated with adaptation of the neuromuscular system. Possible mechanisms underlying changes in lowfrequency depression and their association with neuromuscular adaptation are discussed.

Restoration of frequency-dependent depression of the H-reflex by passive exercise in spinal rats

“…At 10 Hz, the Tx only 30D group (*) differed from the Tx þ Ex 30 group at the Po0.05 level ( þ ), and from the CONTROL at the Po0.01 level ( þ þ ) a lesser extent than able-bodied normals or acutely paralyzed subjects, (2) those with acute paralysis showed similar H-reflex suppression as those within 40 weeks of their SCI, but had decreased frequency-dependent depression after 44 weeks of paralysis (ie there was marked loss of frequency-dependent depression of the H-reflex in the 'chronic' condition), and (3) changes in muscle fatigue were associated with a decrease in H-reflex suppression over time. 13 The results described herein show that frequency-dependent depression of the H-reflex is decreased in the most 'chronic' condition tested, 90 days after Tx. Surprisingly, a similar level of hyper-reflexia was evident even at 30 days (Figure 3), suggesting that hyper-reflexia assumes a fairly 'chronic' level within 30 days after Tx in the rat.…”

“…9,[12][13][14][15] Decreased presynaptic inhibition is frequently linked with decreased low-frequency depression of the H-reflex. 14,21,38 It is thought that the loss of inputs from descending pathways leads to a reorganization of spinal circuitry that promotes hyper-reflexia.…”

“…The physiological changes that have been postulated to contribute to hyper-reflexia include alpha motoneuron hyperexcitability, [1][2][3] changes in the intrinsic properties of alpha motoneurons, [4][5][6][7] reduced post-activation depression of transmission from Ia fibers, 8,9 synapse growth; 10 alterations in morphology of alpha motoneurons, 11 and decreased presynaptic inhibition of Ia terminals. 9,[12][13][14][15] The time course of spinal changes after injury has been proposed to include an early postsynaptic mechanism, possibly involving an increase in excitability and/or receptor upregulation, and a late change involving presynaptic mechanisms possibly involving synaptic growth in spared descending pathways and in reflex pathways. 10 One measure used by numerous investigators to quantify hyper-reflexia is the electrical analogue of the classic tendon jerk reflex, referred to as the Hoffman or H-reflex.…”

“…22,23 However, frequency-dependent depression of the Hreflex is less evident in patients or animals with chronic SCI. 12,13,22,24,25 Previously, we reported the ability of long-term passive exercise therapy to restore frequencydependent depression of the H-reflex in adult rats with complete spinal cord transections. 24,25 Specifically, we found that a period of 3 months of motorized bicycle exercise training (MBET), performed in episodes of 1 h/ day, 5 days/week, was capable of restoring frequencydependent depression of the H-reflex to the level of intact animals.…”

Up-regulation of 5-HT2 receptors is involved in the increased H-reflex amplitude after contusive spinal cord injury

“…Properties of the H-reflex are known to be affected in both humans and rodents after SCI (Lee, et al, 2005, Schindler-Ivens and Shields, 2000, Thompson, et al, 1998, Valero-Cabre and Navarro, 2001. One of these alterations is elevated reflex amplitude that develops over time after SCI (Lee, et al, 2005, Thompson, et al, 1998.…”