Altered patterns of reflex excitability subsequent to contusion injury of the rat spinal cord

Abstract

1. The present study investigated regulation of reflex excitability after experimental contusion injury of the spinal cord. 2. Four measures of H-reflex excitability were evaluated in normal rats and at 6, 28, and 60 days after contusion injury at the T8 level: 1) reflex thresholds, 2) slope of the reflex recruitment curves, 3) maximal plantar H-reflex/maximal plantar M-response (Hmax/Mmax) ratios, and 4) rate-sensitive depression (i.e., the decrease in reflex magnitude relative to repetition rate). 3. Tested as a function of the afferent volley magnitude, the thresholds for reflex initiation fell progressively subsequent to contusion injury. No change was observed at 6 days postinjury, and the decrease at 28 days was not significant. However, by 60 days postinjury, the threshold had decreased by 23% of the maximal afferent volley, and this decrease was significant, [analysis of variance (ANOVA, P < or = 0.01)]. 4. Hmax/Mmax ratios elicited in postcontusion animals at 0.3 Hz were not significantly different from those recorded in normal animals. 5. The slopes of the recruitment curves were markedly reduced subsequent to contusion injury. The decrease was greatest at 6 days postinjury. Although some recovery toward normal occurred at 28 and 60 days postinjury, the slopes of recruitment curves in postcontusion animals remained significantly decreased. 6. H-reflexes elicited at 1-5 Hz were less sensitive to rate depression in postcontusion animals than in normal animals at the same respective frequencies. The decrease was progressive in onset, becoming significant by 28 days postinjury, and of an enduring nature, i.e., still significantly different from normal in the reflexes tested 60 days postinjury. 7. Rate sensitivity of the tibial nerve monosynaptic reflex (MSR) was also compared in normal and postcontusion animals. Rate sensitivity of the tibial MSRs was significantly reduced at 28 and 60 days post-contusion, compared with normal animals. 8. These data indicate that significant changes in lumbar reflex excitability result from midthoracic contusion injury of the spinal cord. These changes include reflex threshold, slope of recruitment, and rate-sensitive depression. Although recruitment slope was most altered in the shortest postinjury interval tested, followed by some recovery, the other changes were progressive in onset and enduring in duration.

Induction of Fos protein immunoreactivity by spinal cord contusion

“…The precise mechanisms by which the effects of injury are distributed throughout the cord are unknown, but similar evidence was found by Yerzierski et al (14), Thomp- son et al (15) and Ruggiero et al (8). Anesthesia is not thought to affect Fos expression; the results showed an effect of surgical stress, but the greater expression of Fos protein following spinal cord contusion suggests that spinal cord injury causes an increase in Fos expression.…”

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

“…This reflex normally undergoes changes with a variety of rhythmic motions such as stepping, 29 walking, 30 running 31 and pedaling. 32 In animals, the H-reflex has been a valuable tool to measure changes in spinal circuitry in both contusion 20,33 and transection models. 23,24 The H-reflex has also been used to assess changes in spinal circuitry in the human, a recent effort concluding that (1) chronically paralyzed subjects showed suppression of H-reflexes to , and all statistical comparisons in this figure made against the Tx ONLY 30D group.…”

Pain following spinal cord injury

“…59 The spinal contusion model, usually evoked by dropping a weight on the exposed spinal cord, produces changes in the excitability of neurons that could be relevant to the development of pain after SCI. 60 It has been demonstrated that animals exhibit features of neuropathic pain at the level of SCI with lowered vocalization thresholds in the dermatomes adjacent to the level of injury. 48 In particular, hypersensitivity was observed for lesions restricted to the central grey matter or the dorsal half of the spinal cord, suggesting that spinal grey matter damage contributes to development of at level neuropathic SCI pain.…”