Postvibration depression of the H-reflex as a result of a dual mechanism -An experimental study in humans

Citation
M. Abbruzzese et al., Postvibration depression of the H-reflex as a result of a dual mechanism -An experimental study in humans, J CL NEURPH, 18(5), 2001, pp. 460-470
Citations number
36
Categorie Soggetti
Neurology
Journal title
JOURNAL OF CLINICAL NEUROPHYSIOLOGY
ISSN journal
07360258 → ACNP
Volume
18
Issue
5
Year of publication
2001
Pages
460 - 470
Database
ISI
SICI code
0736-0258(200109)18:5<460:PDOTHA>2.0.ZU;2-2
Abstract
Changes in amplitude of the soleus H (S-H)-reflex and its neurographic corr elates (P-1 and P-2 waves) after vibration of the soleus muscle have been e valuated as a function of mechanical stimulation frequency, duration of the conditioning train, and test stimulus intensity. Additional experiments ai med at assessing the nervous system mechanisms underlying the postvibration depression (PVD) have been performed. In particular, homonymous (S-HMR or S-H) versus heteronymous (S-HTR) soleus response, evoked respectively by ti bial nerve and femoral nerve electrical stimulation, the effectiveness of s ub-H threshold tibial nerve conditioning volleys on the S-HTR, and the resp ective effects of a brief passive stretching of the quadriceps and soleus m uscles on the recovery of both the S-HMR and S-HTR after vibration of the h omologous muscle were investigated under suitable experimental conditions. It was found that PVD occurs in the absence of changes in amplitude of the Pt wave and the S-HTR, is paralleled by a reduced effectiveness of tibial n erve-conditioning volleys on the S-HTR and is shortened consistently by bri ef passive stretching of the homologous muscle. It follows that PVD may be the result of along-lasting reduction of the transmitter release from la pr esynaptic terminals depending, at least in part, on a protracted postvibrat ion la afferent discharge caused by spindles thixotropy. These findings may provide a better understanding of the pathophysiologic mechanisms underlyi ng spasticity in humans.