These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Central control of reciprocal inhibition during fictive dorsiflexion in man.
    Author: Nielsen J, Crone C, Sinkjaer T, Toft E, Hultborn H.
    Journal: Exp Brain Res; 1995; 104(1):99-106. PubMed ID: 7621944.
    Abstract:
    The size of the soleus Hoffmann reflex (H-reflex) was measured in six healthy human subjects before and after transmission in the common peroneal nerve (CPN) was blocked reversibly by local injection of lidocaine. It was found that the H-reflex at rest increased after the block. When the subjects attempted to perform a dorsiflexion while the CPN was blocked ("fictive dorsi flexion"), the soleus H-reflex was strongly depressed. Stimulation of the CPN proximal to the block elicited a short-latency inhibition of the soleus H-reflex, which was probably mediated by reciprocal Ia interneurones. This inhibition never increased during dorsiflexion relative to rest prior to the CPN block, but after the block a significant increase in inhibition was seen during fictive dorsiflexion in three subjects. Stimulation of the femoral nerve (FN) elicited a short-latency monosynaptic Ia facilitation of the soleus H-reflex. This facilitation was found to decrease during dorsiflexion relative to rest before the block as well as during fictive dorsiflexion after the block. The decrease in the H-reflex during fictive dorsiflexion demonstrates that although an increased Ia-afferent feedback via the gamma-loop may contribute to reciprocal inhibition when transmission in the CPN is intact, a noticeable, centrally mediated inhibition may occur in the absence of this feedback. It is suggested that this inhibition is caused by central facilitation of interneurones mediating disynaptic Ia inhibition as well as interneurones mediating presynaptic inhibition of Ia afferents.
    [Abstract] [Full Text] [Related] [New Search]