The Contribution of Cervical Propriospinal Premotoneurons in Recovering Hemiparetic Stroke Patients

There is evidence in humans that the C3/4 level of the spinal cord is a site for sensorimotor integration, analogous to the C3/4 propriospinal system (PS) in cat. Although the clinical relevance of the putative C3/4 PS in humans is not clear, there is some evidence indicating that drive to upper lim...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of clinical neurophysiology 2004-11, Vol.21 (6), p.426-434
Hauptverfasser: Stinear, James W, Byblow, Winston D
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:There is evidence in humans that the C3/4 level of the spinal cord is a site for sensorimotor integration, analogous to the C3/4 propriospinal system (PS) in cat. Although the clinical relevance of the putative C3/4 PS in humans is not clear, there is some evidence indicating that drive to upper limb muscles via this nonmonosynaptic pathway is upregulated as a compensatory mechanism in stroke and in Parkinsonʼs disease. The authors investigated whether descending drive via the C3/4 PS to affected limb wrist flexors of moderately to well-recovered chronic stroke patients is upregulated compared with controls. The extent of descending drive via the C3/4 PS was assessed in seven patients and seven control subjects during the onset of cocontraction of the biceps brachii and flexor carpi radialis (FCR), during which transcranial magnetic stimulation was used to evoke motor potentials in FCR. Responses were conditioned by subthreshold stimulation of the musculocutaneous nerve. The extent of this facilitation was taken as a measure of the proportion of drive to FCR motoneurons being transmitted via the C3/4 PS. Patients revealed greater facilitation than control subjects, suggesting that descending drive to forearm flexors was being transmitted via the C3/4 PS as a compensation mechanism after stroke.
ISSN:0736-0258
1537-1603
DOI:10.1097/00004691-200411000-00006