Reference : Short-latency autogenic inhibition in patients with Parkinsonian rigidity.
Scientific journals : Article
Human health sciences : Neurology
Short-latency autogenic inhibition in patients with Parkinsonian rigidity.
Delwaide, Paul mailto [Université de Liège - ULg > Services généraux (Faculté de médecine) > Relations académiques et scientifiques (Médecine)]
PEPIN, Jean-Louis mailto [Centre Hospitalier Universitaire de Liège - CHU > > Neurologie CHR]
MAERTENS DE NOORDHOUT, Alain mailto [Centre Hospitalier Universitaire de Liège - CHU > > Neurologie CHR]
Annals of Neurology
Wiley Liss, Inc.
Yes (verified by ORBi)
New York
[en] Aged ; Antiparkinson Agents/pharmacology/therapeutic use ; Female ; H-Reflex/drug effects/physiology ; Humans ; Interneurons/physiology ; Male ; Middle Aged ; Muscle Rigidity/drug therapy/etiology/physiopathology ; Neurons, Afferent/physiology ; Parkinson Disease/complications/drug therapy/physiopathology ; Reflex, Abnormal/drug effects/physiology ; Severity of Illness Index
[en] The spinal Ib interneuron efficacy has been compared in 11 control subjects and 19 patients with parkinsonian rigidity. In normal subjects, gastrocnemius medialis nerve stimulation induces an inhibition of the soleus H reflex for 3 to 8 msec with a peak at 5 msec of 83.72 +/- 7.28% of the control value of H reflex. In parkinsonian patients, inhibition is reduced or even replaced by facilitation, which also peaks at 5 msec. The departures from normal values correlate with rigidity intensity assessed by the Webster scale. Increase in rigidity is associated, first, with a reduction of inhibition and, from a score of 2 or more, with facilitation replacing the normal inhibition. In addition to providing an electrophysiological index of rigidity, reduction in autogenic inhibition might be one of the neurophysiological mechanisms underlying rigidity. In association with the known hyperactivity of the Ia inhibitory interneuron in Parkinson's disease, reduction of activity of Ib interneuron could be explained by an increased activity in the reticularis gigantocellularis nucleus; its efferent tracts both inhibit Ib interneurons and activate Ia interneurons.

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