Transmission of group II heteronymous pathways is enhanced in rigid lower limb of de novo patients with Parkinson's disease

Abstract

A potent heteronymous excitation of quadriceps motoneurones via common peroneal group II afferents has recently been demonstrated in normal subjects. The aim of this study was to investigate whether this group II excitation contributes to rigidity in Parkinson's disease. The early and late facilitations of the quadriceps H reflex elicited by a conditioning volley to the common peroneal nerve (CPN) at twice motor threshold, attributed to non-monosynaptic group I and group II excitations, respectively, were investigated. The comparison was drawn between results obtained in 20 "de novo" patients with Parkinson's disease (hemiparkinsonian, 17; bilateral, three) and 20 age-matched normal subjects. There was no statistically significant effect of "group" (patients/controls), "duration", "global severity" [Unified Parkinson's Disease Rating Scale (UPDRS)] or "side" (unilaterally versus bilaterally affected) factors on either group I or group II facilitations. To further the analysis, the factors of status (affected or non-affected limb), akinesia (lower limb akinesia score) and rigidity (lower limb rigidity score) were entered in a general linear model to explain the variations of the quadriceps H reflex facilitation. Rigidity was the only factor useful in predicting the value of the group II facilitation of the quadriceps H reflex (P < 0.007). Group I and group II facilitation was then compared between the rigid, non-rigid and control lower limbs [multivariate analysis of variance (MANOVA)]. Results are represented as mean +/- SEM (standard error of the mean). Group II facilitation was enhanced in the rigid lower limb of unilaterally affected patients (153.2 +/- 7% of control H reflex) compared with non-rigid lower limbs (124 +/- 4% of control H reflex; P < 0.007) or control lower limbs (126.1 +/- 4.1%; P < 0.01). There was no difference between the non-rigid lower limbs of the unilaterally affected patients and the control lower limbs, but a difference was observed between the rigid lower limbs of unilaterally less affected and bilaterally more affected patients (153.2 +/- 7% and 123.8 +/- 7.5% of control H reflex, respectively; P < 0.04). These results suggest a facilitation of the transmission in the interneuronal pathway activated by group II afferents in rigid lower limb of de novo hemiparkinsonian patients, probably resulting from a change in their descending monoaminergic inhibitory control.

Primary motor cortex of the parkinsonian monkey: altered neuronal responses to muscle stretch

“…Our observation of an elevated LLSR (Figure 2) combined with no change in prevalence or magnitude of stretch-evoked neuronal responses in PTNs is consistent with the view that the alteration in reflex function that mediates the exaggerated LLSR of PD is localized to the spinal cord (Simonetta Moreau et al, 2002; Marchand-Pauvert et al, 2011; Raoul et al, 2012). Several abnormalities in segmental function have been observed in PD and there is no consensus as to which of them contribute most significantly to the LLSR or rigidity.…”

“…For all of these, dysfunction within the BG may affect segmental motor function via descending BG projections to the pedunculopontine nucleus and from there to spinal cord projecting brainstem nuclei (Delwaide et al, 2000). Degeneration of the noradrenergic projection to the spinal cord may also play an important role (Simonetta Moreau et al, 2002). …”

“…It is unclear, however, how this simple model can be reconciled with the abundant evidence that the M1 of parkinsonian subjects has reduced responsiveness to somatosensory inputs as measured by electroencephalography (Rossini et al, 1989; Aminoff et al, 1997; Rickards and Cody, 1997; Lewis and Byblow, 2002; Schrader et al, 2008; Degardin et al, 2009), transcranial magnetic stimulation (Lewis and Byblow, 2002), and functional imaging (Boecker et al, 1999). The alternative model hypothesizes that the exaggerated LLSR of PD is mediated by abnormal function of slow-conducting spinal reflex pathways (Berardelli et al, 1983; Cody et al, 1986; Simonetta Moreau et al, 2002; Marchand-Pauvert et al, 2011; Raoul et al, 2012). …”

Neuroanatomical Study of the A11 Diencephalospinal Pathway in the Non-Human Primate

“…As it has been shown that limb rigidity in patients with PD points to sensorimotor processing damage resulting from a change in their descending monoaminergic inhibitory control [42], we sought to determine the effect of a pro-parkinsonian neurotoxin on the diencephalospinal pathway despite the absence of DAT expression.…”

Transmission in Heteronymous Spinal Pathways Is Modified after Stroke and Related to Motor Incoordination

“…The absence of evidence of group II excitation from quadriceps to soleus in healthy subjects may result from concomitant effects of the recurrent inhibition. In stroke individuals, the increase of group II excitation would probably affect mostly the first part of the inhibition since it has been demonstrated that group II afferents normally have their peak influence from 6 to 20 ms after the onset of the early group I induced facilitation [22], [53], [54], [55]. Our results suggest that recurrent inhibition could also be impaired in itself since the inhibition is reduced at the late ISIs (30 ms and 40 ms ISI) at which the influence of group II excitation must be diminished.…”