The activation of spinal cord neuronal networks generating stepping rhythm in Parkinson’s disease (PD) has received little attention. We examined spinal locomotor circuitry activation in patients with PD using various types of central and peripheral tonic stimulation and compared results to those of age-matched controls. Twenty five patients with mild to moderate stages of PD (1 to 3 on a scale of Hoehn and Yar, 61 ± 9 years) and 22 healthy subjects of similar age took part in investigation.
Subjects lay on their sides with both legs suspended, allowing to perform stepping movements in horizontal plane without external resistance. A remarkable feature of voluntary air-stepping movements in patients was a signiﬁcantly higher frequency of leg oscillations with more short step length than in age-matched controls. However, during normal overground walking cadence and stride length in PD and control subjects were similar, but walking speed of patients was essentially lower. In patients both central (Jendrassik maneuver, Kohnstamm phenomenon, mental task) tonic inﬂuences and peripheral stimulation (muscle vibration) had little if any eﬀect on rhythmic leg responses, whereas in healthy subjects involuntary air-stepping was activated more often. Jendrassik maneuver essentially prolonged passively activated leg oscillations in healthy subjects (in average, on 5-6 oscillations), whereas in PD Jendrassik maneuver did not change the number of oscillations or even reduced its. Kohnstamm phenomenon activated involuntary stepping rhythm in 55% of controls and only in 8% of patients. The muscle vibration caused “air-stepping” in 50% of healthy subjects but only in one patient. In PD dopaminargic treatment enhanced over ground gait speed. Under voluntary “air-stepping” stride length and range of movements in hip and knee joints increased. Medication had no eﬀect on the manifestation of air-stepping movements in PD during both sensory and central tonic stimuli. We argue that the state and the rhythmogenesis capacity of the spinal circuitry are impaired in patients with PD. In particular, the results suggest impaired central pattern generator (CPG) access by sensory and central activations.