Cutaneous reflexes from the foot during gait in hereditary spastic paraparesis.

OBJECTIVE: It is known that P2 cutaneous reflexes from the foot show phase-dependent modulation during gait. The role of the motor cortex and the cortico-spinal tract in these reflexes and their modulation is unknown. Patients with hereditary spastic paraparesis (HSP) have a lesion in the cortico-spinal tract and may show deficits in P2 reflexes and/or their modulation. METHODS: Reflex responses of tibialis anterior and biceps femoris after sural nerve stimulation in 10 HSP-patients were compared with those in 10 healthy subjects. The reflexes were studied at two different moments in the step cycle during walking on a treadmill. RESULTS: Both patients and controls showed a phase-dependent modulation of P2 responses. For the individual muscles, no significant difference in reflex activity was observed between HSP-patients and the controls. However, when all muscles were taken together, the reflex activity for the controls was significantly higher than for the patients. CONCLUSIONS: The results of this study suggest that the cortico-spinal tract is involved in the regulation of the amplitude of the P2 responses and their phase-dependent modulation.

Failed suppression of direct visuomotor activation in Parkinson's disease.

The response times in choice-reaction tasks are faster when the relative spatial positions of stimulus and response match than when they do not match, even when the spatial relation is irrelevant to response choice. This spatial stimulus-response (S--R) compatibility effect (i.e., the Simon effect) is attributed in part to the automatic activation of spatially corresponding responses, which need to be suppressed when the spatial location of stimulus and correct response do not correspond. The present study tested patients with Parkinson's disease and healthy control subjects in a spatial S--R compatibility task in order to investigate whether basal ganglia dysfunction in Parkinson's disease leads to disinhibition of direct visuomotor activation. High-density event-related brain potential recordings were used to chart the cortical activity accompanying attentional orientation and response selection. Response time measures demonstrated a failure to inhibit automatic response activation in Parkinson patients, which was revealed by taking into account a sequence-dependent modulation of the Simon effect. Event-related potential (ERP) recordings demonstrated that visuospatial orientation to target stimuli was accompanied by signal-locked activity above motor areas of the cortex, with similar latencies but an enhanced amplitude in patients compared to control subjects. The results suggest that inhibitory modulation of automatic, stimulus-driven, visuomotor activation occurs after the initial sensory activation of motor cortical areas. The failed inhibition in Parkinson's disease appears therefore related to a disturbance in processes that prevent early attention-related visuomotor activation, within motor areas, from actually evoking a response.

Redundant-signals effects on reaction time, response force, and movement-related potentials in Parkinson's disease.

Studies using transcranial magnetic stimulation have established that patients with Parkinson's disease have increased motor cortex excitability. Relying on current evidence that the redundant-signals effect has its source in the motor system, we investigated whether, as a result of cortical hyperexcitability, Parkinson's disease patients demonstrate an enhancement of this effect. Eight patients with moderately severe Parkinson's disease and nine healthy control subjects participated in a task requiring simple manual responses to visual, auditory, and combined auditory-visual signals. During the task, motor cortex activation was recorded by means of movement-related EEG potentials, while responses were measured via isometric force recordings. The movement-related potentials and the force measures both yielded support for the view that the redundant-signals effect is partially caused in the motor system. However, the facilitatory effect of bimodal as compared to unimodal stimulation (i.e. the redundant-signals effect) was of the same size in Parkinson's disease patients and control subjects, as expressed in latency measures of the movement-related potentials and the force signals. We conclude that the redundant-signals effect is not enhanced in Parkinson's disease and that the mechanisms underlying this effect are probably not influenced by the increased motor cortex excitability found in this disease.