Parkinson's disease (PD) is a neurodegenerative disorder that leads to a progressive decline in motor function. Growing evidence indicates that PD patients also experience an array of sensory problems that negatively impact motor function. This is especially true for proprioceptive deficits, which profoundly degrade motor performance. This review specifically address the relation between proprioception and motor impairments in PD. It is structured around 4 themes: (a) It examines whether the sensitivity of kinaesthetic perception, which is based on proprioceptive inputs, is actually altered in PD. (b) It discusses whether failed processes of proprioceptive-motor integration are central to the motor problems in PD. (c) It presents recent findings focusing on the link between the proprioception and the balance problems in PD. And (d) it discusses the current state of knowledge of how levodopa medication and deep brain stimulation affect proprioceptive and motor function in PD. The authors conclude ...

We investigated how humans with hereditary cerebellar degeneration [spinocerebellar ataxia (SCA) type 6 and 8, n = 9] and age- and sex-matched healthy controls (n = 9) adapted goal-directed arm movements to an unknown external force field. We tested whether learning could be generalized to untrained regions in the workspace, an aspect central to the idea of an internal model, and if any learning could be retained. After removal of the force field, SCA patients showed little or no learning-related aftereffects indicating that repeated force-field exposure never led to successful force compensation. In contrast, healthy control subjects quickly adapted their movements to the new force field. The difference in force adaptation was significant for movements to targets that required both the shoulder and elbow joint (P < 0.001). Moreover, the generalization of learned movements to targets outside the learned workspace was prevented by the cerebellar degeneration (P < 0.01). Retention of force adaptation was significantly lower in SCA patients (P = 0.003). The severity of ataxia in SCA patients correlated negatively with the extent of learning (r = –0.84, P = 0.004). Our findings imply that progressive loss of cerebellar function gradually impairs force adaptation. The failure to generalize learning suggests that cerebellar degeneration prevents the formation of an internal representation of the limb dynamics.

Precise knowledge about limb position and orientation is essential for the ability of the nervous system to plan and control voluntary movement. While it is well established that proprioceptive signals from peripheral receptors are necessary for sensing limb position and motion, it is less clear which supraspinal structures mediate the signals that ultimately lead to the conscious awareness of limb position (kinaesthesia). Recent functional imaging studies have revealed that the cerebellum, but not the basal ganglia, are involved in sensory processing of proprioceptive information induced by passive and active movements. Yet psychophysical studies have suggested a prominent role of the basal ganglia in kinaesthesia. This study addresses this apparent dichotomy by investigating the contributions of the cerebellum and the basal ganglia to the perception of limb position. Using a passive movement task, we examined the elbow position sense in patients with a dysfunction of the basal ganglia (Parkinson’s disease, n = 9), patients with cerebellar degeneration [spinocerebellar ataxia (SCA) types 6 and 8, n = 6] and age‐matched healthy control subjects (n = 11). In comparison with healthy control subjects, Parkinson’s disease patients, but not SCA patients, were significantly impaired in the ability to detect displacements correctly. A 1° forearm displacement was correctly recognized in >75% of trials by control subjects and SCA patients, but only in 55% of Parkinson’s disease patients. Only at 6° displacement did Parkinson’s disease patients exhibit a response rate similar to those of the two other groups. Thresholds for 75% correct responses were 1.03° for controls, 1.15° for cerebellar patients and 2.10° for Parkinson’s disease patients. This kinaesthetic impairment significantly correlated with the severity of disease in Parkinson’s disease patients, as determined by the Unified Parkinson’s Disease Rating Scale (r = –0.7, P = 0.03) and duration of disease (r = –0.7, P = 0.05). In contrast, there was no significant correlation between performance and the daily levodopa equivalent dose. These results imply that an intact cerebro‐basal ganglia loop is essential for awareness of limb position and suggest a selective role of the basal ganglia but not the cerebellum in kinaesthesia.

This study examined whether lesions to the cerebellum obtained in early childhood are better compensated than lesions in middle childhood or adolescence. Since cerebellar lesions might affect motor as well a cognitive performance, posture, upper limb and working memory function were assessed in 22 patients after resection of a cerebellar tumour (age at surgery 1–17 years, minimum 3 years post-surgery). Working memory was only impaired in those patients who had received chemo- or radiation therapy. Postural sway was enhanced in 64% of the patients during dynamic posturography conditions, which relied heavily on vestibular input for equilibrium control. Upper limb function was generally less impaired, but 54% of the patients revealed prolonged deceleration times in an arm pointing task, which probably does not reflect a genuine cerebellar deficit but rather the patients' adopted strategy to avoid overshooting. Age at surgery, time since surgery or lesion volume were poor predictors of motor or cognitive recovery. Brain imaging analysis revealed that lesions of all eight patients with abnormal posture who did not receive chemo- and/or radiation therapy included the fastigial and interposed nuclei (NF and NI). In patients with normal posture, NI and NF were spared. In 11 out of 12 patients with abnormal deceleration time, the region with the highest overlap included the NI and NF and dorsomedial portions of the dentate nuclei in 10 out of 12 patients. We conclude that cerebellar damage inflicted at a young age is not necessarily better compensated. The lesion site is critical for motor recovery, and lesions affecting the deep cerebellar nuclei are not fully compensated at any developmental age in humans.

Background: The importance of assessing proprioceptive function for rehabilitation after neurological or orthopedic injury has long been recognized. Yet, neither the validity nor the accuracy of the available tests is firmly established. Testing typically involves repeated matching of a given joint position with the same or opposite limb where the difference between the 2 positions indicates proprioceptive acuity.Objectives: The aim of this study was to compare position sense acuity between ipsilateral and contralateral matching methods against a psychophysical threshold method to establish the accuracy and relationships between these models.Design: A repeated-measures design was used.Method: Assessment of forearm position sense for a 10-degree reference position in 27 young adults who were healthy.Results: Psychophysical thresholds were revealed to be the most precise and least variable acuity measure. The mean (±SD) threshold (1.05°±0.47°) was significantly lower than mean position errors obtained by both joint position matching tasks (ipsilateral: 1.51°±0.64°; contralateral: 1.84°±0.73°)—a 44% to 75% difference in measurement accuracy. Individual participant position errors correlated poorly with respective thresholds, indicating a lack of concurrent validity. Position errors for both matching methods correlated only mildly with each other.Limitations: The data represent performance of a healthy, young adult cohort. Differences between methods will likely be more pronounced in aging and clinical populations.Conclusions: Threshold testing and joint position matching methods examine different physiological aspects of proprioceptive function. Because threshold testing is based on passive motion, it most closely reflects afferent sensory feedback processing (ie, proprioception). Matching methods require active motion and are consequently influenced by additional sensorimotor processes. Factors such as working memory and transmission between brain hemispheres also influence joint matching task outcomes.