Good vibrations: tactile cueing for freezing of gait in Parkinson's disease.

BACKGROUND: Cueing strategies can alleviate freezing of gait (FOG) in people with Parkinson's disease (PD). We evaluated tactile cueing delivered via vibrating socks, which has the benefit of not being noticeable to bystanders. OBJECTIVE: To evaluate the effect of tactile cueing compared to auditory cueing on FOG. METHODS: Thirty-one persons with PD with FOG performed gait tasks during both ON and OFF state. The effect of open loop and closed loop tactile cueing, as delivered by vibrating socks, was compared to an active control group (auditory cueing) and to a baseline condition (uncued gait). These four conditions were balanced between subjects. Gait tasks were videotaped and annotated for FOG by two experienced raters. Motion data were collected to analyze spatiotemporal gait parameters. Responders were defined as manifesting a relative reduction of > 10% in the percent time frozen compared to uncued gait. RESULTS: The average percent time frozen during uncued gait was 11.2% in ON and 21.5% in OFF state. None of the three tested cueing modalities affected the percentage of time frozen in either the ON (p = 0.20) or OFF state (p = 0.12). The number of FOG episodes and spatiotemporal gait parameters were also not affected. We found that 22 out of 31 subjects responded to cueing, the response to the three types of cueing was highly individual. CONCLUSIONS: Cueing did not improve FOG at the group level; however, tactile as well as auditory cueing improved FOG in many individuals. This highlights the need for a personalized approach when using cueing to treat FOG.

Parkinson's disease patients compensate for balance control asymmetry.

In Parkinson's disease (PD) subtle balance abnormalities can already be detected in early-stage patients. One feature of impaired balance control in PD is asymmetry: one leg produces more corrective joint torque than the other. We hypothesize that in mild to moderately affected PD patients, the least impaired leg compensates for the more impaired leg. Twenty PD patients and eleven healthy matched control subjects participated. Clinical asymmetry was determined by the difference between the left and right body side scores on the Unified Parkinson's Disease Rating Scale. Balance was perturbed with two independent continuous multisine perturbations in the forward-backward direction. Subsequently, we applied closed-loop system identification, which determined the spectral estimate of the stabilizing mechanisms, for each leg. Balance control behavior was similar in PD patients and control subjects at the ankle, but at the hip stiffness was increased. Control subjects exhibited symmetric balance control, but in PD patients the balance contribution of the leg of the clinically least affected body side was higher whereas the leg of the clinically most affected body side contributed less. The ratio between the legs helped to preserve a normal motor output at the ankle. Our results suggest that PD patients compensate for balance control asymmetries by increasing the relative contribution of the leg of their least affected body side. This compensation appears to be successful at the ankle but is accompanied by an increased stiffness at the hip. We discuss the possible implications of these findings for postural stability and fall risk in PD patients.

Event-related mu-rhythm desynchronization during movement observation is impaired in Parkinson's disease.

OBJECTIVE: Patients with Parkinson's disease often experience difficulties in adapting movements and learning alternative movements to compensate for symptoms. Since observation of movement has been demonstrated to lead to the formation of a lasting specific motor memory that resembled that elicited by physical training we hypothesize that mu-rhythm desynchronization in response to movement observation is impaired in Parkinson's disease. METHOD: In a pilot study with nine patients with Parkinson's disease at a Hoehn and Yahr stage of I or II and eleven age-matched controls, we tested this hypothesis by comparing the event related desynchronization (ERD) patterns from the EEG recorded during the observation of hand action and baseline videos. RESULTS: Healthy subjects showed normal bilateral ERD of the mu-rhythm. In patients with Parkinson's disease this distinct ERD pattern was lacking. CONCLUSION: The results of this study suggest that event-related mu-rhythm desynchronization is impaired in Parkinson's disease, even at early stages of the disease. SIGNIFICANCE: Studying event-related mu-rhythm desynchronization dysfunction in Parkinson's disease patients may enhance our understanding of symptoms as impaired motor learning.

Glycopyrrolate for sialorrhea in Parkinson disease: a randomized, double-blind, crossover trial.

BACKGROUND: Sialorrhea affects approximately 75% of patients with Parkinson disease (PD). Sialorrhea is often treated with anticholinergics, but central side effects limit their usefulness. Glycopyrrolate (glycopyrronium bromide) is an anticholinergic drug with a quaternary ammonium structure not able to cross the blood-brain barrier in considerable amounts. Therefore, glycopyrrolate exhibits minimal central side effects, which may be an advantage in patients with PD, of whom a significant portion already experience cognitive deficits. OBJECTIVE: To determine the efficacy and safety of glycopyrrolate in the treatment of sialorrhea in patients with PD. METHODS: We conducted a 4-week, randomized, double-blind, placebo-controlled, crossover trial with oral glycopyrrolate 1 mg 3 times daily in 23 patients with PD. The severity of the sialorrhea was scored on a daily basis by the patients or a caregiver with a sialorrhea scoring scale ranging from 1 (no sialorrhea) to 9 (profuse sialorrhea). RESULTS: The mean (SD) sialorrhea score improved from 4.6 (1.7) with placebo to 3.8 (1.6) with glycopyrrolate (p = 0.011). Nine patients (39.1%) with glycopyrrolate had a clinically relevant improvement of at least 30% vs 1 patient (4.3%) with placebo (p = 0.021). There were no significant differences in adverse events between glycopyrrolate and placebo treatment. CONCLUSIONS: Oral glycopyrrolate 1 mg 3 times daily is an effective and safe therapy for sialorrhea in Parkinson disease. CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that glycopyrrolate 1 mg 3 times daily is more effective than placebo in reducing sialorrhea in patients with Parkinson disease during a 4-week study.

Detecting asymmetries in balance control with system identification: first experimental results from Parkinson patients.

Cognitive processes can influence balance in various ways, but not all changes in postural performance can easily be identified with the naked clinical eye. Various studies have shown that dynamic posturography is able to detect more subtle changes in balance control. For patients with Parkinson's disease (which is typically an asymmetric disease), changes in the symmetry of balance control might provide a sensitive measure of cognitive influences on balance. Here, we describe a new posturography technique that combines dynamic platform perturbations with system identification techniques to detect such asymmetries in balance control of two patients with Parkinson's disease. Results were compared to those of six healthy controls. Our pilot data show clear asymmetries in dynamic balance control, even though patients themselves were not aware of this and had no subjective problems with stability or standing. We also found asymmetries in weight bearing, but the asymmetries in dynamic balance contribution were larger. Finally, asymmetries in weight bearing and dynamic balance in patients were not tightly coupled as in healthy controls. Future studies could incorporate this approach when examining the influence of mental decline on postural regulation.

Impaired antagonist inhibition may contribute to akinesia and bradykinesia in Huntington's disease.

OBJECTIVE: To test the hypothesis that besides impaired agonist facilitation, impaired antagonist inhibition also contributes to delayed initiation (akinesia) and slow execution (bradykinesia) of voluntary movements in Huntington's disease. METHODS: Fifteen patients with Huntington's disease and 11 age-matched controls participated in the study. The amount of agonist facilitation was measured as the increase in soleus H-reflex amplitude prior to ballistic voluntary plantar flexion (soleus contraction). Antagonist inhibition was measured as the decrease in soleus H-reflex prior to ballistic dorsiflexion (tibialis anterior (TA) contraction). The amount of agonist facilitation and antagonist inhibition was correlated with the time needed for motor initiation (reaction time) and movement execution (movement time). RESULTS: Starting 50ms prior to soleus contraction, soleus H-reflex increased in control subjects but less so in patients. Soleus H-reflexes decreased in controls 25ms prior to TA contraction, while this antagonist inhibition was completely lacking in patients. Thus, patients with Huntington's disease not only displayed reduced agonist facilitation, but impaired antagonist inhibition as well. Moreover, more impairment of antagonist inhibition correlated significantly with more severe akinesia and bradykinesia. CONCLUSIONS: Antagonist inhibition prior to and during agonist contractions is markedly impaired in Huntington's disease. This impairment might contribute to motor slowness in these patients.