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Introduction : Autonomic dysfunction is an integral part of Parkinson disease (PD) complex and can be seen both in early and advanced stages. There is a paucity of medicines available to manage autonomic dysfunction in PD and this adds to the considerable morbidity associated with the illness. Areas covered : The pathophysiology and the available therapeutic options of autonomic dysfunction seen in PD are discussed in detail. The potential targets for novel regimens are reviewed and the available literature on the drugs emerging in management of autonomic dysfunction in PD is highlighted. Expert opinion : In the current scenario, there are several drugs that can be tried for constipation viz stool laxatives, prucalopride, prokinetic agents and a high fiber diet. Bladder dysfunction has been treated with β-agonists and with mirabegron, a selective β-3 agonist, the anticholinergic side effects are minimized, and the drug has been found to be effective. Orthostatic hypotension is managed with midodrine while droxidopa is a new drug with promising efficacy. Botulinum toxin works best for management of sialorrhea, but repeated injections are needed.

Background: Parkinson disease (PD) patients have turning impairments that may increase fall risk. Clinics lack specialized kinematic equipment used in gait and turn analysis and require a simple method to evaluate fall risk and advise patients in turning strategy selection., Objectives: To enhance understanding of PD turning strategies and determine if turning can be assessed using a video-recording and categorization method, we compared 180-degree and 90-degree turns as a function of medication status and dual-tasking (DT)., Methods: 21 PD participants (H&Y stage 1-3) in PD-ON and PD-OFF medication states and 16 controls completed 180-degree and 90-degree turn-tasks with and without DT. Video-recordings of tasks permitted classification of 180-degree turns into Few-Step turns (FST) vs. Multi-Step turns (MST) and 90-degree turns into Step vs. Spin-turns. FST were further sub-classified into Twisting vs. Sideways turns and MST into Backward, Festination, Forward or Wheeling turns. Percentages of subtypes were analyzed across groups by task., Results: IN 180-degree tasks, there was an effect of group: FST vs. MST F(2,55) = 9.578, p < .001. PD participants in the off-medication state (PD-OFF) produced significantly more MST with a larger number of different turning subtypes vs. controls or PD on medication (PD-ON). In 90-degree tasks, controls significantly increased their proportion of Step-turns while DT (p < .001), an adaptation not observed in PD-ON or PD-OFF., Conclusions: PD turning impairments may stem from an inability to select a unified turning strategy and to adapt to the turning environment, which may be exacerbated in PD-OFF. Video-analysis may prove beneficial in predicting a clinical course for PD patients by revealing features of turning dysfunction., (Copyright © 2018 Elsevier B.V. All rights reserved.)

In this review, we have gathered all the available evidence to guide medication management after deep brain stimulation (DBS) in Parkinson's disease (PD). Surprisingly, we found that almost no study addressed drug-based management in the postoperative period. Dopaminergic medications are usually reduced, but whether the levodopa or dopamine agonist is to be reduced is left to the personal preference of the treating physician. We have summarized the pros and cons of both approaches. No study on the management of cognitive problems after DBS has been done, and only a few studies have explored the pharmacological management of such DBS-resistant symptoms as voice (amantadine), balance (donepezil) or gait disorders (amantadine, methylphenidate). As for the psychiatric problems so frequently reported in PD patients, researchers have directed their attention to the complex interplay between stimulation and reduction of dopaminergic drugs only recently. In conclusion, studies addressing medical management following DBS are still needed and will certainly contribute to the ultimate success of DBS procedures.

Background: Functional motor impairments including mobility are major reasons for clinical intervention and medication adjustment in symptomatic therapy for Parkinson's disease (PD). Outcome measures used to assess the impact of medication are mostly based on patients' memory or diaries which, considering the gaps between visits, are neither objective nor very reliable., Objective: Investigating the feasibility of using movement features extracted from ecological whole-body kinematics recordings to measure the quantitative and qualitative changes in multiple aspects of mobility after medication changes in PD., Methods: Eleven patients with PD (PwPD) performed mobility tasks in their own home, wearing a full body wireless inertial sensing based motion capture system. Three scripted walking tasks (walking, fast walking, and walk turns) were examined at baseline and two weeks after medication changes. Clinical scales, including investigator-rated clinical global impression of improvement (CGI-I), were collected at both visits., Results: Out of 59 recorded body joint variables, five were identified as pertinent. Changes were represented in vector space as a plot of mean versus peak amplitude. Regression analysis was used to predict clinical improvement or worsening based on these vector features. The predictors were able to explain (>98.5% of variance) patients' clinical global impression of improvement, thus correctly predicting 5 cases of improvement and 2 cases of worsening., Conclusions: This study provided a method of extracting clinically meaningful reports from ecological kinematic data showing changes after drug adjustments. The results are presented using a novel concept called change space that may be more understandable for clinical staff.

Objective: Examine the level of intra- and inter-limb coherency in non-dyskinetic and dyskinetic patients with Parkinson's disease (PD)., Patients & Methods: Using a magnetic tracking system, whole-body 3D movements were assessed in 10 dyskinetic patients with clear monophasic peak-dose levodopa-induced dyskinesia (LID), in 10 non-dyskinetic patients and in 10 control subjects, standing with their arms out. Patients were tested during their best ON period. Coherency in the kinematics of pairs of body segments was assessed by spectral analysis. For each pair examined, we calculated the highest coherency between 0.5 and 3.0Hz and the frequency at which this maximum coherency occurred., Results: Analysis of variance showed that for 34 out of the 44 (77.3%) comparisons we studied, there were significant differences between the means of coherencies of the groups. Typically, the control group had the highest coherency and the patients with LID had the lowest. Patients with LID also tended to have their maximum coherency at higher frequencies than the control and non-dyskinetic patient groups (30 out of 44 comparisons were significant). These trends appeared in all types of inter-segment comparisons, including bilaterally symmetric segments, biomechanically linked segments (in which coherencies were higher overall in all groups, but still different between groups) and in other comparisons, but the trends were not so clear for comparisons involving the feet., Conclusion: LID is indeed incoherent in the frequency domain, suggesting that body segments may be driven by different neural outputs. The challenges of dealing with these incoherent involuntary movements when planning and executing voluntary movements must certainly play a role in motor difficulties observed in patients with LID. The fact that both dyskinetic and non-dyskinetic patients showed less coherency than controls suggests that levodopa may alter postural control by decreasing stiffness and increasing limb independence., (Copyright 2010 Elsevier B.V. All rights reserved.)

The present study characterized involuntary movements associated with levodopa-induced dyskinesias (LID) in patients with Parkinson's disease. We used amplitude, proportional energy, frequency dispersion and sample entropy to determine whether LID movement patterns are truly random, as clinical description seems to suggest, or possess some underlying pattern that is not visible to the naked eye. LID was captured using a magnetic tracker system, which provided 3D rendering of whole-body LID. Patients were instructed to maintain a standing position, with arms extended in front of them. We compared the measurements of the dyskinetic PD group (DPD) with 10 patients without dyskinesias (NDPD) and 10 control subjects. In comparison to the other two groups, movement patterns from the DPD group had significantly higher amplitude, confirming the presence of dyskinesias. In addition, higher frequency components in the power spectrum of velocity were detected, suggestive of higher velocity in LID movement. Furthermore, there was a concentration in narrow frequency bands, which suggested stable oscillatory activity. Finally, sample entropy revealed more regularity in the DPD group. Although not statistically significant, we found that the amplitude from the NDPD group had a tendency to be smaller than those of controls. As well, the spectra were often more dispersed for the NDPD group. In conclusion, the present results suggest that LID cannot be considered as purely random movement since they possess some deterministic pattern of motion. This may provide a way for patients to adapt to these involuntary movements while performing voluntary motor acts.

The influence of peak-dose, levodopa-induced dyskinesias (LID) on manual tracking (MT) was examined in 10 dyskinetic patients with Parkinson's disease (DPD), and compared to 10 age/gender-matched non-dyskinetic patients with Parkinson's disease (NDPD) and 10 healthy controls. Whole-body movement (WBM) and MT performance were recorded simultaneously with a 6-degrees-of-freedom magnetic motion tracker and forearm rotation sensors, respectively. Subjects were asked to match the length of a computer-generated line with a line they controlled via wrist rotation. Results show that DPD patients had greater WBM magnitude at rest and during the motor task, both in displacement and in velocity. All groups displayed some increase in WBM displacement from rest to MT, but only the DPD group had a significant increase in WBM velocity during movement. As for MT performance (determined by assessing the positional mismatch between subjects' and target lines), ERROR in displacement was statistically similar between groups. There was no correlation between ERROR and the magnitude of WBM within the DPD group. The DPD group showed significant increased ERROR when the velocity of the subject's line was compared with that of the velocity of the target line. When two distinct target pace segments were examined (FAST/SLOW), no significant differences were found in ERROR for displacement for either group, but both the NDPD and DPD group showed increased ERROR from SLOW to FAST for velocity. This was accompanied with an increase in WBM velocity only in the DPD group. The lack of increased ERROR during the SLOW tracking portion in the DPD group supports the notion that the dyskinesias themselves were not primarily responsible for the ERROR seen in the patients. When examining the positive or negative values of ERROR (i.e., faster or slower than the target), we found that the increased ERROR in velocity observed in the DPD group was the result of excess velocity rather than bradykinesia, manifested as isolated deviations from the target trace in the DPD group that were coherent in time with increased ERROR in velocity. In conclusion, evidence presented in the present study shows that the LID was not the primary cause of the ERROR seen in the DPD group. Accordingly, we propose that the increased ERROR seen in the DPD group resulted from a mechanism distinct from the one generating LID.

We investigated the likelihood that bradykinesia coexisted with levodopa-induced dyskinesias (LID) in 10 dyskinetic Parkinson's disease patients (DPD). Their motor performance was compared to that of 10 age/gender-matched non-dyskinetic patients (NDPD) and 10 healthy controls. Whole-body movement (WBM) and rapid alternating movements (RAM) at the wrist were recorded simultaneously using 6-degree of freedom magnetic motion tracker and forearm rotational sensors, respectively. WBM was recorded prior to, and while subjects performed pronation-supination movements of their dominant hand with maximal rotational excursion, and as fast as possible for 10s. RANGE, VELOCITY and IRREGULARITY of pronation-supination cycles were quantified to assess motor performance. Results show that DPD patients had greater WBM than NDPD and controls during rest and RAM performance, as expected. There were no differences in motor performance between DPD and NDPD groups for RANGE and VELOCITY, despite significantly longer disease duration for the DPD group (15.5+/-6.2 years versus 6.6+/-2.6 years). However, both the NDPD and DPD groups showed significantly lower RANGE and reduced VELOCITY compared to controls, suggesting the presence of bradykinesia. For IRREGULARITY, DPD patients showed increased fluctuations in pronation-supination cycle amplitude compared to NDPD and controls. However, the lack of correlation between WBM magnitude and IRREGULARITY within the DPD group (Spearman's rank order, rho = 0.31, p > 0.05), suggests that LID were not the primary cause of increased IRREGULARITY. In conclusion, our results demonstrated that bradykinesia can coexist with dyskinesias, suggestive of distinct neural circuits. Our results also demonstrated that the occurrence of LID is not inevitably accompanied with worsening of motor performance.