Parkinson disease and driving: an evidence-based review.
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ABSTRACT:
SUBMITTER: Crizzle AM
PROVIDER: S-EPMC3511919 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:To determine the incidence of and risk factors for driving outcomes in drivers with Parkinson disease (PD).In a prospective cohort study, we ascertained the time until driving cessation, a crash, or a traffic citation using self-report and state Department of Transportation records in 106 licensed, active drivers with PD and 130 controls.Drivers with PD stopped driving earlier than controls, hazard ratio (95% confidence interval) = 7.09 (3.66-13.75), p < 0.001. Cumulative incidence of driving cessation at 2 years after baseline was 17.6% (11.5%-26.5%) for PD and 3.1% (1.2%-8.1%) for controls. No significant differences between groups on times to first crash or citation were detected. However, the number of observed crashes was low. Cox proportional hazards models showed that significant baseline risk factors for driving cessation in PD were older age, preference to be driven by somebody else, positive crash history, use of compensatory strategies, low driving exposure, impairments in visual perception (especially visual processing speed and attention) and cognitive abilities, parkinsonism (especially activities of daily living score and total daily dose of antiparkinsonian medications), and higher error counts on a road test. Within PD, crashes were associated with poorer postural stability and history of driving citations, and citations were associated with younger age and road errors at baseline.Drivers with PD are at a higher risk of driving cessation than elderly control drivers. A battery evaluating motor and nonmotor aspects of PD, driving record, and performance can be useful in assessing future driving outcomes in PD.
| S-EPMC3115811 | biostudies-other
Project description:ObjectiveTo longitudinally assess and predict on-road driving safety in Parkinson disease (PD).MethodsDrivers with PD (n = 67) and healthy controls (n = 110) drove a standardized route in an instrumented vehicle and were invited to return 2 years later. A professional driving expert reviewed drive data and videos to score safety errors.ResultsAt baseline, drivers with PD performed worse on visual, cognitive, and motor tests, and committed more road safety errors compared to controls (median PD 38.0 vs controls 30.5; p < 0.001). A smaller proportion of drivers with PD returned for repeat testing (42.8% vs 62.7%; p < 0.01). At baseline, returnees with PD made fewer errors than nonreturnees with PD (median 34.5 vs 40.0; p < 0.05) and performed similar to control returnees (median 33). Baseline global cognitive performance of returnees with PD was better than that of nonreturnees with PD, but worse than for control returnees (p < 0.05). After 2 years, returnees with PD showed greater cognitive decline and larger increase in error counts than control returnees (median increase PD 13.5 vs controls 3.0; p < 0.001). Driving error count increase in the returnees with PD was predicted by greater error count and worse visual acuity at baseline, and by greater interval worsening of global cognition, Unified Parkinson's Disease Rating Scale activities of daily living score, executive functions, visual processing speed, and attention.ConclusionsDespite drop out of the more impaired drivers within the PD cohort, returning drivers with PD, who drove like controls without PD at baseline, showed many more driving safety errors than controls after 2 years. Driving decline in PD was predicted by baseline driving performance and deterioration of cognitive, visual, and functional abnormalities on follow-up.
| S-EPMC5679414 | biostudies-literature
Project description:ObjectiveTo assess driving performance in Parkinson disease (PD) under low-contrast visibility conditions.MethodsLicensed, active drivers with mild to moderate PD (n = 67, aged 66.2 +/- 9.0 years, median Hoehn-Yahr stage = 2) and controls (n = 51, aged 64.0 +/- 7.2 years) drove in a driving simulator under high- (clear sky) and low-contrast visibility (fog) conditions, leading up to an intersection where an incurring vehicle posed a crash risk in fog.ResultsDrivers with PD had higher SD of lateral position (SDLP) and lane violation counts (LVC) than controls during fog (p < 0.001). Transition from high- to low-contrast visibility condition increased SDLP and LVC more in PD than in controls (p < 0.01). A larger proportion of drivers with PD crashed at the intersection in fog (76.1% vs 37.3%, p < 0.0001). The time to first reaction in response to incursion was longer in drivers with PD compared with controls (median 2.5 vs 2.0 seconds, p < 0.0001). Within the PD group, the strongest predictors of poor driving outcomes under low-contrast visibility conditions were worse scores on measures of visual processing speed and attention, motion perception, contrast sensitivity, visuospatial construction, motor speed, and activities of daily living score.ConclusionsDuring driving simulation under low-contrast visibility conditions, drivers with Parkinson disease (PD) had poorer vehicle control and were at higher risk for crashes, which were primarily predicted by decreased visual perception and cognition; motor dysfunction also contributed. Our results suggest that drivers with PD may be at risk for unsafe driving in low-contrast visibility conditions such as during fog or twilight.
| S-EPMC2764395 | biostudies-literature
Project description:BackgroundIt is unknown whether driving difficulty in Parkinson disease (PD) is attributable to nigrostriatal dopaminergic or extranigral non-dopaminergic neurodegeneration.ObjectiveTo investigate in vivo imaging differences in dopaminergic and cholinergic innervation between PD patients with and without a history of risky driving.MethodsThirty non-demented PD subjects (10 women/20 men) completed a driving survey. These subjects had previously undergone (+)-[(11)C] dihydrotetrabenazine vesicular monoamine transporter 2 and [(11)C] methyl-4-piperidinyl propionate acetylcholinesterase PET imaging. Acetylcholinesterase PET imaging assesses cholinergic terminal integrity with cortical uptake largely reflecting basal forebrain and thalamic uptake principally reflecting pedunculopontine nucleus integrity.ResultsEight of thirty subjects reported a history of risky driving (been pulled over, had a traffic citation, or been in an accident since PD onset) while 22 had no such history (safe drivers). There was no difference in striatal dihydrotetrabenazine vesicular monoamine transporter uptake between risky and safe drivers. There was significantly less thalamic acetylcholinesterase activity in the risky drivers compared to safe drivers (0.0513 ± 0.006 vs. 0.0570 ± 0.006, p = 0.022) but no difference in neocortical acetylcholinesterase activity. Using multivariable logistic regression, decreased thalamic acetylcholinesterase activity remained an independent predictor of risky driving in PD even after controlling for age and disease duration.ConclusionsRisky driving is related to pedunculopontine nucleus-thalamic but not neocortical cholinergic denervation or nigrostriatal dopaminergic denervation in PD. This suggests that degeneration of the pedunculopontine nucleus, a brainstem center responsible for postural and gait control, plays a role in the ability of PD patients to drive.
| S-EPMC3946835 | biostudies-literature
Project description:Parkinson disease (PD) is a chronic neurodegenerative condition that leads to progressive disability. PD-related reductions in muscle strength have been reported to be associated with lower functional performance and balance confidence with an increased risk of falls. Progressive resistance training (PRT) improves strength, balance, and functional abilities. This umbrella review examines the efficacy of PRT regarding muscular strength in PD patients. The PubMed, PEDro, Scopus, and Cochrane Library databases were searched from January 2009 to August 2019 for systematic reviews and meta-analyses conducted in English. The populations included had diagnoses of PD and consisted of males and females aged >18 years old. Outcomes measured were muscle strength and enhanced physical function. Eight papers (six systematic reviews and meta-analyses and two systematic reviews) were considered relevant for qualitative analysis. In six of the eight studies, the reported severity of PD was mild to moderate. Each study analyzed how PRT elicited positive effects on muscle strength in PD patients, suggesting 10 weeks on average of progressive resistance exercises for the upper and lower limbs two to three times per week. However, none of the studies considered the postworkout follow-up, and there was no detailed evidence about the value of PRT in preventing falls. The possibility of PRT exercises being effective for increasing muscle strength in patients with PD, but without comorbidities or severe disability, is discussed. Overall, this review suggests that PRT should be included in rehabilitation programs for PD patients, in combination with balance training for postural control and other types of exercise, in order to preserve cardiorespiratory fitness and improve endurance in daily life activities.
| S-EPMC7270996 | biostudies-literature
Project description:The purpose of this study was to conduct an evidence-based review to determine predictors of fitness to drive and return to driving in persons with traumatic brain injury (TBI). Relevant databases (MEDLINE/PubMed, CINAHL, Cochrane Library, and SCOPUS) were searched for primary articles published before June 2016 using MeSH search terms. Using the American Academy of Neurology's classification criteria, 24 articles were included after reviewing 1998 articles. Studies were rated by class (I⁻IV), with I being the highest level of evidence. Articles were classified according to TBI severity, as well as types of assessments (on-road, simulator and surveys). There were no Class I studies. Based on Class II studies, only Post-traumatic amnesia (PTA) duration was found to be probably predictive of on-road driving performance. There is limited evidence concerning predictors of return to driving. The findings suggest further evidence is needed to identify predictors of on-road driving performance in persons with TBI. Class I studies reporting Level A recommendations for definitive predictors of driving performance in drivers with TBI are needed by policy makers and clinicians to develop evidence-based guidelines.
| S-EPMC6371138 | biostudies-literature
Project description:Mutations in PARK2, encoding Parkin, cause an autosomal recessive form of juvenile Parkinson Disease (JPD). The aim of the present study was to investigate the impact of PARK2 mutations on mitochondrial function and morphology in human skin fibroblasts. We analyzed cells obtained from four patients clinically characterized by JPD, harboring recessive mutations in PARK2. By quantitative PCR we found a reduction (<50%) of PARK2 transcript in all patients but one; however Western Blot analysis demonstrated the virtual absence of Parkin protein in all mutant fibroblasts. Respiration assays showed an increment of oxygen consumption, which was uncoupled to ATP cellular levels. This finding was probably due to presence of altered mitochondrial membrane potential (??m), confirmed by JC-1 analysis. The mitochondrial network was comparable between mutant and control cells but, interestingly, a "chain-like" network was found only in mutant fibroblasts. Dissipation of ??m usually leads to mitochondrial fragmentation in healthy cells and eventually to mitophagy; however, this behavior was not observed in patients' fibroblasts. The absence of mitochondrial fragmentation in mutant Parkin fibroblasts could results in accumulation of damaged mitochondria not targeted to mitophagy. This condition should increase the oxidative stress and lead to cellular dysfunction and death. Our results suggest that PARK2 mutations cause mitochondrial impairment, in particular reduction in ATP cellular levels and alteration of ??m, even in non-neuronal cells and confirm the hypothesis that Parkin holds a pivotal role in pro-fission events.
| S-EPMC4356157 | biostudies-literature
Project description:ObjectiveTo investigate whether cigarette smoking interacts with genes involved in individual susceptibility to xenobiotics for the risk of Parkinson disease (PD).MethodsTwo French population-based case-control studies (513 patients, 1,147 controls) were included as a discovery sample to examine gene-smoking interactions based on 3,179 single nucleotide polymorphisms (SNPs) in 289 genes involved in individual susceptibility to xenobiotics. SNP-by-cigarette smoking interactions were tested in the discovery sample through an empirical Bayes (EB) approach. Nine SNPs were selected for replication in a population-based case-control study from California (410 patients, 845 controls) with standard logistic regression and the EB approach. For SNPs that replicated, we performed pooled analyses including the discovery and replication datasets and computed pooled odds ratios and confidence intervals (CIs) using random-effects meta-analysis.ResultsNine SNPs interacted with smoking in the discovery dataset and were selected for replication. Interactions of smoking with rs4240705 in the RXRA gene and rs1900586 in the SLC17A6 gene were replicated. In pooled analyses (logistic regression), the interactions between smoking and rs4240705-G and rs1900586-G were 1.66 (95% CI 1.28-2.14, p = 1.1 × 10-4, p for heterogeneity = 0.366) and 1.61 (95% CI 1.17-2.21, p = 0.003, p for heterogeneity = 0.616), respectively. For both SNPs, while smoking was significantly less frequent in patients than controls in AA homozygotes, this inverse association disappeared in G allele carriers.ConclusionsWe identified and replicated suggestive gene-by-smoking interactions in PD. The inverse association of smoking with PD was less pronounced in carriers of minor alleles of both RXRA-rs4240705 and SLC17A6-rs1900586. These findings may help identify biological pathways involved in the inverse association between smoking and PD.
| S-EPMC5818012 | biostudies-literature
Project description:Parkinson disease (PD) is a neurological movement disorder resulting primarily from damage to and degeneration of the nigrostriatal dopaminergic pathway. The pathway consists of neural populations in the substantia nigra that project to the striatum of the brain where they release dopamine. Diagnosis of PD is based on the presence of impaired motor features such as asymmetric or unilateral resting tremor, bradykinesia, and rigidity. Nonmotor features including cognitive impairment, sleep disorders, and autonomic dysfunction are also present. No cure for PD has been discovered, and treatment strategies focus on symptomatic management through restoration of dopaminergic activity. However, proposed cell replacement therapies are promising because midbrain dopaminergic neurons have been shown to restore dopaminergic neurotransmission and functionally rescue the dopamine-depleted striatum. In this review, we summarize our current understanding of the molecular pathogenesis of neurodegeneration in PD and discuss the development of new therapeutic strategies that have led to the initiation of exploratory clinical trials. We focus on the applications of stem cells for the treatment of PD and discuss how stem cell research has contributed to an understanding of PD, predicted the efficacy of novel neuroprotective therapeutics, and highlighted what we believe to be the critical areas for future research.
| S-EPMC7663462 | biostudies-literature
Project description:BackgroundDespite advances in both prevention and treatment, traumatic brain injury (TBI) remains one of the most burdensome diseases; 2% of the US population currently lives with disabilities resulting from TBI. Recent advances in the understanding of inflammation and its impact on the pathophysiology of trauma have increased the interest in inflammation as a possible mediator in TBI outcome.ObjectivesThe goal of this systematic review is to address the question: "What is the evidence in humans that inflammation is linked to secondary brain injury?" As the experimental evidence has been well described elsewhere, this review will focus on the clinical evidence for inflammation as a mechanism of secondary brain injury.Data sourcesMedline database (1996-Week 1 June 2014), Pubmed and Google Scholar databases were queried for relevant studies.Study eligibility criteriaStudies were eligible if participants were adults and/or children who sustained moderate or severe TBI in the acute phase of injury, published in English. Studies published in the last decade (since 2004) were preferentially included. Trials could be observational or interventional in nature.Appraisal and synthesis methodsTo address the quality of the studies retrieved, we applied the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) criteria to assess the limitations of the included studies.ResultsTrauma initiates local central nervous system as well as systemic immune activation. Numerous observational studies describe elevation of pro-inflammatory cytokines that are associated with important clinical variables including neurologic outcome and mortality. A small number of clinical trials have included immunomodulating strategies, but no intervention to date has proven effective in improving outcomes after TBI.LimitationsInclusion of studies not initially retrieved by the search terms may have biased our results. Additionally, some reports may have been inadvertently excluded due to use of non-search term key words. Conclusions and Implications of Key Findings Clinical evidence of inflammation causing secondary brain injury in humans is gaining momentum. While inflammation is certainly present, it is not clear from the literature at what juncture inflammation becomes maladaptive, promoting secondary injury rather than facilitating repairand identifying patients with maladaptive inflammation (neuro-inflammation, systemic, or both) after TBI remains elusive. Direct agonism/antagonism represents an exciting target for future study.Level of evidenceSystematic review, level III.
| S-EPMC4297199 | biostudies-literature