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Prepared by: Joanna O’Leary, MD, Marian Livingston, MD, PADRECC, Northwest/Portland
Impact of Specific Executive Functions on Driving Performance in People With Parkinson’s Disease.
Executive cognitive functions are required in complex driving situations. This study evaluates specific executive functions and their association with driving performance in patients with Parkinson’s disease (PD). Nineteen (19) patients with PD (mean age 66.1+/- 5.1 with Hoehn & Yahr stage 2.1 +/- 0.3 and disease duration of 7.5 +/- 4.3 years) were compared to 21 controls (mean age 69.1 +/-3.9). All patients were assessed with mini mental status exam (MMSE) for global cognitive state, Trail Making Test (TMT B-A) for global executive function, TMT Part A for psychomotor speed, Benton Visual Retention Test for visual memory, digit span task for short-term storage capacity, Baddeley’ s Working Memory digit-span task for maintenance of relevant information, Block Design Test for visuo-constructional abilities, Plus Minus Task for mental flexibility, n-back task for updating, and Stroop test for inhibition. All patients were also evaluated with an experimental drive on a specific route in the city of Lyon for one hour using a car equipped with sensors and video recording. A blinded driving instructor evaluated each patient with a version of Test Ride for Investigating Practical Fitness to Drive (TRIP) that evaluates various aspects of driving on a score of 0 to 100 including: (1) operational score that assesses braking and lane position, (2) tactical score which assesses anticipation and speed adaptation, (3) tactical compensation score which assesses gap distance, choice of speed, and anticipatory behavior, and (4) strategic compensation score assessing driving conditions that participants usually avoided. A non-blinded experimenter sat in the back seat and evaluated the patient with an observational grid to code participants’ driving behavior including actions like braking and looking in the rear view mirror with penalty scores for items missed and safety intervention scores for when instructors corrected participants. Participants also evaluated themselves on a scale of 0-10 (0 = bad, 10 = good driving skills). Neurological exam, neuropsychological testing and road tests of PD patients were conducted “on” medication. Cognitive and driving performances in the two groups were compared using 1-tailed analyses. The chi-squared or Fisher exact test was used for categorical variables. A sub-category of drivers determined to be “at risk” if they were within 10% of having the most penalties, 10% with the highest safety interventions made by driving instructor, or 10% with lowest TRIP scores. Comparisons between “at risk” and “safe” drivers were performed using that 2-tailed Mann-Whitney U test. Executive function test results were significantly worse for the PD patients compared to controls in assessment of global cognitive state (MMSE: 27.4 +/- 1.5 for PD patients, 29.3 +/- 0.7 for controls, p=0.0001), psychomotor speed (TMT-A: 51.28 +/-13.23 for PD patients, 39.05 +/- 15.40 for controls, p=0.012), inhibition (Stroop test: 79.24 +/-57.00 for PD patients, 53.86 +/- 16.25 for controls, p=0.017), and visuo-constructional abilities (Block Design Test: 22.89 +/- 6.85 for PD patients, 31.38 +/- 5.70 for controls, p=0.0002). Driving performance was also significantly worse in PD patients than controls (TRIP score 66.34 +/- 9.11 for PD patients, 76.57 +/- 8.48 for controls, p < 0.001) although PD patients fared better in the sub-category of strategic compensation (4.32 +/- 3.22 for PD patients, 1.76 +/- 1.55 for controls, p < 0.001). The non-blinded observational grid results correlated well with the TRIP scores. Eight (8) patients were determined to be “at risk” drivers all of whom were PD patients. There were no significant differences between the demographics of “at risk “ and “safe” driver groups. Cognitive performance was significantly poorer in at-risk drivers than in safe drivers in tests assessing global cognitive state (MMSE: 27.50 +/- 1.20 for at risk, 28.66 +/- 1.47 for safe; p = 0.019), psychomotor speed (TMT- A: 55.88 +/- 15.73 s for at risk, 41.81 +/- 14.35s for safe, p = 0.032), visuo-constructional abilities (Block Design Test score: 20.38 +/- 8.02 for at risk, 29.29 +/- 6.30 for safe, p = 0.007), updating (response time in 2-back condition: 820.02 +/- 173.15 ms for at risk, 693.10 +/- 129.32 ms for safe, p = 0.039), and mental flexibility (shift cost of PMT: 41.19 +/- 26.37 for at risk 19.65 +/-14.09s for safe, p = 0.034). A stepwise discriminant analysis revealed that Block Design score (visuo-constructional ability) and response time in the 2-back test (updating ability) were the two best predictors of driving ability and accounted for 35% of the total variance between “safe” and “at risk” drivers. When medical group status (PD versus non-PD) was also factored in, all three factors together explained 53% of the total variance. This study confirmed the role of visuo-constructional and updating abilities in PD patients who are at risk for unsafe driving. Cognitive assessments to assess driving should include these measures.
Mov Disord 2013;28:1941–1948
PMID: 24114952 [PubMed - as supplied by publisher]
Cortical Effects of Deep Brain Stimulation: Implications for Pathogenesis and Treatment of Parkinson Disease
In a recent JAMA Neurology article, Li and colleagues review the under-appreciated topic of the effects of DBS on the motor cortex. They shift the focus from traditionally debated mechanisms of either decreased or increased basal ganglia output to cortex (via thalamic connections) to an examination of the effects of DBS on the “hyper-direct” cortical to STN pathway. Specifically, antidromic effects of STN stimulation on the motor cortex through this pathway may be important in suppressing the pathological cortical β synchronous oscillations (10-30 Hz) thought to underlie rigidity and bradykinesia in Parkinson Disease. In a PD rat model, Li and colleagues recorded single-unit activity and local field potentials in the motor cortex with STN DBS both on and off. They found antidromic spikes in pyramidal layer V neurons with STN DBS on. They also showed that the improvement in rigidity and bradykinesia was best at lower stimulation frequencies (125 Hz). They hypothesize that the randomness of antidromic impulses to pyramidal neurons through various interneurons and multiple axonal collaterals is the key factor resulting in desynchronization of the pathological beta rhythm. They speculate that there may be a similar GPi-cortical interaction. These findings will have important implications as DBS technology is refined, particularly with regard to cortical activity monitoring in dynamic closed-loop stimulation.
JAMA Neurol. 2014;71(1):100-103. doi: 10.1001/jamaneurol.2013.4221
Published online November 4, 2013.
Isogenic human iPSC Parkinson’s model shows nitrosative stress-induced dysfunction in MEF2-PGC1α transcription
It has been known for some time that Parkinson’s disease has both genetic and environmental risk factors. One such genetic risk factor is the A53T mutation in the protein alpha-synuclein, whereas exposures to herbicides and pesticides are well-established environmental risk factors for Parkinson’s disease. However, there have been relatively few studies in which the combined influences of genetics and environment have been explored. The paper by Ryan et al is one of the few studies that examined the combined influences of a genetic mutation and exposure to herbicides and pesticides on substantia nigra dopamine neurons, which become disabled in Parkinson’s disease. This study is significant because it shows that exposure to environmental toxins greatly increases damage due to oxidative stress in dopamine neurons that also express a genetic mutation for Parkinson’s disease. Moreover, they did their studies in dopamine neurons that were derived from pleuripotent stem cells that were created from skin tissue from Parkinson’s disease patients that had the A53T mutation. The use of a naturally occurring genetic mutation that is expressed by human dopamine neurons is a unique feature of this study. Consequently, this study provides considerable support for the “dual hit” hypothesis that postulates that Parkinson’s disease may be the result of both genetic and environmental influences.
Cell 155:1-14, December, 2013
· Rotation of Committee Chair: Leadership for the clinical care committee rotates amongst the PADRECCs. The Southeastern PADRECC leads the committee for January/February. Committee meets via conference call the first Tuesday of the month at 12pm (EST)
· Standardize and Optimize Clinical Care: Continues to discuss a variety of clinical issues to enhance patient care, the committee continues to provide clinical support to the Consortium network, and work on measures to standardize clinical care across the PADRECC network. Recent agenda items have included ongoing discussion on:
Review of applications in clinical arena for subset of patients, and ways to expand access to CBOCs and remote areas where subspecialty expertise is not available. Research ideas pertaining to the use of home monitoring devices in movement disorders patients.
Development of PMB guideline for clinical use of various toxins
Applications and pitfalls of use
Northwest Service Area Updates
Director: Joe Quinn, MD
The 3 Centers of Excellence (COE’s) from Portland are into year 2 of participation in the National Neurology Telehealth (TH) Program. Susan O’Connor is the lead RN for the Portland group with other team members from the Epilepsy and MS centers and Facility Telehealth Coordinator (FTC). They have worked with the leadership of 2 VA’s ( Spokane and Boise) that have been able to hire an NP to champion with them to provide TH. The 2 NP’s have been to Portland for training in all 3 specialty’s for a week at a time. Tools for measuring outcomes from this project have been developed as well as some educational brochures regarding the centers and what they have to offer. These will all be presented to a national committee for approval before shared.
The Northwest PADRECC has added 2 new consortium sites to their service area:
Billings Montana VA Black Hills HCS
Director: Daniel Rodriquez, MD Director: Laurie Weisensee, MD
Phone: 406-373-3610 Phone: 605-718-1095
Both Dr. Rodriquez and Dr. Weisensee participated in the Northwest PADRECC mini-residency program in Portland spending a week attending clinics, conferences, journal club, grand rounds as well as one on one time with each specialty group from each center of excellence.
Dates to Remember
March 13, 2014
EES/PADRECC Movement Disorder Series
Topic: Etiology & Treatment of Ataxia
April 26-May 3, 2014
American Academy of Neurology-Annual Meeting
May 8, 2014
EES/PADRECC Movement Disorder Series
Topic: Drug Induced Parkinsonism
June 8-12, 2014
18th International Congress of Parkinson’s Disease and Movement Disorders
Movement Disorder Society
July 10, 2014
EES/PADRECC Movement Disorder Series
September 11, 2014
EES/PADRECC Movement Disorder SeriesTopic: TBA
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