1. Speakers
1.1. Bas Bloem
1.1.1. Many movies
1.1.1.1. Some clips from awakenings
1.1.2. Medical Management
1.1.2.1. focus on primary disease process
1.1.2.2. Maybe: Deep brain stimulation could focus on adaptive strategies
1.1.3. Allied health care
1.1.3.1. focus on compensatory strategies
1.1.4. New node
1.1.5. Papers
1.1.5.1. protractedbenefit from paradoxical kinesia in typical and atypical parkinsonism
1.1.5.1.1. Neurol Sci (2010) 31:751-756
1.1.5.1.2. L. Bonnani
1.1.5.2. Snijders et al, Mov Disorders 2010, in press
1.1.5.2.1. cycling to overcome freezing of gait
1.1.5.3. Cycling for freezing of gait: paper New England Journal of MEdicine
1.1.5.3.1. Patients contacting Bas Bloem for tricks they use to overcome freezing after paper
1.1.5.4. van Nimwegen et al, J Neurol 2011, revision pending
1.1.5.4.1. Physical activity in Parkinson Disease
1.1.5.5. Ferraye
1.1.5.5.1. Effects of pedunculopontine nucleus stimulation
1.1.5.5.2. Brain
1.1.5.5.3. Correlation of clinical effect with electrode location
1.1.6. Study
1.1.6.1. ParkFit study
1.1.6.1.1. ParkSafe program
1.1.6.1.2. ParkFit Program
1.1.6.1.3. Design
1.1.6.2. Extensive exercise
1.1.6.2.1. Imaging and extensive physical activity
1.1.6.3. Multimodal exercise
1.1.7. Examples
1.1.7.1. Cues vs 3D cues
1.1.7.2. Dual tasking to IMPROVE performance
1.1.7.2.1. while literature says it makes things worse
1.1.7.2.2. a video example: courtesy of Mariella Graziano
1.1.7.2.3. being able to walk while bouncing a ball
1.1.7.3. visual feedback
1.1.7.3.1. maybe no visual feedback is better than faulty visual feedback for some patients
1.1.7.4. A man who cannot walk - yet he can run
1.1.7.4.1. a Parkinson's disease compensatory strategy
1.1.7.4.2. Clinical: examine arm swing while running
1.1.7.5. Use of side steps as compensatory strategy
1.1.7.5.1. courtesy of Jay Nutt
1.1.7.6. Kicking objects as a trick to walk
1.1.7.7. Being able to play pingpong in a severe off state
1.1.7.8. Walking in a skating movement in order to increase mobility
1.1.7.9. Jumping while moving about the house
1.1.7.10. Dystonia: compensatory mechanisms
1.1.7.10.1. a diving dress as a sensory trick
1.1.7.10.2. Courtesy of Martin Horstink
1.1.7.11. Pisa syndrome
1.1.7.11.1. Dystonia with parkinsonism: a patient that can stand straight when touching the head
1.1.7.12. Retrocollis w PD and dystonia
1.1.7.12.1. touching chin aleviating retrocollis
1.1.7.12.2. Biting on a straw to help compensate
1.1.7.12.3. courtesy of Bart van de Warrenburg
1.1.7.13. External cueing
1.1.7.13.1. nieuwboer et al, JNNP 2007;78:134-140
1.1.7.13.2. Visual cuing
1.1.7.14. Bad compensatory strategies
1.1.7.14.1. I will never fall again
1.1.7.14.2. Risk on falling decreases in end stage PD
1.1.8. "walking in the scanner"
1.1.8.1. fMRI study
1.1.8.2. Thinking about walking
1.1.8.2.1. A behavioral control
1.1.8.2.2. Motor imagery
1.1.8.2.3. Comparison gait vs hand imagery
1.1.8.2.4. Anke Snijders
1.2. Esther Aarts
1.2.1. University of Californisa at Berkeley
1.2.2. Compensation by motivation: how anticipating reward reduces cognitive rigidity in Parkinson's Disease
1.2.3. Dopamine transporter (DaT) SPECT study
1.2.3.1. Background
1.2.3.1.1. motor and cognitive inflexibility
1.2.3.1.2. reward-related impulsivity
1.2.3.1.3. impulsive behavior in PD has often been attributed to dopaminergic overstimulation
1.2.3.2. Hypothesis
1.2.3.2.1. dopamine deplation and reward related impulsivity
1.2.3.3. Rewarded task-switching paradigm
1.2.3.3.1. reward anticipation: high vs low
1.2.3.3.2. cognitive flexibility
1.2.3.4. conclusion
1.2.3.4.1. low baseline dopamine state: increased reward-induced impulsivity
1.2.3.4.2. Task-switching, on low reward
1.2.4. Event related fMRI study
1.2.4.1. Is the above (from SPECT study) related to frontostriatal activity
1.2.4.2. Main effect of reward anticiptaion
1.2.4.3. Conclusion
1.2.4.3.1. patients OFF medication showed a larger beneficial effect of reward on task-switching than ON medication in controls
1.2.4.4. Cools et al, neuropsychopharm 2007
1.2.4.5. Paper
1.2.4.5.1. Zigmond et al TINS 1990
1.3. Henk Berendse
1.3.1. functional connectivity in Parkinson's Disease: the more the
1.3.2. Parkinson's Disease
1.3.2.1. the traditional view
1.3.2.2. Braak et al 2003, Neurobiol Aging 24:197-211
1.3.3. Non-motor symptoms in PD
1.3.4. Synchronization of cortical brain activity
1.3.4.1. changes in local neuronal synchrony
1.3.4.2. synchronization of activity between distributed neuronal populations = functional connectivity
1.3.5. Hypotheses
1.3.5.1. PD is associated with changes in synchronization of neural activity
1.3.5.2. changes in neuronal synchronization in PD will be stage-dependent
1.3.5.3. changes in neuronal synchronization in PD will be correlated with severety of motor and non-motor symptoms
1.3.5.4. changes in neuronal synchronization in PD can be modulated pharmacologically
1.3.6. Experiments
1.3.6.1. MEG 151 channel system
1.3.6.2. Synchronization likelihood (SL)
1.3.6.2.1. statistical interdependency between signals measured at two sensors
1.3.6.3. schematic representation of sensors
1.3.6.3.1. excluding midine sensors from analysis
1.3.6.4. Functional connectivity parameters
1.3.6.4.1. local
1.3.6.4.2. interhemisferic
1.3.6.4.3. intrahemisferic
1.3.6.5. Weighted averages
1.3.6.5.1. local
1.3.6.5.2. interhemisferic
1.3.6.5.3. intrahemispheric
1.3.6.6. predictors of cognitive decline in PD
1.3.6.7. Newly diagnosed drug naive PD
1.3.6.7.1. increased connectivity
1.3.6.7.2. Alpha 1
1.3.6.7.3. Diffusely distributed
1.3.6.7.4. Stoffers et al Neuroimage 2008
1.3.6.7.5. Silberstein et al 2005, Brain 128:1277-1291
1.3.6.8. early to moderate PD
1.3.6.8.1. Increased activity
1.3.6.8.2. What happens when treatment w levodopa
1.3.6.9. Differential effects of DA therapy
1.3.6.9.1. patients with the best levodopa response: reduction in synchronisation likelihood
1.3.6.10. Demented PD patients
1.3.6.10.1. MMSE <=24
1.3.6.11. Conclusions
1.3.6.11.1. PD is characterized by stage-dependent frequency specific changes in functional connectivity
1.3.6.11.2. Dopamine administration modulates functional connectivity changes (not spectral power) in PD
1.3.6.11.3. cholinesterase inhibitors partially resvers spectral power, not loss of functional connectivity
1.3.6.12. Future studies
1.3.6.12.1. longitudinal assesment of changes in neuronal synchronization / predictors of disease course
1.3.6.12.2. comparison w MRI measures of structural (DTI) and functional (fMRI) connectivity
1.3.6.12.3. development of animal model
1.3.6.12.4. monitoring the effects of drug treatment and prediction of treatment response
1.3.7. Literature
1.3.7.1. Stam and van dijk (2002) physica D 163:236-51
1.3.7.2. Montez et al 2006 - neuroimage 33:1117-25
1.4. Peter Praamstra
1.4.1. Questions on Cueing: do patients feel the beat?
1.4.1.1. Does cueing work?
1.4.1.2. What is the physiological basis of cueing
1.4.1.2.1. Kandel & Schwarz, 4th edition 2000
1.4.1.2.2. Goldberg, 1985
1.4.1.2.3. Passingham, 1987, 1993
1.4.1.2.4. Glickstein and stein, 1991
1.4.1.2.5. Schell & Strick 1984
1.4.1.2.6. Context-dependent modulation of movement-related discharge in primate globus pallidus
1.4.1.2.7. Basal ganglia motor control - nonexclusive relation of pallidal discharge to five movement modes
1.4.1.2.8. Self-initiated versus externally triggered movements
1.4.1.2.9. Why is the idea that basal ganglia can be bypassed so established
1.4.1.3. why does cueing need a rethink?
1.4.1.3.1. no notes taken
1.5. Günther Deuschl
1.5.1. some notes
1.5.2. Title: is there a paradox of stereotactic sugery for tremor?
1.5.3. Is there a relation between tremor and voluntary movement
1.5.3.1. Vallbo and Wessberg 1993
1.5.4. Raethjen et al 2002
1.5.4.1. topographical distribution of rhythmic activity
1.5.5. did not take notes on most parts of presentation
1.5.6. The bottleneck of tremors
1.5.6.1. Close to VIM
1.5.6.1.1. Somatotopy of projections within the thalamus
1.5.6.1.2. illinsky et al 2003
1.5.6.2. Herzog et al, Brain 2007
1.5.6.3. Improvement of tremor and ataxia with relation to the caudal Vim Border
1.5.6.3.1. Fasano et al 2011
1.5.6.4. Radiatio prelemnicalis
1.5.6.4.1. Essential tremor: ataxic without stimulation
1.5.6.4.2. Essential tremor: less ataxic tremor with stimulation
1.5.6.4.3. ET: supra threshold stimulation: no tremor, yet restart of ataxia.
1.5.6.5. Chronaxia for tremor and ataxia
1.5.6.5.1. increase stimulation length
1.5.6.5.2. check for intensity you need
1.5.6.5.3. tells about the fibers you are stimulating
1.5.6.5.4. = working in different systems when stimulating ataxia
1.5.7. Summary
1.5.7.1. the central origin of most pathologic tremors is now settled
1.5.7.2. pd tremor has unique clinical characteristics and has also a unique receptor abnormality, a unique system pathophysiology
1.5.7.3. pd tremor seems to be generated within the basal ganglialoop
1.5.7.4. but interventions within the cerebello thalamic pathway are influencing remor
1.6. Lars Timmerman
1.6.1. The rhythm of the beast: pathological oscillatory activity in Parkinsonian tremor.
1.6.2. Where is the tremor in our patient's brain
1.6.2.1. what are the traces of the BEAST?
1.6.2.2. the cerebral oscillatory network of parkinsonian resting tremor
1.6.2.3. Look at normal tremor in EEG
1.6.2.4. Timmermann et al Brain 2003
1.6.2.5. A: coherence atdouble tremor frequency is affected by M1, coherence at tremor frequency is not
1.6.2.6. B: phase triggered averages: alternating pattern at tremor frequence FDI/EDC, M1 shows double tremor frequency
1.6.2.6.1. M1 is primary motor cortex
1.6.2.6.2. FDI/EDC = muscles
1.6.3. Primary motor cortex affected
1.6.3.1. which other brain areas are connected
1.6.3.2. cerebro-cerebral coherence at double tremor frequency
1.6.4. Pathophysiological concept: resting tremor in PD
1.6.4.1. cerebro-cerebral coupling and
1.6.4.2. cerebro-muscular coupling in double the tremor frequency
1.6.4.3. image: timmermann et al Brain 2003
1.6.5. How do we compensate the deficits?
1.6.5.1. the influence of L-Dopa on PD resting tremor
1.6.5.2. EMG and MEG study
1.6.5.3. Dynamic imaging of Coherent Sources, Gross et al 2001
1.6.5.4. pollok et al movement disorders 2009
1.6.5.5. L-Dopa effect: parkinsonian resting tremor: changes in network - decrease in diencephalon premotor cortex and trend in M1/S1-diencephalon and PMC-M1/S1 coupling
1.6.5.6. Most market change: diencephalon and premotor cortex
1.6.6. How does the BEAST look in detail
1.6.6.1. Topography of oscillatory tremor activity in the local...
1.6.6.2. Pattern of pathological tremor-activity in the subthalamic nucleus (STN)
1.6.6.3. Reck et al, EJN 2009
1.6.6.4. Power: calculation with the fast fourier transformation (FFT, transformation of time-series in frequency domain)
1.6.6.5. "Afferent input-causalities" are in general more frequent than "efferent output causalities"
1.6.6.6. Florin et al, neuroimage 2010,
1.6.6.6.1. filtering as an highly negative influence on Granger derived measures.
1.6.6.6.2. Calculation of causalities with Granger derived measures leads to new information
1.6.6.6.3. sPDC is the most robust measure for directionality in neuronal data
1.6.6.7. Can you enforce the BEAST?
1.6.6.7.1. 10 HZ in Parkinson's disease: the true rhythm of the beast?
1.6.6.8. Summary
1.6.6.8.1. not noted
1.7. Rick Helmich
1.7.1. Parkinson's Disease
1.7.2. Resting tremor
1.7.2.1. cardinal symptom of PD, not correlated with dopamine depletion in striatum
1.7.2.2. impaired voluntary motor control "akinesia"
1.7.2.2.1. haslinger et al, brain 2001
1.7.2.2.2. helmich et al j neuroscience 2009
1.7.3. Are the basal ganglia involved in resting tremor?
1.7.3.1. Yes.. but how?
1.7.3.1.1. benabid 1991, koller et al ann neurol 1996, krack etal 1997, lozano et al 1995
1.7.3.1.2. intereventions that can reduce tremor infollowing structures
1.7.4. hypotheses
1.7.4.1. Pathological interaction between basal ganglia and cerebello-thalamic circuit
1.7.4.2. transient tremor-0related signals may be relayed from the basal ganglia to the cerebllo thalamic circuit
1.7.5. Design
1.7.5.1. 36 healthy controls, 23 non-tremor PD patients, 21 tremor dominant PD patients
1.7.5.2. resting state fMRI, combined with EMG recordings
1.7.5.3. DAT scan to measure dopaminergic alterations
1.7.6. Which network produces tremor?
1.7.6.1. EMG recordings correlation with active brain structures
1.7.6.2. SPM of tremor regressor 1 patient
1.7.6.3. Motor cortex involved in production of tremor
1.7.6.4. Tremor amplitude related activity - cerebllo thalamic tract.
1.7.7. How is tremor triggered?
1.7.7.1. Pallidum is activated when the tremor amplitude changes
1.7.8. Tremor "triggers" and tremor "producers"
1.7.8.1. interaction between regions
1.7.8.1.1. seed region in basalganglia
1.7.8.1.2. Altered functional interactions
1.7.9. Is there a dopaminergic correlate for alterations
1.7.9.1. no correlates with striatal dopamine depletion
1.7.9.2. In PD patients with tremor, there's a selective degeneration in retrorubral area, that has projections to globus pallidus interna and externa
1.7.9.2.1. jan et al, EJN 2000
1.7.9.2.2. Bernheimer et al j. neurol Sci 1972
1.7.10. Discussion not noted
2. Mindmap Author
2.1. Paul de Roos, MD
2.2. twitter
2.2.1. www.twitter.com/paulderoos
2.2.2. Tweets on todays conference
2.2.2.1. #cerebralcompensation