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What's the/is there a relation between neurodegeneration and cerebral reorganisation? by Mind Map: What
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What's the/is there a relation between neurodegeneration and cerebral reorganisation?

Interaction of neurodegeneration and cerebral reorganisation

how do the mechanisms which cause neurodegeneration impact cerebral reorganisation?

Cerebral reorganization in Parkinson’s disease Rick Helmich, The disfunction of the striatum affects the healthy cerebello-thalamic circuits which actually produce the resting tremmor., The cerebello-thalamic interacts in the thalamus with the thalamo-sensory cortex tracts., The miss-interpretation of somatosensory information caused by the influence of broken pallido-thalamic tracts over healthy thalamo-cortical tracts., The sensory processing is driven in a "tremorous state" in which cyclical oscillations interrupt normal neuronal activity patterns., increase in neuron sinergism inside the striatum due to the loss of Dopamine., Blurring the connection between cognitive and motor processing, Blurring the somatotopy within motor loop

is there an impact of i.g. iron or alpha-synucleine in reorganisation?

Causes of neurodegeneration, acceleration of cell loss in the SNc, causing nigrostriatal degeneration to both reach a threshold for symptoms in advance of earlier affected brain areas and progress more rapidly than other aspects of the disease

functional pathways that are lost with the degeneration of the striatum

Cerebral reorganization in Parkinson’s disease Rick Helmich, altered connection with primary and secondary Somato-Sensory cortex (impairment in the perception of body's position in space), altered connection with the Pre Motor Area, Skin deafferentation proven by skin byopsies and quantitative sensory testing

interaction between brain areas

Cerebral reorganization in Parkinson’s disease Rick Helmich, The somatosensory processing is altered by motor imagery tasks., Because the Putamen doesn't work distorted sensory maps are sent to premotor area.

Are there predictive factors for a good compensation of neurodegeneration?


Type (genetic, idiopathic or toxic)

Motivation, good cognitive control

Cerebral reorganization in Parkinson’s disease Rick Helmich, The Anterior Cingulate Cortex is an area where motor, motivational and cognitive loops can interract

What are the brain differences between PD patients who compensate and those who not?

Cerebral reorganization in Parkinson’s disease Rick Helmich, Patients least affected with their motor control of an assymetric affected hand do better on visual processing. (the strengthening of occipito-parietal connections), markedly increase in the power of somatosensory cortex to gather data from other sources

forms of clinical Parkinson

Cerebral reorganization in Parkinson’s disease Rick Helmich, Patient with tremor-dominant symptoms do clinically better because they use their tremor as somatosensory cueing. (role of VIM nucleus in the thalamus)

Psychological State

Depression, Cerebral reorganization in Parkinson’s disease Rick Helmich, Depression decreases motor control by lowering Dopamine levels in the Ventral Putamen and decreasing serotoninergic function.

How does cerebral reorganisation work?

Are there any brain areas more prone to organisation than others?

"Cerebral reorganization in Parkinson’s disease" Rick Helmich, The Remapping happens between Parietal lobe and Pallidum and it can be predicted by the dopamine content heterogenity in the Pallidum, enhancement in the Cingulate Motor Area

Is there a connection to the stages of the disease?

Hoehn & Yahr Clinical staging

Braak stages of Lewy Body progression patterns

Is there an active learning process involved or does it happen involuntary?

"Cerebral reorganization in Parkinson’s disease" Rick Helmich, The motivational modulation of cognitive control depends on the dopamine in the striatum and it can be improved by the expectation of a reward.

What compensation mechanisms are there besides motor compensation?

Can the number of neuronal progenitor cells (NPC) inside the patient's brain predict the functional outcome after reorganisation?

Early compensation

How does the brain compensates the damage before symptoms appear?,, "Our results suggest that PD subjects tap into motor reserve, increase the spatial extent of activation and demonstrate NAR to maintain near-normal motor output.",, there is reorganisation of the corticomotor representation of the hand in PD, even at a relatively early stage of the disease, and suggest a dynamic process of reorganisation in the motor cortex due to an increase in the pallidal inhibitory inputs to the thalamo-cortical projections.

Do mutations in the genes with cause the genetic variants of PD affect the (motor) circuits in the brain of healthy mutan carriers?, Mapping preclinical compensation in Parkinson's disease: an imaging genomics approach., "In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction"

Do environmental factors/toxins affect the (motor) circuits of healthy people in fMRI?

Does toxic induced PD in animals has the same compensation mechanisms?

What cases of cerebral reorganisation are described for different neurodegenerative diseases?

i.g. increase in creativity in patients with primary progressive aphasia

How can cerebral reorganisation be influenced?

Can a neuroelectrophysiological technique (DBS,cortical magnetic stimulation) help with the cortical repair?

Can the removal of the pathogenic factor(Iron, Alpha-Sinuclein) increase the brain's chance to reorganisate.

can physical activity lead to structural and functional brain alterations in PD?

Physical exercise administrated in advance protect the animal's basal ganglia from MPTP toxicity, ? Does this happen because of the reorganisation of the frontal cortex especially the Anterior Cingulate Cortex?

What are the effects of reorganisation on the brain function?

Is it a maladaptive process?(like in cardiac insufficiency) Good on the short run but damaging on the long run?

Helmich Dissertation, It seems that it is not maladaptive but completely compensatory because patients with a benign clinical course seem to gather the biggest changes., Although these connectivity changes may help retain cortico-­‐striatal coupling in the face of (dorsolateral) striatal dysfunction, we hypothesized that they may also cause maladaptive changes at other levels of the network, For instance,the cortical area showing cortico-­‐striatal remapping (parietal cortex) also showed reduced functional connectivity with other portions of the motor system (i.e.the motor cortex).

Does motor compensation lead to psychological damage(dementia) on the long-run or does it actually have a protective affect.

The Cognitive and Computational Neuroscience of Categorization, Novelty-Detection

It remains unclear whether the increased visual cortex activity observed during motor imagery in chapter 6 prevents behavioral impairments (making it an instance of compensatory reorganization) or whether it reflects less efficient cortical activation (making it an instance of pathological reorganization).

Methods we could use for our research

Use of fMRI,PET-scan and [F18]Dopamine imaging to see the new motor circuits.

Can it be evaluated by strict paraclinical methods?

using magnetic resonance spectroscopy (MRS, to measure N-­‐acetyl aspartate (NAA) concentrations in the basal ganglia to study it's connectivity

How is the movement control influenced through the neurodegeneration/cerebral reorganisation


thalamic/cortical influence?, These results suggest that a paradigm shift should take place in our view of freezing of gait. PD subjects with freezing of gait have a continuous gait disturbance: the ability to regulate the stride-to-stride variations in gait timing and maintain a stable walking rhythm is markedly impaired in subjects with freezing of gait. In addition, these findings suggest that the inability to control cadence might play an important role in this debilitating phenomenon and highlight the key role of dopamine-mediated pathways in the stride-to-stride regulation of walking., These results suggest that pallidal activity can correlate inversely with the severity of dystonia, perhaps due to activity dependent changes in neuronal function resulting from repeated voluntary movement.


visual control

can certain movements be improved by cerebral reorganisation?

how can the freezing of gait be influenced?, "Overall, the findings suggest a smaller capacity for compensation in patients suffering from FOG. Especially when attention is overloaded, the therapeutic window and the practical applicability of cueing seem more limited."

somatosensory input diminuished

Helmich Dissertation, This suggests  that   the  cortico-­‐striatal  circuit  plays  a  central  role  in  altered  somatosensory  processing  in  PD,  although  it  should   be  kept  in  mind  that  these  changes  may  be  multi-­‐synaptic. ltered thalamic gating of afferent signals to the somatosensory cortex

motor compensation

PD patient cycling, paper Snijders, AH:, In the video accompanying this article, we present another patient with a similarly preserved ability to ride a bicycle, despite marked FOG. It concerns a 57-year- old man who had been treated with bilateral subtha- lamic nucleus stimulation for severe motor fluctuations, 12 years after onset of PD. The home video shows the patient’s severe gait disorder, mainly caused by FOG. However, he can immediately generate smooth cycling, Why is bicycling preserved in some patients with freezing of the gait?, the rotating pedals are presenting tactile cues, more afferent feedbac through tactile cues, there are speciality in cycling: fixed amplitude and timing as well as a length constant could make it easier for PD patients than walking, in PD patients, there could be altered cortical regulation of movement execution. Complex movements like cycling, but also walking upstairs could be preserved, Research ideas about preserved cycling/preserved movements in general in PD Patients, mimicking cycling movements with/without tactil cues under fmri/EEG control, is the motor control different for cycling and walking?, are the tactile cues important for the preserved cycling movement?, Executive function was assessed with Trail-Making Test (TMT) A and B before and after passive leg cycling. Significant improvements on the TMT-B test occurred after passive leg cycling. Furthermore, the difference between times to complete the TMT-B and TMT-A significantly decreased from precycling to postcycling. Improved executive function after passive cycling may be a result of increases in cerebral blood flow. These findings suggest that passive exercise could be a concurrent therapy for cognitive decline in PD., mentally imaging of the preserved movement (cycling movements/walking up the stairs), fMRI, which brain regions and circuits are activated? are they different than those activated under mentally imaging of walking?, could this be a therapeutic strategy?, RESULTS: Following the intervention, the combined treatment group exhibited significantly faster performance of movement sequences than the control group. In addition, the experimental subjects demonstrated higher gains in the mental and motor subsets of the UPDRS and in the cognitive tests. Both groups improved on the activities of daily living scale. CONCLUSIONS: The combination of motor imagery and real practice may be effective in the treatment of PD, especially for reducing bradykinesia. The implementation of this treatment regimen allows for the extension of practice time with negligible risk and low cost., cycling in patients with unilateral FOG, how is the bilateral coordination affected, techniques, fMRI, blood flow changes, while making bilateral hand movements, Posture influences motor imagery: an fMRI study., imagination of walking:, cycling inside a fMRI, Monitoring to get more information about the patients compensation/cueing/preserved movement (skin rate/heart rate), connection to emotion/stress, variation between days, SPECT for measuring the dopamine levels, Voxel based morphometry, are there morphological changes in the gray matter?, EEG/EMG, evocated motoric potential, ergometer monitoring, realtime-walking monitoring, Optic and PET methods allow the measurement of brain activity during real overground walking., HMPAO-SPECT, Hanawaka, Brain functional activity during gait in normal sub- ten Hippokampusregion als Vermitt- ler der räumlichen Orientierung sind jects: a SPECT study., FDG-PECT,, New node,, ambulatoryb EEG, What kinds of preserved movements do exist besides cycling?, identifying how many PD patients do present the preserved cycling, if cueing is important, what is the influence of sensory/auditive/visual cues on the brain circuits/dopamine levels?, Oliver Sacks: Awakenings,, therapeutic idea. tricycles for patients which preserved cycling, What is the role of visual information?, cycling with eyes closed, does it has an impact?

Bas Bloem TEDx

Michael J Fox

de novonmotor skill learning in non-demented PD patients still preserved:





fMRI Imaging of cueing?


How pharmacological manipulation of striatal Dopamine in healthy subjects affects cortical connectivity in resolving different motor/cognitive tasks?