Basal Ganglia

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Basal Ganglia by Mind Map: Basal Ganglia

1. Pathophysiology of dyskinesia in experimental PD

1.1. Picconi et al 2003, pisani et al 2005

1.2. Intermittent TBS over M1 showed that PD patients with LIDs do not have the normal increase in MEP size

1.3. Morgante et al Brain 2006

1.4. Suppa et al 2010

1.4.1. not published yet

2. Functional Circuitry

2.1. picture

2.1.1. picture

2.2. picture

2.3. Functions

3. Functions

3.1. picture

4. Movement analysis of Bradykinesia in PD

4.1. Small first EMG agonis burst, additional bursts (failur to energize movements) during arm and ahnd movements

4.2. failure to match EMG parameters to the size of movements required (inappropriate scaling of movement)

4.3. Difficulty in self-initiated and externally triggered arm movements (more self initiated)

4.4. impairment of individual finger movements more than gross hand movements

5. Bradykinesia and DBS-STN

5.1. Agostino et al JNNP 2008, Agostino et al Mov. Disord 2008

5.2. picture

6. Eyelids movements in PD

6.1. Types

6.1.1. Voluntary

6.1.1.1. internal/external command

6.1.2. spontaneous

6.1.3. Reflex

6.1.3.1. external stimuli (visual, acoustic, kinetic)

6.2. PD patients

6.2.1. slowness in switching between the closing and opening phases of voluntary blinking.

6.2.2. Improvement after dopamine therapy

6.2.3. Agostino et al 2008 Movement Disorders, Bologna et al 2009 Brain

7. Somatosensory discemination: study procedure

7.1. Conte et al Brain 2010

8. Experimental parkinsonism and lessons from surgery

8.1. Putamen,STN and GPi, show an increased neuronal response to peripheral stimulation with impairment of normal filtering of incoming signals.

8.1.1. Picture

9. Synaptic plasticity

9.1. Acitivty dependent modification of the strength or efficacy of synaptic transmission at preexisting synapses (short term and long term plasticity)

9.2. Prescott et al. 2009

9.2.1. Synaptic plasticity at the level of Substantia nigra pars reticulata

9.2.2. Pathophysiology of PD and synaptic plasticity

9.3. Transcranial magnetic stimulation: studies of plasticity

9.3.1. Gilio et al, Mov. Disord 2002

9.3.2. Short-term plasticity is reduced in PD

9.4. Long term plasticity

9.4.1. Measurement with iTBS

9.4.2. Picture

9.4.3. in PD long term potentiation is much less

10. The dorsal premotor cortex (PMd) in PD

10.1. selecting appropriate movements

10.2. suppressing other activities

10.3. Experimental paradigm

10.3.1. record in different areas

10.4. TMS in PD

10.4.1. in PD there's an altered PMd-to M1 activity

11. Bradykinesia

11.1. can be seen as a defect of motor circuit to generate a phasic inhibition of HPi neurons and facilitate cortical activation.

11.2. problems with performing simultaneous movement due to connectivity problem

11.3. picture

12. Rigidity and tremor in PD

12.1. rigidity is not explained by the classical model. Probably also involves disinhibition of brainsem mechanisms and spinal cord

12.2. the abnormal oscillatory activity in the network involving the basal ganglia, the cerebellar... (etc - missed)

12.3. Picture (circuits)

13. Pathophysiology of dystonia

13.1. excessive and sustained muscle contractions causing abnormal postures and involuntary movements

13.2. also cerebellum may be involved

13.3. Neuronal activity in dystonia

13.3.1. Reduced firing rates and altered patterns of neuronal activity in the GPi during pallidal surgery

13.3.2. picture

13.4. Cortical plasticity and connectivity in dystonia

13.4.1. increased excitability of m1 and of brainstem neurons

13.4.2. increased short-term plasticity and long-term plasticity at m1

13.4.3. functional connectivity between PMd and M1 is abnormal. Differently from healthy subjects in dystonia cTBS over PMd had any significant effect on MEPs. The PMd-M1 connectivity is reduced (Huang et al 2010)

13.5. Shared neurophysiological findings of focal organic dystonias

13.5.1. picture