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Basal Ganglia by Mind Map: Basal Ganglia
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Basal Ganglia

Pathophysiology of dyskinesia in experimental PD

Picconi et al 2003, pisani et al 2005

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

Morgante et al Brain 2006

Suppa et al 2010

not published yet

Functional Circuitry

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Functions

Functions

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Movement analysis of Bradykinesia in PD

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

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

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

impairment of individual finger movements more than gross hand movements

Bradykinesia and DBS-STN

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

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Eyelids movements in PD

Types

Voluntary, internal/external command

spontaneous

Reflex, external stimuli (visual, acoustic, kinetic)

PD patients

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

Improvement after dopamine therapy

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

Somatosensory discemination: study procedure

Conte et al Brain 2010

Experimental parkinsonism and lessons from surgery

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

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Synaptic plasticity

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

Prescott et al. 2009

Synaptic plasticity at the level of Substantia nigra pars reticulata

Pathophysiology of PD and synaptic plasticity

Transcranial magnetic stimulation: studies of plasticity

Gilio et al, Mov. Disord 2002

Short-term plasticity is reduced in PD

Long term plasticity

Measurement with iTBS

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in PD long term potentiation is much less

The dorsal premotor cortex (PMd) in PD

selecting appropriate movements

suppressing other activities

Experimental paradigm

record in different areas

TMS in PD

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

Bradykinesia

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

problems with performing simultaneous movement due to connectivity problem

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Rigidity and tremor in PD

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

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

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Pathophysiology of dystonia

excessive and sustained muscle contractions causing abnormal postures and involuntary movements

also cerebellum may be involved

Neuronal activity in dystonia

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

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Cortical plasticity and connectivity in dystonia

increased excitability of m1 and of brainstem neurons

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

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)

Shared neurophysiological findings of focal organic dystonias

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