Lecture 10: Control of Body Movement

Question 1

Discuss the musclotopic organization of the motor cortex

Answer 1

inverted: foot by top of cortex, head by bottom of cortex. area of cortex proportional to number of connections (control of movement)

Question 2

Describe the divisions of the cerebellum

Answer 2

vestibulocerebellum (floculornodular): input from vestibular nuclei, control of eye movements

spinocerebellum (anterior): input from spinocerebellar pathways, such as the DCML, control of posture

corticocerebellum (posterior): input from cortex via pons (pontocerebellar fibers), control of rate of reach and force

Question 3

Describe the basal nuclei

Answer 3

no input from spinal cord, input from cortex/substantia nigra/thalamus, three main nuclei (caudate nucleus (eye movement), putamen nucleus, globus pallidus) (putamen & globus = body movement)

fires before movement occurs therefore slecting movements

Question 4

Is the cerebellar control contra- or ipsi- lateral?

Answer 4

ipsilateral: double crossing by motor efferents and cerebellar efferent

Question 5

Describe the inputs and outputs of the cerebellum

Answer 5

INPUTS:
mossy fibers: synapse indirectly on Purkinje fibers via granule cells first
climbing fibers: synapse directly on Purkinje fibers, modulate responsivity of Purkinje fibers to mossy fibers, fire at low frequencies

OUTPUTS:
Purkinje fibers: only outputs. goes to deep cerebellar nuclei, from there to the thalamus to the motor cortex

Question 6

Describe cerebellar damage

Answer 6

no impairment of intelligence or personality
affects balance, gross motor movement, defects in rate/range/force of movement
damage occurs ipsilaterally

Question 7

Describe the pathways of the basal ganglia, then what happens during Huntington’s and Parkinson’s disease

Answer 7

cortical motor area +caudate/putamen -GPe and GPi
GPe: -GPi/-SubThalamic nucleus (+GPi)
GPi: -thalamus +cortical motor area
direct pathway (GPi) is excitatory, GPe is inhibitory/indirect

Huntington’s disease: hyperkinetic (tremors, jerkiness, shaking): affects caudate/putamen, no longer any inhibition of GPe therefore excitatory

Parkinson’s disease: substantia nigra +D1 to C/P to GPi, -D2 to C/P to GPe. D2 and D1 degenerate, causes decrease of movement.