1
Q
Motor control hierarchy
A
- high: strategy (association areas + basal ganglia)
- middle: tactics (motor cortex + cerebellum)
- low: execution (brain stem + spinal cord)
2
Q
Characteristics of sensorimotor system
A
- Hierarchical control over movement
- cortex—>muscle
- Motor output guided by sensory input
- a lot of it
- Learning changes motor control
- location —> lower hierarchical layers
- plasticity
- nature —> unconscious, child learning to walk
- learning=higher cortical areas
- habitual=lower cortical areas
3
Q
Lateral pathways
A
- Involved in voluntary movements of distal muscles
- under direct cortical control
4
Q
Ventromedial pathways
A
- involved in control of posture and locomotion
- under brain stem control
5
Q
Lower motor neurons
A
- alpha motor neurons
- begin in ventral horn —>ventral root—>mixed nerve—>NMJ
- Alzheimer’s has depleted acetylcholine at NMJ, cortex, hippocampus
- neurotoxins take advantage of acetylcholine in NMJ
- excess acetyl choline in cleft=uncontrollable movement
6
Q
Local feedback
A
- Aa axons send propioceptive information to spinal cord
- affects inhibitory interneurons
- allows one muscle to contract while antagonistic muscle relaxes
7
Q
Corticospinal pathway
A
- lateral pathway
- starts in NEOCORTEX (area 4+6)
- > project to INTERNAL CAPSULE
- > to DIENCEPHELON + THALAMUS
- > base of CEREBRAL PEDUNCLE
- > MEDULLARY PYRAMID
- > decussates at SPINAL CORD
- > descends through lateral columns to form lateral corticospinal tract
- > terminates in VENTRAL HORN
8
Q
Rubrospinal tract
A
- lateral pathway
- originates in RED NUCLEUS of midbrain
- > decussates in PONS
- > parallels corticospinal tract to VENTRAL HORN
9
Q
Lateral pathway lesions (experimental)
A
- deficits in fractionated movement of arms and hands
- unable to move in independent fashion
- recovery of rubrospinal tract in tact
10
Q
Lateral pathway legions (strokes)
A
- tissue dies due to lack of oxygen
- if this occurs in motor cortex or corticospinal tract:
- paralysis in contralateral side (due to decussation)
- some recovery over time due to plasticity of other networks
11
Q
Vestibulospinal pathway
A
- ventromedial pathway
- function to keep head balanced as body moves
- originates in VESTIBULAR NUCLEI
- > projects BILATERALLY down spinal cord as far as lumbar regions
12
Q
Tectospinal pathway
A
- ventromedial pathway
- functions to keep head balanced during movement
- originates in SUPERIOR COLLICULUS
- > descends through medulla
- > decussates in SPINAL CORD
- > projects to cervical regions
13
Q
Reticulospinal pathway
A
- ventromedial pathway
- arises in PONTINE RETICULAR FORMATION
- > descends to MEDULLARY RETICULAR FORMATION
- > divides into 2 tracts (pontine and medullary) which descend IPSILATERALLY to VENTRAL HORN
- pontine tract enhances antigravity reflexes
- ventral horn generally maintains muscle length/tension
14
Q
Paralyzed man who walked again
A
-8mm cut into spinal cord
- Removed olfactory bulb + olfactory ensheathing cells grown in culture
- 100 micro injections of OECs made above and below damaged area
- 4 strips of nerve tissue places across gap
- OECs acted as a pathway to stimulate cells to regenerate
15
Q
Planning of movement
A
- area 4= precentral gyrus = M1
- area 6= anterior to A4
- PMA=premotor area(lateral)—> proximal muscles
- SMA=supplementary motor area(medial)—>distal muscles
- electrical stimulation in area 4 causes twitching is associated region n contralateral side of body
- electrical stimulation in area 6 results in complex movement on either side of body
- prefrontal cortex + parietal cortex send axons to area 6
- area 6 lies at junction where signals encoding WHAT actions are converted to signals that specify HOW an action will be done
16
Q
Area 5+7
A
- posterior parietal
- area 5= receives input from A1,2,3
- area 7=received input from MT
17
Q
Mirror neurons
A
- activated by specific movements
- important for development of social behaviours
- use motor circuits for planning own movement AND understanding actions/goals of others
- area 6-PMA
18
Q
Basal gangli
A
- consists of caudate nucleus, putamen, globus pallidus, subthalamic nucleus and substantia nigra
- striatum= caudate + putamen
- globus pallidus = source of output to thalamus
19
Q
Direct path
A
- cortex->striatum->globus pallidus->ventral lateral nucleus->cortex (SMA)
- net effect=excitation of neurons in SMA
20
Q
Indirect pathway
A
-net effect= excitation of neurons in ventral lateral nucleus
21
Q
Basal ganglia disorders
A
- HYPOkinesia=decreased movement
- Parkinson’s: problems initiating movement
- HYPERkinesia=increased movement
- Huntington’s disease: autosomal disorder
22
Q
Parkinson’s
A
- hyperkinesia
- bradykinesia: slowness of movement
- akinesia: inability to move
- tremors and rigidity
- caused by degeneration of SN
- treated with L-DOPA
23
Q
Huntington’s
A
- hyperkinesia
- dyskinesia: inappropriate movement
- dementia
- caused by genetics (repeat in CAG in telomeres)
- degeneration of striatum
- treated with antipsychotics
24
Q
Initiating movement
A
- M1 output: layer V pyramidal cells
- largest cells called Betz cells
- project to pools of lower interneurons that are excitatory or inhibitory
- excitor neurons will innervate flexors, while inhibit contractors etc
25
Coding movement
- individual pyramidal cells can drive many motor neuron pools from a group of different muscles involved in moving a limb toward desired goal
- bursts of activity occurs before and during voluntary movement
- activity encodes FORCE AND DIRECTION
- movement direction encoded by collective activity of population of neurons
26
Cerebellum
- 10% of total brain volume
- involved in timing sequence of movements (coordination)
- lesions=
- antaxia(uncoordinated movement)
- no resting tremor
- dyssnergia
- dysmetria (lack of precision in distance movement)
- folia like gyri
- molecular layer (outer)
- granule cell layer(inner)
NEURO 2470
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