30/ motor control 2

Question 1

what structures are indirectly involved in influencing movement by regulating function of upper motor neurons

Answer 1

• basal ganglia and cerebellum

Question 2

key components in initiation of movement

Answer 2

• motor cortex - AF4 (telencephalon)
• basal ganglia (forebrain)
• ventral lateral nucleus of thalamus (diencephalon)
• substantia nigra (midbrain)

Question 3

the motor loop

Answer 3

• motor cortex connects to basal ganglia, which in turn feedback to premotor area (area 6) via ventrolateral complex of thalamus (VLo)
• direct and indirect pathway

Question 4

basal ganglia involvement in the direct motor loop

Answer 4

• with no initiating cortical input, globus pallidus internal segment GPi tonically / consciously inhibits VLo
• inputs from many cortical regions converges on the striatum
• when activated by this input, striatum inhibits the inhibitory activity of the GPi, releasing the Vlo to activate area 6 and initiate movement

Question 5

why is the direct pathway set up the way its is

Answer 5

• integration of cortical inputs to trigger a response
• rapid response - engine running, inhibition of inhibition = releasing brake

Question 6

basal ganglia involvement in indirect pathway

Answer 6

• modulates direct pathway
• substantia nigra acts via striatum to maintain balance between inhib/activation of VLo
• excitatory inputs from sn stimulates Vlo actiavtion by activating inhib of GPi through direct path
• in indirect path, GPe inhibits GPi
• but Gpe is inhibited by CP, so VLo inhib
• but inhib input from sn decreases CP inhib of GPe, so GPi inhib, so activation of VLo

Question 7

what % of parkinsons cases are sporadic

Answer 7

85-90%

Question 8

motor symptoms of parkinsons disease

Answer 8

• hypokinesia - partial movement
• bradykinesia - slow movements
• akinesia - no movement
• increased muscle tone - rigid
• resting tremor
• shuffling gait, impaired balance
• face less expressive

Question 9

non motor parkinsons symptoms

Answer 9

• loss of smell
• mood disorders

Question 10

what is parkinsons caused by, what is degeneration marked by

Answer 10

• dopamine loss due to loss of dopaminergic neurons of substantia nigra (alive neurons dont produce less)
• degeneration marked by lewy bodies - intracellular protein aggregates

Question 11

L-dopa treatment for parkinsons

Answer 11

• only lasts about 5 years
• doesnt stop degradation
• eventually too few neurons to keep making dopamine
• side effects: motor response fluctuation increased, dyskinesia (erratic movements)

Question 12

what are the effects of dopamine loss on the basal ganglia

Answer 12

• increased activity of indirect pathway
• decreased activity of direct pathway
• so less inhibition of GPi so its inhibitory activity is increased
• leads to decreased activity of VLo so less motor cortex activation

Question 13

in severe cases, what can be removed in parkinsons patients

Answer 13

• the GPi
• more recently deep brain stimulation to inhibit it

Question 14

huntington background

Answer 14

• rare hereditary, progressive, fatal

Question 15

hd symptoms

Answer 15

• early: hyperkinesia (opposite of pd), dyskinesia, cholera - invol jerking
• late : akinesia, dystonia (muscle spasms), dementia, psychosis

Question 16

hd cause

Answer 16

• autosomal dominant
• initially in indirect pathway of striatum compartments
• subsequently direct pathway components and GPe

Question 17

basal ganglia in hd

Answer 17

• early: degeneration in striatum reduces indirect inputs to GPe
• increases inhib of GPi, VLo disinhib - inappropriate imitation of movement - cholera and hyperkinesis
• later: striatal direct path and GPe neurons degen, releasing GPi to over inhib VLo - akinesis

Question 18

what does the basal ganglia include

Answer 18

• caudate
• putamen
• globus pallidus
• regulated by sn

Question 19

hd and pd overview

Answer 19

• hd: degen of striatum. hyperkinesis then akinesis
• pd degen of sn, hypokinesis

Question 20

info about risk alleles for pd vs hd

Answer 20

• pd: some rare w high penetrance SNCA, others common low penetrance GABA1
• hd: only HTT huntingtin protein - if you have mutation when not if you get the disease

Question 21

info about proteins coded for by risk alleles for pd and hd

Answer 21

• pd: protein degradation pathways (hence lewy bodies) and mitochondria
• hd: HTT - intracellular transport. inclusion bodies in affected neurons

Question 22

what other areas input info about perception of body in space and time

Answer 22

5 and 7

Question 23

cerebellum and motor learning

Answer 23

• modulates upper nms - no direct connection to sc
• learnt execution of planned vol movements
• ball throwing: cerebellum instruct motor cortex w respect to direction, timing and force. based on predictions based on based experience
• compares intended w actual result

Question 24

what is ‘muscle mem’ = motor learning

Answer 24

• strengthens or weakens existing neural pathways
• mem lies in neurons not muscle
• some muscle mem involved in rebuilding quickly

Question 25

cerebellum loop w motor cortex

Answer 25

* cerebellum receives input form many areas if cortex - corticopontocerebellar projection - and sensory info from spinal cord and vestibular system * in turn projects back to motor cortex via thalamus VLo, no direct output to sc * primary function to detect motor error - dif between intended and actual * lesions result in cerebellar ataxia -poorly integrated movement * coordination lost - dyssynergia * alcohol has similar effects, represses cereballar circuits * neurodegen that affect cerebellum - mad cow disease