Chapter 56 Flashcards

1
Q

What is the role of the cerebellum in motor control?

A
  • helps to sequnces the motor activities and also monitors and makes corrective adjustments in the body’s motor acitivities while they are being executed.
  • This allows for smoother and more direct movements.
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2
Q

What are the three anatomical division of the cerebellum?

A
  • anterior lobe
  • posterior lobe
  • flocculonodular lobe
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3
Q

What is the function of the flocculonodular lobe?

A

-works with the vestibular system in controlling body equillibrium

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4
Q

What kind of motor movements is tha lateral zone involved with?

A

-discrete motor movements and the planning of sequential motor movements

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5
Q

What functions is the intermediate zone concerned with?

A

-muscle contractions in distal portions of the upper and lower limbs

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6
Q

What are some of the different inputs into the cerebellum?

A
  • Corticopontocerebellar tract
  • olivocerebellar tract
  • vestibulocerebellar fibers
  • reticulocerebellar fibers
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7
Q

What are the three subdivisions of the reticulocerebellar pathway?

A
  • dorsal spinocerebellar
  • ventral spinocerebellar
  • dorsal columns
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8
Q

What are the three deep nuclei of the cerebellum?

A
  • Dentate
  • Interposed (globos and emboliform)
  • and fastigial
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9
Q

Where do the deep cerebellar nuclei recieve inputs from?

A
  • the cerebellar cortex
  • deep seosry afferent tracts
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10
Q

What is the usual path of signals into the cerebellum?

A
  • Signals enter the cerebellum and are projected to the deep nuclei and the corresponding area of the cotex overlying the deep nucleus.
  • cortex then sends an inhibitory signal to the deep nuclei
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11
Q

What happens to signals that orriginate in the midline (vermis) of the cerebellum? What is the main purpose of this pathway?

A
  • Pass through the fastgial nuclei intot he meduulary and pontile regions of the brainstem
  • controls postural attitudes of the body
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12
Q

What is the order of a pthway that orriginates in the intermediate zone fo the cerebellar hemisphere? What is its function?

A
  • intermediate zone–> interposed nuclei–> VA/VL thalamus–> cerebral cortex–> thalamus–> basal ganglia–> red nucleus and reticular formation
  • helps to coordinate agonist and antagonist muscle contractions (esp. hands, fingers and thumbs)
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13
Q

What is the order of pathways orriginating in the cerebellar cortex? What is its main function?

A

cerebellar cortex–> dentate nucleus–> VA/VL–> cerebral cortex

-coordinates sequential motor activites intiated by the cerebral cortex. (cerebrocerebellar pathway)

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14
Q

What type of sensation trvels via the spinocerebellar tract?

A
  • feedback information on limb position and movement
  • muscle tension, degree and rate of movements, joint position, forces acting on surfaces of the body
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15
Q

What is the purpose of this feedback informatio through the spinocerebellar tract?

A

-to tell the cerebellum:

–intended sequence of movement

–result of that actual movement

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16
Q

What are the two main inputs into the functional unit of the cerebellum?

A
  • mossy fiber
  • climbing fiber
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17
Q

What is the origination of the climbing fiber?

A

-originates in the inferior live and climbs to the cerebellar cortex where it inserts on 5-10 purkinje cells

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18
Q

What is the origination of the mossy fiber?

A

-multiple sources:

–higher brain, brainstema and spinal cord

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19
Q

Where do the mossy fibers insert?

A

-insert on to granule cells (remeber the rosettes?) which then project into the cortex where they interact with purkinje cells

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20
Q

Are the synaptic connections between the mossy fiber and the purkinje cells strong?

A

No

large number of mossy cells are required to excite a single purkinje cell

21
Q

What are the two different action potentials generated in purkinje cells by climbing fibers and mossy fibers?

A
  • Climbing fibers–> complex spikes
  • Mossy fibers–> simple spikes
22
Q

Review the neuronal circuit of the cerebellar function unit- Picture

A
23
Q

How does the turn-on/turn-off signal for the agonist/antagonist muscle intiate?

A

-The cerebellar cortex intiatiates the contraction (agonist) through the non-cerebellar brain stem and cord pathways

24
Q

What happens at the same time the cerebellum is initiating an agonist contraction?

A

Parallel signals are sent via mossy fibers–>deep cerebellar nuclei

The nuclei then send an excitatory signal to the cortex through the CST which supports and further excites the contraction

25
Q

What causes the turn-off signal for the antagonists after movement?

A
  • mossy fiber branches to the granule cells excite purkinje cells which are inhibitory
  • purkinje cells inhibit the effects of the deep nuclei, thereby sotpping trnamission of the excitatory signal to the cortex.
26
Q

What is the basis for the antagonist muscle circuit?

A

-Agonist/antagonist reciprcal circuit in the spinal cord mirror the turn-on and turn-off signals going to the agonists to inhibit then excite the proper antagonistic muscle

(E.g. if your cerebellum is sending the turn-on signal to the brachialis for arm flexion, then interneuons and circuits in the spinal cord are inhibiting the transmission of excitement to the triceps)

27
Q

how does the vestibulocerebellum regulate overall motor control?

A
  • equillibrium management
  • flocculonodular lobe involved
28
Q

How does the spinocerebellum contribute to overall motor control?

A

-coordination of movements of the distal limbs, especially the hands and fingers

29
Q

What areas make up most of the spinocerebellum?

A
  • vermis
  • psoterior and anterior cerebullum
  • intermediate zones on either side of the vermis
30
Q

How does the cerebrocerebellum contribute to overall motor control?

A

-projects planned movements from the cerebral motor cortex and somatosensory areas back to the cerebral cortex to help plan voluntary body and limb movements

31
Q

What areas of the cerebellum make up the cereobrocerebellum?

A

-large lateral zones of the cerebellar hemispheres

32
Q

What kind of motor control do the basal ganglia serve a role in?

A
  • fine, complex motor control (like writing letters of the alphabet)
  • using scissors, hammering nails, shooting a basketball, throwing a baseball etc.
  • pretty much anything that reqires cooridination and is normall performed subconsciously
33
Q

What is the primary functionof the putamen circuit? Where do the inputs main come from? Where does it output to?

A
  • executing learned patterns of movement
  • input from areas adjacent to the promary motor cortex
  • Output to the primary motor cortex or closely associated areas
34
Q

What is the main purpose of the caudate circuit in motor control? Where do signals from theis pathway end up?

A

-integration of the information from the association areas into a usable thought pattern

–> signals end in the prefrontal, premotor, and supplementary motor areas. (almost none go straight to the primary motor cortex)

-this integration allows the motor association areas to come up with a plan very rapidly based on available information

35
Q

What is a good example of the use of the caudate pathway?

A
  • you see a lion so:
  • you turn away from the lion
  • begin running
  • climb a tree

–> all this occured with very little conscious thought becuase the caudate circuit accessed nformation already sotred in memory and then decided what to do based on those previous experiences

36
Q

What is the main difference in outputs of the putamen and caudate pathways?

A
  • putamen pathways go to the motor cortex or close to it to allow execution of a learned movement
  • caudate pathways project to motor association areas for the brain to put together the sequential movement.
37
Q

How does the basal ganglia control timing and scale when doing something like writing a letter?

A

-we dont really know, but what we do know:

–> the basal ganglia determine timing and scale of an action like writing a small leter v. a big letter and writing fast v. slow. –>basal ganglia is able to keep the approximate scaling the same

38
Q

What happens when there is a lesion to the basal ganglia in the posterior parietal cortex?

A

contrallateral neglect.

–>scaling and preception of the contralateral side is absent.

39
Q

What are the 3 major inhibitory neuro transmitters of the basal ganglia?

A
  • Dopamine
  • GABA
  • Serotnin
40
Q

What is a disinihibitory circuit?

A

-inhibition of an inhibitory neuorn–> leading to activation or lack of inhibition of the following neuron

41
Q

What is the general pathway of GABA? in the basal ganglia?

A

-GABA projects from the caudate to the putamen and globus pallidi, then to the substantia nigra

42
Q

In which direction do dopamine trnasmissions flow?

A

-from the substantia nigra to the caudate and putamen

43
Q

Where are ACh inhibitory signals orriginating? Where do they act?

A

-orriginating from the caudate and cortex to the putamen

44
Q

What part of the basal ganglia is either dysfunctional or destroyed in Parkinson disease?

A

Substantia nigra

45
Q

What is the SN no longer releasing that is leading to the presentation manifestation of the illness?

A

Dopamine

46
Q

A patient presents to you with rigidty of body musculature, a 5 Hz tremor of the hand,a akinesia, and poor balance. What structure is no longer functioning properly? What is the pathway involved?

A

Substantia Nigra

-The SN is no longer releasing appropriate amounts of dopamine on to the Striatum, this results in a lack of inhibitory output from the stratum to the medial globus pallidus. This lack of inhibition of the GPm results in over inhibition of the VA/VL thalamus by the GPm, and a lack of excitatory signals being sent to the cortex

47
Q

A 35 year old patient presents to you with progressive cognitive deficits and a whole body choreatic distortional movement. His mother had the same illness, What neurotransmitter is responsible for the signs observed? What is the diagnosis?

A
  • GABA
  • Huntinton disease
48
Q

What is the pathway involved with Huntington disease?

A
  • a decrease in GABA release from the striatum, ruduces the inhibition on the lateral glubus pallidus, this leads to increased activity in the lateral globus pallidus. Increased inhibition from the lateral globus pallidus to the subthalamic nuclei results in a decrese in excitatory transmission from the STN to the GPm. The decreased activity to the GPm results in less inhibition of the VA/VL thalamus leading to hyperexability in the cortex.
  • just know that less gaba in the indirect pathway= more excitable VA/VL
49
Q

Just for completeness, what is the repeating codon seen in Huntinton disease?

A

CAG