8.1 Motor Cortex, Cerebellum and Basal Ganglia Flashcards

1
Q

List 4 important extra-pyramidal structures and state the overall function of these

A

1) Thalamus
2) Basal Ganglia
3) Cerebellum
4) Brain stem

Function to ‘fine tune’ the signals

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2
Q

What are the 4 things our brain must do to allow movement?

A

1) Initial desire to move
2) Initiation
3) planning
4) programming

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3
Q

What 2 systems are involved in planning of movement and state what each does

A

1) Limbic system: this is the where our desire to move originates
2) Prefrontal/premotor and supplementary motor cortex: this is where our attention, understanding and planning of movement occurs

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4
Q

What structure is responsible for Execution of movement?

Where do these signals travel to?

A

Primary motor cortex: sends direct signals to spinal cord

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5
Q

What 3 important structures comprise the limbic system?

Explain the role of each

A

1) Amygdala: emotion
2) Hippocampus: short term memory
3) Thalamus: rely net output of circuit to cortex

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6
Q

How does the Limbic system communicate with the pre-frontal cortex?

A

Via Cingulate gyrus

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7
Q

From the motor cortex, where do signals pass through to generate a response

A

motor cortex ➞ thalamus ➞ pyramidal system ➞ lateral corticospinal tract

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8
Q

The basal ganglia and the cerebellum are both considered _________ structures

A

subcortical

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9
Q

What is the specific role of the basal ganglia and the cerebellum

A

Basal ganglia: fine tune (make the decision regarding correct vs incorrect response)

Cerebellum: coordinate movement (corrects and checks the movement choosen by the basal ganglia)

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10
Q

What tract is the ‘chief organiser and executor of motor function’

Is this Pyramidal or Extrapyramidal?

A

Corticospinal tracts: travel through the pyramids of medulla oblongata and is therfore a pyramidal tract

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11
Q

What 4 tracts comprise the Extrapyramidal tract

A

Rubrospinal

Vestibulospinal

Reticulospinal

Tectospinal

(remember the basal ganglia and cerebellum are considered ‘extrapyramidal structures’ NOT tracts)

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12
Q

Are Extrapyramidal or Pyramidal responsible for movements beyond voluntary control

A

Extrapyramidal

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13
Q

List 4 signs seen in an UMN lesion and explain the reason for each

A

1) Weakness/ spastic paralysis: AP cant propagate from UMN to LMN
2) Increased tone: spasticity caused by overexaggerated stretch reflex
3) Increased tendon reflexes (Hyperreflexia): caused by lack of descending inhibitory pathways
4) Extensor plantars (Babinski sign): because normally extension is inhibited but when UMN is damaged, inhibition is blocked resulting in extension of great toe

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14
Q

List 5 signs seen in an LMN lesion and explain the reason for each

A

1) Weakness: due to loss/decreased innervation to effector muscles
2) Decreased tone: since tone is partially dependent on the monosynaptic reflex arc that links muscle spindles to LMN
3) Loss of tendon reflexes: due to loss/decreased innervation to effector muscles
4) Wasting and atrophy of muscles: due to damage to alpha motor neurones = lack of trophic factors needed by the muscles fibres
5) Fasciculations: spontaneous AP ➞ firing of the motor unit ➞ twitch

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15
Q

Define hyperkinesia and hypokinesia

A

Hyperkinesia: abnormal, involuntary movements

Hypokinesia: reduced movements

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16
Q

What will and will NOT be affected in an extrapyramidal lesions

A

WILL: Impair the regulation of voluntary movement

WILL NOT: affect the strength of movement (no atrophy)

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17
Q

What is a key clinical feature of extrapyramidal lesion and define this

A

Tremor: a rhythmic oscillatory movement that can occur at rest or on movement

Can be normal BUT abnormal may be benign essential tremor, intention tremor, resting tremor

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18
Q

Define Chorea and define Hemiballismus

A

Chorea: rapid irregular, unpredictable, involuntary muscle jerks (nearly always abnormal)

Hemiballismus: unilateral, usually violent, chorea

*** Signs of an extrapyramidal lesions

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19
Q

Define Dystonia

A

Excessive or inappropriate muscle contractions/spasm

*** Sign of an extrapyramidal lesions

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20
Q

Define Bradykinesia and what a progression of this is known as?

A

Bradykinesia is slowness of movement which can progress to akinesia which is absence of movement

*** Sign of an extrapyramidal lesions

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21
Q

Define Tics and state 2 instances when they may occur

A

Fleeting purposeless actions

Can be normal… or may occur in times of stress or in childhood

*** Sign of an extrapyramidal lesions

22
Q

Define Athetosis

A

Involuntary slow writhing movements hands or face

*** Signs of a extrapyramidal lesions

23
Q

What is Tardive dyskinesia and what is it assciated with?

A

An iatrogenic cause of parkinsonism-like effects which has features including oral grimaces, sucking, chewing

Associated with medication

*** Sign of an extrapyramidal lesions

24
Q

Label the image of the basal ganglia

A
25
Q

What is indicated on the image and what is important about this structure?

A

Substantia nigra is where our dopanergic neruons are located (dopamine = NT impt in the motor pathway)

26
Q

What comprises the basal ganglia (broadly speaking)?

A

Consist of multiple deep, sub-cortical nuclei

27
Q

What 5 specific structures comprise the basal ganglia?

A
  1. Caudate
  2. Putamen
  3. Globus pallidus
  4. Substantia nigra (midbrain)
  5. Subthalamic nuclei (ventral thalamus)
28
Q

What are the 4 functions of the basal ganglia?

A

1) Smooth motor movements
2) Amplitude and velocity
3) Posture control
4) Resting muscle tone

29
Q

How does the Basal ganglia influence activity movement

A

Influences activity movement by regulating activity of UMNs (NOTE: these do not project directly onto LMNs)

30
Q

List 3 problems that may occur due to defects of the basal ganglia

A

1) Cause inability to control movement
2) Problems when switching between commands
3) Problems initiating and terminating movements

31
Q

What is the name of the input region on the basal ganglia where projections from the cerebral cortex enter?

A

corpus striatum (= caudate + putamen)

32
Q

What 2 circuits are formed by projections from the CC to the basal ganglia and where do these feedback to?

A

Direct and indirect circuits which feedback to the cerebral cortex via the thalamus

33
Q

What does GPi and GPe stand for?

A

Globus Pallidus Internal and Globus Pallidus External

34
Q

Briefly describe the direct circuit

A

Excitatory…. release neurons from inhibition

35
Q

Briefly describe the Indirect circuit

A

Inhibitory: supress neurons further – a brake on the system

36
Q

Compare the Striatum vs Cortex in terms of their main NT’s

A

Striatum is a complete GABA structure (extremely inhibitory)

Cortex is very glutamatergic (very excitatory)

37
Q

What important NT acts as a filter and decides whether the system progresses or not?

Where does this act?

A

DOPAMINE! acts on the Striatum

38
Q

Describe the response of the GPi to dopamine and where it will be released

A

If we want a movement to progress, we require dopamine to ‘inhibit the inhibitor’ (GPi), making it active.

It does this by simultaneously activating and inhibiting the direct and indirect ganglion.

Dopamine will exist only in the synapse that corresponds to the area of the striatum with the movment we want and when released the GPi is activated leading to subsequent activation of the thalamus and striatum

39
Q

Compare the direct and Indirect pathways in terms of GABA released

A

In the direct pathway LESS GABA is released by the GPi (allowing movement)

In the indirect pathway MORE GABA is released from the GPi (not allowing movement)

40
Q

What is the role of the cerebellum?

A

Like the basal ganglia it influences movements by interaction with UMNs rather than projecting directly to LMNs. It functions to correct and check (fine tune) the movement chosen by the basal ganglia

It is involved in feedback loops with the motor cortex and brain stem nuclei

41
Q

What is the anatomical location of the cerebellum?

A

In the Hindbrain, it is infratentorial (below the tentorium cerebelli) in the posterior fossa

42
Q

How does the cerebellum connect to the brainstem?

A

Connects to the brainstem (pons and medulla) via 3 peduncles (superior, inferior and middle)

43
Q

How are the 2 hemispheres of the cerebellum joined?

What is the function of this structure and what is its clinical relevance?

A

Joined in the middle by the vermis

The vermis determines balance and hence degeneration of the vermis is seen in chronic alcoholics

44
Q

Describe the outer and inner cerebellum, incl what the 2 predominant cell types found here?

A

Outer cerebellar cortex and subcortical cerebellar nuclei

The predominant cell types are purkinje and granule cells

45
Q

What is the specific name given to the white matter of the cerebellum?

A

arbor vitae

46
Q

List 4 specific functions of the cerebellum

A

1) Coordinates smooth skeletal muscle movements
2) Balance
3) Learning and memory
4) Processes sensory information to monitor the course of movement/ feedback

47
Q

List some structures where the cerebellum recieves input from

A

Cerebral cortex, brainstem, ascending pathways, joint position sense, muscle length/tension etc…

48
Q

What 3 structures do outputs from the cerebellum travel to?

A

To brain stem nuclei, thalamus and cerebral cortex

49
Q

List 4 important signs seen is a patient with cerebellar dysfunction and explain each

A

1) Dysdiadochokinesis: inability to perform and sustain a series of repeated movements
2) Ataxia: gross incoordination of movements (gait /rebound
3) Slurred speech: speech may be imprecise slow and distorted
4) Pass pointing (dysmetria): the patient overshoots when touching the examiners finger

50
Q

Why does Pass pointing (dysmetria) occur in cerebellar lesions?

A

In cerebellar lesions (ie. stroke) when patient tries to touch nose then your finger, they will overshoot when they try to touch your finger.

When they try and fix the overshoot they will overcorrect etc… (pendulum movement)

This overcorrection is caused by the basal ganglia. As the cerebllum is not fuctioning correctly the basal ganglia takes over. However, because it cannot do real time-feedback and cannot process responses in the same way the cerebellum can it leads to dysmetria