Lecture 4: Motor systems Flashcards Preview

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Flashcards in Lecture 4: Motor systems Deck (34)
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1
Q

Describe the body representation of in the primary motor cortex. Where is it

A

Different cortical regions of the pre central gyrus (motor homunculus) controls voluntary contraction of specific muscles or groups.

2
Q

What parts of the body in the motor homunculus have the largest representation and why

A

Muscles involved in skilled, complex or delicate movements has more cortical area. These include muscles of mouth/lips for vocalisation and eating as well as the hand/fingers vs the more structural parts of the body.

3
Q

What are pyramidal cells and where are they are found

A

Upper motor neurons with pyramid shaped cell bodies located in the premotor area and primary motor area of cerebral cortex.

4
Q

What is the name of the pyramidal tract and how does it contribute to muscle control

A

Name is Corticospinal pathway. It is a direct motor pathway that provides input to lower motor neurons via axons that extend directly from the cerebral cortex and is used to control the muscles of limbs and trunk.

5
Q

Describe the path of the corticospinal tract up to the point where it splits up

A

Upper motor neurons in the cortex go down through the internal capsule through the cerebral penducle of the midbrain and pons. At the medulla oblongata, the axon bundles of the corticospinal tracts form ventral bulges called pyramids. This is where it starts to split up

6
Q

Compare the point of dessucation for the two tracts of the corticospinal tract. How many axons in each tract

A

At medulla oblongata 85% of axons dessucate to the contralateral (opposite) side in the medulla oblongata. This is the lateral corticospinal tract.
The remaining 15% remain along the ipsilateral (same) side, and eventually dessucate at the spinal segmental level where they synapse with specific neuron- this is called the ventral/Anterior corticospinal tract.

7
Q

What part of the spinal cord do the axons of the corticospinal tract form a tract in before synapsing with lower motor neuron and what type of movement is each tract responsible for

A

The ‘lateral corticospinal’ form the ‘latcort’ tract in the lateral white column of the spinal cord. This tract is responsible for distal parts of limbs responsible for precise agile and highly skilled movements.
The anterior corticospinal tract forms ‘antcort’ tract in the anterior white column of the spinal cord. This tract is responsible for movements of proximal parts of limbs and trunk- posture/core muscle.

8
Q

Why are lower motor neurons considered the ‘final common pathway’. How do they control muscle activity

A

They are the nerves that provide the output from CNS to the skeletal muscle fibres. They receive this information from synapsing with interneurons called local circuit neurons or directly from the upper motor neurons in the brainstem or spinal cord. They are in the anterior grey horn of the spinal cord and exit out of the anterior root of spinal nerves and terminate in skeletal muscle.

9
Q

Why are the pons so enlarged

A

It needs more SA for motor neurons going to the face

10
Q

What happens when there is a lesion in the upper motor neurons of one side (eg. LEFT)

A

Spastic paralysis on the limbs on the other side of the body (RIGHT) as any inhibitory signals from the cortex are removed so the Lower motor neurons are acting on reflex. Muscle tone is increased

11
Q

What happens when there is a lesion in a lower motor neuron on one side (eg LEFT)

A

Flaccid paralysis where there is no neural control at all- voluntary or reflex action of muscle fibres so muscle tone on the same side of the body (LEFT) is decreased/lost

12
Q

When the pyramidal neurons are going through the midbrain and to the pons what happens to the organisation of the fibres looking at it on a cross sectional level

A

In the crus cerebri of the midbrain is is one large bundle in the anterior part but in the pons, the upper motor neurons break into smaller bundles- perhaps because some are going off to the face

13
Q

What 5 parts of the brain are the basal ganglia and what type of colour matter is it

A

The basal ganglia are towards the bottom of the brain in the subcortical grey nuclei. It has the Caudate nucleus, the internal capsule, putamen, Globus pallidus (internal and external) sub-thalamic nucleus and the substantia nigra.

14
Q

What group of basal ganglia make the striatum

A

Caudate nucleus and Putamen

15
Q

How does the pre motor area, basal ganglia system and primary motor area interact.

A

Basal ganglia is used to bring about fine movement control. First the premotor area of the cerebral cortex talks to the basal ganglia system. Then the pre motor cortex talks to the primary motor cortex.

16
Q

What neurotransmitter does is excitory

A

Glutamate

17
Q

What neurotransmitter an inhibitory pathway neural use

A

GABA- gamma amino butyric acid

18
Q

What is the purpose of neurotransmitter dopamine in the substantia nigra to striatum path

A

It keeps the GABAergic fibres primed, ready to fire allowing only a small amount of glutamate/ action potential from the cortex to be propogated along

19
Q

What is purpose of the basal ganglia circuit

A

Improve our ability to engage in movement and to engage in showing our mood. It is particularly involved in the initiation of movement- fine movement control.

20
Q

Describe the circuit starting at cerebral cortex pre motor area state the 5 steps/ pathways to a muscle movement + excite or inhib

A
  1. neurons go from the cerebral cortex to the striatum via excite
  2. 95% of nerves from striatum will go to substantia nigra or into the internal or external segment of the GP (inhib)
  3. A fibre from internal GP goes to the ventral anterior nucleus of the thalamus (inhib)
  4. Thalamus back to cortex (excite) which leads to the activation of upper motor neuron
  5. One last path which is substantia nigra to striatum by dopamine
21
Q

What role does the cerebellum have in movement control

A

Nerves from the cerebellar cortex go to the VA-VL section of thalamus via excite. It is able to bring a cessation of movement. The cerebellum also models future movement and makes adjustments to keep the enacted movement close to the plan by changing muscle tone or direction of movement.

22
Q

What is disrupted in Parkinsons disease and why does this happen

A

The fibres going from sub nigra to striatum carrying dopamine. This happens because the cell bodies producing dopamine in sub nigra die off.

23
Q

What does the disruption in fibres related to Parkinsons disease cause to the gabaergic fibres- pathology

A

The GABAergic fibres in striatum are no longer primed for activation by small signals, so the gabaergic fibres don’t work properly because now a small amount of glutamate isn’t enough to activate it

24
Q

What are the main symptoms of Parkinsons disease

A
  1. They have difficulty expressing their emotion- rigidity of the face. At rest involuntary skeletal contractions interfere with voluntary movement leading to 2. shaking- tremor and
  2. increased muscle tone- rigidity.
  3. Bradykinesia which is slowness of movements because initiation is impaired- but automatic motion is under different circuits not damaged
  4. Hypokinesia is decreasing range of motion.
25
Q

List the treatments available for parkinsons

A

Dopamine replacement, (L-DOPA), Surgical lesions (pallidotomy and thalamotomy) Deep brain stimulation

26
Q

How does a pallidotomy help Parkinsons

A

Artery supplying the internal Globus pallidus nerves is occluded - lesion- so the signals inhibiting the Va-VL of thalamus are stopped. This means that the excitatory pathway to cerebral cortex can give a normal level of glutamate restoring some function.

27
Q

What is better for pallidotomy success

A

doing it only one side of the brain. 2 sides gets some symptoms again.

28
Q

How does L-DOPA help Parkinsons

A

It is the precursor for Dopamine which can cross the blood brain barrier that is taken up by remaining cells in sub nigra and changed to dopamine.

29
Q

How does L-DOPA affect the conc of dopamine compared to normal non parkinsons person

A

Usually Dopamine concentration is kept constant by the brain but the way dosing of L-DOPA leads to wave looking graph where it rises, peaks above the optimal level then declines.

30
Q

why does this dosing pattern of LDOPA a problem

A

Having too little Dopamine leads to the catatonia- stiffness and rigidity symptoms of parkinsons, however above the optimal level, it leads to symptoms of hallucinations, depression and psychosis- symptoms of schizophrenia.

31
Q

What test demonstrates the function of the cerebellum

A

Touch your hand touch your nose because the planning of accuracy of where you touch and being able to stop precisely is what the cerebellum pathway

32
Q

What is the chemistry of the neurotransmitters related to the causing of Parkinsons disease

A

The caudate nucleus of basal nuclei contains neurons that release Ach. And as Dopamine decreases and Ach remains the same there is an imbalance that is thought to cause some of the symptoms of Parkinsons disease

33
Q

What other drugs than L DOPA used to treat parkinsons

A

Drugs that inhibit enzymes that break down dopamine, and drugs that block the effects of Ach at some synapses in the basal nuclei neurons to rebalance Ach and Dopamine

34
Q

How does deep brain stimulation help parkinsons

A

It involves the implantation of electrodes into the subthalamic nucleus. The electrical currents reduce many of the symptoms.