Cortical motor function, basal ganglia and cerebellum Flashcards Preview

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Flashcards in Cortical motor function, basal ganglia and cerebellum Deck (57)
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1
Q

Describe the hierarchical organisation of motor control

A

Higher level areas of hierarchy are involved in more complex tasks (programme and decide on movements, coordinate muscle activity)

Lower level areas of hierarchy perform lower level tasks (execution of movement)

2
Q

What 3 areas make up the motor cortex?

A

Primary Motor Cortex (M1)
Premotor Cortex
Supplementary Motor Area

3
Q

Where is the primary motor cortex (M1, Brodmann area 4) located? What is its function?

A

Precentral gyrus, anterior to the central sulcus

Function: control fine, discrete, precise voluntary movement

4
Q

Describe the somatotopic organisation and homunculus of the primary motor cortex

A

Leg, arm more medial; hand, face and tongue more lateral

Penfield’s motor homunculus: more cortical space is devoted to the face, tongue, and hands than other regions, allowing great variety and precision of movements.

5
Q

The motor cortex gives rise to two lateral pathways for the execution of intentional movements. What are these two motor pathways?

A

Corticospinal tract and Corticobulbar tract

*The planning of voluntary movements and the elaboration of motor commands for their execution is done by the motor cortex which has its outputs via the lateral motor pathways.

6
Q

What does the corticospinal tract consist of? Where do these axons project to?

A

The corticospinal tract consists of the axons of about one million pyramidal cells in layer V of the cortex; over half come from the primary motor cortex (M1, Brodmann area 4) or secondary motor area (MII, Brodmann area 6, premotor cortex and SMA). These axons project to the ventral horns of the spinal cord to alter the activity of alpha and gamma motor neurones.

About 40% of corticospinal tract axons come from the somatosensory cortex (Brodmann areas 1, 2, and 3) or other regions of parietal cortex (Brodmann areas 5 and 7). These axons terminate in the dorsal horns of the spinal cord and regulate sensory input.

7
Q

What are Betz cells?

A

Most of the corticospinal tract consists of fine myelinated and unmyelinated axons with conduction velocities between 1 and 25 m/s. However, there are about 30 000 extremely large pyramidal cells in area 4/PMC, called Betz cells, with big myelinated axons that conduct with velocities of 60–120 m/s

8
Q

Where in the brain do the axons of the corticospinal tract travel down?

A

Axons of the corticospinal tract pack tightly to pass through the internal capsule which lies between the thalamus and the lentiform nucleus and descend into the brainstem.

9
Q

How does the corticobulbar tract arise and what do the axons supply?

A

In the brainstem, the most medial fibres peel off and cross the midline to go to nuclei (trigeminal (V), facial (VII), hypoglossal (XII), and accessory (XI)) of the cranial nerves. These are corticobulbar fibres and are motor to the face, tongue, pharynx, larynx, and sternomastoid and trapezius muscles.

10
Q

What’s the significance of the pyramidal decussation?

A

The remaining corticospinal axons descend through the medulla causing a swelling on its ventral surface (the pyramid);

At the caudal medulla 85% of fibres cross the midline as the pyramidal decussation, giving rise to the lateral corticospinal tract. The remaining ipsilateral axons form the anterior corticospinal tract, which crosses over at spinal cord level.

11
Q

What neurotransmitter do corticospinal tract neurones use? What do they synapse with?

A

Glutamate (excitatory)

They either synapse directly with a motor neurones supplying distal limb muscles, or synapse with interneurons which make polysynaptic connections with a motor neurones of proximal limb muscles and axial muscles. The corticospinal tract inhibits motor neurons disynaptically via Ia inhibitory interneurons.

12
Q

Where is the premotor cortex located? What is its function?

A

Frontal lobe anterior to M1

Function: planning of movements; it is also implicated in movements in response to sensory (mostly visual) cues.

13
Q

Where is the supplementary motor located? What is its function?

A

Frontal lobe anterior to M1, medially
Function:
- planning complex movements
- programming sequencing of movements
- regulates internally driven movements (e.g. speech)
- crucial for movements involving both sides of the body, particularly those that have been learnt.
- becomes active when thinking about a movement before executing that movement (shown by increased cerebral blood flow)

14
Q

Where do SMA and premotor neurones synapse?

A

The secondary motor cortex contains neurons that fire in a way that correlates with the direction and force of a movement.

  • the SMA controls proximal limb muscles directly via its output to the corticospinal tract
  • the premotor area neurons synapse with brainstem reticular neurons that go to axial and proximal limb muscles.
  • both control distal limb muscles via M1.
15
Q

What does the association cortex refer to, and what is its purpose?

A

Brain areas not strictly motor areas as their activity does not correlate with motor output/act;

  • Posterior parietal cortex: ensures movements are targeted accurately to objects in external space
  • Prefrontal cortex: involved in selection of appropriate movements for a particular course of action
16
Q

Lesions above/below the pyramidal decussation causes what kinds of deficits?

A

Corticospinal tract lesions below the pyramidal decussation in primates => ipsilateral motor deficit (below the level of the lesion).
Corticospinal tract lesions above the pyramidal decussation => contralateral motor deficit.

17
Q

Categories the type of signs that may be seen with an upper motor neurone lesion

A

Loss of function (negative signs):

  • Paresis = graded weakness of movements
  • Paralysis (plegia) = complete loss of muscle activity

Increased abnormal motor function (positive signs) due to loss of inhibitory descending inputs:

  • Spasticity = increased muscle tone
  • Hyper-reflexia = exaggerated reflexes
  • Clonus = abnormal oscillatory muscle contraction
  • Babinski sign
18
Q

What’s an apraxia? What is it caused by - what are most common?

A

A disorder of skilled movement => Patients are not paretic but have lost information about how to perform skilled movements

Caused by lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area); stroke and dementia are the most common causes.

19
Q

List the the type of signs that may be seen with a lower motor neuron lesion

A
  • Weakness
  • Hypotonia (reduced muscle tone)
  • Hyporeflexia (reduced reflexes)
  • Muscle atrophy
  • Fasciculations: damaged motor units produce spontaneous action potentials, resulting in a visible twitch
  • Fibrillations: spontaneous twitching of individual muscle fibres; recorded during needle electromyography examination
20
Q

What is motor neuron disease and what are the associated symptoms?

A

Progressive neurodegenerative disorder of the motor system (aka Amyotrophic Lateral Sclerosis (ALS))

Spectrum of disorders:
UMN signs = 
Increased muscle tone (spasticity of limbs and tongue)
Brisk limbs and jaw reflexes 
Babinski’s sign
Loss of dexterity
Dysarthria
Dysphagia
LMN signs = 
Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia
21
Q

State some overall functions of the basal ganglia?

A
  • Elaborating associated movements (e.g. swinging arms when walking; changing facial expression to match emotions)
  • Moderating and coordinating movement (suppressing unwanted movements)
  • Performing movements in order
  • Motor basal ganglia circuitry is responsible for the execution of appropriate prepro- grammed motor sequences during voluntary movements.
22
Q

What is the collective term given to the basal ganglia (and cerebellum)?

A

Classically the basal ganglia constitute part of the extrapyramidal system, on the basis that lesions of the basal ganglia produce quite different symptoms from lesions of the corticospinal tract.

23
Q

Name the structures that comprise the basal ganglia

A

They consist of several extensively interconnected structures, the striatum (the caudate and putamen), the globus pallidus (pars interna and pars externa), the substantia nigra (pars compacta and pars reticulata), and the subthalamic nucleus.

24
Q

Give a brief overview of the inputs and outputs to/from the basal ganglia

A

Most inputs to the basal ganglia are from the cerebral cortex and enter the striatum. The output of the basal ganglia emerges from the pars interna (internal part) of the globus pallidus, and the substantia nigra pars reticulata, to go to the thalamus. The thalamus projects back to the cortex thus closing a loop. The thalamocortical axons return to the same region of cortex which gave rise to the striatal inputs

25
Q

The caudate nucleus and putamen are functionally a single unit but are split anatomically by what?

A

the internal capsule

26
Q

What type of input does the striatum receive from the cortex and name the pathway. How is this input organised?

A
  • Receives excitatory input from the cortex via the glutamatergic corticostriatal pathway.
  • The input is organized topographically so that somatotopy is preserved in the projections from the somatosensory cortex and motor cortex.
27
Q

Corticostriatal axons terminate on what major neuron type in the striatum?

A

Medium spiny neuron (95% of stratal neurones)

28
Q

Describe the two populations of medium spiny neurons in terms of their different connections and neurochemistry

A

Both use GABA as their transmitter, and provide the inhibitory output of the striatum.

Type 1:

  • substance P (SP) and dynorphin (DYN) as co-transmitters
  • expresses dopamine D1 receptors
  • projects to the globus pallidus pars interna (GPi) and substantia nigra pars reticulata (SNpr).

Type 2:

  • enkephalin (ENK) as a co-transmitter
  • expresses D2 dopamine receptors
  • projects to the globus pallidus pars externa (GPe).
29
Q

Medium spiny neurons receive projections via which other pathway/structure? How does it affect the two populations differently?

A

Via the nigrostriatal pathway from the substantia nigra pars compacta (SNpc).

The SNpc uses dopamine as a transmitter. Because the two types of medium spiny neuron express different dopamine receptors they are differently modulated by this input. At the GABA/SP/DYN cells, dopamine acting on D1 receptors enhances the effect of excitatory cortical input. In contrast, the action of dopamine on D2 receptors on GABA/ENK cells is to reduce the effect of cortical excitation.

30
Q

Describe the inputs and outputs of the GPi, SNpr, GPe and thalamus

A
  • Both GPi and SNpr get inhibitory connections from the GABA/SP/DYN population of striatal neurons and excitatory/glutamatergic inputs from the subthalamic nucleus, and both send GABAergic inhibitory outputs to the several thalamic nuclei that project to motor cortex.
  • The GPe receives its striatal connections from the GABA/ ENK medium spiny neurons. The GPe neurons are GABAergic and project mostly to the subthalamic nucleus.
31
Q

Describe two different routes through the basal ganglia circuitry with opposing effects on firing of thalamic and cortical neurons.

A
  1. Direct pathway = uses the GABA/ SP/DYN medium spiny striatal neurons which inhibits GABAergic outflow of the GPi and SNpr to the thalamus. Cortical activation of this pathway increases the firing of thalamic neurons (since inhibiting an inhibition is excitation).
  2. Indirect pathway = starts with the GABA/ENK medium spiny neuron output to the GPe, inhibitory neurons from which go to the STN. The STN excites inhibitory neurons in the GPi and SNpr that go to the thalamus. Corticostriate activation of the indirect path- way results in decreased firing of thalamic neurons.
32
Q

State the importance of having these two pathways

A

This dual circuitry allows the possibility that given movement sequences may be triggered or suppressed by differential activation of direct or indirect pathways respectively.

33
Q

What is effect of the nigrostriatal pathway one the direct and indirect pathways?

A

Dopaminergic neurons of the substantia nigra pars compacta (SNpc) alter their firing pattern in response to stimuli that reward a movement (they have opposite effects on the two populations of medium spiny neurones)

34
Q

What causes Parkinson’s disease?

A

Parkinson’s disease is the neuronal degeneration (progressive depletion) of dopaminergic neurones in the substantia nigra pars compacta

NOTE: symptoms only appear when 80% of the dopamine cells in the substantia nigra have died

35
Q

State the main signs of Parkinson’s disease.

A
Bradykinesia (slow movement) 
Akinesia (difficulty in the initiation of movements) 
Hypomimic face (expressionless face) 
Tremor 
Rigidity (increase in muscle tone)
36
Q

What are the consequences of this with regards to the circuitry of the basal ganglia and how does explain the bradykinesia?

A

Since the normal situation is that dopamine tonically activates the direct pathway via D1 receptors but inhibits the indirect pathway via D2 receptors, the loss of the nigrostriatal pathway leads to an increase in the activity of GABAergic striatal neurons in the indirect pathway and a decrease in the GABAergic striatal neurons in the direct pathway. The overall effect is increased inhibition on the thalamocortical connections that are required for movement.

37
Q

Describe the Parkinsonian gait.

A
Walking slowly
Small steps
Shuffling feet 
Reduced arm swing 
Stooped posture with head and body bent forwards and downwards
38
Q

What is Huntington’s disease caused by?

A

It is an autosomal dominant disease caused by an excessive number of CAG repeats in the coding region of the gene for huntingtin (Htt) (on chromosome 4)

39
Q

What are the main signs of Huntington’s disease and how does the disease progress?

A
  • Choreic movements = rapid, jerky, involuntary movements of the body (hands and face are affected first)
  • Speech impairment
  • Difficulty swallowing
  • Unsteady gait
  • Chorea gradually increases over time until the patients are totally incapacitated by it => Later on the patients will develop cognitive decline and dementia.
  • Note that motor and cognitive symptoms begin between 40 and 50 years of age.
40
Q

What are the consequences of this with regards to the circuitry of the basal ganglia?

A

Degeneration of GABA/ ENK medium spiny neurons of the striatum causes excessive inhibition of the subthalamic nucleus, so increased and inappropriate firing of thalamocortical neurons

chorea is a failure of the indirect pathway to block unwanted movement sequences.

41
Q

The cerebellum consists of 3 anatomically distinct but continuous regions. State what they are? Where do the tonsils arise from?

A

A cerebellar hemisphere on either side, and the vermis connecting them in the middle. Note that each hemisphere is functionally subdivided into lateral and medial portions.

A cerebellar tonsil protrudes from the undersurface of the cerebellum and is continuous with the vermis

42
Q

Each cerebellar hemisphere is further divided into the 3 lobes. What are they?

A

Anterior
Posterior
Flocculonodular

43
Q

What 3 layers make up the cerebellar cortex?

A

Granule cell layer
Piriform layer (with Purkinje cells)
Molecular layer

44
Q

Describe the inputs/outputs of the cells in the cerebellar cortex?

A
  • Inferior olive projects to Purkinje cells via climbing fibres
  • All other input to granule cells via mossy fibres and then onwards via parallel fibres
  • All output from Purkinje cells via deep nuclei
45
Q

What are the three functional divisions of the cerebellum?

A

Vestibulocerbellum
Spinocerebellum
Cerebrocerebellum

46
Q

What is the role of the vestibulocerebellum?

A

Vestibulocerbellum is the flocculonodular lobe
It is connected to vestibular nuclei
Involved in balance, posture and regulation of gait
It is also involved in coordination of head movements with eye movements

47
Q

Which parts of the cerebellum are part of the spinocerebellum?

A

Vermis and intermediate/medial hemisphere

48
Q

From where does the spinocerebellum receive inputs?

A

Afferents from axial portions of the body, visual, auditory and trigeminal inputs => vermis
Afferents from limbs => intermediate hemisphere

49
Q

What are the roles of the spinocerebellum?

A

Coordination of speech
Adjustment of muscle tone
Coordination of limb movement

50
Q

Which part of the cerebellum is part of the cerebrocerebellum?

A

Lateral hemisphere

51
Q

What are the main functions of the cerebrocerebellum?

A
Coordination of skilled movements 
Cognitive function 
Attention 
Processing of language 
Emotional control
52
Q

What are the symptoms of vestibulocerebellar syndrome?

A

This syndrome is similar to vestibular disease

Patients tend to lose their balance with gait ataxia and a tendency to fall (even when patient sitting and eyes open)

53
Q

What are the symptoms of spinocerebellar syndrome?

A

Mainly affects the legs;

It causes abnormal gait and a wide-based stance

54
Q

What’s a cause of spinocerebellar syndrome?

A

Degeneration and atrophy associated with chronic alcoholism

55
Q

Describe the symptoms of cerebrocerebellar syndrome.

A

Damage mainly affects the arms;

  • It affects coordinated movements
  • Speech becomes very hesitant and slow (staccato)
56
Q

What are the main signs of cerebellar dysfunction?

A

Ataxia – general impairments in movement coordination and accuracy

Dysmetria – inappropriate force and distance for target-directed movements

Intention tremor – increasingly oscillatory trajectory of a limb in a target directed movement (nose-finger tracking)

Dysdiadochokinesia – inability to perform rapid alternating movements

Scanning speech – staccato, due to impaired coordination of speech muscles

57
Q

State a hereditary and acquired cause of cerebellar dysfunction

A

Hereditary – Friedreich’s Ataxia

Acquired – Multiple Sclerosis