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Neuro > Motor systems 8. > Flashcards

Motor systems 8. Flashcards

1
Q

Define functional segregation

A

Motor system organised in a number of different areas that control different aspects of movement

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2
Q

Define hierarchical organisation

A

high order 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)

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3
Q

Summarise the motor system hierarchy

A

The primary motor cortex receives info from other cortical areas(non primary) and sends commands to thalamus and brainstem.
The basal ganglia and cerebellum adjust the commands from cortex before they are transmitted to thalamus and brainstem
Thalamus is able to feedback to the motor corticies
The brain stem passes commands from the cerebellum and motor cortex to the spinal cord(can also receive direct signals from cortex) and muscles of face head and neck
Spinal cord then passes commands to the muscles of the body.

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4
Q

What is the location and function of the primary motor cortex?

A

Location: precentral gyrus anterior to the central sulcus in the frontal lobe. Very thin
Function: control fine, discrete, precise voluntary movement
Provide descending signals to execute movement

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5
Q

Discuss the somatotopic organisation of primary motor cortex

A

Penfield’s motor homunculus
The more we use different parts of the body the larger their representation in the cortex. A very distorted representation because different parts of the body are used more than others so a bit different for all of us
Large representation for the hands

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6
Q

What are the two descending motor pathways?

A

Lateral corticospinal pathway

Anterior corticospinal pathway

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7
Q

What are the most important cells in the primary motor cortex?

A

BETZ CELLS
These are also called pyramidal cells and are found in the 5th layer of the grey matter, these are where the corticospinal tracts originate from.

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8
Q

Describe the lateral corticospinal tract

A

Originates within the motor cortex with the Betz cells (really long axons), travel through internal capsule of basal ganglia, upper motor neuron passes through cerebral peduncle of the midbrain, travelling through pons(can’t be seen externally due to transverse fibres)
Undergoes pyramidal decussation in the medulla
UMN descends in contralateral lateral corticospinal pathway to correct spinal level
Synapses to lower motor neuron in ventral horn and this exits via large alpha motor neurones from spinal nerve to musculature.
RIGHT SIDE OF BRAIN = LEFT SIDE OF BODY

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9
Q

Describe the anterior corticospinal tract

A

Made up of remaining 5-10% of motor neurons that dint decussate at the medulla
1) Upper motor neurone emerges from primary motor cortex and travels through internal capsule
2) UMN passes through cerebral peduncle of midbrain, travelling through pons
3) UMN DOES NOT undergo pyramidal decussation in the medulla, remaining ipsilateral
4) UMN descends down ipsilateral half of anterior corticospinal tract to the correct spinal level
5) UMN synapses to LMN in contralateral ventral horn to Lower motor neurone
LMN exits cord via the ventral root, supplies muscles of thorax and intercostals

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10
Q

Corticobulbar pathway?

A

Originates in the head region of the motor cortex
Travels through genu of internal capsule of basal ganglia
Synapse within the brainstem near midline, to hypoglossal nuclues, only 50% decussate and within brain stem
Cranial nerve supply mostly, e.g. supply of glenohyoid muscle
Cranial nerves are the secondary neurons

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11
Q

Location and function of the pre-motor cotex?

A

Location: frontal lobe anterior to M1
Function: planning of movements
Regulates externally cued movements
e.g. seeing an apple and reaching out for it requires moving a body part relative to another body part (intra-personal space) and movement of the body in the environment (extra-personal space)

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12
Q

Supplementary motor area location and function?

A

Location: frontal lobe anterior to M1, medially, superior to pre-motor from a side view
Function: planning complex movements; programming sequencing of movements
Regulates internally driven movements (e.g. speech)
SMA becomes active when thinking about a movement before executing that movement

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13
Q

Discuss the association cortex

A 
Brain areas not strictly motor areas as their activity does not correlate with motor output/act
Posterior parietal cortex(posterior to the somatosensory coretx): ensures movements are targeted accurately to objects in external space
Prefrontal cortex(most anterior in frontal lobe): involved in selection of appropriate movements for a particular course of action
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14
Q

Define lower motor neuron

A

Spinal cord and brainstem

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15
Q

Define Upper motor neuron

A

corticospinal/bulbar

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16
Q

Define pyramidal

A

lateral corticospinal tract

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17
Q

Define extrapyramidal

A

Basal ganglia and cerebellum

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18
Q

What are negative signs regarding upper motor neuron lesion?

A

Loss of function (negative signs):
Paresis: graded weakness of movements
Paralysis (plegia): complete loss of muscle activity

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19
Q

What are positive signs regarding upper motor neuron lesion?

A

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’s sign

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20
Q

What is Babinski’s sign

A

You stroke the plantar surface of the foot and in a normal subject you will see flexion of the toes (they curl downwards - plantar flexion)
In the case of upper motor neurone lesions, the patient will show an EXTENSOR PLANTAR RESPONSE where their toes fan out and their big toe lifts up.

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21
Q

Define Apraxia

A

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

Lesion of inferior parietal lobe, the frontal lobe (premotor cortex, supplementary motor area)

Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes

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22
Q

Symptoms of 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

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23
Q

What is motor neuron disease?

A

Progressive neurodegenerative disorder of the motor system
Spectrum of disorders
Amyotrophic Lateral Sclerosis (ALS) - upper and lower motor neuron signs will present as the disease progresses

24
Q

What are the upper and lower motor neuron signs of MND?

A 
Upper motor neuron signs
Increased muscle tone (spasticity of limbs and tongue)
Brisk limbs and jaw reflexes 
Babinski’s sign
Loss of dexterity
Dysarthria
Dysphagia
Lower motor neuron signs
Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia
25
Q

What is volition?

A

Motor systems produce movements that are adaptive and accomplish a certain goal

26
Q

What are the three parts of the motor cortex?

A

Primary Motor Cortex
Premotor Cortex
Supplementary Motor Area

27
Q

What makes up the association cortex?

A

Frontal Cortex
Parietal Cortex
NOTE: this is not exactly part of the motor pathway but it influences the planning and execution of movements

28
Q

Difference between corticospinal and corticobulbar?

A

Corticospinal Tract – starts in the cortex and exits and innervates the muscles in the arms and legs
Corticobulbar Tract – starts in the cortex then exits and innervates the muscles in the face

29
Q

Which lower motor neurone controls the tongue?

A

Hypoglossal Nerve (CN XII)

30
Q

What might you see in the tongue of an MND patient?

A

Fasciculations and spasticity

31
Q

Size relationship between pre-motor cortex and primary motor cortex?

A

Pre-motor is 6x bigger

32
Q

What is the function of each of these types of pathway?

A 
Lateral 
•	Control of proximal and distal musculature
•	Voluntary movements or arms and legs
Medial
•	Control of axial muscles 
•	Balance and posture
33
Q

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

A

Extrapyramidal

34
Q

What does basal ganglia include?

A

Caudate nucleus
Lentiform nucleus (putamen + external globus pallidus)
Subthalamic nucleus
Substantia nigra
Ventral pallidum, claustrum, nucleus accumbens, nucleus basalis of Meynert

LOOK AT PRINTED DIAGRAMS IN NOTES

35
Q

Functions of 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

36
Q

Where is the basal ganglion located?

A

White matter in the middle of the brain

37
Q

What are the different parts of the basal ganglia?

A

Striatum = caudate + putamen
Globus Pallidus = external segment (GPext) + internal segment (GPint)
Substantia Nigra = pars compacta (SNc) + pars reticulata (SNr)
Subthalamic Nucleus

L00K AT CIRCUITRY DIAGRAM

38
Q

Describe the structure of the direct pathway in the basal ganglia

A

Fibres initially come from the motor cortex to the striatum (caudate and putamen)
Direct Pathway: putamen  globus pallidus internal segment + substantia nigra pars reticulata

39
Q

Describe the structure of the indirect pathway in the basal ganglia.

A

Fibres initially come from the motor cortex to the striatum (caudate and putamen)
Indirect Pathway: putamen to globus pallidus external segment to subthalamic nucleus to globus pallidus internal segment

40
Q

What is the difference in the function of the direct and indirect pathways?

A

Direct Pathway = excitatory on the motor cortex

Indirect Pathway = inhibitory on the motor cortex

41
Q

What extra component modulates the function of the direct and indirect pathways?

A

Nigro-striatal pathway

42
Q

Where do the projections go after leaving the basal ganglion structures?

A

They go to the thalamus
From the thalamus they go to the cortex (supplementary motor area and primary motor area = two regions involved in movement preparation and planning)

43
Q

Describe Parkinson’s disease and summarise its neuropathology

A

“Shaking palsy (paralysis agitans) Involuntary motion, with lessened muscular power, in parts not in action even when supported, with propensity to bend the trunk forward, and to pass from a walking to a running pace: the senses and the intellect being uninjured”

Classically the primary pathology involves the neurodegeneration of the dopaminergic neurons that originate in the substantia nigra and project to the striatum
Symptoms only appear when 80% of neurons are rinsed

44
Q

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

A

The loss of nigro-striatal dopaminergic axons in the caudate and putamen mean that the connection between the striatum (caudate and putamen) and the substantia nigra pars compacta is lost.
This means that the direct pathway is reduced and so the excitation of the motor cortex is reduced.
The lack of excitatory input interferes with the ability of the motor cortex to generate commands for voluntary movement, resulting in poverty of movement.

45
Q

Main motor signs of Parkinson’s disease

A

Bradykinesia-
slowness of (small) movements (doing up buttons, handling a knife)
Hypomimic face -
expressionless, mask-like (absence of movements that normally animate the face)
Akinesia-
difficulty in the initiation of movements because cannot initiate movements internally
Rigidity -
muscle tone increase, causing resistance to externally imposed joint movements
Tremor at rest-
4-7 Hz, starts in one hand (“pill-rolling tremor”); with time spreads to other parts of the body

46
Q

What is the cause of Huntington’s disease?

A

Genetic neurodegenerative disorder
Chromosome 4, autosomal dominant
CAG repeat
Degeneration of GABAergic neurons in the striatum, caudate and then putamen

Reduce GABA-ergic inhibition of GPext so increased inhibitory output from GPext to STN
The facilitatory output from STN to GPint/SNr is reduced
Less inhibitory output from GPint/SNr to the thalamus

47
Q

Motor signs of Huntington’s disease

A

Choreic movements (Chorea)
rapid jerky involuntary movements of the body; hands and face affected first; then legs and rest of body
Speech impairment
Difficulty swallowing
Unsteady gait
Later stages, cognitive decline and dementia

48
Q

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

A

The inhibitory effect of the indirect pathway no longer keeps the direct pathway under control so the cortex will be hyperexcitable.
Patients will continuously have abnormal movements because the cortex is continuously sending involuntary commands for movements.

49
Q

Location of cerebellum?

A

Posterior cranial fossa
Tentorium cerebeli over it
Posterior aspect of the pons connection by transverse fibres

50
Q

State the 3 layers of the cerebellar cortex.

A

Granule cell layer
Purkinje cells
Molecular layer

51
Q

What are the 3 sources of input to the cerebellum?

A

Inferior olive(nuclei in superior medulla) projects to Purkinje cells via climbing fibres
All other input to granule cells via mossy fibres(from cortex/pons OR spinocerebellar tract) and then onwards via parallel fibres
All output from Purkinje cells via deep nuclei

52
Q

What are the 3 divisions of the cerebellum?

A

Vestibulocerebellum
Regulation of gait, posture and equilibrium
Coordination of head movements with eye movements
(lower horizontal)

Spinocerebellum
Coordination of speech
Adjustment of muscle tone
Coordination of limb movements
(medial vertical)
Cerebrocerebellum
Coordination of skilled movements
Cognitive function, attention, 
processing of language
Emotional control
(Lateral cerebellum)
53
Q

Localisation of cerebellar dysfunction

A

Vestibulocerebellar Syndrome:
Damage (tumour) causes syndrome similar to vestibular disease leading to gait ataxia and tendency to fall (even when patient sitting and eyes open)
Vestibulocerebellar disorders causes imbalance when eyes closed, nystagmus and ataxic gate

Spinocerebellar syndrome:
Damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abnormal gait and stance (wide-based)

Cerebrocerebellar or Lateral Cerebellar Syndrome:
Damage affects mainly arms/skilled coordinated movements (tremor) and speech

54
Q

Main signs of cerebellar dysfunction

A

Deficits apparent only upon movement

Ataxia-
General impairments in movement coordination and accuracy. Disturbances of posture or gait: wide-based, staggering (“drunken”) gait
Dysmetria-
Inappropriate force and distance for target-directed movements (knocking over a cup rather than grabbing it)
Intention tremor-
Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)
Dysdiadochokinesia-
Inability to perform rapidly alternating movements, (rapidly pronating and supinating hands and forearms)
Scanning speech-
Staccato, due to impaired coordination of speech muscles

55
Q

What are purkinje cells?

A

Main processing cells, huge dendritic trees with lots of input, flask like shape, receive inputs from granule cells

56
Q

Function of cerebellum?

A

Maintenance of balance and posture:
Postural adjustments to make balance, inputs from vestibular receptors and propioceptors.

Coordination of voluntary movements:
timing and force of different muscle groups

Motor learning:
Fine tune motor programmes to make accurate movements through trial and error

Cognitive function:
Language

57
Q

Summary?

A

Primary motor cortex: issues commands to lower motor nucleus
Premotor cortex and supplementary motor area are responsible for planning and prep of movements
BG and cerebellum are responsible for monitoring, coordination, movements by modifying output of motor cortex

Neuro (17 decks)

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