Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

neuro - yr 2 > motor pathways > Flashcards

motor pathways Flashcards

1
Q

what are the broad principles of motor control

A

fucntional segregation - motor system is organised in a number of different areas that control different aspects of movement

hierarchial organisation - high orders of hierachy are involved in more complex tasks eg programme and decide on meovements, coordinate muscle activity; lower levels perform lower level tasks eg execution of movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

summarise the motor system hierarchy

A

motor cortex recieves signals from other cortical areas and sends commands to the thalamus and the brain stem

cerebellum and basal ganglia adjust the commands recieved from motor cortex

cerebellum provides refining signal - involved in fine mortor activities

brainstem and spinal cord recieve information from the motor cortex (brainstem also from the cerebellum)

brainstem passes info from cortex to spinal cord

spinal cord controls muscles of the body

brainstem controls muscles of the face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where is the primary motor cortex M1 *

A

in the frontal lobe, precentral gyrus anterior to the central sulcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the role of M1 *

A

control fine, discrete precise voluntary movement with input from the cerebellum

provides descending signals to execute movement - activate parts in the motor brain by just thinking about moving - Betz cells in the 5th layer of the cortex project to the lumbar region through the spinal cord

M1 neurons encode the direction of movement, they also encode, by the firing rate, the force of muscle contraction and the velocity with which a force is applied

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe the somatotropic organisation of M1 *

A

Penfield’s motor homunculus

leg supply is more medial in the motor area - supplied by the anterior cerebral artery

lips large for the fine motor control in speech

hands large - fine motor of hands

leg and trunk have smaller representations becasue their muscle patterns are relatively simple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the lateral corticospinal tract *

A

upper motor neuron comes from M1 - travels in the internal capsule through thhe basal ganglia

decussate in the medulla pyramids - R body is supplied by the L brain

travel in the lateral corticospinal tract

project to the ventral horn - synapse - a motor neuron project out via the spinal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the anterior cortical spinal tract *

A

axons from M1 travel and decussate in spinal cord

5% of fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what muscles do the lateral and anterior corticospinal tract supply *

A

anterior - axial muscles in the thorax

lateral - distal parts oif the limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

summarise the corticobulbar pathways

A

motor neurons in teh brainstem in te CN nuclei

axons come from M1

synapse in the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the location of the premotor cortex

A

frontal lobe, anterior to M1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

function of the premotor cortex *

A

planning movements

regulates externally cued movements eg seeing object and reaching for it requires moving body part in relation to another body part (inta-personal space), and movement of body in the environment (extra-personal space)

activity fascilitates many columns in M1 - fascilitating them for movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is te location of the supplementary motor area

A

frontal lobe anterior to M1, more medially than the premotor cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the function of te supplementory motor area *

A

planning complex movements and regulates internally driven movements eg speech

SMA becomes active when thinking about movement seen in fMRI (more blood flow)

stimulation elicits movements involving many muscle groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe the association cortex

A

brain areas not strictly motor areas as activity doesnt corrolate with motorr output/action

posterior parietal cortex - ensures movements are targeted accurately to objects in external space - motor learning and planning. if this is damaged = apraxia

prefrontal cortex and temporal cortex - selection of approproate movements for a particular action - personality input into movement, input previous experience as protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where are lower motor neurons

A

spinal cord - ventral horn

brainstem - bulbar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where are upper motor neurons

A

corticospinal/corticobulbar tract

betz cells and projections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does pyramidal include

A

in the lateral corticospinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does extrapyramidal include

A

basal ganglia

ccerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe the effects of an upper motor neuron lesion *

A

loss of function (-ve signs): paresis - graded weakness of movement, paralysis (plegia) - complete loss of muscle activity (hemiplegia)

increased abdominal motor function (+ve signs) due to loss of inhibitory descending inputs: spastcicty - increased muscle tone, hyper-relexia - exaggereted reflexes, clonus - abnormal oscillatory msucle contraction, Babinski’s sign

no sign of muscle denervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe apraxia *

A

a disorder of skilled movement

not weak - but lost info on how to perfom skilled movements

lesion of inferior parietal lobe or premotor cortex or SMA

stroke and dementia are most common

eg dressing apraxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the effects of lower motor neuron lesions

A

weakness

hypotonia (reduced muscle tone)

hyporeflexia

muscle atrophy - muscle lost innervation so starts to shrink

fasiculations - damaged motor units produce spontaneous AP = visible twitch

fibrillations - spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination

22
Q

summarise the pathophysiology of motor neuron disease*

A

progressive neurodegenerative disorder of the motor system

takes out upper and lower neurons

go from distal (legs) to proximal

kills when resp muscles stop functioning

soectrum of disorders and mutations

Amylotropic lateral sclerosis has a specific pathophysiology

23
Q

what are the upper motor neuron signs of MND *

A

increased muscle tone - spasicity of limbs and tongue - contracted, not functional

brisk limb and jaw reflexes

Babinski’s sign

loss of dexterity - dispraxia

dysarthria - loss of speech

dysphagia - problem eating

24
Q

what are the lower mnotor neuron signs of MND *

A

weakness

muscle wasting

tongue fasciculations and wasting

nasal speech

dysphagia

25
Q

recall the component structures of the basal ganglia *

A

caudate nucleus - look like tadpole

lentiform nucleus made of putamen and external globus pallidus - separated from caudate by internal capsule

subthalamic nucleus

substantia nigra - project to basal ganglia even though in the midbrain

ventral pallidum (dopaminergic neurons) , claustrum (thin grey layer), nucleus accumbens (reward centre), nucleus basalis of Meynert (cholinergic neuron, prject to cortex, important in mem function - lost in dementia)

26
Q

what forms teh straitum *

A

the caudate nucleus

external globus pallidus

putamen

27
Q

describe the nucleus accumbens *

A

dopaminergic

recieve input from mesolimbic

involved in reward

28
Q

why is Parkinson’s a nigrostriatal disease *

A

it is the projections form the nigra to the striatum that are dysfunctional

29
Q

illustrate on a schematic where the components of the basal ganglia are *

A
30
Q

illustrate on an anterior coronal section where the components of the basal ganglia are *

A

1st pic

31
Q

illustrate on a coronal section where the components of the basal ganglia are *

A

2nd pic

32
Q

what is the function of the basal ganglia

A

elaborating associated movements - eg swinging arms to maintain balance, change facial expression to match emotions

moderate and coordinate movement - suppress unwanted movement

perform movements in order

33
Q

describe the circuitary of the basal gangia

A

cortex provides inputs to the striatum

striatum provides inputs to the nigra and internal globus pallidus

external globus pallidus communicates with teh subthalamic nucleus which provides input to the internal globulus pallidus, which inputs to thalamus, which inputs to SMA, which inputs to nigra which communicates with striatum

34
Q

what is the neuropathology of Parkinson’s *

A

deposition of lewy bodies (protein a synuclein)

neurodegeneration of dopaminergic neurons that originate in the nigra and project to the striatum, there is loss of dopaminergic terminals in the putamen and in the caudate - meaning loss of black colour of nigra (normally present because teh nigra retains neuromelanin, a normal byproduct of metabolism in these neurons)

the reduced input to the straitum means there is less inhibition of the internal globus pallidus and nigra = increased inhibitory output from these areas to the thalamus = decreased fascilitation to the motor cortex (SMA) = delays in the initiation of movement - bradykinesia

35
Q

what are the clinical signs of Parkinson’s *

A

tremor of hand

problem initiating movement (akinesia) - basal ganglia input is comprimised

paralysis agitans - invol movement with lesser muscular power

kyphosis

pass from walking to running pace uncontrollably

cognative decline

bradykinaesia - slowness of small movements (doing up buttons, handling a knife)

hypomimic face - expressionless, mask like

rigidity - muscle tone increase, causing resistance to externally imposed joint movements - difficulty pushing down when put hands out

tremor at rest - 4-7Hz, start in 1 hand, pill rolling tremor - rotation around wrist, with time spreads

36
Q

summarise the nigro-straital pathway

A

nigrostriatal neurons go from nigra to striatum

37
Q

what are teh 3 deep nuclei in the cerebellum *

A

fastigial nucleus (involved in balance - has connections with the vestibular and reticular nuclei)

interposed

denate nuclei - voluntary movement - they have projections to the thalamus and the red nucleus

38
Q

what is the pathophysiology of huntington’s *

A

genetic neurodegenreative disorder

on chromosome 4

autosomal dominant

CAG repeat

degeneration of GABAergic interneurons in striatum, caudate and then putamen = reduced GABAergic inhibition of external GP = incraesed inhibitory output from GPe to subthalamic nucleus = reduced fascilitatory output to GPi and nigra is reduced = less inhib output to thalamus

lack if inhibitory control of the thalamus on the motor cortex = unwanted, involuntary movements

35 repeats will give you huntingtons

39
Q

what are the motor signs of Huntington’s *

A

choreic movements - St Vitus’ dance - rapid, jerky involunatry movements - proximal to distal

speech impairment

difficulty swallowing

unsteady gait

cognitive decline and dementia in later stages

40
Q

describe the cellular organisation of the cerrebellum and how this relates to functioning *

A

monocellular layer - few neurons (pial layer)

piriform layer - main processing cells project to nuclei in white mattger of cerebellum

granular layer - small neurons involved in processing

inferior olive projects to purkunje fubres via climbing fibres - they synapse with the dendritic trees

input to granule cells by mossy fibres and then onwards by parallel fibres

output to the thalamus and postural and vestibular centres is via deep nuclei

there are 2 inputs and 1 output

41
Q

what are the 3 divisions of the cerebellum *

A

vestibulocerebellum

spinocerebellum

cerebrocerebellum

42
Q

describe the vestibulocerebellum *

A

regulation of gait, posture and equilibrium

coordinate head movement with eye movement

close connection with superior colliculus in the brainstem

43
Q

describe the spinocerebellum *

A

coordination of speech

adjustment of muscle tone

coordination of limb movements

from inferior cerebral peduncle to spinal cord

44
Q

describe the cerebrocerebellum *

A

coordination of skilled movements

cognitive function and attention

processing language

emotional control

initiation of skilled movements

45
Q

describe vestibulocerebellar syndrome *

A

tumour

causes gait ataxia and tendancy to fall when eyes closed

nystagmus - eyes make repetitive uncontrolled movements

46
Q

describe spinocerebellar syndrome *

A

damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abdominal gait and wide based stance

hypotonia

47
Q

describe cerebrocerebellar or lateral cerebellar syndrome *

A

damage affects arms/skilled coordinated movement = tremor and speech

dysmetria - movements overshoot or undershoot targets

coordination problems = dysdiadochkinesia

48
Q

define ataxia *

A

general inpairments in movement coordination and accuracy

disturbances of posture or gait- wide based, ‘drunken’ staggering gate

49
Q

what are the main signs of cerebellar dysfunction *

A

ataxia

dysmetria - inappropriate force and distance for target-directed movement eg knocking iver cup rather than grabbing it

intention tremor - increasingly oscillatory trajectory of a limb in target directed movement (just by thinking about movement, eg nose-finger tracking)

dysdiadochokinesia - inabilkity to perform rapidly alternating movement - rapidly pronating and supinating hands and forarms

scanning speech - staccato, due to impaired coordination of speech muscles

50
Q

effect of lesions in the SMA *

A

result in lack of spontaneus movements and speech

51
Q

describe connection between the motor areas in the cortex *

A

the SMA and PMA are reciprocally interconnected

both independantly provide reciprical connection to M1

M1 recieves afferents from SMA and PMA and sensory areas

stimulus intensity for M1 is lower than any other area

52
Q

locaation of the basal ganglia *

A

deep in white matter of teh cerebral cortex

neuro - yr 2 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions