motor pathways

Question 1

what are the broad principles of motor control

Answer 1

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

Question 2

summarise the motor system hierarchy

Answer 2

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

Question 3

where is the primary motor cortex M1 *

Answer 3

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

Question 4

what is the role of M1 *

Answer 4

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

Question 5

describe the somatotropic organisation of M1 *

Answer 5

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

Question 6

describe the lateral corticospinal tract *

Answer 6

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

Question 7

describe the anterior cortical spinal tract *

Answer 7

axons from M1 travel and decussate in spinal cord

5% of fibres

Question 8

what muscles do the lateral and anterior corticospinal tract supply *

Answer 8

anterior - axial muscles in the thorax

lateral - distal parts oif the limbs

Question 9

summarise the corticobulbar pathways

Answer 9

motor neurons in teh brainstem in te CN nuclei

axons come from M1

synapse in the brainstem

Question 10

what is the location of the premotor cortex

Answer 10

frontal lobe, anterior to M1

Question 11

function of the premotor cortex *

Answer 11

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

Question 12

what is te location of the supplementary motor area

Answer 12

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

Question 13

what is the function of te supplementory motor area *

Answer 13

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

Question 14

describe the association cortex

Answer 14

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

Question 15

where are lower motor neurons

Answer 15

spinal cord - ventral horn

brainstem - bulbar

Question 16

where are upper motor neurons

Answer 16

corticospinal/corticobulbar tract

betz cells and projections

Question 17

what does pyramidal include

Answer 17

in the lateral corticospinal tract

Question 18

what does extrapyramidal include

Answer 18

basal ganglia

ccerebellum

Question 19

describe the effects of an upper motor neuron lesion *

Answer 19

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

Question 20

describe apraxia *

Answer 20

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

Question 21

what are the effects of lower motor neuron lesions

Answer 21

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

Question 22

summarise the pathophysiology of motor neuron disease*

Answer 22

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

Question 23

what are the upper motor neuron signs of MND *

Answer 23

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

Question 24

what are the lower mnotor neuron signs of MND *

Answer 24

weakness

muscle wasting

tongue fasciculations and wasting

nasal speech

dysphagia

Question 25

recall the component structures of the basal ganglia \*

Answer 25

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)

Question 26

what forms teh straitum \*

Answer 26

the caudate nucleus external globus pallidus putamen

Question 27

describe the nucleus accumbens \*

Answer 27

dopaminergic recieve input from mesolimbic involved in reward

Question 28

why is Parkinson's a nigrostriatal disease \*

Answer 28

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

Question 29

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

Answer 29

Question 30

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

Answer 30

1st pic

Question 31

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

Answer 31

2nd pic

Question 32

what is the function of the basal ganglia

Answer 32

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

Question 33

describe the circuitary of the basal gangia

Answer 33

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

Question 34

what is the neuropathology of Parkinson's \*

Answer 34

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

Question 35

what are the clinical signs of Parkinson's \*

Answer 35

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

Question 36

summarise the nigro-straital pathway

Answer 36

nigrostriatal neurons go from nigra to striatum

Question 37

what are teh 3 deep nuclei in the cerebellum \*

Answer 37

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

Question 38

what is the pathophysiology of huntington's \*

Answer 38

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

Question 39

what are the motor signs of Huntington's \*

Answer 39

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

Question 40

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

Answer 40

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

Question 41

what are the 3 divisions of the cerebellum \*

Answer 41

vestibulocerebellum spinocerebellum cerebrocerebellum

Question 42

describe the vestibulocerebellum \*

Answer 42

regulation of gait, posture and equilibrium coordinate head movement with eye movement close connection with superior colliculus in the brainstem

Question 43

describe the spinocerebellum \*

Answer 43

coordination of speech adjustment of muscle tone coordination of limb movements from inferior cerebral peduncle to spinal cord

Question 44

describe the cerebrocerebellum \*

Answer 44

coordination of skilled movements cognitive function and attention processing language emotional control initiation of skilled movements

Question 45

describe vestibulocerebellar syndrome \*

Answer 45

tumour causes gait ataxia and tendancy to fall when eyes closed nystagmus - eyes make repetitive uncontrolled movements

Question 46

describe spinocerebellar syndrome \*

Answer 46

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

Question 47

describe cerebrocerebellar or lateral cerebellar syndrome \*

Answer 47

damage affects arms/skilled coordinated movement = tremor and speech dysmetria - movements overshoot or undershoot targets coordination problems = dysdiadochkinesia

Question 48

define ataxia \*

Answer 48

general inpairments in movement coordination and accuracy disturbances of posture or gait- wide based, 'drunken' staggering gate

Question 49

what are the main signs of cerebellar dysfunction \*

Answer 49

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

Question 50

effect of lesions in the SMA \*

Answer 50

result in lack of spontaneus movements and speech

Question 51

describe connection between the motor areas in the cortex \*

Answer 51

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

Question 52

locaation of the basal ganglia \*

Answer 52

deep in white matter of teh cerebral cortex