motor pathways Flashcards
what are the broad principles of motor control
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
summarise the motor system hierarchy
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
where is the primary motor cortex M1 *
in the frontal lobe, precentral gyrus anterior to the central sulcus
what is the role of M1 *
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
describe the somatotropic organisation of M1 *
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
describe the lateral corticospinal tract *
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
describe the anterior cortical spinal tract *
axons from M1 travel and decussate in spinal cord
5% of fibres
what muscles do the lateral and anterior corticospinal tract supply *
anterior - axial muscles in the thorax
lateral - distal parts oif the limbs
summarise the corticobulbar pathways
motor neurons in teh brainstem in te CN nuclei
axons come from M1
synapse in the brainstem
what is the location of the premotor cortex
frontal lobe, anterior to M1
function of the premotor cortex *
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
what is te location of the supplementary motor area
frontal lobe anterior to M1, more medially than the premotor cortex
what is the function of te supplementory motor area *
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
describe the association cortex
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
where are lower motor neurons
spinal cord - ventral horn
brainstem - bulbar
where are upper motor neurons
corticospinal/corticobulbar tract
betz cells and projections
what does pyramidal include
in the lateral corticospinal tract
what does extrapyramidal include
basal ganglia
ccerebellum
describe the effects of an upper motor neuron lesion *
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
describe apraxia *
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
what are the effects of lower motor neuron lesions
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
summarise the pathophysiology of motor neuron disease*
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
what are the upper motor neuron signs of MND *
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
what are the lower mnotor neuron signs of MND *
weakness
muscle wasting
tongue fasciculations and wasting
nasal speech
dysphagia
recall the component structures of the basal ganglia *
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)
what forms teh straitum *
the caudate nucleus
external globus pallidus
putamen
describe the nucleus accumbens *
dopaminergic
recieve input from mesolimbic
involved in reward
why is Parkinson’s a nigrostriatal disease *
it is the projections form the nigra to the striatum that are dysfunctional
illustrate on a schematic where the components of the basal ganglia are *
illustrate on an anterior coronal section where the components of the basal ganglia are *
1st pic
illustrate on a coronal section where the components of the basal ganglia are *
2nd pic
what is the function of the basal ganglia
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
describe the circuitary of the basal gangia
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
what is the neuropathology of Parkinson’s *
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
what are the clinical signs of Parkinson’s *
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
summarise the nigro-straital pathway
nigrostriatal neurons go from nigra to striatum
what are teh 3 deep nuclei in the cerebellum *
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
what is the pathophysiology of huntington’s *
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
what are the motor signs of Huntington’s *
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
describe the cellular organisation of the cerrebellum and how this relates to functioning *
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
what are the 3 divisions of the cerebellum *
vestibulocerebellum
spinocerebellum
cerebrocerebellum
describe the vestibulocerebellum *
regulation of gait, posture and equilibrium
coordinate head movement with eye movement
close connection with superior colliculus in the brainstem
describe the spinocerebellum *
coordination of speech
adjustment of muscle tone
coordination of limb movements
from inferior cerebral peduncle to spinal cord
describe the cerebrocerebellum *
coordination of skilled movements
cognitive function and attention
processing language
emotional control
initiation of skilled movements
describe vestibulocerebellar syndrome *
tumour
causes gait ataxia and tendancy to fall when eyes closed
nystagmus - eyes make repetitive uncontrolled movements
describe spinocerebellar syndrome *
damage (degeneration and atrophy associated with chronic alcoholism) affects mainly legs, causes abdominal gait and wide based stance
hypotonia
describe cerebrocerebellar or lateral cerebellar syndrome *
damage affects arms/skilled coordinated movement = tremor and speech
dysmetria - movements overshoot or undershoot targets
coordination problems = dysdiadochkinesia
define ataxia *
general inpairments in movement coordination and accuracy
disturbances of posture or gait- wide based, ‘drunken’ staggering gate
what are the main signs of cerebellar dysfunction *
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
effect of lesions in the SMA *
result in lack of spontaneus movements and speech
describe connection between the motor areas in the cortex *
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
locaation of the basal ganglia *
deep in white matter of teh cerebral cortex
