Motor learning & Neuro syndromes COPY Flashcards
THE MOTOR PATHWAY
i) what is the first question you ask when you see a motor problem?
ii) where to UMN and LMN run from and to?
iii) what is each step of the motor pathway starting from the motor cortex and ending in the motor end plate of the muscle? (7 stages) (where do the fibres decussate? where do UMN synapse to LMN?)
i) is it an upper motor neuron or lower motor neuron problem? ii) UMN run from the motor cortex in the brain to the spinal cord and LMN run from the anterior horn of the spinal cord to the muscle iii) motor cortex -> internal capsule -> brainstem -> decussate in the spinal cord –> synapse at the anterior horn of the spinal cord -> LMN -> motor end plate of the muscle
where to UMN synapse to LMNs?
in the anterior horn of the spinal cord
ORGANISATION OF THE MOTOR NERVOUS SYSTEM
i) what are the UMNs responsible for?
ii) what is the brainstem responsible for? iii) what is the basal ganglia responsible for?
iv) what is the cerebellum responsible for?
v) where do the descending systems feed into and what does this allow?
I) UMNs from motor cortex involved in plan and initiation of voluntary movement
ii) brainstem for basic movement and posture control iii) basal ganglia is the selector - select the muscle to move
iv) cerebellum co-ordinates the movements
v) desc systems feed into local circuit neurons (allows reflex co-ord) or feed into motor neuron pools (LMNs) which synapse to muscles
DESECENDING MOTOR PATHWAYS
i) where do the voluntary aspects lay positionally in the spinal cord?
ii) give two examples of voluntary tracts
iii) where do involuntary aspects lay positionally in the spinal cord?
iv) give three examples of involuntary tracts
i) voluntary tracts lay lateral in spinal cord
ii) vol tracts = rubrospinal and corticospinal
iii) involuntary tracts lay ventromedially
iv) invol tracts = reticulospinal, tectospinal and vestibulospinal
DESCENDING PATHWAYS i) which two tracts control head and neck movement? ii) which two tracts activate extensor muscles in the arms and legs and allow upright balance and posture? iii) which tract activates flexor muscles in the arms?
i) tectospinal and medial vestibulospinal ii) lateral vestibulospinal and reticulospinal iii) rubrospinal
name three techniques that can used to evoke a response in someone that seems unresponsive? what area is activated to evoke a response in the limbs?
1) supraorbital pressure (above eyelid) 2) nail bed stimulation 3) sternal stimulation activation of the reticular formation by noxious stimuli will evoke a response in the limbs
DECORTICATE POSTURE i) is the lesion above or below the red nucleus? is the rubrospinal tract therefore in tact? ii) what pathology is this seen in? iii) why do you get arm flexion? iv) how many points in GCS do you get for this posture?
I) lesion above the red nucleus therefore the rubrospinal tract is in tact ii) seen in stroke iii) get arm flexion because there is damage to the corticospinal tract but the rubrospinal tract is preserved so you get arm flexion iv) 2 points
DECEREBRATE POSTURE i) is the lesion above or below the red nucleus? is the rubrospinal tract therefore in tact? ii) which tracts are left functioning and therefore predominate here iii) what posture is seen?
i) lesion is below the red nucleus therefore RS tract is not in tact ii) loss of RS tract causes lateral vestibular and reticular spinal tract left to work iii) get all four limbs extended as LV and reticular tracts are involved extensor muscles
STROKE i) what is the predominant brain area and/or tract that is damaged? ii) what is the typical posture seen? why is this? iii) name three other signs that may be seen (tone and reflexes) iv) does the patient maintain posture? v) is there loss of descending inhibition?
i) motor cortex and/or corticospinal tract is damaged ii) typical postures are preserved upper limb flexion and lower limb extension due to vestibule and reticulospinal tracts still active iii) increased tone, brisk reflexes and extensor/babinski reflex iv) yes the patient will maintain posture v) there is loss of descending inhibition
will an UMN problem take the brakes off or put the brakes on? - what is seen in a UMN lesion (2) - what is the babinski reflex?
an UMN problem will take the brakes off - UMN lesions see brisk lesions and tone in the arm - babinski reflex is stroke bottom of the foot and normally toes will flex (curl in) but abnormal is fanning (extension) of toes
LOSS OF DESCENDING INHIBITION i) which motor neurons modulate spinal inhibitory interneurons? ii) if UMN are damaged what actions do you get? iii) what is seen when there is damage to the corticospinal tract later in life? iv) why do children get the spinal extensor response (extension of toes on babinski test?
i) UMN modulate spinal inhibitory INs ii) damage to UMN causes brisk reflexes and spasticity (increased tone) iii) damage to CS tract later in life causes babinski sign to revert back to baby (extend toes rather than flex) iv) children get extension of toes on stroking as the CS tract isn’t developed until age two and this is what inhibits the spinal extensor response
CORTICOBULBAR PATHWAY
i) what does it connect?
ii) what is it comprised of?
iii) what do the nerves pass to?
i) connects the motor cortex and medullary pyramids
ii) comprised of UMN of cranial nerves
iii) nerves pass to muscles and sensations in the face
STROKE FACIAL PALSY i) what side of the face do you get problems on in relation to the side of the lesion? why is this? ii) why is it possible for the top part of the face to be unaffected? iii) are the eyes affected in stroke? ie can you still raise your eyebrows? iv) what palsy occurs when LMNs are severed? how is this characterised?
i) get problems on the contralateral side to the brain lesion as the corticospinal tract decussates in the medullary pyramids ii) the top part of the face can be spared as it is bilaterally innervated by UMNs iii) eyes are not affected in stroke - you can still raise your eyebrows iv) severing LMN causes bells palsy = problems with the whole one side of face
MOTOR HOMUNCULUS i) info from which part of the body is represented in the medial part of the hemisphere? ii) where do CS tract that originate medially therefore head to? iii) why can you see symptoms spread through the body during a seizure?
i) information from the lower limbs is represented medially ii) CS tracts originating medially therefore head to the lower limb area iii) see symptoms spread through body during a seizure as the electrical activity spreads through the cortex and affects each different area represented in each part of the cortex
how does a parasaggital meningioma present? why does it present like this?
PS meningioma presents with bilateral leg weakness and spasticity as its sits between the two hemispheres so it pushes on both motor cortices (lower limb information lays medially)
MIDDLE CEREBRAL ARTERY OCCLUSION i) what will a proximal lesion affect and what symptom will this manifest as? ii) what will a distal lesion cause? what area may be spared? iii) which body part brain regions travel through the internal capsule? what will a lesion affecting the internal capsule therefore cause?
i) proximal MCA lesion will affect the internal capsule and leg area = causing complete hemiparesis ii) distal MCA lesion may spare the leg area but may cause swelling and ischaemia iii) the head, face and leg all travel through the internal capsule so a lesion here will cause problems in all of them
ANTERIOR CEREBRAL ARTERY OCCLUSION i) what does the ant ceb artery supply? ii) occlusion here will cause paresis is what body area? iii) may also see abulia - what is this?
I) supplies the medial part of the frontal lobes (inc the leg area and personality areas) ii) occulusion may cause leg paresis iii) abulia is impairment to make decisions and act independently
SEIZURE ‘MARCH’ I) what is this aka? ii) what is it? describe iii) what is it strongly associated with?
i) aka Jacksonian seizure ii) partial onset simple motor seizure that becomes more generalised eg starts in one part of body and spreads to face (along motor homunculus) iii) strongly associated with structural abnormality in or close to the motor cortex
POSTERIOR PARIETAL CORTEX i) what brain areas are found here? what do they represent? ii) what is it responsible for? iii) what does damage here result in?
i) brain areas 5 (somatosensory afferents) and area 7 (visual pathway afferents) ii) response for information that needs further refinement and exploratory movement such as turning an object in your hand/looking/ feeling iii) damage results in neglect
what brain area is responsible for exploratory movements eg looking and feeling?
posterior parietal cortex
ASSOCIATION CORTICES what are the i) parietal ii) temporal iii) occipital lobes responsible for? iv) where do all these feed forward to?
I) parietal = sensation ii) temporal = vestibular information and hearing iii) occipital = vision iv) all feed forward to frontal lobe
PREMOTOR AREA i) what brain area is this found in? ii) what is it involved in? iii) give an example of what this area is responsible for iv) where does it receive inputs from? v) what do lesions in this area cause?
i) found in area 6 ii) involved in visually guided movement and postural/proximal limb muscles iii) involved in grasping iv) receives inputs from the cerebellum v) lesions in this area cause decreased fine dexterity eg you cant grab things
what brain area may be affected if you have decreased fine dexerity and cant grab things?
the pre motor area
what does the supplementary motor area allow? where does it feed into? when finger movements are mentally rehearsed and not actually performed - which brain area is activated?
- SMA allows following of complex finger movements - feeds into M1 motor cortex - when finger movements are mentally rehearsed only you see SMA activation but not M1
BEREITSCHAFTSPOTENTIAL I)what is the bereitschaftspotential? ii) how can this be measured? iii) in voluntary movement - signals from which brain area will be picked up before signals from the primary motor cortex? iv) what type of patients can the BSP be seen in? v) how long usually is this?
i) time gap between thinking about a movement and actually doing it - ii) can be recorded by measuring time from supplementary motor cortex activation to motor activation iii) in voluntary movement there are signals from the supplem motor cortex before the primary motor cortex iv) seen in patients with functional movement disorders v) usually 500-1000ms
APRAXIA i) what is it? ii) how is it characterised? iii) are motor pathways in tact? iv) damage to which brain areas causes it?
i) inability to carry out purposeful movement in the absence of paralysis ii) characterised by difficulty in the sequencing and execution of movement iii) motor pathways are in tact but cant do complex movements iv) due to damage between parietal and frontal lobes
TYPES OF APRAXIA - what is: i) ideational ii) ideomotor what brain areas do each involve?
i) ideational is unable to report the sequence eg asked to show how to make a sandwich and cant do it ii) ideomotor is unable to use a tool eg show me how t use a pair of scissors ideational involves parietal and ideomotor involves SMA and motor area
TASK SPECIFIC DYSTONIAS i) what type of processing goes wrong here? ii) how is it characterised? iii) what causes this to happen? iv) is it a sensory or motor problem? v) define dystonia
i) sensory processing goes wrong ii) characterised by abnormal sustained muscle contraction leading to sustained postures iii) caused by repeated and extended use of the hand which can result in changes in the functional organisation of brain areas relating to sensory processing and motor control iv) manifestation is motor but the primary abnormality is due to disrupted sensory processing v) dystonia is a sustained muscle contraction that produces twisting, repetitive movement or abnormal postures
which brain area allows you to see movement in the lower face of someone who has just had a stroke when you tell them a joke? why is this?
the anterior cingulate gyrus - the emotional pathways are not damaged
what tract is this?
corticospinal tract
which tract is this?
what does it predominantly innervate?
rubrospinal tract
predominantly innervates flexors of upper limbs
which tract originates from here?
name the specific area it originates from
where do the fibres decussate?
the tectospinal tract
orignate from the superior colliculus
fibres decussate straight away in the midbrain
what type of posturing is this?
is this caused by a lesion above or below the red nucleus?
decorticate posturing
caused by a lesion above the red nucleus
what type of posturing is this?
is this caused by a lesion above or below the red nucleus?
decerebrate posturing
caused by a lesion below the red nucleus
occulusion of which vessel will cause a stroke and result in this posture?
middle ceb artery stroke
what conditions are characterised by facial palsy A and B?
why is only the bottom half of the face affected in A?
A = stroke
B = bells palsy
only bottom half of face is affected in stroke as the top is bilaterally innervated by UMNs
what is this?
how does it present? (2)
parasaggital meningioma
presents as bilateral leg weakness and spasicity
which arteries supply the
i) red
ii) blue
iii) green
areas of the brain?
i) middle cerebral
ii) anterior cerebral
iii) posterior cerebral
what type of stroke has caused this?
anterior cerebral stroke
