Week 6 Motor Control (Dr Roger Newport) uCorticospinal Damage Hemiparesis u Cerebellar Damage Ataxia...
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Transcript of Week 6 Motor Control (Dr Roger Newport) uCorticospinal Damage Hemiparesis u Cerebellar Damage Ataxia...
Week 6 Motor Control(Dr Roger Newport)
Corticospinal DamageHemiparesis
Cerebellar Damage Ataxia Timing IssuesMotor Learning
Basal Ganglia DamageParkinson’s DiseaseHuntingdon’s Chorea
Cortical DamageApraxia
Corticospinal DamageHemiparesis and Hemiplegia
Definitions
Hemiplegia: Paralysis Hemiparesis: Weakness
The most common and obvious sign of stroke, butcan be caused by a variety of reasons including:tumoursInfection (e.g. meningitis / encephalitis)Metabolic imbalancecongenital disorders
Always as a result of damage to the corticospinal tract
Corticospinal TractOriginates in Primary MotorCortex and neighboring regions
Passes through Corona RadiataInternal CapsuleCerebral PedunclesPonsPyramidsCrosses in the Pyramidal DecussationForms Anterior and LateralCorticospinal tracts
Doctor,I’ve had a stroke
but you can’t affordto give me a scan
Can we tellwhere my lesion is?
Yes, if we follow afew basic rules
How can we tell where in the tract the damage is?
RULE NUMBER 2 There is usually only one lesion. Bilateral lesions do occur, but then there are bilateral signs
RULE NUMBER 1 There are 4 major sites causing hemiparesis: (1) Cortex (2) Internal Capsule (3) Corona Radiata(4) Brainstem
RULE NUMBER 3 If it is below the neck there will be no facial weakness.
Doctor,my lesion is in my spinal cord
How do I know?
Doctor,my lesion is in my spinal cord
How do I know?
Because I have nofacial weakness
DecussationM
idbr
ain
Pon
sM
edul
la
Facialnuclei
To right limbsTo left limbs
FromRight Cortex
FromLeft Cortex
SC
X
Cortical damage does not affect the entire side of the face. Because of the bilateral innervation of the upper third of the face, only the lower two-thirds of the face would be affected by cortical damage
UncrossedCorticobulbarfibreTo Upper
Facial Muscles
To LowerFacial Muscles
Facialnervefibres
Crossed corticobulbar fibre
X &UnXinput
UnXinputonly
L Cortex R Cortex
Left-sided upper motor neurone facial weakness.
RULE NUMBER 4 The face is always weak on the same side as the arm and leg if it is an upper motor neurone facial weakness -except when the lesion is in the pons
A lesion in the pons can result in crossed hemiparesis, i.e. contralateral limb weakness and ipsilateral facial weakness
Doctor,my lesion is in my spinal cord
How do I know?
Doctor,my lesion is in
my ponsHow do I know?
Because I have have crossed hemiparesis
DecussationM
idbr
ain
Pon
sM
edul
la
Facialnuclei
To right limbsTo left limbs
FromRight Cortex
FromLeft Cortex
SC
To theR face
X
RULE NUMBER 4 The face is always weak on the same side as the arm and leg if it is an upper motor neurone facial weakness -except when the lesion is in the pons
RULE NUMBER 5 If the lesion is above the neck then it is on the opposite side to the hemiparesis. EVERYTHING, absolutely everything crosses if it’s going to the hemispheres. Your left brain receives sensation and visual input from the right side and sends out its motor output to the right side.
RULE NUMBER 7: THE LAW OF EXPECTATIONS
If there is a left sided hemiparesis, which is an easy thing to observe: it follows that you can expect to find (if there is not a brainstem lesion):
Left-sided upper motor neurone facial weakness. Left-sided sensory loss Left homonymous hemianopia (can be cortical or subcortical)If the lesion is in the cortex you expect cortical signs
Left Hemisphere–Aphasia –Right hemiparesis –Right-sided sensory loss –Right visual field defect –Apraxia–Dysarthria (speech) –3Rs Difficulty
Right Hemisphere–Extinction of left-sided stimuli –Left hemiparesis –Left-sided sensory loss –Left visual field defect –Poor left conjugate gaze –Spatial disorientation
Look at the eyes! Eyes look at involved hemisphere Eyes look away from the Hemiparesis
Doctor,my lesion is in
my cortexHow do I know?
Doctor,my lesion is in
my cortexHow do I know?
Because I haveuneven arm and leg weakness and show
cortical signs
X
But what if the brainstemand pons have been ruled
out and there are nocortical signs?
Remaining Candidates:Internal capsuleCorona radiata
Corona Radiata Internal capsule
These fibres funnel through the internal capsule which lies between the thalamus and basal ganglia on their way to the brainstem.
Fibres descending from the cortex are called the ‘corona radiata’
cortex
C.R.
I.C.
ToLMN
Bra
inst
em
Reticular formation
The reticulospinal tracts are two long descending pathways associated with the control of movements and posture. The lateral reticulospinal tract inhibit extensors.
cortex
C.R.
I.C.
ToLMN
Bra
inst
em
Reticular formation
X
Bra
inst
em
Reticular formation
So if input to the reticular nuclei is interrupted (as happens with a lesion of the internal capsule) extensor reflexes are no longer inhibited - result: the Babinski sign.
Normal plantar reflex Babinski extensor reflex
Up
Fanningtoes}
Doctor,my lesion is in
my internal capsuleHow do I know?
Because I haveequal arm and leg weakness and showthe Babinski sign
Doctor,my lesion is in
my internal capsuleHow do I know?
cortex
C.R.
I.C.
ToLMN
Bra
inst
em
Reticular formation
X X
X
Facial Weakness? Spinal cordNo
Yes
FW same side as limb W? PonsNo
Internal CapsuleYes
Yes
Leg and arm equal?
No
Cortical signs?
Ipsilateral damage
Contralateraldamage
Where is my lesion: summary?
Cortex
Corona Radiata
Yes
No
But there is more to motor control than the corticospinal tract.
Thalamus
If you want to speak to the cortex, you’ll have to go through the thalamus
Much more.
Major components of the motor system
Transforming sensoryinput into plans for
voluntary movementInitiating and directing voluntary movement
Movement learning,motivation and initiation
Motor learning,timing and coordination
The Cerebellum: where is it and what does it do?
Thought to be involved in:BalanceCoordinating movementTiming of movementsTiming of discontinuous movementsMotor learning - acquiring and maintaining
Sources of cerebellar injuriesToxins (ethanol, chemotherapy, anticonvulsants, ethanol).Autoantibodies (paraneoplastic cerebellar degeneration ) Structural lesions (strokes, MS, tumors, etc)Inherited cerebellar degenerations ( e.g. Freidreich's ataxia)
Diagnosis usually by MRI
Vermis
Paravermis
LateralHemispheres
AnteriorLobe
PosteriorLobe
The cerebellum - basic divisions
Flocculus
Postural instability e.g. fall to ipsilesional sideTruncal ataxiaPostural control and adjustmente.g. Romberg signGait ataxiaExtensor rigidityNystagmus Eye deviation if unilateral
Cerebellar Ataxia
Midline effects
}
Cerebellar Ataxia
Hemispheric effects
Asynergia Decomposition of movement
DysarthiaJerky speech pattern
Dysmetriainability to stop a movement at desired point
Dysdiadochokinesiainability to perform rapidly alternating movements
Hypotoniadecreased muscle tone, pendular knee jerk
Intention Tremorusually evident during powerful movements, but absent or diminished with rest (contrast basal ganglia disorders)
Remember : Lesions to the cerebellum do not destroy movement, they disrupt it.Ataxia = disordered movement
The Cerebellum and TimingCerebellum is thought be involved in the timing of movements because cerebellum lights up in PET study of complex/novel timing tasks (Penhune et al. 1998) cerebellar patients are imparied at tasks like tapping along to a metronome beat
Two basic models:
40 Hz25 ms
Pacemaker10 pulses = 250 ms
20 pulses = 500 ms
30 pulses = 750 ms
Clock counter modelPacemaker produces output to counterLonger intervals represented by more pacemaker outputs in counter
250 ms 500 ms 750 ms
Interval modelDifferent intervals represented by distinct elementsEach corresponds to a specific duration
Multiple timer model
Must be independent (interval) timers for each effector (finger/hand/limb etc.) as unilateral cerebellar damage gives rise to unimanual timing deficit, but bimanual tapping improves performance.
Ivry, R.B. & Richardson, T. (2002).
Spencer et al (2003): Cerebellum is only responsible for stop-start movements, not continuous motion.
Continuous movements
can be set going and left
Discontinuous movements
have a specific temporal goal
This is what is controlledby the cerebellum.
The Cerebellum and Motor LearningThe Cerebellum is thought to be involved in motor learning and the maintenance of movement accuracy because patients with cerebellar lesions are impaired at learning novel motor tasks.
Evidence from prism adaptation ( e.g. Thach et al., 1992)
No Prisms
Prisms On
Prisms Off
Example data
CORTEX
InferiorOlive
Spinal Cord
Cerebellum
Corticospinal T
ract
ErrorCorrection
Feedback from actual movement
Spin
o-ce
rebe
llar
T
ract
The Feedback Circuit: One theory of how the cerebellum might correct movement
The basal gangliaa collection of nuclei deep in the white matter of the cerebral cortex.
They include: CaudatePutamenglobus pallidussubstantia nigrasubthalamic nucleus
(the caudate nucleus and the putamen taken together all known as the striatum)
The main input to the Basal Ganglia is exitatory from the frontal cortex (especially from the supplementary motor area SMA) The striatum (C+P) inhibit the Globus Pallidus whose output to the thalamus is also inhibitory The thalamic output to the cortex is exitatory. Striatum activity is modulated by the Substantia Nigra
There’s more:Direct and indirect loops.Direct RouteStriatum - GPi - Th - cortexIndirect Route detours via GPe and SN.
The release of dopamine stimulates D and inhibits InD routes
-ve
+ve +ve
-ve
+veMod -ve)
-ve
What is the function of the Basal Ganglia?
Slow postural adjustments? - BG damage can cause postural disturbances
Initiating movements? - BG patients can struggle to start movements
Gate Keeper / Brake Regulator (e.g. Gazzaniga et al.)?BG acts in a regulatory way to facilitate desired voluntary movements and inhibit unwanted, often reflexive, movements
The direct route enables the preferred actionThe indirect route suppresses unwanted movements
Activity in the BG increases in anticipation of an intended movement
Gate Keeper or Brake Regulator?
Lesions in specific nuclei tend to produce characteristic deficits.the slow and steady loss of dopaminergic neurons in SNpc leads to:
Parkinson's disease, 3 symptoms usually associated with Parkinson's are:Tremor (+ve) most apparent at restRigidity (+ve) due to simultaneous contraction of flexors an extensorsBradykinesia (ive) difficulty initiating voluntary movement
Akinesia illustrates intentional aspect of BG function
-ve
+ve
-ve
+veX
Remember the role of the GPi is inhibitory
-ve
-ve
Fixed by removal of STN
Whereas degeneration of the caudate and putamen (inhibitory) leads to:
Huntington's disease, or chorea, a hereditary disease of unwanted movements. produces continuous dance-like movements of the face and limbs A related disorder is hemiballismus, flailing movements of one arm and leg, which is caused by damage (i.e., stroke) to the subthalamic nucleus.
+ve
-ve
Remember the role of the GPi is inhibitory
-veX-ve +ve
Action systemAction system
Three component approachThree component approach
1. Perceptual processes1. Perceptual processes
vision, proprioception, haptics, vestibular, vision, proprioception, haptics, vestibular, auditoryauditory
2. Cognitive processes2. Cognitive processes
attention, semantic memory, decision-making, attention, semantic memory, decision-making, response selection, motor representationsresponse selection, motor representations
3. Motor processes3. Motor processes
convert movement plan into motor response, convert movement plan into motor response, control muscle activationcontrol muscle activation
Apraxia has an exclusionary definition:Apraxia has an exclusionary definition:
It is a disorder of skilled movement that cannot be attributed to It is a disorder of skilled movement that cannot be attributed to basic level sensory, motor or cognitive disturbancesbasic level sensory, motor or cognitive disturbances
It is therefore a disorder of It is therefore a disorder of high-levelhigh-level perceptual, cognitive and/or perceptual, cognitive and/or motor systemsmotor systems
What is apraxia?
Apraxia
Some basic tests for apraxia
But watch out for confounds
SMAPrimaryMotorcortex
PrimaryVisualcortex
(Broca’s area)
Primaryauditory ortex
(Wernicke’s area) Angular gyrus
(ArcuateFasciculus)
Brain areas involved
Main types of Apraxia
Ideational apraxiainability to produce a coherent action sequence - Kimura Box Impairment in the concept of an actionability to imitate gestures / produce movements on command spared
Thought to occur when the motor programming area is destroyed by damage to the supramarginal gyrus, impairing the conceptual representation of an action and leading to deficits in using tools or performing an action to verbal command while imitation is spared (Koski (on web))
Ideomotor apraxiaImpairment in the performance of skilled pantomime movements on verbal command or in imitationmost commonly caused by parietal damage in the dominant hemisphere (LH). In this case bilateral apraxia results. (In rare cases a lesion to the right-hemisphere SMA or to the corpus callosum may also produce ideomotor apraxia. In this case the apraxia is restricted to the left limb.)
Ideomotor apraxia occurs when the motor programming area is disconnected from the premotor and motor regions, so that the patient can conceptualize but not actually execute the action,demonstrating spared recognition of tools but deficientability to use them appropriately or to imitate actions.
Ideomotor apraxia (cont.)
Can be ok with ipsilesional limbHave greatest difficulty when imitating transitive movements (tool use)Several types of errorsUse body parts instead of imagined tool (e.g. scissors)Perseverative errors (do previous pantomime)Sequencing (e.g open door twist before reach or pull before twist)
Impairment in knowing how,rather than what to do
Most characteristic are spatial errors1. Postural (e.g. wrong grip)2. Spatial orientation (e.g. not cutting in one plane)3. Spatial movement
(e.g screwdriver shoulder not wrist)
2 forms of ideomotor apraxia (Heilman and Rothi, 1993)
1. Loss of praxicons in supramarginal or angular gyrusPerform poorly to command, cannot comprehend gestures
2. Disconnection of praxicons from premotor and motor areas (caused by lesions anterior to SMG/AG.
Praxicons stored in dominant inferior parietal lobe
Praxicon = stored spatiomotor gesture representations which provide the ‘‘time-space-form picture of the movement’’
(Liepmann & Maas, 1907) a ‘movement formula’ if you like
But, Ochipa et al (1990)Patient could comprehendPanto and panto to command, but not imitate transitive gestures
AG
SMA
DirectNon-lexical
Output praxicon
2 route model
Semantics (learnt actions)}SMG/AG
Auditory Analysis
Auditory/verbal input(command)
Innervatory patterns(motor plan)
(SMA)
Visual Analysis
Visual input(gesture or object)
Input praxicon
Motor sytems
lexicalroute
Input praxicon unable to recognise/comprehend gestures, but can do so to verbal command
Between input and output praxicon able to recognise, but not produce object gestures, but can do so to verbal command
Output praxicon can recognise/comprehend, but can’t produce
Any of above can still imitate meaningful and meaningless gestures
Direct route can do meaningful gestures only
Input praxicon unable to recognise/comprehend gestures, but can do so to verbal command
Between input and able to recognise, but not produce object output praxicon gestures, but can do so to verbal command
Output praxicon can recognise/comprehend, but can’t produce
Any of above can still imitate meaningful and meaningless gestures
Direct route can do meaningful gestures only
Quick review
Damage to:
DirectNon-lexical
Output praxicon
2 route model
Semantics (learnt actions)}SMG/AG
Auditory Analysis
Auditory/verbal input(command)
Innervatory patterns(motor plan)
(SMA)
Visual Analysis
Visual input(gesture or object)
Input praxicon
Motor sytems
lexicalroute
Another patient that causes problems for this model is BG (Buxbaum, 2000) who can do tool-use gestures, but not other gestures, but whose meaningless imitation is worse than meaningful imitation
Problem is when a patient can do meaningless imitation, but not meaningful imitation(MF (Bartolo, 2001))
Buxbaum 2000
Dynamic interplay between knowledge of tool use and stored learnt gestures and body-centred representations of how to do actions (the body schema). The boxes on the left can supplement or boost the damaged processes of the right hand box.
Direct routeLexical routeIn
PP
C
A closer look at Patient BG:
gestures nearly normally with tool in handAnd recognises gestures quite well gesture representations can be accessed by visual input more deficient in imitating meaningless gesture-like movementsthan spatially matched meaningful gesture analogues direct route damaged?
But, unable to gesture to command , to sight of object or imitation output praxicon damaged?
difficulty in matching gestures (but not objects), especially when a spatial transformation is requireddeficient processes not conceptual or visual,but spatiomotor
more parsimonious explanation:BG’s pattern reflects damage to a unitary set of procedures or representations common to both lexical and direct routes(Buxbaum, 2000).
One possibility is dual lesions to both lexical and direct route
1. What is the basis for the relative integrity of BG’s tool use?
2. Why does she fail to use the direct route upon provision of a model to be imitated?
Apraxia summary
2 main types of apraxia
2-route model explains most functional characteristics of ideomotor apraxia are covered by the 2-route model, but
Cannot account for dissociation between being able to perform meaningless, but not meaningful gestures (patient MF (Bartolo))
Cannot account for preserved tool-use gesture with impaired other geture and impaired meaningless imitation (patient BG (Buxbaum)