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)