Presentation on theme: "Week 6 Motor Control Corticospinal Damage Hemiparesis"— Presentation transcript:
1Week 6 Motor Control Corticospinal Damage Hemiparesis (Dr Roger Newport)Corticospinal DamageHemiparesisCerebellar DamageAtaxiaTiming IssuesMotor LearningBasal Ganglia DamageParkinson’s DiseaseHuntingdon’s ChoreaCortical DamageApraxia
2Corticospinal Damage Hemiparesis and Hemiplegia Definitions Hemiplegia: ParalysisHemiparesis: WeaknessThe most common and obvious sign of stroke, butcan be caused by a variety of reasons including:tumoursInfection (e.g. meningitis / encephalitis)Metabolic imbalancecongenital disordersAlways as a result of damage to the corticospinal tract
3Corticospinal Tract Originates in Primary Motor Cortex and neighboring regionsPasses through Corona RadiataInternal CapsuleCerebral PedunclesPonsPyramidsCrosses in the Pyramidal DecussationForms Anterior and LateralCorticospinal tracts
4How can we tell where in the tract the damage is? Doctor,I’ve had a strokebut you can’t affordto give me a scanYes, if we follow afew basic rulesCan we tellwhere my lesion is?
5RULE NUMBER 1There are 4 major sites causing hemiparesis:(1) Cortex(2) Internal Capsule(3) Corona Radiata(4) BrainstemRULE NUMBER 2There is usually only one lesion.Bilateral lesions do occur, but then there are bilateral signsRULE NUMBER 3If it is below the neck there will be no facial weakness.
6Doctor, my lesion is in my spinal cord How do I know? Doctor, DecussationMidbrainPonsMedullaFacialnucleiTo right limbsTo left limbsFromRight CortexLeft CortexSCXBecause I have nofacial weakness
7Left-sided upper motor neurone facial weakness. 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 damageTo UpperFacial MusclesTo LowerFacialnervefibresCrossed corticobulbar fibreX &UnXinputUnXonlyL CortexR CortexUncrossedCorticobulbarfibre
8RULE NUMBER 4The 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 ponsA lesion in the pons can result in crossed hemiparesis, i.e. contralateral limb weakness and ipsilateral facial weakness
9Doctor, my lesion is in my spinal cord How do I know? Doctor, my ponsHow do I know?DecussationMidbrainPonsMedullaFacialnucleiTo right limbsTo left limbsFromRight CortexLeft CortexSCTo theR faceXBecause I have havecrossed hemiparesis
10RULE NUMBER 4The 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 ponsRULE NUMBER 5If 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.
11RULE 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 lossLeft homonymous hemianopia (can be cortical or subcortical)If the lesion is in the cortex you expect cortical signs
12Left Hemisphere Right Hemisphere Aphasia Right hemiparesisRight-sided sensory lossRight visual field defectApraxiaDysarthria (speech)3Rs DifficultyRight HemisphereExtinction of left-sided stimuliLeft hemiparesisLeft-sided sensory lossLeft visual field defectPoor left conjugate gazeSpatial disorientationLook at the eyes!Eyes look at involved hemisphereEyes look away from the Hemiparesis
13But what if the brainstem and pons have been ruled Doctor,my lesion is inmy cortexHow do I know?Because I haveuneven arm and legweakness and showcortical signsXDoctor,my lesion is inmy cortexHow do I know?But what if the brainstemand pons have been ruledout and there are nocortical signs?Corona RadiataInternal capsuleRemaining Candidates:Internal capsuleCorona radiata
14Fibres descending from the cortex are called the ‘corona radiata’ C.R.I.C.ToLMNBrainstemReticularformationThese fibres funnel through the internal capsule which lies between the thalamus and basal ganglia on their way to the brainstem.The reticulospinal tracts are two long descending pathways associated with the control of movements and posture. The lateral reticulospinal tract inhibit extensors.
15So 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.cortexC.R.I.C.ToLMNBrainstemReticularformationXNormal plantar reflexBabinski extensor reflexUpFanningtoes}
16Doctor,my lesion is inmy internal capsuleHow do I know?Doctor,my lesion is inmy internal capsuleHow do I know?cortexC.R.I.C.ToLMNBrainstemReticularformationBecause I haveequal arm and legweakness and showthe Babinski signX
17Where is my lesion: summary? Spinal cordNoIpsilateral damageFacial Weakness?YesFW same side as limb W?PonsNoYesLeg and arm equal?ContralateraldamageInternal CapsuleYesNoCortical signs?CortexCorona RadiataYesNo
18But there is more to motor control than the corticospinal tract. ThalamusIf you want to speak to the cortex, you’ll have to go through the thalamusMuch more.Major components of the motor systemTransforming sensoryinput into plans forvoluntary movementInitiating and directingvoluntary movementMovement learning,motivation and initiationMotor learning,timing and coordination
19The Cerebellum: where is it and what does it do? Thought to be involved in:BalanceCoordinating movementTiming of movementsTiming of discontinuous movementsMotor learning - acquiring and maintainingSources 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
21} Cerebellar Ataxia Midline effects Postural instability e.g. fall to ipsilesional sideTruncal ataxiaPostural control and adjustmente.g. Romberg signGait ataxiaExtensor rigidityNystagmusEye deviation if unilateral
22Cerebellar Ataxia Hemispheric effects Asynergia Dysarthia Dysmetria Decomposition of movementDysarthiaJerky speech patternDysmetriainability to stop a movement at desired pointDysdiadochokinesiainability to perform rapidly alternating movementsHypotoniadecreased muscle tone, pendular knee jerkIntention 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
23The Cerebellum and Timing Cerebellum is thought be involved in the timing of movements becausecerebellum 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 beatTwo basic models:40 Hz25 msPacemaker10 pulses = 250 ms20 pulses = 500 ms30 pulses = 750 msClock counter modelPacemaker produces output to counterLonger intervals represented by more pacemaker outputs in counter250 ms500 ms750 msInterval modelDifferent intervals represented by distinct elementsEach corresponds to a specific duration
24Multiple timer modelMust 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).
25Spencer et al (2003): Cerebellum is only responsible for stop-start movements, not continuous motion.Continuous movementscan be set going and leftDiscontinuous movementshave a specific temporal goalThis is what is controlledby the cerebellum.
26The Cerebellum and Motor Learning The 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 PrismsPrisms OnPrisms OffExample data
27The Feedback Circuit: CORTEX Inferior Olive Spinal Cord Cerebellum One theory of how the cerebellum might correct movementCORTEXInferiorOliveSpinal CordCerebellumCorticospinal TractErrorCorrectionFeedback fromactual movementcerebellarSpino-Tract
28The 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)
29 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 NigraThere’s more:Direct and indirect loops.Direct RouteStriatum - GPi - Th - cortexIndirect Routedetours via GPe and SN.The release of dopamine stimulates D and inhibits InD routes+ve+ve-ve-ve-ve+veMod -ve)
30 What is the function of the Basal Ganglia? Slow postural adjustments? - BG damage can cause postural disturbancesInitiating movements? - BG patients can struggle to start movementsGate Keeper / Brake Regulator (e.g. Gazzaniga et al.)?BG acts in a regulatory way to facilitate desired voluntary movements and inhibit unwanted, often reflexive, movementsThe direct route enables the preferred actionThe indirect route suppresses unwanted movementsActivity in the BG increases in anticipation of an intended movementGate Keeper or Brake Regulator?
31X +ve -ve -ve -ve +ve -ve Fixed by removal of STN 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 movementAkinesia illustrates intentional aspect of BG function+ve-ve-ve-ve+veX-veFixed by removal of STNRemember the role of the GPi is inhibitory
32X +ve -ve -ve +ve -ve Remember the role of the GPi is inhibitory 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 limbsA related disorder is hemiballismus, flailing movements of one arm and leg, which is caused by damage (i.e., stroke) to the subthalamic nucleus.+ve-veX-ve+ve-veRemember the role of the GPi is inhibitory
33Apraxia What is apraxia? Apraxia has an exclusionary definition: It is a disorder of skilled movement that cannot be attributed to basic level sensory, motor or cognitive disturbancesIt is therefore a disorder of high-level perceptual, cognitive and/or motor systemsWhat is apraxia?ApraxiaAction system Three component approach1. Perceptual processes vision, proprioception, haptics, vestibular, auditory2. Cognitive processes attention, semantic memory, decision-making, response selection, motor representations3. Motor processes convert movement plan into motor response, control muscle activation
36Brain areas involved Primary (Arcuate Motor Fasciculus) SMA cortex (Broca’s area)PrimaryauditoryortexPrimaryVisualcortexAngular gyrus(Wernicke’s area)
37Main types of ApraxiaIdeational apraxiainability to produce a coherent action sequence - Kimura BoxImpairment in the concept of an actionability to imitate gestures / produce movements on command sparedThought 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))
38Ideomotor 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.
39Ideomotor 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)Most characteristic are spatial errorsPostural (e.g. wrong grip)Spatial orientation (e.g. not cutting in one plane)Spatial movement(e.g screwdriver shoulder not wrist)Impairment in knowing how,rather than what to do
402 forms of ideomotor apraxia (Heilman and Rothi, 1993) Loss of praxicons in supramarginal or angular gyrusPerform poorly to command, cannot comprehend gestures2. Disconnection of praxicons from premotor and motor areas (caused by lesions anterior to SMG/AG.AGSMAPraxicon = stored spatiomotor gesture representations which provide the ‘‘time-space-form picture of the movement’’ (Liepmann & Maas, 1907)a ‘movement formula’ if you likeBut, Ochipa et al (1990)Patient could comprehendPanto and panto to command, but not imitate transitive gesturesPraxicons stored in dominant inferior parietal lobe
41} Output praxicon 2 route model SMG/AG Auditory Analysis Semantics (learnt actions)}SMG/AGAuditory AnalysisAuditory/verbal input(command)Innervatory patterns(motor plan)(SMA)Visual AnalysisVisual input(gesture or object)Input praxiconMotor sytemslexicalrouteDirectNon-lexicalAny of above can still imitate meaningful and meaningless gesturesInput praxicon unable to recognise/comprehend gestures, but can do so to verbal commandBetween input and output praxicon able to recognise, but not produce object gestures, but can do so to verbal commandOutput praxicon can recognise/comprehend, but can’t produceDirect route can do meaningful gestures only
42Quick reviewDamage to:Input praxicon unable to recognise/comprehend gestures, but can do so to verbal commandBetween input and able to recognise, but not produce objectoutput praxicon gestures, but can do so to verbal commandOutput praxicon can recognise/comprehend, but can’t produceAny of above can still imitate meaningful and meaningless gesturesDirect route can do meaningful gestures only
43} Output praxicon 2 route model SMG/AG Auditory Analysis Semantics (learnt actions)}SMG/AGAuditory AnalysisAuditory/verbal input(command)Innervatory patterns(motor plan)(SMA)Visual AnalysisVisual input(gesture or object)Input praxiconMotor sytemslexicalrouteDirectNon-lexicalProblem is when a patient can do meaningless imitation, but not meaningful imitation(MF (Bartolo, 2001))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
44Lexical routeDirect routeIn PPCBuxbaum 2000Dynamic 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.
45A closer look at Patient BG: gestures nearly normally with tool in handAnd recognises gestures quite well gesture representations can be accessed by visual inputmore 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 imitationoutput praxicon damaged?difficulty in matching gestures (but not objects),especially when a spatial transformation is requireddeficient processes not conceptual or visual,but spatiomotor
461. 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?One possibility is dual lesions to both lexical and direct routemore parsimonious explanation:BG’s pattern reflects damage to a unitary set of procedures or representations common to both lexical and direct routes(Buxbaum, 2000).
47Apraxia summary2 main types of apraxia2-route model explains most functional characteristics of ideomotor apraxia are covered by the 2-route model, butCannot 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)