Presentation on theme: "Week 6 Motor Control (Dr Roger Newport) uCorticospinal Damage Hemiparesis u Cerebellar Damage Ataxia Timing Issues Motor Learning uBasal Ganglia Damage."— Presentation transcript:
Week 6 Motor Control (Dr Roger Newport) uCorticospinal Damage Hemiparesis u Cerebellar Damage Ataxia Timing Issues Motor Learning uBasal Ganglia Damage Parkinsons Disease Huntingdons Chorea uCortical Damage Apraxia
Corticospinal Damage Hemiparesis and Hemiplegia Definitions Hemiplegia: Paralysis Hemiparesis: Weakness The most common and obvious sign of stroke, but can be caused by a variety of reasons including: tumours Infection (e.g. meningitis / encephalitis) Metabolic imbalance congenital disorders Always as a result of damage to the corticospinal tract
Corticospinal Tract Originates in Primary Motor Cortex and neighboring regions Passes through Corona Radiata Internal Capsule Cerebral Peduncles Pons Pyramids Crosses in the Pyramidal Decussation Forms Anterior and Lateral Corticospinal tracts
Doctor, Ive had a stroke but you cant afford to give me a scan Can we tell where my lesion is? Yes, if we follow a few 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 no facial weakness Decussation Midbrain Pons Medulla Facial nuclei To right limbsTo left limbs From Right Cortex From Left 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 Uncrossed Corticobulbar fibre To Upper Facial Muscles To Lower Facial Muscles Facialnerve fibres Crossed corticobulbar fibre X &UnX input UnX input only L CortexR 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 pons How do I know? Because I have have crossed hemiparesis Decussation Midbrain Pons Medulla Facial nuclei To right limbsTo left limbs From Right Cortex From Left Cortex SC To the R 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 its 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 cortex How do I know? Doctor, my lesion is in my cortex How do I know? Because I have uneven arm and leg weakness and show cortical signs X But what if the brainstem and pons have been ruled out and there are no cortical signs? Remaining Candidates: Internal capsule Corona 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. To LMN Brainstem 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. To LMN Brainstem Reticular formation X Brainstem 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 reflexBabinski extensor reflex Up Fanning toes }
Doctor, my lesion is in my internal capsule How do I know? Because I have equal arm and leg weakness and show the Babinski sign Doctor, my lesion is in my internal capsule How do I know? cortex C.R. I.C. To LMN Brainstem Reticular formation X X X
Facial Weakness? Spinal cord No Yes FW same side as limb W? Pons No Internal Capsule Yes Leg and arm equal? No Cortical signs? Ipsilateral damage Contralateral damage 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, youll have to go through the thalamus Much more. Major components of the motor system Transforming sensory input into plans for voluntary movement Initiating 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: Balance Coordinating movement Timing of movements Timing of discontinuous movements Motor learning - acquiring and maintaining Sources of cerebellar injuries Toxins (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
Postural instability e.g. fall to ipsilesional side Truncal ataxia Postural control and adjustment e.g. Romberg sign Gait ataxia Extensor rigidity Nystagmus Eye deviation if unilateral Cerebellar Ataxia Midline effects }
Cerebellar Ataxia Hemispheric effects Asynergia Decomposition of movement Dysarthia Jerky speech pattern Dysmetria inability to stop a movement at desired point Dysdiadochokinesia inability to perform rapidly alternating movements Hypotonia decreased muscle tone, pendular knee jerk Intention Tremor usually 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 Timing Cerebellum 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 Hz 25 ms Pacemaker 10 pulses = 250 ms 20 pulses = 500 ms 30 pulses = 750 ms Clock counter model Pacemaker produces output to counter Longer intervals represented by more pacemaker outputs in counter 250 ms500 ms750 ms Interval model Different intervals represented by distinct elements Each 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 controlled by the cerebellum.
The 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 Prisms Prisms On Prisms Off Example data
CORTEX Inferior Olive Spinal Cord Cerebellum Corticospinal Tract Error Correction Feedback from actual movement Spino- cerebellar Tract The Feedback Circuit: One theory of how the cerebellum might correct movement
The basal ganglia a collection of nuclei deep in the white matter of the cerebral cortex. They include: Caudate Putamen globus pallidus substantia nigra subthalamic 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 Theres more: Direct and indirect loops. Direct Route Striatum - GPi - Th - cortex Indirect Route detours via GPe and SN. The release of dopamine stimulates D and inhibits InD routes -ve +ve -ve +ve Mod -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 action The 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 rest Rigidity (+ve) due to simultaneous contraction of flexors an extensors Bradykinesia (ive) difficulty initiating voluntary movement Akinesia illustrates intentional aspect of BG function -ve +ve -ve +ve X Remember the role of the GPi is inhibitory -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 -ve X +ve
Action system Action system Three component approach Three component approach 1. Perceptual processes vision, proprioception, haptics, vestibular, auditory vision, proprioception, haptics, vestibular, auditory 2. Cognitive processes attention, semantic memory, decision-making, response selection, motor representations attention, semantic memory, decision-making, response selection, motor representations 3. Motor processes convert movement plan into motor response, control muscle activation convert movement plan into motor response, control muscle activation Apraxia has an exclusionary definition: It is a disorder of skilled movement that cannot be attributed to basic level sensory, motor or cognitive disturbances It is therefore a disorder of high-level perceptual, cognitive and/or motor systems What is apraxia? Apraxia
Some basic tests for apraxia
But watch out for confounds
SMA Primary Motor cortex Primary Visual cortex (Brocas area) Primary auditory ortex (Wernickes area) Angular gyrus (Arcuate Fasciculus) Brain areas involved
Main types of Apraxia Ideational apraxia inability to produce a coherent action sequence - Kimura Box Impairment in the concept of an action ability 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 apraxia Impairment in the performance of skilled pantomime movements on verbal command or in imitation most 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 deficient ability to use them appropriately or to imitate actions.
Ideomotor apraxia (cont.) Can be ok with ipsilesional limb Have greatest difficulty when imitating transitive movements (tool use) Several types of errors Use 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 errors 1.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 gyrus Perform 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 comprehend Panto and panto to command, but not imitate transitive gestures AG SMA
Direct Non-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 lexical route 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 cant produce Any of above can still imitate meaningful and meaningless gestures Direct route can do meaningful gestures only
Input praxiconunable to recognise/comprehend gestures, but can do so to verbal command Between input andable to recognise, but not produce object output praxicon gestures, but can do so to verbal command Output praxiconcan recognise/comprehend, but cant produce Any of above can still imitate meaningful and meaningless gestures Direct routecan do meaningful gestures only Quick review Damage to:
Direct Non-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 lexical route 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 route In PPC
A closer look at Patient BG: gestures nearly normally with tool in hand And recognises gestures quite well gesture representations can be accessed by visual input more deficient in imitating meaningless gesture-like movements than 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 required deficient processes not conceptual or visual,but spatiomotor
more parsimonious explanation: BGs 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 BGs 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)