Motor Learning and Neurological Syndromes PDF
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Brighton and Sussex Medical School
Dr. J. Ganesalingam
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Summary
These lecture notes cover motor learning and neurological syndromes. The document outlines the hierarchical motor control system, identifies the motor cortex representation, describes the role of the cerebellum and basal ganglia, and recognizes common signs of impairment in the motor control system.
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Motor learning and Neurological syndromes Dr J. Ganesalingam Learning objectives • To outline the hierarchical motor control system • To identify the motor cortex representation • To describe the role of the cerebellum and basal ganglia • To recognise common signs of impairment in the motor contro...
Motor learning and Neurological syndromes Dr J. Ganesalingam Learning objectives • To outline the hierarchical motor control system • To identify the motor cortex representation • To describe the role of the cerebellum and basal ganglia • To recognise common signs of impairment in the motor control system. Contents • • • • • Broad overview of motor control Voluntary descending pathways Involuntary descending pathways Motor cortex representation Brief mention of role of cerebellum and basal ganglia. • Illustrate each with Neurological syndromes Simple motor pathway Upper and Lower motor neuron Hierarchial motor control Cortical motor control centres Actions Brainstem motor control centres Complex movements Central pattern generators Motor interneurons Motor neurons Muscles Simple movements Hierarchial motor control Basal ganglia Thalamus Cerebellum Basal ganglia: Selector of muscle groups Cerebellum: Conductor and comparator Cortical motor control centres Brainstem motor control centres Central pattern generators Actions – intentional movements Complex movements Chewing, eating, walking, standing Motor interneurons Motor neurons Muscles Simple movements Twitching of muscles Types of movements • Passive – Low tone ( Lesion in cerebellum, lower motor neuron) – Cogwheel rigidity (Lesion in Basal ganglia) – Spasticity (Lesion in Corticospinal tracts) • Reflexive – Areflexia, Hyporeflexia (lower motor neuron lesion) – Hypereflexia (upper motor neuron) • Stereotyped – Examples are chewing, swallowing, vomiting, walking, • Self-generated – Volitional – Emotional Reflexive movements Loss of descending inhibition Babinski Reflex -VE A- Normal (flexor) B- Abnormal (extensor) Altered excitability of spinal inhibitory interneurons Brisk reflexes increased tone to rapid passive muscle stretching= spasticity Contrast with damage to motor neuron – reduced tone loss of reflexes muscle wasting (Corticospinal tracts not fully developed until age 2, inhibit spinal extensor response) Descending motor pathways Voluntary voluntary involuntary Tectospinal tract Allows us to direct head and eyes to move to a target that has caught our attention in the visual field – e.g danger, threat. Vestibulospinal tract Useful for guiding head and neck movements to keep the eyes stable as the body is moved. Reticulospinal tract Important in maintaining the posture and balance Descending pathways • Tectospinal and medial vestibulospinal – Control head and neck movements. • Lateral vestibulospinal and reticulospinal – Activate extensor muscles in arms and legs. Stereotypy Locomotive movements Central pattern generators: Rhythmic activation of different muscle groups to generate a desired repetitive movement e.g walking Self-generated movements Emotional Stroke – facial palsy Role of anterior cingulate gyrus A normal smile can be elicited by emotion even when the corticobulbar connections are not in tact (causing UMN CN VII weakness) Self-generated movements Volitional The pyramidal or corticospinal tract Internal Capsule Betz Cells Pyramidal tract derives its name from decussation in medullary pyramids Only cortical tract to directly synapse with motor neurons Predominantly derived from cells in layer V (not exclusively Betz cells) Brodmans Area 4 (and 6) 90% fibres crossed in lateral CST but individual variation may account for different deficits in strokes 90% Corticospinal tracts Rubrospinal tract This is a small and rudimentary pathway in humans responsible for flexion in the upper limbs. This becomes apparent when the corticospinal tract is lesioned. Descending Tracts- Posturing in Coma DECORTICATE POSTURING Lesion above red nucleus DECEREBRATE POSTURING Lesion below red nucleus Damage to motor cortex and corticospinal tract-humans Middle cerebral artery stroke Typical Posturesome preserved upper limb flexion and lower limb extension Increased tone (spasticity), Brisk Reflexes, Extensor Plantar/Babinski reflex, Clonus But patient maintains a posture Motor Homunculus Somatotopic organisation Every part of the body is represented in the primary motor cortex these representations are arranged somatotopically -- the foot is next to the leg which is next to the trunk which is next to the arm and the hand. The amount of brain matter devoted to any particular body part represents the amount of control that the primary motor cortex has over that body part. This disproportionate map of the body in the motor cortex is called the motor homunculus. This map may not be fixed and may be malleable. Eg Parasagittal Meningioma By pressing on foot/leg area of both motor cortices it presents as bilateral leg weakness and spasticity Blood Supply to the Brain And Stroke Syndromes Anterior Cerebral artery Coronal Middle Cerebral artery (MCA) Posterior Cerebral artery Anterior choroidal artery Branch of Internal Carotid, rarely MCA Boundaries subject to anatomical variation and collateral supply Transverse Middle Cerebral artery occlusion LEG HAND FACE Proximal lesion affects internal capsule Complete hemiparesis Distal lesion may spare leg area of motor cortex (though secondary swelling and ischaemia may compromise function) Anterior Cerebral Artery Stroke Supplies medial part of frontal lobes including leg area of motor cortex • Crural (leg) paresis > arm paresis • Frontal signs (eg, abulia) Abulia:- Loss or impairment of the ability to make decisions or act independently Seizure ‘March’ (Jacksonian seizure) Partial onset simple motor seizure becoming secondarily generalised Strongly associated with structural abnormality in or close to motor cortex Posterior Parietal Cortex Area 5- somatosensory afferents Area 7- visual pathway afferents Mental body/ environment image Damage results in neglect (can perceive but do not attend) Exploratory movements Eg turning object in hand (looking and feeling) Perceptual motor dysfunction Visual Auditory somato sensory Hetero modal vestibular Gustatory Motor planning Association cortices Frontal lobe • Prefrontal cortex – Involved in planning and decision making • Premotor area – Involved in sensory guidance of movement and controls the more proximal movements and truncal movements of the body. – Mirror neurons – imitation/learning • Supplementary motor area – Selecting movements based on remembered sequence of movements/complex movements – Bimanual tasks – Imagery Premotor Area (PMA) Importance in control of Visually guided movements Eg orientation of hand in relation to object to be grasped (Prehension) Damage may also causePerseveration of motor activity despite lack of success PMA receives input from the cerebellum and is involved in planning movements based on external (especially visual) cues; it is involved mostly in control of postural and proximal limb muscles. Lesions of PMA disrupt learned responses to visual cues • Simple finger flexion – only M1 activation • Sequence of complex finger movements – M1 + SMA activation ~ • Mental rehearsal of finger movements (Rowland) – only SMA activation ~ The 'Bereitschaftspotential' attributed to activation of the supplementary motor area (SMA) precedes the 'motor potential' of the primary motor cortex (M1) by about 5001000 ms during self-initiated movements. If a simple action like moving our hand is prepared for more than a half second in our brain, at what moment do we consciously decide to perform this action? Intuitively, we feel it is much less that a half second. If this is right, and the preparation of an action begins much earlier as the conscious decision to perform this action, can we have a free will ? In humans:wide interconnections between sensory and motor association areas -damage causes Apraxia Apraxia: Inability to carryout purposeful movements in the absence of paralysis or paresis. Great difficulty in the sequencing and execution of movements. Types of apraxia • Ideational (parietal): unable to report the sequence – Show me how to make a peanut butter sandwich? • Ideomotor (SMA): unable to use the tool – Show me how to hold and use a pair of scissors Aberrant sensory processingTask specific dystonias Repeated and extended use of the hand results in changes in the functional organisation of brain areas related to sensory processing and motor control. Can be altered by ‘sensory tricks’ musician’s dystonia Although the manifestation is motor, the primary abnormality is likely to be disrupted sensory processing probably mediated by the basal ganglia Dystonia- sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions. If only occurs with certain actions, said to be ‘task specific’. writers cramp Hierarchial motor control Basal ganglia Thalamus Cerebellum Basal ganglia: Selector of muscle groups Cerebellum: Conductor and comparator Cortical motor control centres Brainstem motor control centres Central pattern generators Actions – intentional movements Complex movements Chewing, eating, walking, standing Motor interneurons Motor neurons Muscles Simple movements Twitching of muscles Learning objectives • To outline the hierarchial motor control system • To identify the motor cortex representation • To describe the role of the cerebellum and basal ganglia • To recognise common signs of impairment in the motor control system. References Good starting point for extra reading. Neuroscience: Exploring the brain. Bear, Connors, Paradiso