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control of movement by the CNS - motor neurons found in anterior horns medial column - trunk, lateral column - proximal then distal limbs - motor unit = motoneuron + all the muscle fibres it innervates - 3 types of muscle fibres slow oxidative - slow twitch, low force, lots of myoglobin/mitochondria, non-fatiguing fast oxidative/glycolytic - moderate twitch, force, etc... fatigues slowly (minutes) fast glycolytic - fast twitch, large force, little myoglob / mito, fatigues quickly (<1 min) - the faster the fibre, the larger diameter of the motoneuron that innervates it smaller neurons more easily excited by summated EPSPs slow motor units recruited by low levels of synaptic input fast motor units recruited by high levels of excitatory synaptic input - one action potential –> one twitch (100-300 ms) for effective action, need summation of twitches summation of twitches = tetanic contraction (6-10 imp/s or more) maximal summation (maximal force output) = fused tetanus (30-40 imp/s) all this happens because APs are coming so fast Ca can’t be sequestered - motor units, when first recruited, fire at 6-10 imp/s fire at faster rates only in brief bursts to increase speed of contraction - Renshaw cells inhibitory glycinergic interneurons adjacent to motor nuclei excited by collateral branches of motoneuron axons (cholinergic input) provide inhibitory feedback to limit discharge rates to below 35-40 imp/s - gamma motoneurons smallest motoneurons, easy to excite, innervate muscle spindle intrafusal fibres adjust sensitivity of muscle spindle, modifying perception of stretch - alpha motoneurons larger motoneurons, innervate extrafusal work-producing fibres - recruitment first gamma, then slow, then fast to increase force: increase m.u. discharge rates, or recruit more (and faster) m.u.’s - motoneuron bistability when strongly excited, maintain memb. pot. just below threshold decays to normal after about 40 s. useful in maintaining tonic contraction (eg. postural muscles) - length-tension relationship maximum tetanic tension produced at a particular muscle length this corresponds to length where actin and myosin can form the most cross-bridges longer or shorter lengths produces progressively weaker contractions - physiological tremor roughly 10Hz fine tremor observable in outstretched fingers synchronous discharge in newly recruited motor units (firing at 10 imp/s) greater tremor with greater synchrony of discharge - cortical myoclonus uncontrolled twitching and jerking of limb muscles drive comes from hyperexcitable cortex (genetic or post-ischemic) spinal reflexes - stretch reflex stimulus: passive stretch by load or antagonist muscle response: active contraction of muscle sensory organ: muscle spindle (inside capsule, wrapped around intrafusal fibres) afferents: Ia - big, fast, sensitive to changes in stretch II - smaller, slower, sensitive to static stretch function: postural stabilization, suppressed during movement - Golgi tendon reflex stimulus: excessive force in tendon (active tension in muscle) response: relaxation of muscle sensory organ: Golgi tendon organ - distorted by force of active contraction afferents: Ib - slightly slower than Ia, slowly-adapting, synapse on interneurons in intermediate zone, which inhibit alpha-motoneurons of same muscle function: prevent movement, control tension, suppressed during movement? - flexion withdrawal reflex stimulus: noxious injury of limb response: flex joints proximal to stimulus, extend distal joints sensory organ: ? afferents: A, C nociceptor - small diameter, slow, multisynaptic path (interneurons), commissural interneurons carry signal for contralateral extension function: avoid bad things - reciprocal inhibition basic property of intermediate zone eg. activation of flexors elicits inhibition of extensors suppressed when co-contraction is desired (ie. for joint stiffness) - Babinski sign extensor thrust reflex (in foot) influenced by corticospinal tract if this is damaged, reflex pattern switched to flexion withdrawal - presynaptic inhibition main mechanism for regulating and switching reflex afferents when one route to a motor nucleus is inhibited, another can be disinhibited acts via... glycine or GABA or depolarization? - reflex adaptation can be rerouted via a different pathway (eg. Babinski) can adjust gain (output per unit input) - Hoffman reflex peripheral nerves have both afferent and efferent fibres stimulate one nerve, get two muscle responses faster M-wave due to stimulation of motor neuron slower H-wave due to stimulation of Ia afferents (reflex arc) for an increasing stimulus, get H-wave first (25V) then M-wave (40V) further increase, M-wave increases but H-wave decreases (60-90V) due to: refractory motoneurons, Renshaw inhibition, more Ib inhibition? orthodromic activity in sensory neuron collides with antidromic activity in motoneuron posture - types of postural activity tonic maintenance of ‘antigravity’ body configuration stabilization during movement - skeletal support, mechanical, centre of gravity shift (every limb movement requires ‘anticipatory postural adjustment’ in rest of body) - postural maintenance organized in reticular formation (pons and medulla) 3 sensory sources: somatosensory (esp. proprioceptive), vestibular, visual - proprioceptive reflexes stretch and tendon reflexes stabilize joints, but narrow operating range large perturbation -> ‘automatic postural reaction’ (programmed response, not reflex) eg. decerebrate cate with labyrinths removed (head up -> sit, head down -> crouch) - vestibulospinal reflex stimulus: downward deviation of head to one side response: ‘downhill’ limbs extend afferents: otolith afferents -> lateral vestibulospinal tract -> ipsilateral extensors function: maintain upright posture - vestibulocollic reflex afferents: semicircular canal and otolith afferents to vestibular nucleus efferents: medial vestibular nuclei -> neck motor nuclei function: stabilize head w.r.t. trunk (eg. while walking) - vestibulo-ocular reflex stimulus: head rotation response: compensatory eye movement afferents: semicircular canal afferents efferents: superior vestibular nucleus -> MLF -> extraocular muscles - visual postural reflexes low effect, operates at low frequencies (<0.3 Hz)? complement to vestibular reflexes which respond to higher frequencies align body axis with visual perception of vertical - automatic postural reaction centrally programmed response to restore grossly perturbed centre of gravity subjugates local reflexes, coordinates action across entire body organized within reticular formation of medulla and pons - sensory substitutions closing eyes doubles postural sway, compensated by lightly touching stable surface visual and somatosensory inputs constantly reweighted according to congruence with vestibular (gravitational) reference persistant visual / vestibular incongruence can lead to motion sickness - red nucleus midbrain centre for discrete distal synergies, not part of posture / locomotion rubrospinal tract projects to contralateral intermediate zone and motor nuclei probably responsible for most basic hand movements in humans - synergy group of muscles contracting together for a specific purpose reticulospinal synergies are very widespread (eg. for support postures) rubrospinal (and corticospinal) synergies are highly localized - decerebrate rigidity brainstem transection b/w vestibular complex and red nucleus net increase in reticulospinal activity -> extensor stretch reflexes facilitated higher centres (red nucleus, motor cortex) normally suppress postural drive - reticular activating system cholinergic - control of posture and goal-directed movements controls corical excitability - EEG changes affective changes to sensory stimuli esp. pain - changes in sleep/wake cycle motor control of ‘vital reflexes’: circulation, respiration, swallow, cough - brainstem stroke contralateral involvement of body, ipsilateral involvement of face medial medullary syndrome: ipsilateral paresis, atrophy and fibrillation of tongue, contralateral hemiplegia sparing the face, contralateral loss of position and vibration central pattern generator - reflexes vs. central pattern generation opposing reflexes can create alternating action through sensory feedback eg. 1914 “Reciprocal inhibition underlies rhythmic behaviour of walking -- sensory basis of reflexes underlies rhythmic movements” CPG creates ocillation without sensory feedback eg. 1960's - deafferented locust flight produces fictive motor patterns in the absence of all sensory input - effects of deafferentation on locust flight cycle frequency decreases due to increased depressor-elevator interval - CPG behaviour depends on intrinsic membrane properties of cells endogenous bursting cells - timing inputs plateau potential cells (start with depol, stop with hyperpol) - memory, tonic drive postinhibitory rebound - synchronize CPGs spike freq. adaptation during constant depol. - mechanisms of rhythm generation pacemaker - eg. vertebrate breathing reciprocal inhibition / half-centre oscillators - eg. lamprey swimming not just network wiring, but also different properties of individual cells types of coupling: pacemaker/follower vs. reciprocal inhibition - lamprey locomotor network E-interneurons excite all ipsi I, L, M neurons I- interneurons inhibit all contra I, L, M neurons stretch receptors (SR) excite ipsi and inhibit contra reticulospinal (RS) neurons receive all sensory and higher input, excite all spinal stuff - sensory control of CPG adaption to imposed movements sensory (stretch) input matches CPG rate to rate of imposed movements - spike frequency regulation large slow afterhyperpolarization (sAHP) means fewer spikes in burst Ca dependent K channels cause sAHP and terminate NMDA plateau potentials many factors determine burst onset and end: NMDAR, low voltage Ca channels stretch receptors start (excitatory) and stop (inhibitory) the burst synaptic excitation from excitatory neurons (ie. reticulospinal neurons?) - visuo-vestibular control of lamprey “roll-control” like extensor motor reflex vestibular input excites contra eyes and ipsi reticulospinal neurons response is corrected motor roll - synaptic modulation postsynaptic metabotropic glutamate receptors mediate RS –> increased freq of CPG postsynaptic Group I do that... presynaptic Group II and III can inhibit glu release - vertebrate models of CPGs spinal cord much more complex CPG involved in locomotion, breathing, etc. half-centre organization found in cat spinal cord human central CPG - maybe involving STN and GP (eg. Parkinsonian tremor) - significance of all this spinal cord recovery may benefit from activation of CPGs below lesion site electrical stim, pharm. tx, weight-bearing treadmill training... can enhance recovery cortical motor control - motor cortex large layer 5 pyramidal cells (Betz cells) project via corticospinal/bulbar tracts direct synapses on motoneurons mostly to distal limb and speech motor nuclei premotor (area 6), motor (area 4), posterior parietal (areas 5 and 7) somatotopic organization... regional ‘concentric’ plan around distal foci (fingers, toes) - distal-axial gradient distal muscles tend to be deep in central sulcus while axial closer to premotor cortex - multiple representation single motor nuclei represented by columns of neurons at many loci each cortial locus represents a different synergy muscles participating in the most synergies have biggest representation - cortical column functional unit of cortex about 1mm across, goes through all layers stimulation anywhere in column gives same motor response - motor cortex maps synergies cells in one column may fire when muscle is active in a specific movement (synergy) same cells may be silent when same muscle participates in a different movement not necessary to represent every possible muscle synergy finite set of cardinal synergies, which can be combined and weighted - coding direction of reach many cortical columns contribute to generation of reach each will be active for reaches over a range of directions one direction coded by ratio of activity across the pop. of neurons (population coding) - somatosensory inputs only sensory input with direct access to motor cortex cutaneous input from somatosensory association areas, related to posture and motion proprioceptive input direct from thalamus (and form somatic assoc. cortex) - transcortical reflexes stretch reflex - same as spinal reflex but longer latency and more modifiable proprioceptive signals from one muscle trigger contractions in others helps to syncronize actions at several joints eg. grasp reflex slipping object in fingers activates mechanoreceptors direction of slip computed in somatosensory association areas increased finger tension triggered in motor cortex - stroke eg. cerebrovascular infarct deep in white matter or interal capsule both corticobulbar and corticospinal tracts damaged corticospinal - muscle weakness or paresis corticobulbar - spasticity - spasticity hyperactive spinal stretch reflexes (velocity sensitive) excessive resistance to passive stretch of muscles - premotor areas set of regions projecting into motor cortex, but also to brainstem and spinal cord select motor cortical synergies in proper sequence preparatory role: coordinate postural support and focal limb movements - postural integration every cortical movement must be supported by ‘anticipatory postural adjustments’ postural programs in brainstem reticular formation are activated or suppressed by premotor cortex, in parallel with motor cortical activation - preparatory activity related to ‘working memory’.. premotor neurons often inactive during actual movement active during prep: selecting appropriate cortical and postural synergies - motor field one corticospinal axon synapses with a set of motor nuclei (>1 spinal segment) set of muscles influenced constitutes the motor field weighting of synaptic strength: some nuclei influenced more than others (some silent) - cortical plasticity representation fo muscles in motor cortex changes with use sustained vigorous activity in one column leads to expansion into adjacent territory sustained somatosensory inputs to motor cortex increase their synaptic influence (long-term potentiation) - premotor areas cingulate motor area (CMA): 2 representations of body within cingulate sulcus supplementary motor area (SMA) premotor cortex: dorsal and ventral parts Broca’s area: ventral premotor cortex in left hemisphere - supplementary motor area (SMA) on medial wall of hemisphere somatotopic representation of body, less detail than motor cortex processes internal ‘volitional’ signals that drive movements controls bilateral coordination of limbs when diff. motions done on each side - cingulate motor area (CMA) gross somatotopic representation within cingulate sulcus processes emotional and motivational drive to movements ‘limbic motor center’, important in many epileptic seizures also contributes to corticospinal tract - lateral-medial differences medial premotor zones (SMA, CMA) process internal, volitional drives to move lateral premotor zones process sensory drives to move (learned sensory cues) eg. door knob, sound of boss’ footsteps, etc each premotor locus processes different kinds fo information - premotor cortex processes sensory inputs, esp. visual and auditory, for cueing movement phases activates cortical synergies in proper sequence many loci in premotor cortex project to same motor cortical synergies dorsal vs. ventral portion? - ventral premotor cortex Broca’s areas - organizes sequences of phonemes for speech, hand movement sequences fo writing ‘mirror neurons’ found in this zone stroke here may result in aphasia - can’t synthesize grammatical/coherent phrases input from Wernicke’s area - mirror neurons elicit specific movement in motor cortex eg. hand gesture receive parietal postural info and temporal lobe visual discrimination of the gesture neuron activated by the sight of someone else performing the gesture - reach and grasp frontal motor areas need to know: current position of arm and hand location of target object relative to hand shape and orientation of object all this comes from neurons in parietal and temporal lobes parietal lesion: misdirection of arm, lack of hand pre-shaping - parietal cortex representation of body image, specific limb posture (eg. hand configuration) in post. parietal lobe, neurons either respond to spatial location of targets w.r.t hand, or to shape of objects that match a specific hand posture needed for spatial guidance, hand shaping - lateralization R side parietal lesion can result in left-sided hemineglect L side lesion can cause ideomotor apraxia (problem with purposeful movements) - due to disruption of path b/w ideation centre and motor centre (memories for skilled movements found in left angular gyrus) left frontal (Broca’s) area for speech, right side for prosody (rhythm and tone) - alien hand syndrome lesion in medial premotor/prefrontal region loss of volitional inhibitory control over sensorimotor loops in lateral frontal lobe sensory drives free to elicit movements without willed ‘permission’ cerebellum - role in motor system not essential... agenesis -> delayed motor devel, perpetual clumsiness cerebellum is ‘conductor’ of motor system, doesn’t generate any actual movements - structure cortex - receives most of input nuclei - provide excitatory output to motor centres cortex inhibits deep nuclei via Purkinje cells (GABA) - cortex (input) 3 layers: granular, Purkinje, molecular granule cells receive input from mossy fibres (spinal cord, brainstem, cortex, sensory (dynamic), and motor signals) each input projects to a region, but lots of overlap and mixing project axons up to molecular region, then form parallel fibres to interact /w Purkinje Purkinje cells in middle layer inhibit deep cerebellar nuclei (GABA) dendritic tree flattened like an outstretched hand (looks like a bush in parasagittal plane, twig in coronal plane) each parasagittal band of Purkinje cells activated by specific coincidence of inputs - cerebellar nuclei spontaneously active, tonically excited all motor centres (brainstem and thalamic) fastigial nucleus - posture and locomotion (brainstem) interposed nuclei - reach and grasp (red nucleus and motor cortex) dentate nucleus - fine skills (writing, speech, etc.) - regulating the CPGs a cluster of Purkinje cells activated at specific instant in motor performance they inhibit a targe zone in the cerebellar nuclei target sensorimotor area is disfacilitated, bringing some action to precise ending - cerebellar dysfunction motor elements drag on, can’t stop at precise phase in movement ataxia - movements not balanced or coordinated dysmetria - movements overshoot target adiodokokinesis - can’t make fast transitions between opposing motions - motor adaptation when set of Purkinje cells is overactive, climbing fibre system discharges direct powerful depolarization of Purkinje followed by inhibition therefore increased vacilitation by cerebellar nuclei of targe sensorimotor areas climbing fibres cause long-term depression of parallel fibre-Purkinje synapses - inferior olive lesion loss of abilit to adapt motor programs to new conditions eg. throwing darts while wearing eye prism -> displacement error continues indicates that parietal cortex can’t perform visuomotor recalibration w/o cerebellum basal ganglia - regulates flow of ‘volitional’ drive to premotor centres - 2 tiers of nuclei striatum - caudate, putatmen, nucleus accumbens pallidum - globus pallidus (internal) and substantia nigra (pars reticulata) - striatum (input tier) excitatory input (glutamate) from cerebral cortex and centeromedian thalamus topographic projection from cortex: motor cortex -> putamen prefrontal/parietal -> caudate limbic cortex -> n. accumbens thalamus conveys reticular formation input - pallidum (output tier) tonically inhibits (GABA) premotor centers resting discharge rate of 70-90 imp/s premotor centres activated by disinhibition - forms a reiterative loop cortex -> striatum -> pallidum -> thalamus -> premotor cortex -> cortex - direct pathway (GO) striatum inhibits pallidum removes inhibition from thalamus, permits motor activity - indirect pathway (STOP) striatum inhibits GPe, which inhibits STN STN excites pallidal output, which inhibits thalamus and prevents motor activity - direct / indirect antagonism focusing - paths act on different cells adjusting speed or force - paths act on same cell - striatal modulation substantia nigra (SNc) dopaminergic neurons project to striatum striatum chooses motor act, guided by cortical and reticular inputs - dopamine and plasticity dopaminergic neurons respond preferentially to reward-related stimuli necessary for synaptic plasticity in striatum (motivational component) - Parkinson’s disease loss of dopaminergic neurons in substantia nigra and VTA ? also loss of noradrenergic neurons in locus ceruleus also loss of cholinergic neurons in pedunculopontine nucleus symptoms: akinesia, bradykinesia, tremor, cogwheel rigidity, postural instability too much STOP, not enough GO - automatic routines automatic chaining of motor elements into a habitual routine is lost in PD each element in the sequence msut be individually commanded replacing lost internal cues with external stimuli can help (eg. stripes on floor) - Huntington’s disease genetic disorder, chr 4, huntingtin >40 CAGs loss of striatal neurons in indirect (STOP) pathway unopposed GO pathway, excessive movement triggered in premotor centres chronic involuntary movement of limbs, face and mouth (chorea) - hemiballismus discrete lesion in subthalamic nucleus disinhibition of pallidum, spontaneous proximal limb movements - dystonia sustained muscle activity producing abnormal posture focal, segmental or generalized combination of dysfunction in basal ganglia and in cortex focal can be use-dependent - eg. musicians and writeres can sometimes stop with sensory stimulus - geste antagonistique - pedunculopontine nucleus glutamatergic neurons (mesencephalic locomotor centre) receive pallidal output cholinergic neurons part of reticular activating system, up to 50% loss in PD dysfunction in PPN may be responsible for rigidity in PD