Higher motor control

Higher motor control

1. Task of motor system: Visual info, proprioceptive feedback from limbs & postural adjustments= What? Where? How?

   • Hypokinetic disorders of BG= parkinsons= conscious of difficulty of getting them started.
   • Lesion in cerebellum: distances misjudged and trajectory incorrect- hand to be guided.

2. Cerebellum

   • Cerebellar neurones & connections
     • Deep nuclei: 4 are presented, fastigal to vestibular nuclei, interpositus to red nucleus & dentate to thalamas and cerebral cortex.
     • Climbing fibres: unique single fibre= ivy branch= release aspartate= excitatory- DN. Come from IO. Also excite deep nuclei. Fire infrequently. complex spike= signal to whole tree.
     • Mossy fibres: Lower layers of cortex-large terminal structures, synapse in glomeruli with granule cells- bifurcate & send parallel fibres in opposite directions.
     • Carry info: directly: muscle spindles Indirectly: visual, spinal & auditory afferents via precerebellar nuclei. >Parallel fibres excite other interneurons causing lateral inhibition.
     • Purkinje cell- huge dendritic tree, 15million. Output of cortex, inhib output to DN. Active at rest. Input for 1/2mill parallel.
   • Higher hierarchical level: Refine actions; spinocerebellum & larger part neocerebellum (cortico). neuronal crystal structure.
   • Cerebellar circuit: 1 set of inputs: the climbing fibres (extraordinarily precise) and second system: mossy fibres; equally abundant, diffuse & non-specific.
     • Cerebellum learns but teaches as well: modify the behaviour of circuits in brainstem. -Error decorrelation: predict the retinal slip
   • Cerebellar damage: vestibulocerebellum: difficulties postural corrdination. Spinocerebellum: impaired gait. Cerebrocerebellum: defects in initiation.
     • -Cerebellar ataxia: movements jerky. -Dysynergia: no synergistic multijoint movement. -Dysmetria: inaccuracy in range and direction of joints. >Injury: slow & uncoordinated.

3. Primary motor cortex

   • Two thalamic nuclei: ventrolateral: projects to 1o cortex & ventroanterior: projects to premotor area.
   • Ascending input: comes from BG, cerebellum & reticular formation & project to centromedial nucleus. Output: corticospinal tract, travel to cord indirectly via red nucleus, colliculus & Rf. Mainly to BG & cerebellum, (via relays in pons and inferior olive). Indirect routes termed extrapyramidal path.
   • Cortical influence on SC: big cells in layer V= Betz cells- descend into corticospinal tract (30% extraP) and corticobulbar. Lesions: paresis & loss of skilled movements- in extremities- flaccid paralysis (motor).
   • Jacksonian epilepsy= twitching start at one location (finger) and progress inwards (arm); epileptic focus on one cortical region can spread.

4. Basal Ganglia

   • Corpus striatum; lies in mesencephalon; globus pallidus, putamen, caudate nucleus= striatum.
   • Connections: sn pars reticulata VA and VL areas of thalamus and to the motor cortex. 2nd output route from SNpr: to superioir colliculus. Striato-pallidal & striato-nigral: GABAergic & dendritic spines = glutamate secreting fibres from cortex. 5-HT from raphe nucleus, endings releasing SP & inhib cholinergic from interneurons. Main pathways: send to corpus striatum, and limbic via nucleus accumbens. > striosomes (spiny neurones)= project to SNpc.
     • Final inhib output= SNpr & GPi= fire tonically act via disinhibition
   • Parkinsons: damage to DA pathway linking SN & putamen.
     • -Akinesia: absence of expressive movements. Strong emotional stimulus- normal movements made. -Difficulty in initiating movements. -Bradykinesia: rigidity & slowness. -Hypokinetic disorder, rise to ballismus= limbs thrown violently.
     • -Treat? manipulate dysfunctional neural pathway: atrophy of SN & DA deficiency= excitation of GPi by subthalamic nucleus GP inhibits thalamus. Underlie paucity of movement and psychomotor retardation. Pallidotomy lifts inhib influence of thalamus, DBS prevents excessive activation of GP. -DOPA precursor for DA; as defect in transmission: SN putamen. Some benefit from DBS.
   • -Hungtingdon: progressive, affected by BG- spontaneous movements- chorea. atheetosis. Inhibitory projection from external GP to subthalamus increased. >Basal ganglia actions: Lesions give defects execution not initiation. disinhibition: movements occur when tonic inhibition removed.

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