--- module: 028-02 language: en chapter: 28 title: "Motor Control, Reflexes, Cerebellum, and Basal Nuclei" module_title: "Motor-unit physiology, lesion localisation, and adaptive movement control" source_sha256: 943f8611c7bc27cedfb339141998be98e378cd76173517f8163481a45ff1a11a --- # Motor units, localisation, and adaptive control ## Hierarchical force recruitment ### Units differ in size, speed, fatigue, threshold ### Size principle: small fatigue-resistant first #### Smooth economical output, reserve preserved ### Rate coding fuses twitches ### Fatigue: more units and drive, more effort ### Surface EMG records summed activity, not force ### Needle examination samples single units #### Denervation gives fibrillation potentials #### Reinnervation gives larger longer units ## Neuromuscular safety margin ### Each impulse releases surplus acetylcholine ### Postsynaptic receptor loss: fatigable weakness ### Presynaptic failure may improve with repetition #### Calcium accumulates with activation ### Myasthenia: ocular, bulbar, neck, proximal #### Sensation and pupils spared #### Respiratory and swallowing crises ### Botulinum toxin blocks acetylcholine release #### Local use for dystonia and spasticity ## Localising weakness ### Upper motor neuron: pyramidal pattern #### Acute lesions may show low tone first ### Lower motor neuron: root, plexus, nerve pattern #### Root lesions add radicular pain ### Junction disease: fatigability, no early atrophy ### Myopathy: symmetric proximal weakness ### Functional weakness: positive inconsistency #### Genuine, treatable, uses preserved pathways ## Tone and reflex physiology ### Tone: mechanics, activation, reflex gain, state ### Spasticity rises with velocity and direction ### Rigidity uniform, smooth or ratcheting ### Paratonia varies with attention ### Hyperreflexia: raised gain, not strong muscle ### Clonus: self-sustaining stretch cycle ### Reinforcement can reveal a present reflex ### Asymmetry with weakness localises ## Spinal networks and pattern generation ### Withdrawal recruits by stimulus location ### Reflex effects are task dependent ### Pattern generators need supraspinal start #### Load, hip position, skin input adapt gait ### Cord lesion: segmental at, long-tract below ### Hemicord: ipsilateral motor, contralateral pain ### Central cervical lesion: arms more than legs ## Cerebellar prediction and error ### Compares command copy with feedback ### Feed-forward learning outruns slow feedback ### Climbing fibres teach, mossy fibres give context ### Plasticity updates internal models ### Signs worsen near the target #### Predictive braking and scaling fail #### Dysmetria, decomposition, intention tremor ### Midline: stance, trunk, gait ### Drugs, stroke, immune, nutritional causes ## Basal-ganglia selection and reinforcement ### Output tonically inhibits thalamus, brainstem ### Selection releases desired, holds competitors ### Hyperdirect pathway speeds global stopping ### Dopamine loss slows initiation and scaling #### Strength retained, starting impaired #### External cues bypass automatic control ### Bradykinesia decrements with repetition ### Levodopa fluctuates as buffering declines ### Deep-brain stimulation does not cure ### Phenomenology determines cause and treatment ## Posture, gait, and dual-task reserve ### Balance integrates many systems ### Compensation fails in dark or on uneven ground #### Recreate fall conditions safely ### Gait begins with weight shift ### Freezing at doorways, turns, competing demands ### Dual-task slowing predicts reduced reserve ### Devices help only when fitted and used ## Rehabilitation and adaptive control ### Restitution, compensation, prevention, adaptation ### Careless repetition is insufficient ### Error size must be tolerable #### Too little: no teaching signal #### Too much: fear and compensatory habits ### Variable practice improves transfer ### Rest and sleep consolidate learning ### Spasticity treatment targets specific goals ### Formulation beyond a single strength grade