MOTOR FUNCTION
MOTOR CONTROL
Components for motor control: normal postural tone and muscle tone, postural mechanisms, selective movements and coordination
Sensory and motor systems are interdependent. Movement guided by:
Input from sensory system: close-loop or reflex controlled
OR
Triggered by a sensory cue or internal desire to move: open-loop or volitional movement
Ability to make dynamic postural adjustments and to direct body and limb movements with intention and in purposeful activity.
Highest areas of motor control: prefrontal cortex, supplementary motor area, premotor cortex and basal ganglia. Concerned with initiation, planning and programming of movements. Desire originates in limbic system and parietal cortex – which is then translated into movement by the basal ganglia and their cortical projections.
BASAL GANGLIA
Complex movement disorders e.g. Parkinson’s disease, Huntington’s disease, choreoathetoid cerebral palsy and many others
Abnormal involuntary movements such as chorea, dystonia, akinesia, bradykinesia, rigidity
Damage alters the ability to activate or suppress movements
CEREBRUM
Achieved by comparing intended movement from motor areas in cortex with actual movement as detected by activation of muscle afferents and interneurons in spinal cord.
Useful in learning new movements and correct timing
Responsible for the coordination of movement, stores motor information
DAMAGE
Hypotonia (caused by reduced input from deep cerebellar nuclei neurones)
Incoordination / ataxia (presentation varies with where cerebellar damage occurs)
Breakdown in coordination of movement without weakness.
Dysarthria - slurred speech due to oral muscular incoordination
Nystagmus - rapid jerky eye movements
MOTOR CORTEX AND DESCENDING MOTOR TRACTS
Role: cortical execution of movements
UMN – executes movement/function. Motor pathway above anterior horn cell (CNS)
LMN – synapses and initiates movement. PNS – anterior horn cell, motor nerve root, brachial plexus and peripheral nerves.
PATHWAYS
Corticospinal tract :
Originates in the primary motor cortex, but also in premotor and somatosensory cortices.
Synapse directly onto the motor neuron in the brainstem cranial nerve nuclei and anterior horn (ventral) of spinal cord.
Vestibulospinal tract, tectospinal tract, reticulospinal tract, rubrospinal tract
Originate from subcortical structures and have more complex synaptic distribution with both motor and interneurons.
Can cause hypotonia or flaccidity (Important: hypotonia can also be due to acute UMN lesion)
Interruption of signals to muscles decreases or prevents muscle contraction – decrease in tone
Weakness, wasting, hypotonia and/or reduced or absent reflexes
A complete lesion of peripheral nerve interrupts all the axons in nerve and produces paralysis
Denervation of skeletal muscle produces atrophy
Positive signs: (primary signs)
Increased stretch reflexes/spasticity
Negative signs: (secondary signs)
Slowness of movement
Loss of dexterity
Abnormal muscle synergies (post stroke)
Hypertonia
Weakness