Nolte Chapter 18: Overview of Motor Systems
The combinations of one motor neuron and all the muscle fibers it innervates is referred to as a motor
unit. Lowe rmotor neurons are found in the anterior horn of the spinal cord.
Red fibers (type I) are thin, contain abundant mitochondria, and contract weakly and slowly and have a
long endurance. These are innervated by the smallerst lower motor neurons
White fibers (Type II) are larger, contain relatively few mitochondria, and contract in briefer, more
powerful twitches. Type IIb uses glycolysis almost exclusively and IIa uses a combination of oxidative
metabolism and glycolysis and fatigue and intermediate rates. Innervated by the largest lower motor
neurons.
Neurons that give rise to descending pathways are known as upper motor neurons
Stretching a muscle stimulates its muscle spindles, whose afferent fibers end on motor neurons, which
in turn causes the muscle to contract.
Networks of interneurons act as pattern generators for rhythmic movements and can persist in the
absence of afferent inputs.
Upper motor neurons affect the activity of lower motor neurons. They are in the cortex and brainstem.
The ones in the brainstem control muscles of the face, head, and neck.
The vestibulospinal tract mediates postural adjustments and head movements.
The corticospinal tract is the principal mediator of voluntary movements.Lateral corticospinal crosses at
pyramids. Anterior corticospinal crosses at appropriate level of spinal cord. Coricobulbar goes from
cortex to brainstem motor neurons.
The reticulospinal and rubrospinal tracts are principal alternative routes for the mediation of voluntary
movements (the rubrospinal originates in the red nucleus which is involved in reaching and grasping
with the limbs). Maintain posture during movement as well.
The tectospinal tract descends from the superior colliculus to cervical levels of the spinal cord and is
responsible for the reflec of turning the head in reponse to visual and other stimuli.
It is thought that association areas of the cortex decide that a movement is called for, premotor devises
a plan, and the motor cortex issues those commands.
The basal ganglia and cerebellum act primarily by affecting the motor and premotor cortex. Basal
ganglia might be responsible for intiation and the cerebellum for sensorimotor coordination.
On the anterior wall of the central sulcus is the somatopically mapped primary motor cortex. This area
contains giant pyramidal cells called Betz cells, whose axons descend to the spinal cord through the
medullary pyramids. However, these cells only account for 3% of the corticospinal tract’s fibers. Half the
fibers come from motor cortex and the other hald ceom frome frontal motor areas and the parietal
lobe, particularly somatosensory cortex.
Premotor cortex is just anterior to primary motor and supplementary is on the medial surface of the
hemisphere, just anterior to the representation of the foot in primary motor cortex. These areas provide
the anterior third of the corticospinal tract (primary motor is posterior) and both project to primary
motor. Stimulating these areas requires much more activity in order to elicit movements. That’s because
these areas are thought to be involved with more complex movements. However, if you remove Primary
motor, stimulation of SMA will not cause hand movements, but will cause trunk movements. Both SMA
and PMC receive sets up inputs appropriate for planning movements, prominently including projections
from prefrontal cortex and parietal association cortex (information about the spatial relationships
between body parts and the outside world). Both regions change their levels of activity before
movements and even if movements are only contemplated.
Premotor seems to be guided by external stimuli, whereas SMA is more involved in planning and
learning complex, internally generated movements. Premotor shows set-related activity (changed in
baseline before movement).
Corticospinal passes through the posterior limb of the internal capsule.
A good heuristic: large diameter fibers are more likely to end directly on lower motor neurons.
Projections to sensory nuclei might serve to compensate somehow for the altered afferent activity
caused by an impending movement.
Alpha-gamma coactivation – if only the alpha motor neurons were activated, during the resulting
contraction the muscle spindles would be “destretched” and hence inactive. Activating the gamma
motor neurons as well serves to maintain spindle sensitivity throughout the movement.
A surprisingly minimal chronic motor deficit arises from a total loss of corticospinal function. However,
there is an inability to use fingers individually.
If lesions of medial portions of the meduallary reticular formation are added to the corticospinal lesion,
a severe and permanent disability of the axial muscles results.
Reticulospinal and rubrospinal tract can compensate for the role normally played by the corticospinal
tract in most aspects of voluntary movement.
Henneman’s Size Principle – with low-level excitation of a motor pool, smallest are first recruited and
move up to larger neurons with more excitation. Due to higher density of synaptic terminals on smaller
motor neurons and that input resistance is larger due to surface area for larger neurons.
Lower motor neuron syndrome is associated with weakeness/paralysis, decreased superficial reflexes,
hypoactive deep reflexes, decreased tone, fasiculations, and atrophy.
Upper motor neuron sysndrom is associated with weakness, spasticity (increased tone, hyperatice
reflex, clonus), babinksi’s sign, and loss of fine voluntary movements.
Pyarmidal cells are mainly coming from Layer V and is considered to be the output layer. The input layer
(IV) is usually made up of granular cells. However, Primary motor is agranular, in that it almost totally
lacks granule cells and has an enlarged layer V due to its massive outputs.
Apraxia is the inability to execute learned purposeful movements.