The execution of movements that are more complex than spinal reflexes depends upon the activation of networks of neurons in the motor cortex and brainstem. Motor areas of the cerebral cortex direct purposeful, voluntary movement, whilst neurons located in brainstem nuclei direct automatic movements such as postural control. Because the brainstem nuclei and cortical motor areas communicate directly with the local controls of the spinal cord they are known as the descending pathways.
The primary motor cortex , which is located in the precentral gyrus, contains large neurons (pyramidal neurons) that make direct connections to local circuits in the spinal cord. Some neurons synapse directly onto somatic efferent neurons, and so have earned the clinical term upper motor neurons. In this terminology, somatic efferent neurons projecting to skeletal muscle are considered lower motor neurons.
In addition to cortical upper motor neurons, there are also upper motor neurons whose cell bodies are located in brainstem nuclei. For the most part, these brainstem pathways project to spinal cord circuits involved in automatic movements. For example, the vestibulospinal neurons and reticulospinal neurons project to spinal neurons controlling proximal muscles and are responsible for postural control.
To understand how damage to the descending
pathways affects motor function, it is important to know the path
taken by the axons of certain upper motor neurons. The figure
represents a schematic frontal section of the brain and spinal
cord. The axons of upper motor neurons located in the primary
motor cortex coalesce into a bundle that descends through the
cerebrum and is known as the internal capsule. The axons
continue along the ventral surface of the medulla in raised
triangular bumps known as the pyramids. In the medulla,
axons of cells that project to somatic efferent neurons that
innervate the limbs cross over to the opposite side of the body
(this crossing over is known poetically as the “decussation of the
pyramids”), and travel in a bundle known as the lateral
corticospinal tract. The ventral horn of the spinal cord has
a somatotopic organization
such that the somatic efferent neurons controlling distal muscles
are located laterally, whilst those that control proximal muscles
are located medially.
The vast majority (roughly 90%) of axons that project from the motor cortex to the spinal cord are contained in the lateral corticospinal tract. The 10% of cells that project to proximal muscles have axons that do not cross at the medulla, and travel in the anterior corticospinal tract in the spinal cord. Axons of the anterior corticospinal tract cross over when they reach the level of the spinal cord where they form synapses. Often these cells make a bilateral projection, branching and innervating neurons on both sides of the spinal cord. A significant amount of the descending pathway input to neurons controlling proximal muscles is contributed by the brainstem pathways, which also make bilateral projections. The inset shows a cross-section of the spinal cord, illustrating the locations of the lateral and anterior corticospinal tracts.
Damage to neurons of the corticospinal tracts affects motor control in different ways, depending on the location of damage. If a stroke causes a lesion in the primary motor cortex, motor function on the opposite side of the body will be affected. If on the other hand, there is damage to the lateral spinal cord (where the lateral corticospinal tract axons are located), this will cause a motor deficit in the limbs on the same side of the body. Deficits in motor behavior are more pronounced for the limbs than for the trunk, probably because there are several parallel pathways of descending innervation to the proximal muscles (bilateral projections of the anterior corticospinal tracts as well as inputs from brainstem pathways).
Damage to upper motor neurons causes two kinds of effects. The predominant effect initially is a loss of motor function. There may be paralysis, or paresis, which means partial paralysis. The loss of control is more pronounced for distal muscles, causing a lack of dexterity. These changes due to loss of function are referred to as negative signs. After some time, positive signs due to increased abnormal motor function will emerge. Spasticity is the term used to describe the positive signs that occur in upper motor neuron disorders. There is hypertonia (increased muscle tone, stiffness), hyperreflexia (exaggerated reflexes), and an oscillatory movement known as clonus. In a patient with clonus, a muscle stretch elicits alternating contractions of agonist and antagonist muscle groups. The hypothesis is that spasticity is due to a loss of inhibitory descending input that keeps the stretch reflex from being over-active.
Spasticity may result from a brain damaging stroke or spinal cord injury, but it most commonly occurs in the context of cerebral palsy. Cerebral palsy is a developmental disorder that results from descending pathway damage that may occur prior to or just after birth.
Click on the answer you think is correct.
A stroke causes damage in the left primary motor cortex. Which of the following would be most affected?
|movements of the left hand||movements of the right hand|
|movements of the left shoulder||movements of the right shoulder|