Which spinal tracts decussate

The tract continues down into the medulla where it forms two large collections of axons known as the pyramids ; the pyramids create visible ridges on the exterior surface of the brainstem. The fibers that have decussated form the lateral corticospinal tract ; they will enter the spinal cordand thus cause movementon the side of the body that is contralateral to the hemisphere of the brain in which they originated. Most of the axons of the anterior corticospinal tract will decussate in the spinal cord just before they synapse with lower motor neurons.

The fibers of these two different branches of the corticospinal tract preferentially stimulate activity in different types of muscles. The lateral corticospinal tract primarily controls the movement of muscles in the limbs, while the anterior corticospinal tract is involved with movement of the muscles of the trunk, neck, and shoulders. As they travel down to the spinal cord, corticospinal tract neurons send off many collateral fibers that make connections in a number of areas including the basal ganglia , thalamus , various sensory nuclei , etc.

Additionally, corticospinal tract fibers terminate in various places in the spinal cord, including the posterior horn which is normally involved in processing sensory information. These diverse connections suggest that the functions of the corticospinal tract are likely diverse as well, and that defining it as having movement as its sole function is an oversimplification. When the upper motor neurons of the corticospinal tract are damaged, it can lead to a collection of deficits sometimes called upper motor neuron syndrome.

When such an injury occurs, it often results in a state of paralysis or severe weakness immediately following the event, usually on the side of the body opposite to the location of the injury. After several days, function begins to return, but some abnormalities persist.

The patient often displays spasticity, which involves increased muscle tone and hyperactive reflexes; motor control may also be decreased.

As mentioned above, after damage to the corticospinal tract the ability to make crude movements generally returns but some deficit in fine finger movements may remain. Also, patients may display other abnormal reflexes; the best known of these is the Babinski sign.

When the sole of the foot is stroked it generally causes the toes in adults to curl inwards; in someone with damage to the corticospinal tract the toes fan outwards, an abnormal movement referred to as the Babinski sign after neurologist Joseph Babinski. In infants, it is normal to observe the Babinski sign due to the fact that the corticospinal tract is not yet fully myelinated.

Thus, the lack of a Babinski sign in infants is considered abnormal and potentially problematic, while the presence of a Babinski sign is adults is pathological and indicates possible corticospinal tract damage. Nolte J. Philadelphia, PA. The descending tracts transmit this information to lower motor neurons, allowing it to reach muscles. This will become particularly relevant during the discussion of pathologies that present in the motor pathways.

There are many motor tracts in the spinal cord. Some of these are under conscious control and others under unconscious, reflexive or responsive control. These motor tracts can be grouped functionally into pyramidal and extrapyramidal tracts.

These functional groups contain several anatomical tracts , one for each side of the body:. The pyramidal tracts are named as such due to their course through the pyramids of the medulla oblongata. The pyramidal tracts are responsible for the conscious, voluntary control of the body and face muscles. The fourth cortical area the CST communicates with is the posterior parietal cortex for integration with and modulation of incoming sensory information.

Neurons exiting the cerebral cortex in one of the three major regions above converge to form the white matter structure in the brain known as the internal capsule. The internal capsule is located between the basal ganglia and thalamus; two highly vascularised structures in the deep brain.

After passing through the internal capsule, the fibres continue to pass down through the centre of the crus cerebri of the midbrain, before entering the pons and medulla. As the CST passes through the caudal medulla , it divides into the lateral and anterior corticospinal tracts:. These tracts then descend into the spinal cord, terminating in the ventral horn of the spinal cord where they synapse onto LMNs to supply the peripheral musculature.

The anterior CST remains ipsilateral and descends only to the cervical and upper thoracic spinal cord, where they decussate at the level of the nerve root they supply. Arising from the lateral aspect of the primary motor cortex the cephalic region of the motor homunculus , the CBTs receive mostly the same inputs as the CSTs.

They follow a similar path but terminate in the brainstem at the motor nuclei rather than continuing down to the spinal cord. In the brainstem, they synapse on the cranial nerve motor nuclei, which are LMN structures that supply the head and neck muscles. It is important to understand the clinical implication of damage to the CBTs.

This is the case for all head and neck muscle cranial nerve nuclei except:. The extrapyramidal tracts all originate in the brainstem and do not pass through the pyramids. These tracts all carry motor fibres to the spinal cord that allow for unconscious, reflexive or responsive movement of muscles to control balance, locomotion, posture and tone.

The rubrospinal tract begins in the red nucleus , where fibres immediately decussate and descend through the pons and medulla and into the spinal cord. It is thought that the rubrospinal tracts supply upper limb flexors as well as trunk flexors. Disinhibition of the rubrospinal tract leads to upper limb flexion. The tectospinal tract begins in the tectum, or roof of the midbrain, where the superior and inferior colliculi are located.

Collectively, the two superior and two inferior colliculi are referred to as corpora quadrigemina. Together, the colliculi send information about sights and sounds to the tectospinal tract, which decussates soon after leaving these structures, to supply muscles of the head and neck for reflexive localisation of these stimuli.

You will notice that UMN lesions present with hypertonia and spastic paralysis , whereas LMN lesions are usually associated with hypotonia and flaccid paralysis. This is because of the impaired ability for motor neurons to regulate descending signals, giving rise to disordered spinal reflexes.

To understand more, we must integrate what we know about the central nervous system: as much as it is involved with activating pathways, it can also suppress pathway activity. That is, the corticospinal tract also helps in conscious inhibition of muscle lack of the signal. If we sever the UMNs of the corticospinal tract, there is a loss of inhibitory tone of muscles.

The effect of this is two-fold on a simple level; there is much more to it! This leads to the hypertonia and spastic paralysis we see in UMNs. If LMNs are damaged or lost, there is nothing to tell the muscles to contract, with resultant hypotonia and flaccid paralysis.

We have discussed that the upper half of the face receives a bilateral cortical supply , whereas the lower half of the face receives contralateral cortical supply only. The paralysis in an UMN facial lesion will classically be spastic. The paralysis of a LMN facial lesion is flaccid. Now that we understand the rubrospinal tract and the role it plays in adjusting flexor tone in the upper limb, we can discuss decorticate versus decerebrate posturing.

Both types of posture involve lower limb extension. Decerebrate posturing refers to an adopted posture of upper limb extension. This occurs when a lesion below the red nucleus prevents the red nucleus from activating the upper limb flexors, resulting in upper limb extension. Decorticate posturing refers to an adopted position of upper limb flexion. This occurs when a lesion above the red nucleus prevents inhibitory tone of the red nucleus, allowing it to cause flexion of the upper limb.

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