Introduction

The corticospinal tract, AKA, the pyramidal tract, is the major neuronal pathway providing voluntary motor function. This tract connects the cortex to the spinal cord to enable movement of the distal extremities.[1] As the corticospinal tract travels down the brain stem, a majority of its fibers decussate to the contralateral side within the medulla then continues to travel down the spinal cord to provide innervation to the distal extremities and muscle groups. Various collateral pathways exist which do not follow this pathway, leading to variability amongst individuals. This structure continues to develop after birth, with maturation taking place during puberty, due to rising levels of androgens. Clinically, the corticospinal tract is important in ischemic infarcts, rehabilitation, and various neurodegenerative disorders.

Structure and Function

The corticospinal tract originates primarily from the frontoparietal cortices, including the primary motor cortex, secondary motor area, and somatosensory cortex.[2] The corticospinal tracts then come together to form bundles, which travel through the internal capsule and cerebral peduncles. The bundles then travel down to the brainstem.[3] As the tract reaches the pons, the bundles take on a more compact structure and continue to condense as they descend. As a result, the neural structure of the corticospinal tract takes up more surface area in the upper pons than in the lower pons.[4] As the corticospinal tract continues to travel down into the medulla, 75 to 90% of the fibers will decussate to the contralateral side via the pyramidal decussation.[5][3] The 5 to 15% of fibers that do not decussate within the pyramidal decussation make up the anterior corticospinal tract. This tract extends into the spinal cord, but only travels down to the levels of the lower thoracic cord. Various collaterals also exist for the corticospinal tract, with the aberrant pyramidal tract being the most representative. The aberrant pyramidal tract separates from the corticospinal tract within the midbrain and pons, then descends through the medial lemniscus.[6] This collateral pathway may provide an alternative motor pathway in the case of a cerebral infarct, which will be a topic of discussion below.[2]

After leaving the brainstem and entering the spinal cord, the fibers run down through the anterior and lateral corticospinal tract. When they get to their target level, the fibers of the anterior corticospinal tract decussate through the anterior white commissure before synapsing to a neuron in the anterior horn of the gray matter. The lateral corticospinal tract fibers have previously decussated at the level of the pyramid and synapse at a neuron on the anterior horn when they get to the appropriate level. These neurons, known as anterior horn cells, then project to the limbs and axial muscles to provide voluntary motor function.[3] 

Embryology

During embryologic development, there is an overgrowth of axons distributed throughout the cortex, which incorporate into the corticospinal tract, and as development progresses, many of these axons are eliminated. Gray matter development begins a few weeks after the corticospinal tract axons reach the spinal cord. As growth continues, the corticospinal tract axons will reach the lower part of the cervical spinal cord by 24 weeks gestation.[3][7] After birth, the corticospinal tract continues to develop. The tract is then refined, and motor control develops. The research proposes that refinement of the corticospinal tract happens through the elimination of transient termination and growth within the gray matter of the spinal cord.; this is followed by developing control of the corticospinal tract’s role in voluntary motor function.[2] The tract continues development through puberty, which is when the gender differences in white matter emerge. Studies have shown that androgens play a role in axonal development through the proliferation of neural cell bodies and the prevention of cell death following axonal injury. As a result, the development of white matter in males and females diverges during adolescence.[8]

Physiologic Variants

Due to the complex nature of the corticospinal tract, many physiologic variants exist. The collateral pathway known as the aberrant pyramidal tract has been observed in some patients as traveling through the medial lemniscus from the midbrain to the pons until it reached the medulla where it rejoined the corticospinal tract.[6] Variants have also been observed between men and women following puberty, due to surges in androgens. The neuroprotective nature of testosterone leads to physiologic differences between individuals following adolescence.[8] Studies have shown anatomical and physiologic differences of this structure exist across individuals, and those differences are a continued topic of research.

Clinical Significance

Knowledge of the corticospinal tract is of the utmost importance in many clinical scenarios. Preservation and recovery of the corticospinal tract are necessary for the recovery of impaired motor function following a brain injury.[2] During the event of an acute ischemic stroke, hypo-perfused tissue may be potentially salvageable through timely reperfusion therapy. Areas where the corticospinal tract is contained within a small, dense area, such as the pons, have shown less of a correlation between motor impairment and the size of the ischemic lesion. Studies have proven that the extent of motor impairment during acute ischemic stroke depends on the extent of the corticospinal tract involved in the lesion.[1][4][9][4] Motor paralysis is a debilitating result of an ischemic infarct, for which rehabilitation has proven to be the most effective treatment modality.[10] Patients who have the highest degree of improvement following an acute ischemic stroke had superior integrity of the corticospinal tract than those with fewer improvements during rehabilitation.

Damage to the corticospinal tract has correlations with neuromyelitis optica (NMO) and multiple sclerosis (MS). Both autoimmune diseases involve an inflammatory process that causes extensive damage to neurologic structures involved in the corticospinal tract resulting in extensive neurologic disability, including optic neuritis and transverse myelitis.[11][12]

Compromise of the corticospinal tract during development presents may present as a tract that is completely absent, hypoplastic, or malformed. Disorders with the absence of corticospinal tracts include anencephaly, where there is a failure of the rostral neural tube to close; congenital aqueduct stenosis with a narrowing of the cerebral aqueduct; and microcephaly, which is a defect in proliferation. Underdeveloped corticospinal tracts present in lissencephaly, a defect in migration leading to absent gyration, Walker-Warburg syndrome, migration deficiencies yielding cerebro-ocular dysplasia with muscular atrophy; holoprosencephaly, and the failure of the brain hemispheres to separate. Corticospinal tract malformations usually involve diffuse brain malformation and are most often associated with an abnormal trajectory of the pathway.[3] These pathologies present with a range of problems, including the lack of motor control due to the involvement of the corticospinal tract.