The pyramids are two elongated swellings on the ventral aspect of the medulla. Each pyramid contains approximately 1,000,000 CORTICOSPINAL AXONS. As the name suggests, these axons arise from the cerebral cortex and descend to terminate within the spinal cord. The cortical cells that give rise to corticospinal axons are called Betz cells. As corticospinal axons descend from the cortex, they course through the internal capsule, the cerebral peduncle of the midbrain, and the ventral pons (you will learn about these structures later in the course so dont worry about them now) and onto the ventral surface of the medulla as the pyramids (see below).
When corticospinal axons reach the medulla they lie within the pyramids. The pyramids are just big fiber bundles that lie on the ventral surface of the caudal medulla. The fibers in the pyramids are corticospinal. It is important to REMEMBER: THERE HAS BEEN NO CROSSING YET! in this system. The cell bodies of corticospinal axons within the pyramids lie within the IPSILATERAL cerebral cortex.
At the most caudal pole of the pyramids the corticospinal axons cross over the midline and now continue their descent on the contralateral (to the cell of origin) side. This crossover point is called the PYRAMIDAL DECUSSATION. The crossing fibers enter the lateral funiculus of the spinal cord where they are called the LATERAL CORTICOSPINAL TRACT (corticospinal is not good enough, you have to call them lateral corticospinal; LCST - remember this one??). LCST axons exit the tract to terminate upon neurons in the spinal cord gray matter along its entire length. Some of the spinal cord neurons that receive direct input from lateral corticospinal fibers send axons into the ventral root to innervate striated muscles that move the arms and legs. In such instances only two neurons and one synapse are involved (monosynaptic). Lateral corticospinal tract axons also end upon spinal cord neurons that do not directly innervate muscle, but instead synapse upon lower motor neurons. Such cells are called interneurons. A pathway involving a lateral corticospinal axon, an interneuron and a lower motor neuron is disynaptic.
Lets review! The cells of origin of the corticospinal tract lie in the ipsilateral cerebral cortex. In contrast, the cells of origin of the lateral corticospinal tract lie in the contralateral cerebral cortex. REMEMBERthe lateral corticospinal tract is the part of the corticospinal system in the spinal cord. It is important to remember that damage to the corticospinal fibers rostral to the pyramidal decussation results in contralateral motor deficits, while lesions in the spinal cord (i.e., caudal to the decussation) result in ipsilateral deficits. Clinicians refer to the motor deficit resulting from a lesion of the corticospinal tract as hemiplegia (plegia =paralysis) or hemiparesis (weakness). For instance, they would say that a lesion of the LEFT corticospinal tract in the internal capsule (rostral to the pyramidal decussation) results in a RIGHT hemiplegia (involves the right arm, trunk and leg) while a lesion of the LEFT lateral corticospinal tract at C1 (in the spinal cord and therefore caudal to the decussation) results in LEFT hemiplegia. Since the motor neurons that directly innervated the muscle are OK, there is no muscle atrophy. This is important.
A unilateral lesion of the lateral corticospinal tract results in motor deficits ipsilateral to the lesion. Interrupting the tract does NOT result in muscle atrophy, since the neurons innervating muscle are NOT dead. For example, if the LEFT lateral corticospinal tract is interrupted at Cl, then the LEFT arm, trunk and leg are affected. This is because the lateral corticospinal tract influences the musculature on the same (ipsilateral) side of the body. If the lesion involves the LEFT lateral corticospinal tract at T3, then only the LEFT trunk and leg are affected, since the spinal cord motor neurons that innervate the muscles of the arms still receive corticospinal input.
As mentioned above, the term hemiplegia is commonly used by clinicians when discussing the effects of lesions of the corticospinal tract anywhere from the cortex to the medulla, and of the lateral corticospinal tract anywhere in the spinal cord. Cerebrovascular accidents (strokes) commonly damage the corticospinal tract in the motor cortex or the posterior limb of the internal capsule (a compact bundle of axons through which almost all neural traffic to and from the cortex passes). The term stroke is poorly defined and has different meanings to different users. It generally implies the abrupt onset of neurological deficits as the result of cerebrovascular disease. As such, it includes the manifestations of cerebral hemorrhage (Gr. blood bursting forth; may be arterial, venus or capillary) cerebral infarction (L. to stuff into; area of tissue undergoes necrosis [death] following cessation of blood supply) and intracranial and extracranial thrombosis (Gr. clot condition; when a thrombus is detached from its original site and found in another site it is called a thrombotic embolis [Gr. embole=throwing in]).
As you have already learned, immediately following a lesion involving corticospinal or lateral corticospinal fibers, there is a period of flaccid paralysis (spinal shock). After a period of days to weeks, muscle tone (spasticity) and muscle reflexes return and increase. There will also be a Babinski sign, (extension of the big toe and fanning of the others in response to firmly stroking the sole of the foot; the plantar reflexes are extensor). There will also be clonus.
You need to keep in mind that lesions of the corticospinal tract do not destroy motor neurons that DIRECTLY innervate muscle. THUS, THERE IS NO DEATH OR ATROPHY OF MUSCLE. Corticospinal tract neurons are referred to as UPPER MOTOR NEURONS since they do not innervate muscle directly. In contrast, neurons in the ventral horn that DIRECTLY innervate muscle are called LOWER MOTOR NEURONS (LMN). When these neurons die there is ATROPHY OF THE MUSCLE.
In my humble opinion, the corticospinal tract is the most important pathway in clinical neurology. I will ask you about this tract every time I see you, even after you graduate! In other words, if you forget any neuroanatomy, DO NOT forget the following points:
1. the pathway is crossed.
2. lesions anywhere rostral to the decussation (cortex, internal capsule, cerebral peduncle, basilar pons, rostral two-thirds of pyramid) result in contralateral deficits.
3. lesions involving this system in the spinal cord (i.e., the lateral corticospinal tract) result in ipsilateral deficits below the level of the lesion.
4. corticospinal neurons are upper motor neurons; and therefore their death does NOT result in muscle atrophy.