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Pyramidal and extrapyramidal tracts

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Pyramidal and extrapyramidal tracts

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Pyramidal and extrapyramidal tracts

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Lesions above the pontine reticular formation and lateral vestibular nucleus but below the midbrain cause , a dramatic increase in extensor tone.

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A 20-year-old man comes to the emergency department because of a head injury while working at a construction site. He is currently immobilized on a spineboard and his body is extremely stiff. His arms are flexed at his sides, his fists are clenched on his chest, and his legs are extended with pointed toes. Increased activity in which of the following motor tracts best explains the patient’s physical findings? 

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In order for you to flex your bicep in the mirror, your brain and brainstem has to send a motor signal through the spinal cord to the muscles in the body.

These motor signals are carried through two tracts, the pyramidal and extrapyramidal tracts.

Neurons in the pyramidal tract are composed of upper motor neurons that directly innervate lower motor neurons in the anterior horn of the spinal cord.

Neurons in the extrapyramidal tract do not directly innervate lower motor neurons, but instead help coordinate muscle movement by indirectly activating or inhibiting groups of lower motor neurons through interneurons.

These groups of lower motor neurons usually innervate multiple muscles that share the same function, usually either flexors or extensors.

The pyramidal pathway is the primary pathway that carries out motor commands for voluntary movement. And it can be broken down into two main tracts, the corticospinal tract and the corticobulbar tract.

The corticospinal tract originates in the motor cortex where the cell bodies of the upper motor neurons are located.

The axons of these neurons travel together as fibers through the internal capsule to reach the brainstem where they form the medullary pyramids on the ventral surface of the brainstem.

At the level of the medulla, these fibers divide, and 90% of them form the lateral corticospinal tract which cross over to the opposite side of the medulla at the pyramidal decussation, while the remaining 10% of them form the anterior corticospinal tract which does not cross over just yet, and both tracts then travel through the spinal cord.

Neurons from the lateral corticospinal tract synapse on lower motor neurons in the anterior horn, while the neurons in the anterior corticospinal tract cross over in the spinal cord first before they synapse on the lower motor neurons in the anterior horn.

The upper motor neurons activate the lower motor neurons which leave the spinal cord and innervate the different skeletal muscles.

The lateral corticospinal tract controls the muscles of the limbs while the anterior corticospinal tract controls those in the trunk.

The corticobulbar tract also starts in the motor cortex where the upper motor neurons are located.

The axons of these upper motor neurons form the cortical bulbar tract which travels lateral to the corticospinal tract to reach the brainstem.

These axons will depart the tract and synapse directly with the contralateral lower motor neurons for Cranial Nerves V, VII, XI, and XII at their corresponding levels of the Pons and medulla.

Some of the upper motor neurons branch into two fibers which synapse with both the ipsilateral and contralateral motor nuclei.

These include cranial nerves V, which controls the muscles for chewing, XI, which controls the muscles of the neck, and the part of VII that innervates the muscles in the upper half of the face.

This means the muscles innervated by these nerves receive motor signals from the motor cortex from both hemispheres of the brain.

The upper motor neurons of cranial nerve VII that control the lower half of the face, and cranial nerve XII, which control tongue movement, crossover in the brainstem without branching and only synapse with the contralateral nuclei.

Sources
  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2018)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Recrudescence of Deficits After Stroke" JAMA Neurology (2017)
  6. "" Malaria Journal (2005)