Pathways focus session week 5 Flashcards
Where does the corticospinal tract originate?
What is the function of neurons in this tract?
Corticospinal pathway: This is one of the motor pathways responsible for driving and modulating the activity of motor neurons. It originates in the precentral gyrus and is of great importance as it is responsible for control of refined, precise voluntary movements. To accomplish this control, the corticospinal pathway mainly innervates motor neurons that will supply flexor musculature of the distal extremities.
Explain the pathway of the corticospinal tract beginning at the precentral gyrus of the cortex.
Where do these fibers decussate?
The corticospinal pathway is described as a “two-neuron chain” (upper and lower motor neuron). The upper motor neuron (UMN) s a pyramidal cell in the cerebral cortex (pre central gyrus). The myelinated axons of these upper motor neurons descend via the ipsilateral internal capsule, down through the middle third of the crus cerebri in the midbrain. From the midbrain they reach the pons and the fibers coalesce on the ventral surface to continue downward to the pyramids of the ventral medulla. More caudally in the medulla, at the spinomedullary junction, most of the corticospinal fibers (~85%) decussate (a.k.a. pyramidal decussation) to become the lateral corticospinal tract which is located in the lateral aspect of the spinal cord. At this point, the axons are still part of the same neurons at the pathway’s origin in the precentral gyrus.
These axons continue to descend but some will leave the lateral corticospinal tract at each level of the spinal cord to synapse on lower motor neurons (LMN) in the ventral horn of the spinal cord.
From here, the axons of LMNs extend outward in the ventral roots at each spinal level and course through spinal nerves (and then peripheral nerves) to reach their targets, namely muscle fibers. One Alpha motor neuron (same as LMN) and all of the muscle fibers it innervates is a motor unit. The size of motor unit (i.e. how many muscle fibers a single motor neuron innervates) affects the amount of force generation and fine motor control for a given muscle.
What are the sites of potential damage of an UMN in the corticospinal tract?
Explain how a patient would present acutely and chronically with an UMN lesion of the corticospinal tract.
Upper Motor Neuron Lesions (Corticospinal damage) :
1) Site of Potential Damage
a) UMN in the Cortex
b) Axons in the internal capsule, brainstem, or spinal cord
2) Patient Presentation
a) Acute: “Spinal Shock”: Flaccid Paralysis (resembling a lower motor neuron lesion), Hyoptonia and Hyporeflexia
b) Chronic:
i. Spastic paralysis/paresis (Paresis/paralysis in this lesion is difficulty particularly with performing refined movements)
ii. Hyperreflexia (exaggerated or increased DTRs e.g. knee jerk)
1. Contractures and spasticity are associated with the hyperreflexic state.
iii. Hypertonia (increased muscle tone)
iv. Babinski sign in the foot (upgoing toe: elicited with a firm stroke of the sole of the foot from the heel to the toe). Plantar flexion is the normal response though it is normal for children less than 1 year to exhibit a Babinski sign.
v. Disuse Atrophy: muscle wasting from inability to use muscles affectively. do not have fine control
What are the sites of potential damage of an LMN in the corticospinal tract?
Explain how a patient would present acutely and chronically with an LMN lesion of the corticospinal tract.
Lower Motor Neuron Lesions
1) Site of Potential Damage:
a) Ventral horn motor neuron
b) Axons of the LMN in a ventral root, spinal nerve, or peripheral nerve
c) Cranial nerve motor neurons or their axons
2) Patient Presentation
a) Acute: Flaccid Paralysis (no activation of muscle fibers), Hyoptonia and Hyporeflexia, Fasciculations and Fibrillations (EMG)
a. Fibrillation is asynchronous firing of muscle fibers measured with EMG recording electrodes. It is caused by denervation hypersensitivity resulting from spread of acetylcholine receptors along the fiber after degeneration of the presynaptic terminal of a motor end-plate.
b. Fasciculations are the clinical manifestation of fibrillation. They can be felt or observed as contractures beneath the skin. These initial effects subside over periods of days to weeks.
b) Chronic: Flaccid Paralysis, Hyoptonia and Hyporeflexia, and very severe atrophy (Denervation atrophy implies trophic factors from the neuron which influence muscle metabolism and maintenance have been lost). This atrophy is more severe than the disuse atrophy observed in UMN lesions.
Explain where the signs/symptoms of a lesion of the corticospinal tract will present in the following locations:
spinal cord
brainstem
cortex
What parts of the body will be affected if a lesion is in each of these locations?
Spinal cord lesions (i.e. lesions inferior (or caudal) to the spinomedullary junction/medullary pyramid) produce ipsilateral upper and/or lower motor neuron signs. The location of the lesion within the cord (e.g. cervical v. thoracic) will determine the part(s) of the body affected.
Above the spinomedullary junction (i.e. brainstem and cortex) - corticospinal (i.e. UMN) signs and symptoms will be contralateral to the location of the lesion.
What are the functions of neurons in the dorsal column-lemniscal pathway?
What peripheral receptors are involved?
This pathway is responsible for conscious proprioception, 2 pt discrimination, and vibratory sense. The pathway is an ascending chain of three neurons in sequence. The peripheral receptors for these modalities are muscle spindles, cutaneous Meissner’s and Pacinian corpusles, and Golgi tendon organs respectively.
Explain the travel/pathway of axons of the dorsal column-lemninscal pathway.
The Pathway: Centrally directed processes of the primary (1°) neurons in the dorsal root ganglia send large myelinated fibers into the spinal cord. Ascending branches of these fibers enter the dorsal columns, specifically the fasciculus gracilis (fibers from the leg) and a more laterally located fasciculus cuneatus (which appears as fibers from the upper limb enter the cord more rostrally). These primary fibers ascend to the spinomedullary junction where they synapse ipsilaterally with second order (2°) neurons located in the nucleus gracilis and nucleus cuneatus respectively.
Axons of these second order neurons decussate (cross midline) at the spinomedullary junction by curving ventrally as internal arcuate fibers. These axons ascend through the brainstem as the medial lemniscus. This tract is identifiable in all levels of the brainstem, although its position and somatotopy change.
The secondary fibers synapse with third order (3°) neurons in the thalamus. The synaptic relay occurs in the ventral posterior nucleus (VPL) of the thalamus. These third order neurons project through the internal capsule to the postcentral gyrus of the cerebral cortex.
What are the potential sites of damage to the dorsal column pathway?
On what side of the body do symptoms of spinal cord lesions present (relative to the lesion)?
What is a sensory level?
On what side of the body do symptoms of lesions above the spinomedullary jucntion present (relative to the lesion)?
Dorsal column lesions produce loss of vibratory, 2-pt discrimination, and position (conscious proprioception) sense.
Spinal Cord Lesions: produce effects ipsilateral to the location of the lesion at all segments below the affected level. Sensory loss below a certain level and extending downward is referred to as a “sensory level” by neurologists. Examples:
- A lesion to the dorsal columns in the cervical cord would likely affect both the fasciculus gracilis and cuneatus thus affecting sensation in both the legs and the arms.
- A lesion to the mid-thoracic level of the cord would spare fibers from the arm (which would enter the cord above the level of the lesion), thus the sensory level would be on the thoracic wall and extend downward to the legs (e.g. a T10 spinal cord injury would result in sensory loss beginning around the umbilicus and extending downward to the legs.)
- Small lesions (e.g. demyelination) could affect either the fasciculus gracilis or cuneatus in isolation thus restricting sensory loss to the arm or the leg.
Lesions above the Spinomedullary Junction: Lesions in the brainstem (medial lemniscus) or higher (i.e. thalamus, internal capsule, or postcentral gyrus) all produce contralateral loss of vibration, 2 pt discrimination, and proprioception. This is because at any level above the decussation of fibers at the spinomedullary junction, the information coming from the opposite side of the body is interrupted.
What modalities does the lateral spinothalamic pathway convey?
How many neurons are considered to be in the “chain” of this pathway?
What kind of axons (myelinated, unmyelinated) are in the central and peripheral processes of these cells?
What kind of receptors are in this pathway?
The lateral spinothalamic pathway is for perception and localization of pain (and temperature) by virtue of its somatotopic representation in the postcentral gyrus. This pathway is coined the “fast-pain” pathway to distinguish these pain sensations from the more noxious affect of painful stimuli which is regarded as “slow pain”. In a neurological exam, testing cutaneous sensation with a cold object or a pointed object (i.e. a broken applicator stick or tongue depressor) is very useful for assessing sensory loss due to either peripheral nerve lesion or lesions to the central pathway described here. The sensitivity and spatial resolution for “fast” pain/temperature make this an excellent modality for dermatome mapping.
The lateral spinothalamic pathway is an ascending three-neuron chain. The central and peripheral processes of these cells consist of unmyelinated and small myelinated axons. The receptors are mainly free nerve endings along with a lesser number of other specialized cutaneous receptors.
Explain the pathway of axons in the lateral spinothalamic tract.
Centrally directed processes of the primary (1°) neurons in the dorsal root ganglia enter the spinal cord and immediately branch in a small intersegmental tract (Tract of Lissauer) to synapse in the dorsal horn across several segments. This spread of the primary neuron to multiple segments is related to withdrawal reflexes and illustrates the importance of pain sensation as a protective mechanism. Cells upon which the primary neurons synapse are the secondary (2°) neurons which send axons into the ascending pathway. Fibers of the second order (2°) neuron decussate in the spinal cord at the anterior white commissure (just anterior to the central canal of the cord). The decussating fibers enter the anterolateral region of the cord and turn upward to ascend in the lateral fasciculus. Here the fibers are designated as the lateral spinothalamic tract. The tract stays in an anterolateral position in the cord, relocates more laterally through the entire brainstem, and finally synapses in the ventral posterior lateral (VPL) nucleus of the thalamus on the third order (3°) neurons. The axons of the third order neurons project through the internal capsule to the postcentral gyrus of the cerebral cortex in a somatotopic fashion.
What are the potential sites of damage to the lateral spinothalamic pathway?
On what side of the body (relative to the lesion) will symptoms of lesions of the lateral spinothalamic pathway in the spinal cord present?
The brainstem/above the brainstem?
Lesions of the lateral spinothalamic pathway in the brainstem or above as with the other two long tracts, produce contralateral signs on the body. Specifically for this pathway, these are contralateral losses of pain and temperature sensation.
This pathway differs, however, in that lesions in the spinal cord also produce contralateral pain and temperature loss below the level of the lesion. This is because the decussation of the fibers in the cord is so close to the level of entry of the primary pain and temperature afferents. The “sensory level” produced by a lesion to this pathway also differs. It does consist of sensory loss that proceeds from the proximity of the lesion downward, but it differs from the dorsal column pathway in these ways: 1) the sensory level is contralateral to the location of the lesion; and 2) the sensory loss starts 1 to 2 segments below the location of the lesion. This second difference occurs because fibers entering at the level of the lesion escape damage since they branch upward and synapse at higher levels (~1-2 segments) of the cord and then decussate above the lesion. While tests of the lateral spinothalamic pain pathway are called “pin” in the jargon of many neurologists, cold or pointed objects other than pins are more commonly used to map out the sensory losses described above.
Compare and Contrast a MCA stroke with an ACA stroke. What are the patients symptoms in each?
The ACA supplies regions of the cortex where the leg and foot are represented versus the MCA which supplies cortical areas where the arm and face are represented. Strokes in either of these vessels would result in UMN signs and sensory losses in respective regions of the body which are contralateral to the location of the lesion.
Compare and Contrast a ASA (anterior spinal artery) stroke with an PSA (posterior spinal artery) stroke. What are the patients symptoms in each?
There are two posterior spinal arteries which each supply the region of the dorsal columns on either the right or left side. The single anterior spinal artery supplies the entire anterior 2/3rds of the spinal cord. An anterior spinal artery stroke would affect the bilateral corticospinal and lateral spinothalamic pathways as well as the lower motor neurons (LMNs) at the level of the lesion. A stroke affecting one of the posterior spinal arteries would impact the dorsal column pathway on that side.
