Neuroanatomy Lecture #39: Corticospinal And Cotricobulbar Fibers

Front 1

The Corticospinal tract helps initiate and control motor activity. Name the 3 areas in the brain involved in its fxn and their relation to one another.

Back 1

• Prefrontal Cortex
• Premotor Cortex
• Primary Motor Cortex

The lateral area of the Prefrontal cortex sends axons to the Premotor cortex which communicates with the Primary motor cortex to excite LMNs

Front 2

Primary Motor Cortex:
• Brodmann's area
• overlaps with this gyrus and lobule
• Its Pyramidal cells in cortical layer 5 excite LMNs in these parts of the CNS (2)
• How its cells mediating muscular movement of the body are organized

Back 2

Primary Motor Cortex:
• B-4

• Overlaps with the Precentral gyrus and anterior paracentral lobule

• Excite LMNs in the brain stem and spinal cord

• Its cells are organized into a somatotopic fxnal map called a homunculus, a representation of the body fxnally mapped across nervous tissue.

Front 3

Name the areas from which the Primary motor cortex receives input and whether this connection is direct or indirect (6)

Back 3

• Premotor cortex
• Premotor cortex (direct)
• Primary somatosensory cortex (direct)
• Posterior parietal cortex (direct)
• Basal ganglia (via thalamus and premotor area)
• Cerebellum (via Thalamus)

Front 4

Describe cortical activity for the following types of sequences and give an example of each
• Simple
• Complex
• Imagined

Back 4

• Simple
- Primary motor and somatosensory cortices
- ex. repeated flexion and extension of a finger

• Complex
- Primary motor & somatosenory cortices and the Medial premotor/Supplementary motor area
- ex. repeated flexion and extension of fingers in succession

• Imagined
- Only the Medial premotor/Supplementary motor area is active
- ex. mental rehearsal of a sequence

Front 5

The Lateral Cortical Spinal Tract
• Main fxn
• Starting location
• Ending location and the pre- and post- synaptic neurons involved

Back 5

The Lateral Cortical Spinal Tract
• Voluntary contraction of distal flexor muscles
• Start - Layer 5 of the Pre-central gyrus and Paracentral lobule
• End - Contralateral ventral/anterior horn of the spinal cord
- Pre-synaptic neurons are the UMNs
- Post-synaptic neurons are the α- and γ- LMNs

Front 6

Describe the route of the Corticalspinal Tract (8 Steps)

Back 6

1. Cerebra cortex
2. Corona radiata
3. Posterior limb of the Internal Capsule
4. Crus cerebri
5. Basilar pons
6. Medullary pyramids
7. Coticalspinal tracts in spinal cord
8. Synapsing on the α- and γ- LMNs in the contralateral ventral/anterior horn of the spinal cord

Front 7

The three possible routes/destinations of cortical spinal fibers

Back 7

• Decussate in the caudal medulla, forming the lateral corticalspinal tract
• Not decussate and continue ipsilaterally down the spinal column to form the anterior corticalspinal tract
• Terminate in the gray matter to regulate sensory inputs

Front 8

Upper Motor Neurons
• Responsible for forming these tracts
• Arise from this area of the cortex
• The neurotransmitter it releases and the receptors the NT binds
• Effect of lesion rostral to decussation
• Effect of lesion caudal to decussation

Back 8

Upper Motor Neurons
• Corticalspinal and Cotricobulbar Tracts
• Layer 5 of the Primary motor cortex
• Glutamate, which binds AMPA receptors
• Rostral lesion: contralateral paresis
• Caudal lesion: Ipsilateral paresis

Front 9

LMN Lesions
• Effect on muscles and sidedness
• Effect on reflexes
• Effect on Muscle tone
• Sick/dying LMNs exhibit this activity and are recognized as this on a EMG
• Two examples of LMN syndrome

Back 9

LMN Lesions
• Paralysis or paresis on ipsilateral side
• Hyporeflexia or Areflexia
• Hypotonia or Atonia
• They exhibit fasciculations, seen on an EMG as fibrillations
• ALS and Peripheral nerve trauma

Front 10

UMN Lesions
• Initial damage leads to this kind of a state and causes these sx (2)
• Three common signs

Back 10

UMN Lesions
• Leads to a transient state called shock and causes Flaccidity & Areflexia
• Three common signs
- Extensor plantar response / (+)Babinski sign
- Spasticity/Hypertonia
- Hyperreflexia: brisker than normal deep tendon reflexes w/ possible clonic responses

Front 11

Paraplegia
• Etiology
• Presentation
- 3 main signs
- Below level of the lesion, early & late observations with muscles
- Below the level of the lesion, this information lost

Back 11

Paraplegia
• Bilateral spinal cord injury due to a traumatic event impairing cells within the spinal cord (cutting, bruising, compression, laceration)

• Presentation
- Hyperreflexia, Extensor plantar reflex/+Babinski sign, Spastic paralysis
- Flaccid paralysis followed by spasticity (days to weeks later)
- somatosensory info is lost

Front 12

Corticobulbar fibers
• Starting location
• Ending location
• General idea about the route
• Function/Muscles it innervates

Back 12

Corticobulbar Fibers
• Layer 5 of the ventrolateral precentral gyrus, motor cortex
• Motor nuclei of cranial nerves in the brain stem
• There are several bundles of cortical fibers that travel different routes, depending on which cranial nerve the fibers target

•Fxns to iNN muscles in the head and back of the neck. These areas include the eyes and mouth

Front 13

An infarction in the posterior limb of the internal capsule causes damage to these fibers and system

Back 13

Damages the spinocortical fibers, the corticobulbar fibers and the somatosensory system

To damage these areas, which part of the internal capsule is affected?

Front 14

Corticospinal Tract damage:
• causes this syndrome, included sidedness
• Sidedness of somatosensory loss

Back 14

Corticospnal Tract damage:
• UMN syndrome on the contralateral side
• Somatosensory loss on contralateral side

Front 15

Corticobulbar fiber damage:
• Presentation if hypoglossal nucleus iNN is affected

Back 15

The Corticobulbar tract iNN the contralateral hypoglossal nucleus. Damage to the tract de-innervates the contralateral genioglossus muscles.

Presentation: Upon tongue protrusion, the tongue will deviate
- contralateral to the side of tract damage
- ipsilateral to the side of muscle de-innervation

Front 16

Corticobulbar fiber damage:
• Presentation if PPRF iNN is affected

Back 16

The Corticobulbar Tract iNN the contralateral PPRF. The PPRF will iNN the Abducens Nucleus (for Lateral rectus muscle) of the contralateral side and the Oculomotor Nucleus (for the Medial rectus muscle) of the ipsilateral side (side in which the Corticobulbar tract originated). Damage to the tract will de-iNN the contralateral PPRF and ultimately affect the fxn of the contralateral lateral rectus and ipsilateral medial rectus muscles.

Presentation: The eyes will deviate towards the side of the lesion, towards the side of the damaged corticobulbar tract

Front 17

Corticobulbar fiber damage:
• Describe the iNN of the Facial Nucleus
• Presentation for a Central facial lesion vs a Peripheral facial lesion


• An example of a LMN Syndrome that includes the facial nucleus

Back 17

The Facial Nucleus has an upper and a lower part, each iNN by the ventrolateral primary motor cortex
- The Upper portion is bilaterally iNN and controls upper facial muscles
- The Lower portion is contralaterally iNN (unilateral) and controls lower facial muscles

• A central facial lesion would affect the iNN of the upper and lower facial nuclei however since the upper facial nuclei is bilaterally iNN, only the lower muscles would be paralyzed - the patient would still be able to wrinkly their forehead.

In a Peripheral facial lesion, CN VII is damaged and both upper and lower facial nuclei would be damaged causing hemifacial paralysis

• An example of a LMN syndrome is Bell's palsy