Corticospinal Tract & Corticonuclear (Corticobulbar) Fibers Study Guide
Corticospinal Tract
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Two neuron pathways:
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UMN – pyramidal cells of cerebral cortex
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LMN – neurons in anterior horn of spinal cord
Neurotransmitter:
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Glutamate (+)
Function:
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Lateral
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Voluntary motor control of extremities
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* Fractionation
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Particularly important in fine control of digits of hand
Anterior
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Voluntary motor control of axial musculature
Origin
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Cerebral Cortex
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Primary motor (Both Corticospinal tracts), Premotor (Ant Corticospinal
tract only)
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Course
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Cerebral Cortex (primary motor and/or premotor cortex)  corona radiata &
posterior limb of internal capsule  cerebral peduncles of midbrain  anterior
pons  pyramids of medulla  lateral funiculus of SC (lateral corticospinal
tract) or anterior funiculus of SC (anterior corticospinal tract)  lower motor
neurons in ventral horn of SC
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Termination
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Spinal Cord (primarily laminae VI-IX)
Lesions
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Myasthenia Gravis
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Moderate to profound weakness of skeletal muscles; caused by circulating
antibodies that react with postsynaptic nicotinic acetylcholine receptors.
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Patients with this present with progressive fatigability throughout the day.
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Ocular muscles effected – 85% of pts
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Symptoms: weakness in limb muscles, facial/oral weakness, diplopia, ptosis,
dysphagia, dysarthria
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Lateral Corticospinal Tract Lesion
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Ipsilateral UMN signs (Lesion below the level of decussation)
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Contralateral UMN signs (Lesion above the level of decussation)
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Tumors or MS affect the lateral corticospinal tract
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Symptoms: weakness, hypotonia, hyperflexia
Any lesion in SC will result in ipsilateral UMN signs because the deccussation occurs at
the medulla (SC is below the level of deccussation)
Corticonuclear (Corticobulbar) Fibers
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Two neuron pathway:
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UMN – cells of cerebral cortex
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LMN – motor cranial nerve nuclei in brainstem
Fibers influence motor nuclei of oculomotor, trochlear, trigeminal, abducens, facial,
glossopharyngeal, vagus, accessory, & hypoglossal nerves
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Function
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Controls muscles of face, head & neck
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Initiation and control of voluntary & fine movements
Neurotransmitter
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Glutamate (+)
Innervated by the cranial motor nuclei (V, VII, XII), nucleus ambiguus (IX and X) & by
accessory nucleus
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DOES NOT innervate nuclei for nerves III, IV, and VI
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Fibers do NOT project to the oculomotor, trochlear, and abducens DIRECTLY (from
frontal eye fields to terminate in mesencephalon [sup colliculus] and then relay input to
the motor nuclei
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Origin
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Precentral gyrus - somatomotor cortex, area 4 (primary motor cortex)
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Frontal eye fields - areas 6 and 8
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Postcentral gyrus - areas 3, 1, 2 (some)
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Course
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Precentral gyrus  descends through corona radiata  genu of internal capsule
(few fibers in the posterior limb of the internal capsule)  crus cerebri 
brainstem
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Major Structures
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Precentral gyrus, corona radiate, genu of internal capsule, posterior limb of
internal capsule, cerebral peduncles (midbrain), brainstem (medulla & pons),
cranial nerve nuclei
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Termination
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Frontal eye fields
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Rostral Interstitial Nucleus of the MLF
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Paramedian Pontine Reticular Formation
Precentral gyrus
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Brainstem motor nuclei: CN V (bilateral), CN VII (contralateral), CN XII
(contralateral tongue)
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Nucleus Ambiguus (bilateral): CN IX, CN X (soft palate, pharynx, larynx)
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Accessory Nucleus (bilateral): CN XI
Upper half of the facial motor nucleus receives BILATERAL corticonuclear projections
Lower half of the facial motor nucleus receives only CONTRALATERAL projections
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Pseudobulbar Palsy
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Bilateral lesion
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Inability to control facial movements
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Caused by variety of neurological disorders (ALS, MS, Parkinson’s)
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Symptoms: Dysphagia, Dysarthria, Paresis of tongue, loss of emotional control
One-and-a-Half Syndrome
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Results from unilateral lesion of the paramedian pontine reticular formation
(PPRF) and the ipsilateral MLF
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Loss of ipsilateral abduction (lateral rectus), adduction & contralateral loss of
adduction (EYE MOVEMENT)
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Only remaining horizontal movement is contralateral abduction