Year I Neurosciences SystemMotor Pathways: Corticospinal and Motor Pathways: Corticobulbar (nuclear)Dr. Vijaya KumariMonday, March 16, 2009 8:00 – 9:50 AMTuesday, March 17, 2009 1:00 – 2:50 PM

MOTOR PATHWAYS: CORTICOSPINAL ANDMOTOR PATHWAYS: CORTICOSPINAL AND CORTICONUCLEAR (BULBAR) TRACTSCORTICONUCLEAR (BULBAR) TRACTS

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I. OVERVIEW OF REGULATION OF MOTOR ACTIVITY

A. Contractions of skeletal muscles can be: 1) reflex, 2) voluntary- stereotyped movements for locomotion and postural regulation, or 3) voluntary- to accomplish finely skilled non-repetitive movements.

B.The lowest level of CNS responsible for muscle contractions are the spinal and cranial lower motor neurons (LMNs) that are the final common pathways to skeletal muscles.

C.Reflex activation of LMNs is triggered by sensory stimuli and occurs at the cord or brain stem levels. Voluntary activations of LMNs are initiated by upper motor neurons (UMNs) arising at higher levels: brain stem motor centers and motor cortex. The UMNs synapse on the LMNs to regulate them.

II. LOWER MOTOR NEURONS (LMNS)

A. TYPES OF LOWER MOTOR NEURONS 1. LMNs consist of the alpha and gamma motor neurons in the spinal cord and brain stem,

their axons and branches that innervate muscle fibers in skeletal muscles.2. Of these, the alpha motor neurons make muscle fibers contract and ensure health and

survival of skeletal muscles. Gamma motor neurons are concerned with the normal functions of the neuromuscular spindles and stretch reflexes.

3. Both are activated by the UMNs.

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LEARNING OBJECTIVESLEARNING OBJECTIVES

Understand the anatomical organization of lower motor neuron and upper motor neuron pathways that control motor activity.

Learn the signs and symptoms typical of upper and lower motor neuron lesions. Know the detailed anatomical arrangements of corticospinal and corticonuclear

tracts. Be able to distinguish a central facial paralysis from a peripheral facial

paralysis. Understand the anatomical basis of regulation of voluntary horizontal conjugate

movements of the eyes.

B. LOCATIONS OF LMNS :1. Anterior horn cells that innervate the skeletal muscles of the neck, trunk and limbs. 2. Cranial motor nuclei in the brain stem that innervate skeletal muscles of the head and neck

(III, IV, V, VI, VII, IX, X, XI, XII). C. EXTENT OF LMNS:

1. Neuronal cell body, i.e., anterior horn cells and cranial motor nuclei2. Motor axons in the spinal ventral roots, spinal nerves and cranial motor and mixed

nerves 3. Motor axons in plexuses, nerves, and their branches4. Neuromuscular junction5.5. It is important to keep this complete extent in mind, since pathology anywhere from and

including the anterior horn/cranial motor nuclei to skeletal muscles can give rise to a LMN lesion.

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CRANIAL NERVE COMPONENTS AND NUCLEI

LEVEL MOTOR SENSORY PARASYMPATHETIC

MIDBRAIN 3, 4 5 (mesencephalic nu) 3 (Edinger-Westphall nu)

PONS 5, 6, 7 5 (main sensory and spinal)8 (cochlear and vestibular

nu)

7 (Superior salivary nu)

MEDULLA 9, 10 (Nu.ambiguus)

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7, 9, 10 (Nu. solitarius);5 (spinal nu);

8 (Cochlear and vestibular nu)

9 (Inferior Salivary nu)10 (dorsal nu);

CERVICAL SPNAL CORD

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CRANIAL NERVE/S MAJOR SKELETAL MUSCLES SUPPLIED

III, IV and VI Extraocular muscles + LPSV Muscles of mastication

VII Muscles of facial expressionIX, X Muscles of the pharynx, larynx and

soft palateXI Trapezius and SternocleidomastoidXII Extrinsic and intrinsic muscles of the

tongue

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CRANIAL NERVE NUCLEI

III. BRAIN AREAS CONCERNED WITH THE REGULATION OF LMNs

A. UPPER MOTOR NEURONS (UMNS)

These are neurons that exist at a higher level of the CNS and give rise to pathways ending on the LMNs. The concept is that the LMNs are regulated by the UMNs. The UMNs include:1. Cerebral cortex

a) Influences the LMNs by way of descending pathways.b) Descending pathways are referred to as the “pyramidal" tracts or system since parts of

these tracts pass through the medullar pyramids on their way to the spinal cord. The pyramidal tracts are made up of:i. Corticospinal tracts that end in the spinal cord.ii. Corticonuclear (corticobulbar) tracts that end in the brain

c) These are the only known direct pathways from the cerebral cortex to the LMNs in the spinal cord and brain stem.

d) These pathways enable us to initiate non-stereotyped voluntary motor activity upon command or desire to move, esp. of a fine skilled kind that uses the fingers and hand and the muscles involved in speech.

e) This control is largely exerted on the contralateral musculature, with some bilateral control.

2.2. Motor centers located in the brain stem a) Red nucleus, believed to be small in size in the human, gives rise to rubrospinal tracts.

The red nucleus in turn receives input from the cerebral cortex by way of corticorubral pathways.

b) Reticular formation in the medulla and pons gives rise to descending tracts, the pontine and medullary reticulospinal tracts. Their motor functions are controlled by corticoreticular tracts.

c) Vestibular nuclei respond to vestibular stimuli elicited by movements and changes in position of the head. They give rise to medial and lateral vestibulospinal tracts.

d) These pathways provide a motor system parallel to the pyramidal system for activation of the LMNs. They descend through the brain stem and spinal cord and synapse on the LMNs. Note that they do not directly connect the cortex and the LMNs.

e) These pathways are believed to regulate postural adjustments and non-skilled repetitive stereotyped motor activity of axial and proximal muscles of the limb. The degree to which they play a role in fine skilled movements is not clear.

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B. OTHER MOTOR REGULATORY CENTERS

1.1. Cerebellum Cerebellum a) Cerebellum does not initiate motor activity but plays a key role before and during motor

activity.b) Cerebellum “coordinates” muscle contractions to produce smooth movements by

regulating the sequence, rate, force of contractions of agonists and antagonists.c) Cerebellar hemispheres regulate ipsilateral limb muscles; vermis regulates the trunk,

neck and proximal limb muscles.d) Cerebellum does not have tracts that end on the LMNs directly. It acts through

bidirectional connections between it and the cerebral cortex, and between it and the brain stem motor centers.

2.2. Basal nuclei (ganglia)Basal nuclei (ganglia)a)Often referred to by neurologists as the “extrapyramidal system”.b) BN do not initiate motor activity.c)When the cortex starts a motor activity, BN come into play to ensure that the desired

activity is sustained and any unwanted movements are eliminated.d) BN do not have tracts that end on the LMNs directly, although some recent findings

challenge this traditional notion. BN act through bidirectional connections with the motor cortex to regulate its activity.

IV.IV. ORGANIZATION OF THE PYRAMIDAL SYSTEM (TRACTS)ORGANIZATION OF THE PYRAMIDAL SYSTEM (TRACTS)

The term pyramidal system is applied to the tracts that pass through the pyramids. These include the corticospinal and the corticonuclear (bulbar) tracts. They arise in the cerebral cortex; the former innervate the anterior horn cells, and the latter, the cranial nerve motor nuclei.

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L.L.CorticospinalCorticospinal TT

A. Corticospinal TA. Corticospinal T

Rubrospinal Rubrospinal TT

L.L.ReticulospinalReticulospinal TT

M. Reticulospinal TM. Reticulospinal T

Vestibulospinal TVestibulospinal T

Spinal cord white matter Spinal cord white matter –– Descending motor tracts: UMNsDescending motor tracts: UMNs

A. MOTOR CORTEX

1. Higher level motor “association” corticesa) The planning and programming of motor activity (includes the selection of muscles to

contract and relax, the sequence of these actions, etc.), precedes the activation of the motor cortices and are believed to occur in the supplementary motor area (SMA) and the premotor area (PMA).

b) SMA is on the medial surface of the frontal lobe anterior to the paracentral lobule and the PMA occupies the posterior part of the superior frontal gyrus.

c) Dynamic imaging studies have shown increases in blood flow to these areas prior to the increase in the PCG or when a subject mentally rehearses the sequence of a movement.

d) The PMA and SMA in turn activate the neurons in the relevant parts of the primary motor cortex depending on the body part involved in the voluntary activity.

2. Primary motor cortexa) Primary motor cortex (PMC) gives origin to the corticospinal and corticonuclear tracts.

Neurons of origin are found largely in the in the precentral gyrus (PCG) and the paracentral lobule.

b) The remaining axons come from the general sensory cortex, the sensory association areas in the parietal lobe and some from the PMA and SMA.

c) In the PMC, there is a somatotopic representation of body parts:i. Body is represented in an upside-down orientation, with the feet and legs in the

paracentral lobule, and the hands and face at the lower end of the precentral gyrus near the lateral sulcus.

ii. Area of the cortex devoted to body parts is not proportionate to their sizes but to the complexity of motor functions subserved by each. For example, the hand, especially the thumb, and structures involved in speech, i.e., tongue, lips and larynx, are represented over a larger area of the cortex compared to the trunk or the lower limb.

iii. Another notable feature of the PMC is that its vascular supply comes from the middle and anterior cerebral arteries. Each artery supplies specific somatotopic areas represented in the precentral gyrus.

B. CORTICOSPINAL TRACT

1. Origin and coursea) Axons of the neurons gather subcortically in the corona radiata. b) Below the corona, the tract condenses into a compact bundle traveling in the posterior

limb of the internal capsule.i. Here, it is placed between the caudate nucleus and the

thalamus medially and the lentiform nucleus laterally. ii. A somatotopic arrangement is believed to exist in the

posterior limb of the internal capsule, with the fibers destined for the upper limb anterior to those for the lower limb.

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c) The corticospinal tract passes through the middle three-fifths of the crus cerebri. Upper limb fibers are more medial to the ones destined for the lower limb.

d) The tract traverses the ventral part of the pons where the fiber bundles are dispersed among the pontine nuclei, without any clear somatotopic localization.

e) Axons gather in the upper medulla to form the pyramid. 75% to 90% of the axons cross in the pyramidal or motor decussation at the junction of the medulla and spinal cord to

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form the lateral corticospinal tract and enter the lateral funiculus. The remaining fibers descend uncrossed in the medial part of the ventral funiculus as the anterior corticospinal tract.

4. Termination of corticospinal tractsa) Lateral corticospinal tract

i. Found throughout the cord in the lateral funiculus.ii. Axons leave the tract at all levels and terminate by synapsing on the LMNs in the

anterior horn on the same side as the tract (contralateral to the side of their origin). They largely end on neurons that innervate muscles in the distal parts of the limbs.

iii. At any level below the decussation, esp. at the level of the spinal cord, damage to the tract will affect the LMNs and skeletal muscles of the same side as the tract.

iv. However, above the level of the pyramids, damage to this pathway will produce contralateral UMN signs and symptoms because of the pyramidal decussation.

b) Anterior corticospinal tracti. This tract is found at the cervical and upper thoracic levels of the cord

only.ii. Many of its axons end contralateral to the side of origin, by crossing in the

white commissure, and synapse on the medial group of motor neurons in the anterior horn. A significant number of axons are believed to remain without crossing, and synapse on the LMNs of the ipsilateral side. Thus, the tract ends bilaterally.

iii. This tract affords bilateral and simultaneous activation of the LMNs in the medial group of anterior horn cells that innervate axial muscles (i.e., of neck and trunk).

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1185% Crossed =Lat. Corticospinal T

15% Uncrossed = Ant. Corticospinal T

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C. CORTICONUCLEAR (CORTICOBULBAR)TRACTS

1. Origin and Coursea) As described earlier, the corticonuclear tracts are the equivalents of the corticospinal

tracts and end on and control the cranial motor nuclei that innervate the skeletal muscles of the head and neck.

b) Exception: Control of III, IV and VI nuclei that work in pairs is different from that of other cranial motor nuclei, are controlled by other cortical areas and is described under a separate heading.

c) The tracts originate from PMC from the area that represents the face and head region, close to the lateral sulcus. In addition, contributions come from the PMA, SMA, the general sensory cortex and the sensory association areas in the parietal lobe.

d) These axons travel with the corticospinal tracts parts of the way.i. In the corona radiata, they are intermingled with the corticospinal tracts.ii. In the internal capsule, the corticonuclear tract lies in the posterior limb, anterior to

the corticospinal fibers representing the upper limb.Note: Older literature placed these tracts in the genu but more recent tractography studies show that they are located in the posterior limb.

iii. In the middle three-fifths of the crus cerebri, they are medial to the corticospinal fibers representing the upper limb

iv. In the basal part of the pons and the pyramid, the corticospinal and corticonuclear tracts are intermingled and indistinguishable.

e) In contrast to the corticospinal tract, axons leave the corticonuclear tract at all levels of the brain stem to terminate on cranial motor nuclei.

f) In contrast to the corticospinal tract, the corticonuclear tracts do not extend much below the medulla except to innervate the nucleus of XI in the upper cervical cord.

2. TerminationThere are three patterns of innervations of cranial motor nuclei.a) Bilateral: V, IX, X and XI

i. Some corticonuclear tracts end bilaterally on cranial motor nerve nuclei. In the middle third of the pons, crossed and uncrossed fibers end on V motor nuclei.

ii. In the medulla crossed and uncrossed fibers end on the nucleus ambiguus of IX and X.

iii. At C2-C5 cord levels, crossed and uncrossed axons end on XI nucleus.b) Partly bilateral and partly contralateral: VII

i. The facial nucleus is located in the lower pons and is functionally divided into two parts: an upper group of neurons that innervate frontalis and orbicularis oculi, i.e., upper facial muscles, and a lower group of neurons that innervate levator anguli oris, levator labii superioris etc., i.e., lower facial muscles.

ii. Of these, the neurons that regulate the upper face receive bilateral innervation from the corticonuclear tracts.

iii. Neurons that regulate the lower face receive strictly contralateral input from the corticonuclear tract.

iv. Thus, the upper face (forehead) is dually controlled by both sides; whereas, the lower face (muscles below the eye) is dependent on the contralateral face area in PCG and contralateral corticonuclear tract for activation and is vulnerable to unilateral lesions.

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c) Contralateral i. Hypoglossal nucleus is contralaterally innervated by the corticonuclear tracts. ii. This means that each hypoglossal nucleus depends on the contralateral cortex and

corticonucler tract for activation.

V.V. FUNCTIONS OF THE UPPER MOTOR NEURONSFUNCTIONS OF THE UPPER MOTOR NEURONS

A. CORTICOSPINAL TRACTS

Corticospinal tracts are essential for voluntary control of contralateral skeletal muscles of the neck, trunk and limbs. They initiate voluntary activity, in response to sensory perception, thoughts, emotions, memory or commands. Corticospinal tracts are predominantly involved in rapid finely coordinated non-stereotyped skilled movements involving small muscles, especially of the hand, as in playing the piano, and muscles involved in speech.

B. CORTICONUCLEAR TRACTS

Corticonuclear tracts similarly control the voluntary contractions of the muscles of the head innervated by cranial nerves V, VII, IX, X, XI and XII. The corticonuclear tracts exert largely bilateral control (except for lower face and muscles innervated by XI) since most of the muscles involved such as the jaw, laryngeal, pharyngeal and palatine muscles need to be activated simultaneously on both sides for the normal functioning of these visceral structures.

C. UMN PATHWAYS FROM BRAIN STEM CENTERS

As mentioned earlier, these pathways are known to regulate motor activity, primarily of a non-skilled variety, involved in postural adjustments and more automatic motor activities such as walking. Their roles in skilled voluntary activity are not clear. Isolated lesions of these centers/pathways are rare. It is sufficient for you to know that lesions that affect the corticospinal tracts are likely to also involve these pathways and that the combined deficits contribute to the full-blown UMN paralysis.

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CORTICONUCLEAR TRACTS

Upper face

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VI.VI. SIGNS AND SYMPTOMS OF A LMN PARALYSISSIGNS AND SYMPTOMS OF A LMN PARALYSIS

A. Lesions of any part of the LMN lead to a lower motor neuron type of paralysis, limited to the muscles innervated by the corresponding neurons/nerves. Remember that the LMN is essential for the contraction and sustenance of skeletal muscles. They are the so-called “final common pathway” to skeletal muscles.

B. A LMN lesion may involve:1. Anterior horn cells (poliomyelitis, anterior spinal artery syndrome)2. Brain stem motor nuclei (infarcts/ischemia) 3. Ventral roots of spinal nerves (prolapsed intervertebral disc)4. Spinal nerves, plexuses (cervical rib) 5. Peripheral nerves (peripheral neuropathies, entrapment syndromes)6. Cranial nerves (compression by tumors/aneurysms)

C. A LMN syndrome is characterized by symptoms and signs that include:1. Loss/diminution of contractile strength of the affected skeletal muscle/s. This is

referred to as weakness or paralysis. LMN paralysis tends to be not widely distributed as a hemiplegia but is more likely to affect a limb or parts of a limb, as in poliomyelitis.

2. The paralyzed muscles lose their resting state of partial contraction, or tone. This leads to hypotonia or complete loss of tone, called atonia or flaccidity.

3. Deep tendon reflexes (DTR’s) mediated by the muscles are diminished or lost: hyporeflexia or areflexia.

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4. Since the skeletal muscle depends on the LMNs for survival, the denervated muscle fibers degenerate and disappear, replaced by connective tissue. This results in muscle atrophy that sets in fairly rapidly and is irreversible.

5. During the stage of atrophy, the denervated muscles exhibit contractions of groups of muscle fibers visible to the naked eye (fasciculation) and twitching of individual muscle fibers, not visibly apparent but detected on electromyography (fibrillation)

.VII.VII. SIGNS AND SYMPTOMS OF AN UMN PARALYSISSIGNS AND SYMPTOMS OF AN UMN PARALYSIS

A. An UMN disorder will deprive the LMNs of the control normally exerted by the UMNs. The LMNs and their connections to skeletal muscles remain intact, but muscle strength, voluntary activity, tone and reflexes are all modified by this loss of control.

B. Symptoms and signs of UMN lesions include : 1. Loss of strength (weakness) and voluntary movements (paralysis) in the affected

muscles on the contralateral side since most pathology tends to be unilateral. Bilateral involvement of the UMNs as in ALS will lead to bilateral paralysis of the muscles innervated.

2. Since UMNs occupy compact areas in many parts of their course, small lesions are likely to deprive a large number of LMNs of their control. The results are usually manifested in one half of the body (hemiplegia), both lower extremities (paraplegia), or one limb (monoplegia). The result is a loss of strength leading to weakness of the affected parts of the body. You may also come across the term “paresis” which refers to partial weakness.

3. Paralysis predominantly affects the distal parts of the extremities and makes it impossible or difficult to perform highly coordinated and skilled voluntary movements such as playing the piano. Larger proximal limb muscles and axial muscles are often spared or recover from the insult. Similarly, paralysis tends to be greater in extensors of the upper limb and flexors of the lower limbs.

4. Tone in an UMN lesion is increased, leading to a state called spasticity, sometimes embellished as a “clasp-knife” phenomenon. Hypertonia is greater in flexors of the upper limbs and extensors of the lower limbs, leading to the typical posture of flexed upper limbs and hyperextended lower limbs of hemiplegia and a “circumduction gait”. Patient is disabled not only by the weakness but by the spasticity as well.

5. The increase in tone is associated with exaggerated DTR’s, or hyperreflexia, with/without clonus.

6. Absence of profound muscular atrophy (except for long-term disuse atrophy) and absence of fasciculations or fibrillations.

7. Abnormal or extensor plantar reflex (Babinski sign) - dorsiflexion of the big toe and abduction of the other toes when the lateral border of the sole of the foot is stimulated with a dull pointed object. This is believed to represent a release phenomenon from the inhibition normally exerted on the flexor response by the UMNs.

8. Diminished or absent superficial (abdominal, cremaster) reflexes.9. Spinal shock: In complete and acute lesions that transect the spinal cord (trauma,

transverse myelitis, infiltrating intrinsic tumors), there is a 2-3 week period immediately following the damage that is characterized as “spinal shock”. This is believed to result from a rapid loss of the UMN control. This stage is associated with:(a). Flaccid paralysis of all the muscles below the level of the lesion(b). Loss of bladder and bowel functions

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(c). Hypotonia and areflexiaAfter 2-3 weeks, spinal shock is replaced by the typical hypertonia, spasticity and hyperreflexia described above. Neurologists are less definitive whether a similar phenomenon is consistently observed in acute brain injury.

10. All UMN lesions above the level of the cord will also affect the corticonuclear tracts. Because of the bilateral innervation of most cranial nerve nuclei, it is uncommon to detect paralysis of the innervated muscles as a result of unilateral lesions (see exception below). There may be a small reduction in the strength of these muscles on both sides due to loss of bilateral innervation from the lesioned side. Bilateral involvement of the UMNs as in ALS leads to bilateral paralysis of the muscles innervated, esp. those of the pharynx, larynx, tongue and palate.

C. Examples of lesions affecting the facial UMN pathways:

1. Hemispheric stroke2. Infarct/ischemia/compression at the level of the midbrain3. Infarct/ischemia/compression at the level of the medulla of the midbrain

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LMN (Peripheral) ParalysisLMN (Peripheral) ParalysisLeft 7 Nucleus/nerveLeft 7 Nucleus/nerve

UMN (Central) ParalysisUMN (Central) ParalysisRight corticonuclear tracts Right corticonuclear tracts above lower ponsabove lower pons

4. Exception: Bilateral sparing of the upper face (possibly with some minimal weakness), associated with contralateral lower facial paralysis is the typical feature of lesions anywhere above the level of the facial nucleus, i.e., cortex to lower pons. Expect a lower facial paralysis contralateral to pathologies in the cortex affecting the face region, subcortical white matter in corona radiata, posterior limb of the internal capsule, midbrain and upper and middle thirds of the pons.

5. This is in sharp contrast to a facial paralysis such as the Bell's palsy resulting from involvement of the nerve, or a facial paralysis due to a lesion affecting the facial nucleus in the pons, or compression of the nerve by an acoustic neuroma in the cranial cavity. In these cases, the subsequent paralysis will be of the LMN type and will involve the entire face on the same (ipsilateral) side of the lesion.

VIII.VIII. REGULATION OF CONJUGATE EYE MOVEMENTS REGULATION OF CONJUGATE EYE MOVEMENTS

A. CONJUGATE EYE MOVEMENT

1. Voluntary eye movements can be in the horizontal or the vertical plane and normally occur in a conjugate manner, i.e., both eyes moving in the same direction.

2. There are two major systems of conjugate eye movements: a) Saccades that are rapid movements that redirect gaze to each new stationary object of

interest to place it on the fovea. There are many types: intentional, memory-guided, stimulus-induced, etc. The rapid phase of nystagmus is a saccade elicited by activity in the FEFs to bring the eyes to look straight ahead.

b) Smooth pursuit movements track moving objects, again in an attempt to place them on the fovea.

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B. PATHWAYS FOR SACCADES IN THE HORIZONTAL PLANE

1. Pathways for horizontal saccades are the best understood. These involve muscles and cranial nerves that move the eyes laterally and medially. For each eye the lateral rectus (LR) is the abductor and the medial rectus (MR) is the adductor. The LR is innervated by cranial nerve VI (Abducent) and MR by cranial nerve III (Oculomotor).

2. Under normal conditions, eyes move in a conjugate fashion. This means that to look to the right, we use the right LR (abduction) and the left MR (adduction). For this, we need to activate our right VI and the left III nerve. To look to the left, we use the left LR and the right MR through activation of the left VI and the right III nerves.

3. The motor commands for these movements are generated by the frontal eye fields (FEF) in the posterior part of the middle frontal gyrus.

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4. From FEF, a descending pathway reaches the pons by ill-defined routes. 5. In the pons, axons cross and end on the opposite side in the "center for horizontal

(lateral) gaze" in the paramedian pontine reticular formation (PPRF), located near the VI nucleus.

6.6. PPRF sends axons to the VI nucleus on the same side to activate the lateral rectus muscle on the same side, i.e., the side opposite to that of the frontal eye field concerned.

7. Axons of VI nucleus leave by way of the VI nerve to innervate the LR muscle of the same side. Some axons cross to the opposite side to enter the medial longitudinal fasciculus (MLF) to reach III nucleus on the opposite side, i.e., same side as the corresponding frontal eye fields. This results in activation of the opposite MR muscle.

8. Activation of frontal eye fields on one side will result in contractions of the LR on the opposite side and the MR on the same side.

9. The result is a horizontal conjugate deviation of both eyes to the opposite side.

C. PATHOLOGY OF HORIZONTAL CONJUGATE GAZE With Any type of pathology that destroys the FEF of one side, the patient will be unable to move both eyes to the opposite side due to absent or reduced activity of the injured FEF. 1. Unopposed activity of the intact eye fields will produce spontaneous

deviation of eyes toward the side of the lesion. This is typically seen in coma resulting from a cortical lesion involving the frontal eye fields. If the cortical lesion extends to the motor cortex and results in contralateral hemiplegia, eyes will look away from the hemiplegia.

2. A unilateral brain stem lesion at the level of the pons that involves the PPRF and the VI nucleus will result in an inability to move the eyes to the side of the lesion. Normal activity of the intact PPRF and VI nucleus on the opposite side will lead to a drift of the patient’s eyes to the side opposite to the lesion. If the pontine lesion affects the

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corticospinal tracts and leads to hemiplegia on the opposite side, eyes will look toward the hemiplegic side.

3. Demyelination of MLF, often occurring in multiple sclerosis, results in a failure of the ipsilateral eye to adduct as the contralateral eye is being abducted, a condition referred to as "internuclear ophthalmoplegia (INO)".

Control of Horizontal Conjugate Gaze

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Lesion #1: Rt. Frontal

Eye fields/Frontal

lobe

Lesions Affecting Horizontal Conjugate Gaze

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Lesion #2:Left

PPRF/LOWER PONS

Lesions Affecting Horizontal Conjugate Gaze

IX.IX. EEXAMPLESXAMPLES OFOF UMN UMN ANDAND LMN LMN LESIONSLESIONS

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Lesions Affecting Horizontal Conjugate Gaze

Lesion #3:Right MLF

See PowerPoint slides

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