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65 Cards in this Set

  • Front
  • Back
Dyskinesia, ataxia, bradykinesia, akinesia, hypokinesia, hyperkinesia
Dyskinesia – Literally means dys - abnormal and kinesia – movement.
This very general term is often used to imply an abnormal movement associated with a lesion of the Basal Ganglia.
Bradykinesia – movements are slowed down (from brady – slow).
Common disorder in Parkinson’s Disease and a large variety of disorders collected together under the umbrella of Parkinsonism.
Akinesia – absence of movements (from a – without and kinesia - movement).
Hypokinesia – decrease in amount of movements
Hyperkinesia – increase in amount of movements
Planning and execution of movement
Plan and program:
-Sensory association and prefrontal cortex sends info to basal ganglia, cerebrocerebellum, and pre & supplementary motor cortex
-Basal ganglia and cerebrocerebellum feed info to pre & motor cortex
-Pre & supplementary motor cortex and cerebro-cerebellum feed into primary motor cortex (executive motor area)
-primary motor cortex feeds to brainstem motor nuclei (executive motor area), spinal cord and cranial nerve motor nuclei, and vestibulo and spino-cerebellum
-brainstem motor nuclei also feed to spinal cord and cranial nerve motor nuclei
-spinal cord and cranial nerve motor nuclei give sensory input and feedback which goes to primary motor cortex, sensory association, and prefrontal cortex, and vestibulo and spino-cerebellum
Alpha motor neurons
exert final control over muscle
-aka LMN and final common pathway
Basal ganglia and cerebellum role in movement
Help Plan and Organize Movements But Do Not Project Directly to Lower Motor Neurons
-Structures that project to motor neurons are called Executive Motor Areas
General principles of motor system
The motor system is somatotopically organized
-structures organized as map of body
Reflexes are the basis for complex movements
There are medial and lateral descending systems
-Control coarse vs fine movements
-Axial/proximal vs distal musculature
Most brain structures represent the contralateral body
-Cerebellum is ipsilateral
-Know where the pathways run and where the decussations are
Extensors and flexors are physiological
-i.e., refer to work against gravity
Anatomical Flexors & Extensors May Not Be Physiological Flexors & Extensors
Hip & knee extensors stand us up against gravity
-They are both anatomical and physiological extensors (e.g., quadriceps)
Foot extensors, which dorsiflex the foot, are wired (in the spinal cord) like the hip and knee flexors
Arm flexors are wired like leg extensors
-They work against gravity
-They are anatomical flexors but physiological flexors & extensors (e.g., biceps)
Cortical lesions manifest themselves in physiological extensors, not anatomical ones
-Flexor posturing
-Babinski sign
Arms flexed & legs extended
Cortical or CST damage
-Release of Red nucleus excites upper limb flexors
-Release of reticulo- and vestibulospinal tracts excite leg extensors
Decorticate (flexor) posturing
Arms flexed & legs extended
Cortical or CST damage
-Release of Red nucleus excites upper limb flexors
-Release of reticulo- and vestibulospinal tracts excite leg extensors
Develop over time
Decerebrate (extensor) posturing
Arms & legs extended in response to painful stimulus
-Upper Brainstem damage
-Release of reticulo- and vestibulospinal that excite both upper and lower limb extensors
Develop over time
Babinski sign
Normal adult response is ventroflexion
-A skin reflex that works to support body against gravity as foot touches the ground
Pathological response is extension (dorsiflexion)
-part of a flexion reflex in response to painful stimulus
CST suppresses dorsiflexion to non- painful stimuli
Lesion of CST releases flexion reflex
Executive motor areas
Primary Motor Cortex (Area 4)
Brainstem nuclei that send axons to spinal cord to control movement
Divided into medial and lateral systems
The cerebellum and basal ganglia are not included
Lateral descending motor system
Lat. Corticospinal
-Distal limb musculature
-Terminate only contralaterally
-Terminate in a few segments
-Terminate on motor neurons and interneurons
Terminations of the lateral
systems are in the dorsolateral
ventral horn and intermediate zone

They are always unilateral
Medial descending motor system
Ant corticospinal tract
Sup Colliculus
Vestibular N.
Reticular Formation
-Axial and proximal musculature
-Terminates both ipsi- and contralaterally
-Terminates over many segments
-Terminates on interneurons
Terminations of the medial
systems are in the ventromedial
ventral horn and intermediate zone

They are usually bilateral
Emotional motor system
Neocortical & Limbic Inputs Influence Movement via the Lateral & Medial Systems
Medial descending pathways from brainstem
The Tectospinal fibers arise from neurons in the Superior Colliculus and their axons cross immediately in the midbrain to descend in the ventral medial brainstem and spinal cord. When Tectospinal fibers arrive in the spinal cord they innervate the medial ventral horn on both sides.

The Vestibulospinal fibers arise from two vestibular nuclei that may be grouped together to innervate the medial ventral horn on both sides. Bilateral
The Reticulospinal tract arises from the reticular formation in the pons and medulla to descend in the ventral cord. These fibers descend the entire length of the spinal cord to innervate the medial ventral horn on both sides. Ipsilateral

All terminate on interneurons
Reticular formation
Runs through the core of the brainstem
Midbrain and rostral
Pons involved in arousal
and attention

Caudal pons and medulla
give rise to reticulo-
spinal tracts
The Reticulospinal
tracts originate in
magnocellular RF
in the pons & medulla

They regulate axial &
proximal musculature

They are involved in
postural adjustments
& coarse movements of
the head, trunk
& proximal limbs

Descending projections from large cell (medial)
Tectospinal tract
The Tectospinal tract mediates visual influences on movement, especially during the tracking of objects in visual space
Major influence is on neck and upper trunk musculature
Originates in Superior Colliculus
It decussates in midbrain & travels contralaterally
Vestibulospinal tract
The vestibulospinal
tracts mediate
vestibular influences
(sense of balance, location & movement of head) on movement, especially for
postural adjustment
Both the lateral and the medial vestibulospinal tracts are part of the medial descending system

Medial vestibular n. projects bilaterally
Anterior corticospinal tract
The anterior corticospinal tract contains corticospinal fibers that do not decussate in the pyramid. These fibers represent about 15% of the corticospinal tract.
Note the anterior corticospinal tract innervates the medial ventral horn on both sides of the spinal cord. It is also part of the medial descending system.
The anterior corticospinal tract has a direct effect on bilateral proximal limb and trunk movements. It also stimulates the reticular formation to provide cortical supervision and command of the reticulospinal tract
Red nucleus
The Red Nucleus Is the Only Brainstem Nucleus Contribution to the Lateral Descending System
The largest cells of the red nucleus are the magnocellular cells
-These form the rubrospinal tract.
-Travel in lateral column
-We don’t really know what rubrospinal projections do
-They could direct well-learned movements
-Their predominant effect is to excite upper limb flexors
-This is visible in decorticate rigidity

The parvocellular
portion of the Red
nucleus projects to the inferior olive
Primary motor cortex
Primary Motor Cortex Is the Main Contributor to the Lateral CST Somatosensory cortex contributes fibers that terminate in the dorsal horn and modulate ascending sensory inputs
Fibers running in the internal capsule
Note the anterior limb funnels fibers between the medial caudate and lateral putamen. It contains fibers from the anterior subdivision of the thalamus to the frontal and prefrontal cortex.
The corticobulbar tract passes in the genu.
The posterior limb funnels fibers between the medial thalamus and lateral lentiform nucleus (here the globus pallidus and the putamen are shown). The corticospinal fibers travel within the posterior limb of the internal capsule. From medial to lateral the somatotopic organization is ATL – (arms, trunk, legs). The posterior limb also includes somatosensory information traveling to the thalamus (VPL and VPM) and from the thalamus to the primary sensory cortex. The most posterior regions of the posterior limb include auditory and visual radiations.
Damage to corticospinal tract
Increased tone in leg extensors and arm flexors (decorticate rigidity)
Increased resistance to passive movement
Increased deep tendon reflexes
-Varies with speed of movement
-Clasp knife response
-Inverse stretch reflex –
Upper vs lower motor neuron syndrome
-Corticospinal tract and its neurons of origin
-Paralysis or paresis
-Hyperreflexia of deep tendon reflexes
-Spasticity – Increased Tone
-Babinski sign
-Loss of ability to perform fine movement
-Acute spinal shock evolves to spasticity

-Alpha Motor Neurons and their axons
-Paralysis or paresis
-Loss of muscle tone
-Loss of reflexes or hyporeflexia with partial injury
-Fasciculation and fibrillation
-Muscle atrophy
Premotor cortex
Neurons in the Premotor Cortex Are Involved in the Preparation for Movement and Help Select Movements Based on External Cues.
Prior to a stimulus there is no activity in the premotor cortex or PMA as shown by the neuron recording in the top panel.
With a light stimulus (external cue) there is immediate activation to form a rapid motor plan to move the upper limb.
With the completion of the plan the PMA neuron returns to baseline.
Supplementary motor cortex
Supplementary Motor Cortex Creates Internal Representations and Memories of Movements

Simple Movements Activate Only Primary Motor
& Somatosensory Cortex

Complex Movements Activate Primary,
Pre & Supplementary Motor Cortex

Mentally Planning Complex Movements Activates
Supplementary Motor Cortex
Motor thalamus
The Motor thalamus is in the rostral part of the ventral tier
-Ventral Anterior n
-Ventrolateral n
--Vlo Basal Ganglia input
--VLc Cerebellar input
--VLc is equivalent to VIM in humans
Spasticity vs rigidity
Spasticity: CST
-Increased tone in leg extensors and arm flexors (decorticate rigidity)
-Increased resistance to passive movement
-Increased deep tendon reflexes
--Varies with speed of movement
--Clasp knife
--Inverse stretch reflex

Rigidity: BG
-Increased tone in both flexors and extensors
-Increased resistance to passive movement
--Lead pipe – limb stays where placed
--Cog wheel (Parkinson’s)
-Limbs stay where placed
Muscle strength tests
0/5: Paralysis - no muscle contraction
1/5: muscle contraction flicker, but no observed movement
2/5: Severe Paresis: - movement possible, but failure against gravity, this is a severe weakness or paresis
3/5: moderate paresis - movement possible against gravity but failure against resistance applied by the examiner
4/5: minor paresis - movement possible against some applied resistance,
5/5: Normal Strength
Two types of muscle fiber
Fast or White fibers:
Fast Fatigable Type 2 fibers or fast-twitch, (2B)
-glycogen rich (anaerobic - less myoglobin and fewer mitochondria). Lightly stained for oxidative enzymes.
-Rapidly generate highest contractile force but rapidly fatigue (make up about two thirds of the fibers in typical muscles).
Fast Fatigue Resistant (2A)
Intermediate fibers:
-intermediate size and exhibit myoglobin/cytochrome content and mitochondrial numbers between the other two types.
-Moderate force generated and moderately fatigue resistant.

Slow or Red fibers – Fatigue Resistant:
-Type 1 fibers or slow-twitch,
-high quantity of myoglobin (hence red), mitochondria and therefore rich capillary beds (aerobic dependent). Darkly stained for oxidative enzymes (NADH-TR)
-Highly resistant to fatigue but generate low muscle tension
make up about one third of the fibers in typical limb muscles
Innervation of Muscle
The synapse between motor neurons and muscle is called the neuromuscular junction (NMJ)
-The NMJ is also called the the “motor end plate”
Acetylcholine is neurotransmitter released from motor neuron terminals
-It activates nicotinic Ach receptors on muscle
-The pharmacology of nicotinic receptors is clinically important
Each muscle cell is innervated by only one neuron
Motor neurons supply trophic factors needed for muscle survival

There are two types of motor fibers
-Alpha motoneurons – skeletal muscle (extrafusal fibers)
-Gamma motoneurons – muscle spindle (intrafusal fibers)
There are several types of sensory endings
-Muscle spindles - stretch receptors,
--Aa & Ab fast axons
-Golgi Tendon Organs - muscle tension receptors
--Aa axons
-Mechanoreceptors A b
-Fast pain - Ad
-Second pain - C
Motor unit
An α motor neuron and the muscle fibers it innervates
-Large motor neurons innervate many different muscle fibers
-Small motor neurons innervate only a few muscle fibers
-The muscle cell needs trophic factors released from the neuron terminal to survive
--These trophic factors also determine the physiological properties of the muscle
A pool of motor neurons innervates a whole muscle
-The Pool of Motor Neurons That Innervate a Whole Muscle Are Found in Multisegmental Columns
Contractile Tension (force) in a single muscle fiber is dependent on the firing rate of the innervating LMN
Low firing frequencies create a small amount of tension
Higher firing frequencies produce larger tension
At higher firing rates, the muscle doesn’t have time to relax, so the tension created by each new contraction is added to the preexisting tension until tetanus is produced
-Tetanus - the muscle remains locked in a sustained position of contraction without stretch
The size principle
The black line shows dynamic changes in whole muscle tension as a task begins and continues and red lines to indicate the size of motor units participating in the task. The task begins with small motor units (short red lines). Note as more force is required and the whole muscle tension increases the size of the added motor units (illustrated by the length of the red line) also increases.

Small motor neurons are activated by small currents (excitatory synaptic inputs)
Large motor neurons need larger currents
Therefore, smaller motor neurons (units) are activated first by low levels of excitatory input
Reflex overview
Self-corrective responses to bring system back to some set point
Reflex circuits organize movement so the brain doesn’t have to pay attention to every detail
Descending influences modulate reflex circuitry
Different upper motor neuron lesions lead to well-described alterations in reflexes
-They are diagnostic
Muscle spindles
-Input about stretch from muscle spindle via Aα fiber
-Terminates on alpha motor neuron
Reciprocal inhibitory innervation relaxes antagonist
Projects to spinal cord, somatosensory cortex & cerebellum
Has efferent control to alter sensitivity
Intrafusal muscle fibers
Intrafusal fibers have striated, contractile ends
-Like regular muscle fiber
Middle of fiber can stretch, like a rubber band
-Stretch of whole muscle pulls on middle
-Contraction of its own ends will stretch middle
-Sensory receptors wrapped around middle to detect stretch
Motor and sensory innervation of muscle spindles
gamma- Motor firing can
modify sensory fiber
-dynamic and static

Aα fibers most sensitive to active stretch and
respond best when
stretch is happening

Aβ fibers most sensitive to
sustained stretch
Respond at low threshold to light stimulus
Functions of muscle spindle
Detects stretch (length) of muscle
-Rate of stretch
-Absolute length
Gamma motor input controls sensitivity
-Dynamic γ increases sensitivity to ongoing stretch
-Static γ increases sensitivity to maintained stretch
-Allows spindle to respond even while muscle is shortening
--α and γ motor neurons are activated together
--Normally, intra & extrafusal fibers contract together
Responses of a alpha muscle spindle
With a continuous heavy load placed on muscle there is rapid A alpha firing rapidly reporting Muscle Stretch. As stretch (or load on the muscle) is maintained the sensory fibers continue to report maintained stretch.
Deep Tendon Reflex: A brief hammer tap on a tendon lengthens the whole muscle and the A alpha briefly reports a burst of stretch information.
Rhythmic pulling of a muscle elicits waves of A alpha feedback
A rapid release of a heavy load stops A alpha firing until the spindle can be reset by gamma motoneurons. The reset spindle fires at a background baseline low frequency waiting for a new stimulus of muscle stretch to increase the frequency of firing.
Responses of gamma motor neuron
Without gamma motoneurons the spindle cannot be reset with whole muscle contraction.
The figure on the right shows how the gamma motoneuron resets or retightens the spindle so it can again report stretch. The gamma motor neurons can regulate the gain of muscle spindles so that they can operate efficiently at any length of the parent muscle.
Descending control of LMN and reflexes
The typical effect of descending cortical UMN activity is to inhibit stretch reflexes
-This allows for more intentional control of movement
Cortical UMN lesions release stretch reflexes and increase muscle tone
-Especially in leg extensors and arm flexors
These effects are due to the influences of intact reticulo and vestibulospinal pathways
Rhytmic sustained muscular contraction brought about by stretching
-Literally, a tiny “tumult”
-Rhythmic series of agonist and antagonist contraction cycles resembling mini limb seizures
-Typically seen after UMN lesion
-Reflects uncontrolled cycling of stretch reflex
The Golgi Tendon Organ
GTO (golgi tendon organs) are located within the dense regular connective tissue where the muscles connects with the tendon. Sensory axons intermingle with the collagen fibers. As the muscle contracts there is a tremendous load placed on the collagen fibers (tensile strength). The GTO measures muscle contraction by measuring how hard the muscle is pulling the tendon.

Detect muscle tension (force of contraction), especially at the onset of contraction
-Tension information detected by the GTO is complimentary to length information detected by muscle spindles
-Information provides negative feedback to the spinal cord LMN
-Ascends in dorsal columns and spinocerebellar tracts
Innervated by Aβ sensory axons
Normally, GTO feedback helps muscles contract smoothly
-Ultimately, Golgi tendon sensory fibers may prevent tissue damage by setting limits on strength of muscle contraction
Clasp-knife response may be pathological manifestation of inverse stretch reflex
Inverse stretch reflex
Originates in Golgi tendon organ
Disynaptic inhibtion of homonymous muscle
-Inhibits the alpha motor neuron preventing tension overload
Excitation to antagonist muscles

The Inverse Stretch Reflex Is Only Apparent After UNM Lesions
-Cog wheel rigidity
-clasp knife reflex
Renshaw cells
Govern the Motor Neurons Locally Through Recurrent Inhibition

Recurrent collateral from motor neuron activates Renshaw cell
Renshaw cell innervates the motor neuron that activates it
-Inhibits firing of motor neuron that activated it
-acts as a brake
Renshaw cells use GABA as a neurotransmitter
-Virtually all inhibitory interneurons use GABA as a neurotransmitter

Explain why benzodiazepines can be effective muscle relaxers
Flexion reflexes
Noxious (painful) stimuli activate primarily free nerve endings in skin (Aδ)
Graded according to intensity of stimulus
Complex Response
-Ipsilateral activation of synergistic flexors
--Inhibition of extensors
-Contralateral effects reciprocal
--Inhibition of flexors and excitation of extensors
-Multisegmental via propriospinal interneurons
Overrides other reflexes to pull endangered limb away from threat
The circuitry of the flexion reflex includes crossed reciprocal innervation of flexors and extensors.
This pathway permits the opposite lower limb to support weight (extensor activation for standing) to compensate for opposite leg flexion – leg withdrawal
The Flexion Reflex
Demonstrates Intersegmental
Integration Mediated by the collateral branches of Long Propriospinal Sensory Axons
Vestibular reflexes
Evoked by changes in position of head
-Vestibular information from semicircular canals
Acts on neck and limbs
-Act on neck to keep head aligned with respect to gravity
-Prepare upper limbs to block a fall
--Activation of anatomical extensors
Neck reflexes
Visual stimuli and auditory stimuli evoke protective movements
- Evoked response results in bending or turning the neck
Visual tracking also supported by these relfexes
Affects arm, leg, and neck muscle in a coordinated fashion
Integrated with vestibular reflexes
Postural adjustments
Postural Adjustments are elicited in response to three kinds of sensory input
-Muscle and joint proprioceptor feedback
-Vestibular system feedback
-Visual stimuli
Anatomy of pupillary light reflex
This slide illustrates the anatomy of the pupillary light reflex. Axons of retinal ganglion cells make up the afferent limb of this pathway. Upon exiting the retina, retinal ganglion cell axons follow the usual route (i.e., optic nerve, optic chiasm, optic tract), however, instead of synapsing in the LGN, the axons of cells involved in the pupillary light reflex continue on to enter the brachium of the superior colliculus enroute to their site of termination, the pretectal nucleus. The pretectal nucleus is found at the level of the posterior commissure, just anterior to the superior colliculus and just posterior to the thalamus (i.e., the midbrain-diencephalon junction).
The efferent limb begins at the pretectal nucleus. Fibers exit the pretectal nucleus and project bilaterally to the Edinger-Westphal nucleus, the preganglionic parasympathetic component of the oculomotor complex. The preganglionic fibers exit as part of Cranial Nerve III (oculomotor nerve) enroute to the ciliary ganglion (located near the eye within the orbit). The postganglionic fibers enter the eye as the short ciliary nerve and innervate the pupillary sphincter (constrictor).
Direct and consensual pupillary light reflex
Constriction of the illuminated pupil is referred to as the direct response. Constriction of the other pupil is called the consensual response
Afferent pupillary light reflex
The bottom panel shows an abnormal response. In this case, illuminating the subject’s left eye fails to produce constriction of either pupil. This pattern of result, i.e., direct (right eye) and consensual (left eye) response when the right eye is illuminated but no response in either eye when the left eye is illuminated, points to a deficit in the afferent limb of the pathway originating on the left side. Such a patient would be diagnosed as having a left afferent pupillary defect (LAPD). The mirror symmetric pattern would, of course, be diagnostic of a right afferent pupillary defect (RAPD).

Afferent defects need not be all-or-none, as in the case of total blindness in one eye. Lesions of the afferent limb that produce partial visual impairment are associated with differences in the magnitude of the light reflex induced by illumination of the two eyes. Inflammation of the optic nerve (optic neuritis) is condition that might lead to a partial visual impairment.
This slide shows the results of an examination that would indicate a partial afferent defect on the right side. Weaker (constricts to 4mm vs 2mm) direct and consensual responses produced when light is shone in the right eye (bottom panel) indicates that the right afferent limb has less light detecting capability than the left.
Efferent pupillary light reflex
A lesion of the efferent limb of the pathway is one that is located anywhere from the pretectum to the short ciliary nerve. Use the pathway figure to confirm that a lesion of the efferent limb will obliterate (or diminish) both the direct and consensual responses for the pupil of one eye. Note that this pattern is quite distinct from that produced by a lesion of the afferent limb.
This slide shows a hypothetical efferent lesion of CNIII (oculomotor nerve)
The most common efferent pupillary defect is Adie’s syndrome, which is associated with denervation of the intraocular muscles innervated by the ciliary ganglion (both the pupillary sphincter and the ciliary muscle). Viral ciliary ganglionitis is thought to be a cause.
Afferent vs efferent pupillary light reflex lesions
Afferent Lesion
(to optic nerve)
Light on pupil ipsi to lesion
-direct response? NO
-consensual response? NO

Light on pupil contra to lesion
-direct response? YES
-consensual response? YES

Efferent Lesion
Light on pupil ipsi to lesion
-direct response? NO
-consensual response? YES

Light on pupil contra to lesion
-direct response? YES
-consensual response? NO
Anatomy of sympathetic pupillary dilation
The sympathetic chain involves the hypothalamus and mediates effects that are secondary to arousal. One of these is dilation of the pupils. Beginning in the hypothalamus, this relatively long pathway goes into the cervical spinal cord and synapses on cells in the intermediolateral zone. From there, it’s to the superior cervical ganglion, and then to the pupillary dilator via the long ciliary nerves.
Near reflex
1.Convergence. Contraction of the medial recti (extraocular muscles that cause nasal rotation of the eyes) to make the eyes converge. Convergence is necessary to put the image of a near object on the fovea. The nearer the object, the more convergence needed.
2)Accommodation. Contraction of the ciliary muscle causes the lens to become more spherical (increasing refractive power). The nearer the object, the greater the refractive power needed to focus the image on the retina.
3)Constriction of the pupil. The amount of pupillary constriction depends on the nearness of the object. Constriction of the pupil limits the amount of light that reaches the retina from surrounding objects. The effect (like with the aperture on a camera) is to increase the depth of field.

Note that the efferent pathway to the ciliary muscle (accommodation) and the pupillary sphincter (pupillary constriction) are the same beginning with the Edinger-Westphal nucleus. Both muscles are innervated by the short ciliary nerves, the output of the ciliary ganglion, which receives its input from E-W nucleus. As a result, lesions that affect the pupillary light reflex are also likely to affect accommodation (e.g. Adie’s syndrome -See above).
Argyll-Robertson pupil
This is named after the physician who noted that a patient could show normal pupillary constriction associated with the near response but a poor or absent light reflex. Despite sharing part of the efferent pathway to the pupillary sphincter, anatomical differences elsewhere make it possible for a lesion to impair one without the affecting the other. In the past, light-near dissociation was a good diagnostic for neurosyphillus and is also a component of syndromes associated with midbrain lesions (e.g. Parinaud’s syndrome).
Rectus and oblique eye muscles
medial rectus, lateral rectus (CN VI), inferior rectus, and superior rectus.

inferior oblique (up) and superior oblique (CN IV) (down)
Abducens nerve palsy

Trochlear nerve palsy
causes the right eye to deviate in the nasal direction as compared to the left (normal) eye

When the superior oblique is impaired the eye deviates upward and extorts (rotates clockwise from the patient’s perspective) as compared to the normal eye.
Occulomotor nerve gaze palsy
Down and out
Coordinated conjugate eye movements
It is important to note that, in addition to innervating the lateral rectus muscle (via CNVI), the abducens nucleus indirectly influences the action of the medial rectus on the opposite side to allow for coordinated conjugate movements. This is accomplished via a projection that crosses the midline (shown in purple) and terminates in the oculomotor nucleus (III). These so-called internuclear fibers travel in what’s called the medial longitudinal fasciculus (MLF) enroute from the abducens to the oculomotor nucleus. As we’ll see shortly, disruption of these internuclear fibers creates a clinical condition known as internuclear opthalmoplegia.
Internuclear opthalmoplegia
Example of right internuclear opthalmoplegia: This woman is first asked to look to her right (top photo), which she does fine. She is then asked to look to the left (bottom photo). Note that the left eye abducts just fine, but the right eye shows incomplete adduction (Compare to above adduction).
The lesion is one that affects the internuclear fibers that run in the MLF from the abducens to the oculomotor complex.
One and a half lesion
The lesion shown here is extensive enough to encroach upon the both sets of internuclear fibers (both MLFs) as well as the PPRF and abducens nucleus of one side. In this case, we have bilateral internuclear opthalmoplegia and a unilateral deficit in abduction (right eye). The only movement this patient would be able to make is that of abducting the left eye. She is unable to look to the right at all (top photo). Upon looking to the left (bottom photo), she is only able to abduct the left eye.
Voluntary control of eye movement
Like all voluntary movements, the motor plan for producing a volutary eye movement begins in cortex. The eye movement motor command is first formed in an area of frontal cortex known as the frontal eye fields (FEF). The frontal eye fields receive inputs from visual cortex and uses this information to begin elaborating a plan to move the eyes to a visual target. Note that the system is contralateralized such that activity in the right FEF corresponds to a leftward saccade and vice versa.
Some terminology:
The FEF is part of what is called the supranuclear part of the gaze control pathway. The motor nuclei and brainstem gaze centers already presented are compose the internuclear part of the pathway, while the cranial nerves compose the infranuclear component of the gaze control pathway.
Discerning a supranuclear problem
The way to diagnose this is to check for an intact vestibulo-ocular-reflex, which must go through the same pontine regions (internuclear path). Thus, when the head is rotated to the left (as shown below), the eyes can counterrotate to the right indicating that these areas are intact. In this case the lesion was to the left internal capsule which cut off the fibers from frontal eye fields to the SC. Thus, the lesion was contralateral to the deficit which is also characteristic of supranuclear horizontal palsies.