Brainstem and eye movements

Question 1

Vestibulospinal tract

Answer 1

Paraveterbral extensors and proximal limb extensors (posture and balance)

Lateral: from the ipsilateral lateral vestibular nucleus through the lateral funiculus and throughout the spinal cord to the ipsilateral ventral horn. controls muscles to maintain upright posture and balance

Medial: from the ipsilateral and contralateral median vestibular nuclei through the anterior funiculus in the cervical spinal cord to the ipsilateral ventral horn. Controls head position in association with vestibular stimuli

Question 2

Reticulospinal tract

Answer 2

Through gamma MNs, maintaining posture and modulating muscle tone

arises bilaterally from the pontine and medullary areas, travels thorugh the lateral and anterior funiculi, throughout the spinal cord, and to the ipsilateral ventral horns and intermediate zone. Controls movement and posture control and modulates sensory activity

Question 3

Tectospinal tract

Answer 3

Head movements for orienting reactions
Head movement in response to sound or light is controlled by the tectospinal tract. There is no muscle below neck-shoulder level innervated by the tectospinal tract.

arises from the contralateral superior colliculus, held within the anterior funiculus, travels through the cervical spinal cord, and terminates at the ipsilateral ventral horn. functions in head position in association with eye movement.

Question 4

Rubrospinal Tract

Answer 4

arises from the midbrain contralateral red nucleus, carried in the lateral funiculus, travels throughout the spinal cord, and terminates in the ipsilateral ventral horn. function in movement control

goal-directed movements
through interneurons on MNs
control distal limb muscles
innervating proximal limb flexors (upper limb)
Humans w/ corticospinal lesion, it provides remaining function to control distal muscles

If a lesion in the mid-brain below (or caudal to) the red nucleus, the rubrospinal tract is interrupted between the red nucleus and the spinal cord, you will see the patient with decerebrate rigidity. If the lesion above or rostral to the red nucleus, the cortical inhibition on the red nucleus is interrupted, the patient shows decorticate rigidity

Question 5

Decerebrate Rigidity

Answer 5

Patient has extended upper and lower limbs and neck.
Patients with trauma, vascular disease or tumors may present this way. Section through the neural axis between the superior and inferior colliculi produces decerebrate rigidity. The tonic over-activity due to the un-inhibited influence of reticulospinal tract and vestibulospinal tract (by the cortex) without rubrospinal influence due to the rostral location of the red nuclei

If a lesion in the mid-brain below (or caudal to) the red nucleus, the rubrospinal tract is interrupted between the red nucleus and the spinal cord, you will see the patient with decerebrate rigidity. If the lesion above or rostral to the red nucleus, the cortical inhibition on the red nucleus is interrupted, the patient shows decorticate rigidity

Question 6

Decorticate Rigidity

Answer 6

Patient has flexion of upper limbs and extension of lower limbs and trunk muscles.
Section through neural axis rostral to superior colliculus.
The resulting unchecked rubrospinal drive overexcites flexor motor neurons which in humans is limited to upper limbs (due to the interrupted cortical inhibitory influence to the red nuclei), in addition to the tonic over-activity of reticulospinal tract and vestibulospinal tract

This lesion interrupts the cortical inhibition to all three descending medial tracts and the rubrospinal tract (the only brainstem lateral tract)

If a lesion in the mid-brain below (or caudal to) the red nucleus, the rubrospinal tract is interrupted between the red nucleus and the spinal cord, you will see the patient with decerebrate rigidity. If the lesion above or rostral to the red nucleus, the cortical inhibition on the red nucleus is interrupted, the patient shows decorticate rigidity (see next two slids).

Question 7

CN III Palsy

Answer 7

Lateral strabismus caused by unopposed action of the lateral rectus muscle.
Inability to direct the eye medially or vertically.
Drooping of the upper eyelid (ptosis) – as a result of levator palpebrae palsy.
Dilation of the pupil, enhanced by unopposed action of the dilator pupillae muscle in the iris.
The ciliary muscle does not contract to allow the lens to increase in thickness for focusing on near objects.

Question 8

CN IV - Superior Oblique Palsy

Answer 8

Causes vertical diplopia, which is maximal when the eye is directed downward and inward.
Patients experience difficulty in walking downstairs.
Rare
isolated lesion of the trochlear nerve as a manifestation of a peripheral neuropathy (e.g., in diabetes mellitus)
occasional persistent complication of head injury.

Question 9

CN VI – Lateral Rectus Palsy

Answer 9

Causes medial squint (or strabismus) with an inability to direct the affected eye laterally.
Lesions to the abducens nucleus paralyze the contralateral medial rectus. Patient cannot direct the gaze to the side of the lesion.
A nuclear lesion may also involve the nearby nucleus or axons of the facial nerve, causing paralysis of all the ipsilateral facial muscles.

CN VI (right side) neuron (and the PPRF – the center controls horizontal eye movements) sends the axon across to the contralateral side through the (left) MFL to control CN III neuron (left side) - the LMN directly innervates and controls (left) medial rectus

Question 10

Saccade

Answer 10

ballistic movements shift fovea rapidly to visual target

Keep the fovea on a visual target in the environment

Question 11

Smooth pursuit

Answer 11

keep image of moving target on fovea

Keep the fovea on a visual target in the environment

Works by calculating how fast object is moving and moves eyes accordingly. Keeps moving objects on the fovea.
Smooth pursuit requires a moving target - verbal command or imagined object won’t work.
Movements are slower than saccades - max velocity about 100o/sec.
Although both saccadic and smooth pursuit movements use same brainstem centers for horizontal and vertical gaze, the central control systems are different.
Central control of smooth pursuit is ipsilateral.

Frontal eye fields is important for initiating pursuits movements.
Parieto-temporo-occipial junction provides sensory information needed to guide pursuit movements.
Motion sensitive neurons in the junction calculate velocity of the target which is sent to cerebellum (flocculus & vermis) via the pontine nuclei.
The junction (the area among BA 39, BA 19, BA 17) provide continuous signal designed to keep image of target on fovea.
Cerebellar velocity signals correlated with pursuit are sent to PPRF and medial vestibular nucleus which also drives horizontal gaze.

Question 12

Vergence movements

Answer 12

move eyes in opposite directions so that image is positioned on both foveas (convergence for near and divergence for far)

Keep the fovea on a visual target in the environment

Question 13

Vestibulo-ocular reflex

Answer 13

movements hold images still on fovea during head movements with accelerations

Stabilize the eye during head (or body) movement

VOR needs head movement to trigger the reflex, also adapts quick (with continuous movement).

Question 14

Optokinetic movements

Answer 14

hold images during sustained head (or body) movement & supplements VOR

Stabilize the eye during head (or body) movement

Optokinetic movements help as a supplement to VOR

Question 15

Visual Fixation (Foveation)

Answer 15

The fixation system holds the eye still during intent gaze.
Neural center (fixation zone): most rostral portion of the superior colliculus.
Fixation requires active suppression of eye movements.
Pre-motor neurons in the fixation zone inhibit saccades.

Question 16

Conjugate movements

Answer 16

Both eyes move in the same direction by contracting and relaxing different muscles.
Saccade, smooth pursuit, vestibulo-ocular reflex, and optokinetic movements.

Question 17

Disconjugate eye movement - vergence system

Answer 17

Converge: eyes move toward each other when object is near
Diverge: eyes move away from each other when object is farther away

Question 18

Vergence Movements

Answer 18

Near Triad
To look from a distant object to a closer one, three actions are yoked
Eyes converge by simultaneous contraction of both MR muscles (a disconjugate movement).
Pupil is constricted increasing depth of field of eye.
Accommodation - curvature of lens is increased, which increases refractive power of lens to focus near object on fovea

Neural Center of Vergence
Premotor neurons related to vergence are in the midbrain of the supraoculomotor area (SOA) close to (rostral to) the Oculomotor Nucleus.
Cells of SOA project to medial and lateral rectus motor neurons (Somatic MN).
Cells of SOA also project to motor neurons of the Edinger-Westphal nucleus that controls the pupil and lens (Viseral MN - parasympathetic).
Vergence and Saccade operate independently:
A lesion in the pontine center for lateral saccade will impair horizontal saccades, NOT convergence movement in horizontal plane

Question 19

Neural Circuits for Saccades

Answer 19

Center for Vertical Saccades - the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) in the midbrain
Center for Horizontal Saccades – the paramedian pontine reticular formation (PPRF)
Both centers provide coordination between oculomotor and abducens nuclei for saccadic and smooth pursuit movements – their movements initiated by different cortical centers, BUT share same somatic LMNs (III + VI) and ocular muscles (MR + LR)
Cortical control of horizontal & vertical saccades work through superior colliculus

Question 20

Saccadic System

Answer 20

Purpose of saccade is to move the eye as rapidly as possible from one fixation point to another
Preprogrammed rapid movements occurring in a fraction of a second and up to 800o per sec (duration <100 ms)
Visual feedback cannot modify the saccade - successive saccades are necessary
Vision is suppressed during a saccade.
Cortical control is contralateral

Question 21

Neurons Involved in Saccade

Answer 21

Burst neurons relay signals from the cortex and provide velocity component. Also provide inhibition to ipsilateral medial rectus and contralateral lateral rectus.
Abducens motor neurons project excitation to ipsilateral lateral rectus
The interneurons project to contralateral CN III - medial rectus through MLF.
Ominpause neurons inhibit burst neurons to prevent unwanted movements but are inhibited during saccade.
Abducens and oculomotor motor neuron signals contains both velocity and position signals to eye muscles.
Position signal provided by neurons in nucleus prepositus hypoglossi.

Question 22

Cortical Control of Gaze Centers

Answer 22

The brainstem saccade generator receives a command from the superior colliculus. The colliculus receives direct excitatory projections from the FEF and the lateral parietal area and an inhibitory projection from the substantia nigra. The substantia nigra is suppressed by the caudate nucleus, which in turn is excited by the FEF. Thus the FEF directly excites the colliculus and indirectly release it from suppression by the substantia nigra. Cortical areas controlling saccades are in purple, the intermediate supranuclear structures in blue, and the brain stem reticular formation (i.e., RiMLF and PPRF) in brown.

Question 23

Cortical Control of Saccades

Answer 23

Centers for Horizontal (PPRF) and Vertical (RiMLF) gaze receive commands from superior colliculus (SC).
Sub-cortical center - SC receives
excitatory commands from frontal eye field (FEF) and parietal cortex and
inhibitory commands from substantia nigra.
Substantia nigra is inhibited by caudate which is excited by FEF.
Saccade centers also receive commands directly from contralateral FEF

Question 24

Horner’s Syndrome

Answer 24

Lesions in central (A or B) or peripheral (C) sympathetic pathway can produce Horner’s Syndrome

A -occlusion of the posterior inferior cerebellar artery (Wallenberg)
B -tumor in the lung apex or occlusion of anterior spinal artery
C -lesion associated with the carotid artery

miosis: reduction in pupil diameter due to unopposed action of parasympathetic innervation
ptosis: drooping of eyelid due to loss of innervation to superior tarsal muscle
enophthalmos: apparent sinking of eyeball in socket because of the interrupted innervation
anhidrosis: lack of sweating on affected side

Question 25

Medial medullary syndrome

Answer 25

or inferior alternating hemiplegia

Occlusion of a medullary branch of the vertebral artery

Lesions to ventromedial medulla, including pyramid and axons of hypoglossal nerve

Contralateral hemiplegia
Ipsilateral hypoglossal palsy
Contralateral impaired position sensation

Question 26

Wallenberg’s syndrome

Answer 26

or lateral medullary syndrome

Occlusion of a medullary branch of the posterior inferior cerebellar A.

Infarcted area includes the inferior cerebellar peduncle and vestibular nuclei, nucleus ambiguus, the spinal trigeminal tract and spinothalamic tract

Vertigo, ataxia; ipsilateral impaired palate and vocal cord; loss of pain and thermal sensation in contralateral body and ipsilateral face; ipsilateral Horner’s syndrome

Question 27

Millard-Gubler syndrome

Answer 27

Occlusion of a pontine branch of the basilar artery

Lesion to corticospinal and abducens nerve

Contralateral hemiparesis
Ipsilateral medial strabismus or squint

Another “crossed” or alternating hemiplegia
in the pons

Question 28

Weber’s syndrome

Answer 28

or superior alternating hemiplegia

Occlusion of a branch of the posterior cerebral artery

Lesion to corticospinal tract, oculomotor nerves

Contralateral hemiparesis
Ipsilateral paralysis of ocular muscles (except LR & SO) – unable to raise the upper eyelid and lateral strabismus, dilation of the pupil

Lesion extended farther dorsally to cerebellar efferent fibers causes a tremor – the condition is known as Benedikt’s syndrome

Question 29

Nystagmus

Answer 29

involuntary rhythmic oscillations of the eyes; biphasic oscillations with an initial slow component responsible for their genesis and continuation.

Question 30

Parinaud’s syndrome

Answer 30

paralysis of upward gaze and of convergence

Lesions that involve the general vicinity of CN III nuclei, such as top of the basilar artery embolic stroke, may cause deficits in vertical eye movements. Masses in the vicinity of the aqueduct, such as pineal tumors, may compress the various nuclear groups subserving vertical eye movements and their connections with the oculomotor and trochlear nuclei, leading to impairment in vertical eye movements, especially upgaze

Question 31

Foville’s syndrome

Answer 31

caused by a dorsally located infarction in the caudal part of the pons, comprises ipsilateral CN VI palsy and lower motor neuron facial palsy, with contralateral hemiplegia. The limb paralysis recovers because most of the descending motor fibers are ventral to the infarct.

Question 32

one-and-a half syndrome

Answer 32

In the one-and-a half syndrome, there is a lesion of one abducens nucleus, as well as the crossed connections to both MLFs. Thus, in a right-sided lesion, neither eye can look to the right on attempted right conjugate gaze. On attempted left conjugate gaze, only the left eye moves, as its lateral rectus function is preserved.

Question 33

Internuclear ophthalmoplegia, also called MLF syndrome

Answer 33

caused by a tiny lesion in one medial longitudinal fasciculus (MLF) at a level between the nuclei of CNs III and VI. The usual cause is multiple sclerosis. Interruption of the fibers going from the abducens nucleus (the interneuron within the PPRF) of the opposite side to the oculomotor nucleus of the same side causes an inability to adduct the eye on the side of the lesion. These abnormalities are evident only when the patient is asked to gaze to the side opposite that of the lesion; contraction of the medial rectus occurs normally with convergence of the eyes for looking at a near object (because the SOA is located in the rostral midbrain. These premotor neurons and the CN III LMNs and the muscles are not affected). A somewhat larger lesion can involve both medial longitudinal fasiculi, causing bilateral internuclear ophthalmoplegia.

Question 34

doll’s eyes phenomenon

Answer 34

which is a vestibule-ocular reflex uncomplicated by voluntary eye movements, is another clinical sign useful in the diagnosis of coma. If the vestibular apparatus, nuclei, and nerve; the medial longitudinal fasciculus; and the abducens and oculomotor nuclei are all intact, movement of the head will be accompanied by conjugate movement of the eyes in the opposite direction. Losses of caloric responses and of the oculocephalic reflex are two signs that can contribute to a diagnosis of brainstem death.

Question 35

rubrospinal tract

Answer 35

The main lateral descending pathway from the brainstem is the rubrospinal tract, which originates in the magnocellular portion of the red nucleus in the midbrain. Rubrospinal fibers descend through the medullar to the dorsal part of the lateral column of the spinal cord. In cats and monkeys the rubrospinal tract is important in the control of distal limb muscles used for manipulating objects

Question 36

strabismus

Answer 36

Defective alignment of the eyes is called squint or strabismus. A malfunction of one or more of the extraocluar muscles causes a paralytic squint. If paralysis is complete, it is not usually difficult to decide which muscle or group of muscles is not working. When only weakness (paresis) is present, however, the squint may be apparent only when the eye is attempting to move in the direction of action of the affected muscle

Question 37

Babinski Sign

Answer 37

An important neurologic examination based upon what the big toe does when the sole of the foot is stimulated. If the big toe goes up, that may mean trouble.

One of the normal reflexes in infants. Reflexes are responses that occur when the body receives a certain stimulus. The Babinski reflex occurs after the sole of the foot has been firmly stroked. The big toe then moves upward or toward the top surface of the foot. The other toes fan out. Absence of this reflex indicates paresis or paralysis in the tested side

The Babinski sign is known by a number of other names: the plantar response (because the sole is the plantar surface of the foot), the toe or big toe sign or phenomenon, and the Babinski reflex, response or phenomenon.

It is common but wrong to say that the Babinski sign is positive or negative; it is present or absent.

Question 38

Caloric testing

Answer 38

The caloric test is used when there is a reason to suspect a tumor of the vestibulocochlear nerve or a lesion that interrupts the vestibular pathway in the brainstem. This procedure separately tests the pathway from each internal ear. The head is positioned so that the lateral semicircular duct is in a vertical plane, and the external acoustic meatus is irrigated with warm (40oC) or cold (30oC) water to induce convection currents in the endolymph. The ampulla of the duct is near the bone that is undergoing a change of temperature, and the endolymph “rises” or “falls”, depending on whether it is warmed or cooled. In a conscious subject, the procedure causes nystagmus if the vestibular pathway for the side tested is intact. This nystagmus is a series of slow conjugate eye movements (driven by the vestibular nuclei), each followed by a rapid movement (driven by the FEF in the cerebral cortex) to restore the original direction of gaze. This relationship is encapsulated in the mnemonic COWS: Cold water produces nystagmus beating to the Opposite side (fast component of nystagmus, as a result of inhibition to the vestibular sensors); Warm water produces nystagmus beating to the Same side (which stimulates the vestibular sensors). See Figure 3 the top center tracing of eye movements.
In a comatose patient with intact pathways in the brainstem, caloric stimulation with warm water makes the eye deviate to the opposite side; cold water cause a conjugate deviation toward the cooled side. The deviation is the isolated slow component of a nystagmus (still responding to the input from the brainstem). The fast component (controlled by the FEF), which is a voluntary compensation, is prevented by the absence of consciousness (interrupted control from the cortical area).