Brain Stem

Chapter 13Brainstem II: Eye Movements and

Pupillary Control

Abnormalities of pupils and eye movements are often warning signs of pathology in brainstem or cranial nerves so careful evaluation is necessary.

Extraocular muscles produce eye movements.Internal ocular muscles control pupil size and lens accommodation.

Nuclear and infranuclear pathways involve nuclei of CN III, IV, & VI; peripheral nerves from these nuclei and eye movement muscles.

Supranuclear pathways include brainstem and forebrain circuits that control eye movements via connections with CN III, IV, & VI nuclei.

Eye Movements and Extraocular muscles

Rectus Muscles Superior and Inferior Oblique

Dual Actions of Superior Rectus Dual Actions of Superior Oblique

Extraocular Nerves and Nuclei

Oculomotor nerve (CN III) divides in 2: superior division goes to the superior rectus and levator palpebrae superioris (eyelid elevation); inferior division goes to medial rectus, inferior rectus, and inferior oblique. Also carries preganglionic para- sympathetics to the pupillary contrictor muscles and ciliary muscles of lens

Trochlear (CN IV) innervates the superior oblique muscleAbducens (CN VI) innervates the lateral rectus

Oculomotor nucleus consists of several subnuclei and is located at level of superior colliculus and red nucleus.Edinger-Westphal nucleus is site of parasympathetic preganglionic neurons.Unilateral lesions of the oculomotor nucleus affect the ipsilateral and contralateral eye since some axons cross in brainstem before nerve exits.

Trochlear nucleus in caudal midbrain at level of inferior colliculusTrochlear nerves are the only cranial nerves to exit dorsal surface of brainstem. They cross after exiting.

Abducens nuclei lie on floor of 4th ventricle at level of mid-to-lower pons.Axons travel ventrally to exit at the pontomedullary junction.

Diplopia (double vision)

Possible causes:Mechanical problems such as orbital fracture with muscle entrapmentExtraocular muscle disorder such as from thyroid disease or myositisNeuromuscular junction disorder such as myasthenia gravisDamage to CN III, IV, or VI, their nuclei or connecting pathways

In young children where visual pathways are still developing, congenital eye muscle weakness can produce strabismus that over time causes suppression of one image resulting in amblyopia (decreased vision in one eye). Early correction is critical for proper function of both eyes.

Oculomotor Palsy

Damage of oculomotor nerve or nucleus causes paralysis of all extraocular muscles except for lateral rectus and superior oblique.Only eye movement remaining is abduction, depression and intorsion.Result is that eye may take “down and out” position at rest.Paralysis of levator palpebrae will cause eyelid closure (ptosis).Common causes of oculomotor palsy include diabetic neuropathy, head trauma, compression of CN III by Pcomm aneurysm or by herniation of the uncus over the tentorial notch caused by unilateral expanding mass lesion.

Painful oculomotor palsy involving the pupil is usually due to aneurysm.Complete oculomotor palsy that spares the pupil is usually caused by diabetic neuropathy.Partial oculomotor palsy sparing the pupil may be caused by aneurysm.

Trochlear Palsy

Produces elevation of eye; patients often tuck chin and tilt head away from affected eye to correct diplopia.TN is most commonly injured CN in head trauma; tumor, infection and aneurysm can also damage TN.

Abducens Palsy

Produces horizontal diplopia; patients often turn head toward affected eye.AN especially susceptible to downward traction caused by elevated ICP, so AP is often an important early sign of supratentorial or infratentorial tumors, hydrocephalus and other intracranial lesions.Other causes of AP: head trauma, infection neoplasm, inflammation, aneurysm, and diabetic neuropathy.

The Pupils and Other Ocular Autonomic Pathways

Pupils under both parasympathetic (constriction) and sympathetic (dilation) control.Light reflex: optic nerve>optic tract>pretectal area; pretectal neurons> bilateral Edinger-Westphal nuclei>ciliary ganglion>constrictor musclesDirect response and consensual response.

Bilateral pupillary constriction also occurs via a slightly different pathway during the accommodation response.Accommodation response includes pupillary constriction, accommodation of lens ciliary muscle, and convergence of eyes.Accommodation requires activation of visual cortex (recognize closer object).

Lens is normally under tension from suspensory ligament.Ciliary muscle acts as sphincter and when contracted causes suspensory ligament to relax producing a more rounded lens for near focus.

Sympathetic pathway for pupillary dilation involves connections from hypothalamus via lateral brainstem to thoracic cord T1-T2 sympathetic preganglionic neurons whose axons go to superior cervical ganglion. Neurons of SCG project to pupillary dilator muscles of eye.Sympathetic path also controls superior tarsal muscle which elevates the upper eyelid, giving a wide-eyed stare.Sympathetic axons traveling with these also innervate sweat glands of face and neck; when damaged this gives Horner’s syndrome

Pupillary Abnormalities

Causes include peripheral or central lesions, sympathetic or parasympathetic lesions, or disorders of iris muscle or visual pathways.Pupillary abnormalities can be bilateral or unilateral.Unilateral abnormality produces pupil asymmetry = anisocoria

1. Oculomotor LesionsUnilateral dilated pupil (when large = blown pupil)Decreased or absent direct and consensual light response

2. Horner’s SyndromeDisruption of sympathetic paths to eye and facePtosis, miosis (constriction), and anhydrosisImpaired dilation responseDirect and consensual light response intact; following dilation

slowed

Locations for lesions causing Horner’s Syndrome:Lateral brainstem, spinal cord, T1 & T2 roots, sympathetic chain,

carotid plexus, cavernous sinus, orbit.

3. Afferent Pupillary Defect (Marcus Gunn Pupil)Direct light response in one eye is absent while the consensual response

in that eye is normal.Caused by lesion in retina, optic nerve or eye.

4. Benign AnisocoriaIn about 20% of general population there is a slight pupillary

asymmetry which can vary over time.

5. Pharmacological Miosis (constriction) and Mydriasis (dilation)Opiates cause bilateral pinpoint pupils.Barbiturates cause small pupils.Anticholinergic agents like atropine or scopolamine cause dilation.Anticholinesterase agents (sarin, nerve gas) cause constriction.

6. Light-Near DissociationPupils constrict much less in response to light than to

accommodation.Classic example is Argyll Robertson pupil typically associated with

neurosyphilis in which pupils are small and irregular andshow light-near dissociation.

LND also seen in diabetic neuropathy and Parinaud’s syndrome(compression of dorsal midbrain).

Ptosis (drooping eyelid)

Eye opening involves levator palpebrae superior (CN III) and Muller’ssmooth muscle in upper eyelid (sympathetic control); frontalismuscle of forehead (CN VII) also plays accessory role.

Eyelid closure done by orbicularis oculi muscle (CN VII).Common causes of ptosis:

Horner’s syndromeoculomotor nerve palsymyasthenia gravisredundant skin folds that occur with aging (pseudoptosis)

Cavernous Sinus & Orbital ApexCN III, IV, and VI pass through CS and lesions here produce

characteristic syndromes that often affect eye movements.Cavernous sinus is a group of venus sinusoids on either side

of the pituitary that receives venous blood from the eyeand adjacent areas of cortex.

5 CN branches run through the CS:CN III, IV, VI and V (ophthalmic and maxillary divisions).Sympathetics going to pupil travel through CS also.

Coronal planeLooking from front to back

Orbital apex is the region just caudal to the eye where most all of thenerves, arteries and veins of the orbit converge beforepassing into the optic canal & superior orbital fissure.

Cavernous Sinus SyndromeLesions of CS can affect one or more nerves passing through.Complete lesion causes complete loss of eye movement and

fixed, dilated pupil, and sensory loss in V1/V2 dermatomesof trigeminal.

Orbital apex lesions are likely to also include the optic nerve andalso often produce proptosis, bulging eye due to masseffect in the orbit.

Causes of CS Syndrome:metastatic tumornasopharyngeal tumormeningiomapituitary tumoraneurysm of intracavernous carotidcavernous carotid ateriovenous fistulabacterial infection causing CS thrombosis

Orbital Apex SyndromeCommon causes:

metastatic tumorsorbital cellulitis (bacterial infection)orbital myositisfungal infection

Both CS and OA Syndromes are medical emergencies requiring immediate treatment due to carotid artery involvement.

Supranuclear Control of Eye Movements

Brainstem, cerebellum and forebrain all contribute to control of eyemovements via effects on CN nuclei III, IV, and VI.

3 main types of eye movements:Horizontal eye movementsVertical eye movementsVergence eye movements

Types of Eye Movement1. Saccades – rapid eye movements directed at targets in visual field2. Smooth pursuit – slower movements following objects in visual field3. Vergence – movements to maintain visual fixation on objects moving toward or away from viewer4. Reflex – including optokinetic nystagmus & vestibulo-ocular reflex

Nystagmus: rhythmic form of reflex eye movement in one direction interrupted by fast saccade-like movement in the opposite

direction (a few beats are normal when patient turns eyes far to side, continued beats or beats when eyes turned small amount is abnormal.

Brainstem Pathways for Control ofHorizontal Eye Movements

Brainstem Circuits forHorizontal Eye Movements

Controlled by lateral rectus (CN VI) and medial rectus (CN III).MLF interconnects nuclei of III, IV, VI and vestibular nuclei.This interconnection makes conjugate eye movements possible.Nucleus VI acts as horizontal gaze center by controlling movement of both eyes by projecting to the ipsilateral lateral rectus and the contralateral III nucleus.Pontine tegmentum near nucleus VI has the paramedian pontine reticular formation that projects to nucleus VI to activate lateral gaze.

Brainstem Lesions Affecting Horizontal Gaze

MLF lesions interrupt input to medial rectus so the eye ipsilateral to the lesion does not fully adduct on attempted horizontal gaze; there is also often nystagmus in the contralateral eye.This syndrome is called internuclear ophthalmoplegia (INO)

Common causes of INO: multiple sclerosis pontine infarct tumors near MLF

Brainstem Circuits for Vertical Eye Movements

Vertical eye movements mediated by superior and inferior rectus and superior and inferior oblique muscles.Centers controlling vertical eye movement located in rostral midbrain reticular formation and pretectal area.

Ventral region mediates downgaze.Dorsal region mediates upgaze.

Locked-in syndrome caused by large pontine infarct/hemorrhage often damages corticospinal tracts bilaterally and nucleus VI, thereby eliminating body movement and horizontal eye movement; patient can then communicate only via vertical eye movements.

Brainstem Circuits for Vergence Eye Movements

Convergence is produced by medial recti muscles and divergence by lateral recti muscles.Exact location of brainstem vergence centers not known, but neurons in

midbrain reticular formation appear to be involved.Visual cortex and parietal cortex involved as part of the accommodation

response.

Parinaud’s Syndrome

Includes a group of eye abnormalities caused by compression of the dorsalmidbrain and pretectal area:

1. Impairment of upgaze2. Large, irregular pupils that do not react to light but may react to accommodation3. Eyelid abnormalities ranging from bilateral lid retraction to ptosis4. Impaired convergence

Most common cause is pineal tumor and hydrocephalus.Hydrocephalus can cause dilation of the suprapineal recess of the 3rd

ventricle which pushes downward on the tectum.Hydrocephalus in children can produce the bilateral “setting-sun sign” in which the eyes are deviated inward due to CN VI palsy and downward due to Parinaud’s Syndrome.

Forebrain Control of Eye Movements

Multiple paths descend from forebrain and affect eye movements.These paths project either directly to brainstem nuclei involved with eye movements or relay via the superior colliculus.Frontal eye fields appear to be in area 6.FEF generates saccades in the contralateral direction via connections to contralateral PPRF.Parieto-occipital-temporal cortex functions in smooth pursuit eye movements in ipsilateral direction via connections with the vestibular nuclei, cerebellum, and PPRF.Inputs from visual cortex and visual association cortex influence FEF activity.Basal ganglia also appear to play a role in eye movements.

Right-Way Eyes and Wrong-Way Eyes

Cerebral cortex lesions may impair eye movements in the contralateral direction and so produce eyes directed toward the lesion side.This gaze preference is typically accompanied by muscle weakness contralateral to the lesion side so that eyes look away from the side of paralysis. This is the typical “right-way eyes.”Certain lesions/abnormalities can cause eyes to look toward the side of paralysis, which is “wrong-way eyes.”Causes of “wrong-way eyes”: 1. Cortical seizures can drive eyes in contralateral direction by activating FEFs, while causing weakness on the contralateral side of body controlled by seizing cortex. 2. Thalamic hemorrhage can disrupt corticospinal paths of internal capsule and also cause eyes to deviate toward the side of weakness. This may be accompanied by coma. 3. Pontine basis and tegmentum lesion which damages corticospinal fibers can also damage VI nucleus or PPRF causing ipsilateral gaze weakness.

Cerebellar, Vestibular and Spinal Control of Voluntary and Reflex Eye Movements

Two common reflex eye movements:1. Optokinetic nystagmus (OKN) – can be triggered in patient by moving a thick ribbon with vertical stripes horizontally in front of the eyes. Eyes alternate between smooth pursuit movements in the direction of stripe movement and backup saccades in the opposite direction. Sometimes called “train nystagmus” because it can be observed in the eyes of train passengers as they view passing scenery while on a moving train. Slow phase (smooth pursuit) mediated by ipsilateral posterior cortex via connections to vestibular nuclei and cerebellum projecting to the PPRF and nucleus VI. Fast phase (saccades) mediated by FEFs projecting to contralateral PPRFLesions of frontal cortex disrupt fast phase of OKN while lesions of posterior cortex disrupt smooth pursuit movements.

2. Vestibulo-Ocular Reflex (VOR) – stabilizes eyes on visual image during head and body movements. Vestibular nuclei inputs via MLF control extraocular nuclei. Tested using oculocephalic maneuver or cold water calorics. While prone head is rotated and eyes should move opposite to direction of head turning. Cold water irrigation of ear should produce nystagmus with eyes beating in contralateral direction.