midbrain

what is included in the midbrain tectum?

superior and inferior colliculi - also called the corpora quadrigemina

superior colliculus

superficial layers - recieve direct RGC axonal input

deeper layers - sensory (visual, auditory, somatosensory and motor functions

visual & auditory orienting reflexes

90% of optic nerve fibers travel to LGN for conscious visual processing

10% goes to superior collicus and the pretectal nucleus via brachium of superior colliculus

2 pathways: tectobulbar and tectospinal

tectobulbar pathway

CONTRALATERAL

optic tract fiber → superior (& inferior) colliculus → cranial nerve nuclei

• eye closures V2 - blinking

• eye movement  CN 3 4 6

• head turning CN 6 and C2-C4

tectospinal pathway

CONTRALATERAL

optic tract fiber → superior (& inferior) colliculus → motor neurons of anteriror gray column of spinal cord

body movements C5 forward

brachium of superior colliculus

arm of the superior collliculus

crus cerebri (aka basis pedunculli)

location: ventral of the midbrain

includes:

• corticopontine fibers from occipital, parietal, temporal lobes

• corticospinal tract: voluntary movement of contralateral body

• corticobulbar tract: bilateral voluntary movement ABOVE neck - except tongue and face (if one side has lesion, the other side still work)

• corticopontine fibers from frontal lobe: coordination of movement thru communication w cerebellum

oculomotor naming

• fascicles: when traveling in the midbrain

• - nerves: after it leaves the midbrain

anatomical locations of 4 nuclei in midbrain

• these nuclei are ventral to the cerebral aqueduct

• The oculomotor nuclear complex is located at the level of the superior colliculus, ventral to the periaqueductal gray matter, and dorsal to the medial part of the red nucleus.

• trochlear nucleus is located inferiorly to oculomotor nucleus, associate w CN4

red nucleus function

motor coordination and balance

Edinger-Wesphal nucleus

a nuclei of oculomotor nerve responsible for pupil constriction and accommodation

trochlear nucleus

control CONTRALATERAL superior oblique muscle

crosses at the superior medullary velum, the trochlear nucleus becomes trochlear NERVE and is ipsilateral

the course of CN 3

fasicular (EW nucleus or oculomotor nucleus) → subarachnoid segment → intracavernous segment → intraorbital segment

intracavernous segment has which nerves and arteries

Mnemonic CATOOM

C: cavernous portion of intracavernous artery

A: abducens nerve

T: trochlear nerve

O: oculomotor nerve

O: ophthalmic division CN V1

M: maxillary division CN V2

superior orbital fissure

contains CN 3, 4, V1, 6, ophthalmic vein

optic canal

contains CN 2, opthalmic artery

CN 3 intraorbital segment

• superior division:

oculomotor nucleus → oculomotor nerve → levator palpebrae superioris / superior rectus

• inferior division:

oculomotor nucleus → oculomotor nerve → medial rectus / inferior rectus / inferior oblique

Parasympathetic: Edinger-Wesphal nucleus (pregang)→ nerve of inferior oblique → ciliary ganglion (postgang) → ciliary muscle (constrict / dilate)

lesion at the ciliary gang will not affect eye movements, just dilation/constriction

lesion anywhere in the course can cause CN 3 paresis

superior divisional CN 3 paresis : upper eyelids ptosis, limited supraduction

parasympathetic functions of CN3

parasympathetic fibers of CN3 originated from EW nucleus → synapse at the ciliary ganglion in the orbit → innervates constrictor pupillae and dilator pupillae

does sympathetic pathway make a synapse at ciliary ganglion?

sympathetic (innervating blood vessels, not iris dilators) & sensory fibers (from corneam iris, ciliary muscles) pass thru ciliary ganglion WITHOUT synapse

short ciliary nerves

• efferent fibers

• contain parasympathetic, sympathetic and sensory fibers, pierces the sclera around optic nerve to supply the globe

majority of short ciliary nerve supply ciliary muscles (accommodation at NEAR), 3% supply iris sphincters (30:1 ratio)

tonic pupil

pupil does not react to light and may constrict SLOWLY to near target during accommodation

not associated w EOM problem or 3rd nerve palsy, ptosis

ciliary ganglion pathology

parasympathetic innervation to the eye

EW nucleus in midbrain → oculomotor nerve → inf division → parasympathetic root → ciliary ganglion → short ciliary nerves → one of these: 

iris sphincter → pupil mitosis (constriction @N&D)

ciliary muscle → accommodation (constriction @N)

sympathetic innervation to the eye

ophthalmic division V1→ nasociliary nerve (branch of V1) → one of these:

• long ciliary nerve → iris dilator → dilate iris

• sympathetic root → ciliary ganglion (NO synapse) → short ciliary nerves → choroidal and conjunctival blood vessels → vasoconstriction

which CN are involved in pupillary light reflex? and their functions.

CN 2 - carrying sensory signal to the midbrain (afferent)

CN 3 - carrying motor signals to the pupillary sphincter muscles (efferent). begins at the EW nucleus

Afferent pupillary light reflex pathway

pupillary fibers starts at RGC → optic nerve → cross at optic chiasm → optic tract →  branch off at posterior 3rd of optic tract → brachium of superior colliculus → terminate in pretectal area (olivary pretectal nucleus) of midbrain → half of the fibers innervate the IPSILATERAL EW Nucleus, the other half cross in the posterior commissure to innervate the CONTRALATERAL EW

Efferent pupillary light reflex pathway

efferent fibers from EW neurons (pregang) travel in the superficial dorsomedial aspect of the IPSILATERAL oculumotor nerve to reach the ciliary ganglion (postgang) → axons from ciliary gang travel in the short ciliary nerve (30:1 ratio of innervating ciliary muscle : iris sphincters)

iris sphincter

miosis = pupil constriction at both near and distance

direct and consensual pupillary response

when light is shone into 1 pupil, expect:

• direct response from ipsilateral pupil

• consensual response from contralateral pupil

why is there a consensual response in pupil?

1. nasal retinal fibers cross in the chiasm

2. about half the fibers from each pretectal nucleus cross in the posterior commissure

will lesion on posterior commissure affect consensual response?

yes, because the contralateral eye will not receive any light signal from the pretectal area

CN 3 accomodation pathway

parasympathetic component of CN 3 innervates ciliary muscle → zonular fiber relax → lens becomes more round → accommdation

near responses triad

pupil constriction

accommodation

convergence

→ they do not share the same efferent pathway meaning they can be abolished independently

will low vision patient have near response?

yes because vision is not a prerequisite for near response, it can be observed in the blind when they fixate on a near object

what happen when there is a lesion at OD optic nerve?

APD of OD will be observed. There will be no direct response but consensual response is ok 

what happen when there is a lesion at left optic tract?

APD in the contralateral eye will be observed since this is after the crossing at chiasm and it has more fibers

does lesion in the LGN cause APD?

no because LGN is not involved in pupil light reflex pathway

does lesion in area 17 cause APD?

no because area 17 is not involved in pupil light reflex pathway

is RAPD commmonly associated w vision loss?

most cases will cause low vision acuity, low color vision, and other vision related issues.

lesions on optic tracts do NOT cause vision problems.

is it possible to have RAPD without any vision loss?

yes, lesions on optic tracts do not cause vision impairment

can RAPD be checked if one pupil iis fixed due to injury or inflammation?

the pupil on the fixed eye will not have any constriction/dilation, but can still check for consensual of the contralateral eye

is RAPD associated w anisocoria?

APD is afferent pathway and anisocira is a efferent pathway (motor) - they don’t really associate

how many ciliary nerve are there?

2 long (sensory and sympathetic nerve)

6-10 short (sensory, sympathetic, and parasympathetic fibers)

quantifying RAPD using neutral density filters

RAPD can be detected when it’s 0.6 log unit or greater, smaller RAPD requires more skills/experience

is RAPD expected in unilateral cataract?

not in regular cataract

dense cataract cause RAPD in opposite eye because the cataract eye does not get the regular amount of light to the retina → weak ligh response for both direct and consensual → opposite eye appears to have APD but it doesn’t actually have one

APD in patching

up to 1.5 log units in unoccluded eye because of that unoccluded eye has become less senstive to light → weaker response comparing to the the patched eye which has become more sensitive to light

Why is pupillary testing important?

because the superficial location of the pupillary fibers make them vulneratble for compression lesions such as aneurysm causing efferent pupillary effects. when involved 3rd nerve palsy it becomes life threatening

efferent pupillary defect

disruption in the efferent pathway (EW nuclei → CN3 fascicle/nerve → ciliary gang/short ciliary nerve) cause poor direct and consensual resposnes and a poor near response

damage in CN3 could involve some or all of EOM and or levator dysfunction

what happens when there is a lesion in the ciliary ganglion or short ciliary nerve?

efferent pathway is disrupted

Acute phase: poor rxn to light w sectoral palsy of the iris sphincter

Chronic phase: about 8wks after onset, strong and tonic pupillary response to near (light-near dissociation-LND) 

peripheral light-near dissociation symptoms

• reduced or absent pupil constriction to light

• slow tonic pupil constriction to near stimuli, slow-redilation when looking from near to far

• sectoral paresis of pupil, vermiform movement(worm-like twitching)

• no ptosis or motility problems → other CN 3 problems

• idiopathic → Adie tonic pipil (unilateral)

mechanism of peripheral light-near dissociation

injury to ciliary ganglion / short ciliary nerves that innervate the sphincter, over time they get regenerated (2 types: accommodation fibers innervate ciliary muscle and pupillary fibers innervate sphincter 30:1 ratio) but since there is a heck more accommodation fibers than pupillary fibers (sphincter), some of the accommodation inaccurately innervate the sphincter → inefficient regular pupil constriction but tiny response at near light response due to having a few of the accommondation fibers there.

upper eyelid innervation

CN 3: innervates the levator muscle of the upper eyelid, allow it to raise voluntarily

CN 7: innervates the orbicularis muscle to close the eye

Sympathetic nerves innervate the Mullers muscle

oculomotor sub-nuclei

• central subnucleus: bilateral innervation to levator superioris muscle (keeps the eye lids up)

• medial subnucleus: contralateral innervation to superior rectus muscle

• lateral subnuclei: 

  • dorsal: ipsilateral innervation to inferior rectus muscle

  • intermediate: ipsilateral innervation to inferior oblique muscle

  • ventral: ipsilateral innervation to medial rectus muscle

what happen if there is a lesion at the central subnucleus of the oculomotor nerve?

bilateral ptosis will be observed

what happen if there is a lesion at the lateral subnuclei or medial subnuclei?

bilateral effects will be observed because the subnuclei are very close to each other

3rd nerve palsy symptoms

def: complete damage of 3rd nerve

symptoms:

• lids Droopy (ptosis)

• pupil Dilated

• eye Down and out → cause Diplopia

causes of 3rd nerve palsy

• nucleus lesion: rare, complete unilateral 3rd nerve palsy w bilateral SR weakness and bilateral ptosis

• fascicular lesion: thường hay bị chung với mấy bệnh thần kinh khác -  contralateral hemiparesis (Weber’s), contralateral ataxia and tremor (Benedikt’s)

• subarachnoid: typically isolated, may have headache / pain, need to rule out aneurysms (the 3rd nerve is compressed)

• cavernous: CN 4,6,V1, V2, horner’s, pain

• orbital apex: proptosis (eye bulging), visual loss, cranial nerve 4,6,V1, horners, pain

anisocoria

pupil size of each eye is not equal

• if the difference between each pupil is the same in both bright and dim, it is physiological (no need to worry)

• if pupil size difference is greater in dim light, the small pupil is the problem, then it can be mechanical restriction to dilation or Horner’s

• if pupil size difference is greater in bright light, the big pupil is the problem, check for ptosis and EOM:

  • if yes to either: 3rd nerve palsy

  • if no to both: check for tonic pupil, can also be damage in mydriatic agent in iris

dorsal midbrain syndrome

aka Parinaud’s syndrome

upgaze palsy

pupil’s light-near dissociation

tegmental midbrain syndrome

ipsilateral 3rd nerve palsy

red nucleus is affected: contralateral ataxia, involuntary movement

ventral midbrain syndrome

aka Weber syndrome

ipsilateral 3rd nerve palsy

contralateral hemiplegia (movement weakness in the lower face, arm, and leg)

trochlear nucleus and fascicle

• fibers from the nucleus course dorsally and DECUSSATE before exiting the brainstem immediately below inferior colliculus

• the only cranial nerve to exit dorsally

portions of trochlear nerve

• cisternal portion

• cavernous sinus portion

• orbital portion

which muscle does the CN 4 innervate?

ipsilateral superior oblique muscle

which muscle does the trochlear nucleus innervate?

contralateral superior oblique

contralateral SO Muscle paresis and ipsilateral Horner’s localize the lesion where?

midbrain (CN 4 nucleus / fascicles BEFORE decussation)

4th nerve palsy

Superior: the affected eye is higher

Oblique: head tilts opposite to the affected eye

• pt adopts the head tilt to the opposite side to the affected eye to reduce diplopia

ex: OD is raised higher, head tilts to the left → lesion at the right 4th nerve

Parks-Bielschowsky 3 step test

Right eye hyper at primary gaze

Hyper worse on left gaze

Hyper worse on right head tilt

do 3 cover tests

superior oblique muscle actions

intorsion

depression

abduction

example of 4th nerve palsy

long standing case