All about oculomotor nervE....

1. By- Sinchana S Kumbar

3. Intro:
The oculomotor nerve is the third of 12 pairs of cranial nerves
in the brain.
This nerve is responsible for eyeball and eyelid movement.
 The oculomotor nerve involves two separate components, each
of which has a distinct function.
somatic motor component
visceral motor component

4.  Somatic motor component - Supplies four extraocular muscles in the eye
and the upper eyelid's levator palpebrae superioris with motor
(movement) fibers.
- It controls the muscles that allow for visual tracking and fixation by
the eye.
Visceral motor component - controls parasympathetic innervation
(nerves related to involuntary actions) of the ciliary muscles and
constrictor papillae, aiding ACCOMMODATION and pupillary light
reflexes.

5. Course of III CN
ORIGIN - The oculomotor nerve originates from the anterior aspect
of the midbrain.
 It moves anteriorly, passing below the posterior cerebral artery, and
above the superior cerebellar artery.
 The nerve pierces the dura mater and enters the lateral aspect of
the cavernous sinus.
 Within the cavernous sinus, it receives sympathetic branches from
the internal carotid plexus.
These fibres do not combine with the oculomotor nerve – they
merely travel within its sheath.

6. The nerve leaves the cranial cavity via the superior orbital
fissure. At this point, it divides into superior and inferior
branches.
Once within the orbital cavity, both branches innervate
accessory structures of the eye:
a. Superior branch: Motor innervation to the superior rectus
and levator palpabrae superioris. Sympathetic fibres run with
the superior branch to innervate the superior tarsal muscle.
b. Inferior branch: Motor innervation to the inferior rectus,
medial rectus and inferior oblique. Parasympathetic fibres to
the ciliary ganglion, which ultimately innervates the sphincter
pupillae and ciliary muscles.

10. 1. The oculomotor nerve (CN III) arises from the anterior aspect
of midbrain. There are two nuclei for the oculomotor nerve:
• The oculomotor nucleus originates at the level of the superior
colliculus. The muscles it controls are the striated muscle in
levator palpebrae superioris and all extraocular muscles except
for the superior oblique muscle and the lateral rectus muscle.
• The Edinger-Westphal nucleus supplies parasympathetic fibers
to the eye via the ciliary ganglion, and thus controls the sphincter
pupillae muscle (affecting pupil constriction) and the ciliary
muscle (affecting accommodation).
Nuclei Of Oculomotor Nerve

13. Parasympathetic Functions
There are two structures in the eye that receive parasympathetic
innervation from the oculomotor nerve:
Sphincter pupillae – Constricts the pupil, reducing the amount of light
entering the eye.
Ciliary muscles – Contracts, causes the lens to become more spherical,
and thus more adapted to short range vision.
The parasympathetic fibres travel in the inferior branch of the
oculomotor nerve. Within the orbit, they branch off and synapse in
the ciliary ganglion. The fibres are carried from the ganglion to the eye
via the short ciliary nerves.

15. These structures
innervates:
SR
IR
MR
IO
LPS
Sphincter pupillae
Ciliaris muscle

16. Cn 3 i
Cn 3 s
Cn 6
Cn 4

17. It is one of the extraocular muscles.
It is innervated by the superior division of the oculomotor
nerve
Functions – Elevation
Intorsion
Adduction
Superior Rectus

18. The superior division of oculomotor nerve passes upward
lateral to the optic nerve and enters the superior rectus
muscle .
Then it pierces and terminates by supplying to the LPS

19. SR palsy commonly is of congenital origin.
The paralyzed eye is affected primarily in elevation and
abduction. Elevation is normal in adduction.
When superior rectus palsy has been present for long
periods, elevation from primary position and adduction may
also become limited.
 The ipsilateral inferior rectus and the contralateral inferior
oblique muscles overact, and a small excyclotropia usually
is present.
 The paralyzed eye is hypotropic in primary position, and
Bell’s phenomenon is absent.

21. Inferior rectus
 Innervated by inferior branch of III CN
 It depresses, adducts, and helps extort (rotate laterally) the eye
Attachments: Originates from the inferior part of the common
tendinous ring, and attaches to the inferior and anterior aspect of
the sclera.
The Inferior division of the ouculomotor nerve divides intio 3
branches , which supplies the IR,MR and IO
The branch IR runs forward

22. The patient fixates with the paralyzed eye. Note right hypotropia and
pseudoptosis in the primary position, and secondary overaction of the
superior oblique and superior rectus muscles.

23. The diagnosis is made on the basis of the prism and cover test
in the diagnostic positions and on examination of ductions and
versions.
 The deviation is greatest on attempts to look downward with
the affected eye in abduction
Diagnosis

24. Medial rectus
Attachments: Originates from the medial part of the common
tendinous ring, and attaches to the anterio-medial aspect of the
sclera.
Actions: Adducts the eyeball.
Innervation : the branch to the MR passes medially below the
Optic nerve .

25. An isolated paralysis of the medial rectus muscle without
involvement of other muscles supplied by cranial nerve III is very
rare.
With this type of paralysis the greatest defect of ocular motility
occurs when the affected eye moves into adduction.
 Since the action of the antagonistic lateral rectus muscle is
unopposed, an exotropia usually is present in primary position.

26. Right medial rectus paralysis. Exotropia in primary
position and overaction of left lateral rectus muscle

28. The differential diagnosis of an isolated medial rectus paralysis
includes internuclear ophthalmoplegia
Diagnosis

29. Inferior oblique
Attachments: Originates from the anterior aspect of the orbital floor.
Attaches to the sclera of the eye, posterior to the lateral rectus.
Actions: Elevates, abducts and laterally rotates the eyeball.
Innervation: Oculomotor nerve (CN III).
The branch to the IO , is the longest branch , that passes
forward close to the orbital floor and lateral to the IR muscle , the nerve
enters the post. Border of the Oblique muscle

30. The inferior oblique muscle is least likely to become paralyzed.
The onset is usually congenital but trauma has been mentioned as a
cause.
 In primary position the affected eye may be hypotropic or the
unaffected eye hypertropic, depending on whether the patient fixates
with the nonparalyzed or paralyzed eye.
Causes

31. The forced duction test is necessary in making this diagnosis, since the
prevalence of Brown syndrome is far greater than paralysis of the inferior
oblique muscle and since the defect of ocular motility is clinically similar.
However, with Brown syndrome the involved eye is frequently depressed
more severely in adduction than it is with inferior oblique paralysis.
Diagnosis

32. LPS
Attachment: The levator palpebrae superioris originates on the
lesser wing of the sphenoid bone, just above the optic foramen.
It broadens and becomes the levator aponeurosis.
Function: Elevates eye lid
Innervation: The sup. Division of the oculomotor nerve passes
upward lateral to the optic nerve . By supplying to SR ,the
nerve pierces the muscle and terminates by supplying the LPS

34. Damage to its innervation, can cause Ptosis - The drooping of
the eyelid.
Ptosis can also be caused by damage to the adjoining superior
tarsal muscle, or its sympathetic innervation.
Such damage to the sympathetic supply occurs in Horner's
syndrome, and presents as a partial ptosis.
Clinical condition:

36. Parasympathetically III CN
These are postganglionic fibres travel to the ciliary and sphincter
pupillae muscles in the short ciliary nerves and innervate
two eye muscles:
1.Sphincter pupillae - constricts the pupil, a movement known
as Miosis
2.Ciliaris muscle - releasing tension on the Zonular fibres, making
the lens more convex, also known as accommodation.

37. Sphincter pupillae
Muscle contracts the pupil ,and the dilator pupilae muscle
dilates it.
Coloured part of the eye
Its inner edge forms the margin of the pupil
Functions - In humans, it functions to constrict the pupil in
bright light or during accomodation
Innervation – Parasympathetically.

38. .

39. Examination
When performing a pupillary exam - illuminate pupils indirectly /
directly to see what is happening.
Observe the pupil size and shape at rest, looking for anisocoria (one
pupil larger than the other)
Observe the direct response (constriction of the illuminated pupil)
Observe the consensual response (constriction of the opposite pupil)
Check for accommodation (constriction of pupil when viewing a
close object)

40. Pupillary responses & tests…
1. Efferent pupillary defect – (size and shape) the patient has
to look at the distant object , then room is darkened and the
direct reflex of pupil is then tested with different intensities
- if both the pupil gets constricted then There is no efferent
pupillary defect .
2. Afferent pupillary defect(Swinging Flash test) – examiner
has to indirectly illuminates 1 eye then quickly switches to
another eye - 2 pupils are always of EQUAL diameter -
afferent is good

41. Clinical conditions…
Anisocoria:
> Refers to the asymmetric sizes of pupils
> Physiologic anisocoria is very common and a normal
variant in up to 20% of the population. The variation should be no more
than 1mm and both eyes should react to light normally.
RAPD - is a defect in the direct response. It is due to damage in optic
nerve or severe retinal disease.
Its diagnosis…..

42. Swinging Flashlight Test:> 10-15 times swinging should be done(10sec)
> Swing a light back and forth in front of the two
pupils and compare the reaction to stimulation in both eyes.
> When light reaches a pupil there should be a
normal direct and consensual response.
> An RAPD is diagnosed by observing
paradoxical dilatation when light is directly shone in the affected pupil after
being shown in the healthy pupil.
>>> Helps to distinguish decreased vision and RAPD.
Some causes of a RAPD include:
optic neuritis , ischemic optic disease or retinal disease , severe glaucoma
causing , trauma to optic nerve , direct optic nerve damage , retinal detachment
, very severe macular degeneration , retinal infection.

44. Adie's (Tonic) Pupil: Common in women (but also can be
present in men)
• Either no or sluggish response to light (both direct and
consensual responses)
• Thought to be caused from de- innervation in the
postganglionic parasympathetic nerve
Associated with Holmes-Adie syndrome described .

45. Ciliary muscle
The Ciliary ganglion is a para sympatheticlly innervated
structure located in the posterior orbit.
Fibres from Edinger – westpal nucleus , it travels in the
oculomotor nerve along its outer edge , and enter the ciliary
ganglion .
Function – Accommodation , Trabecular meshwork pore size
Innervation-The ciliary muscle receives only parasympathetic
fibers from the short ciliary nerves that arise from the ciliary
ganglion. These postganglionic fibers are part of cranial nerve
III .

46.  Presynaptic parasympathetic signals that originate in
the Edinger-Westphal nucleus are carried by cranial nerve
III and travel through the ciliary ganglion.
 Parasympathetic activation of the M3 muscarinic
receptors causes ciliary muscle contraction, the effect of
contraction is to decrease the diameter of the ring of ciliary
muscle.
 The zonule fibers relax and the lens becomes more
spherical, increasing its power to refract light for near
vision.

47. Accommodation
changes in lens shape for light focusing.
the ciliary muscle contracts.
Converging of eyes occurs.
Trabecular meshwork pore size:
 Contraction and relaxation of the longitudinal fibers, which insert
into the trabecular meshwork in the anterior chamber of the eye,
cause an increase and decrease in the meshwork pore size,
respectively, facilitating and impeding aqueous humour flow into
the canal of Schlemm.

48. Clinical condition
Glaucoma - Open-angle glaucoma (OAG) and closed-angle
glaucoma (CAG) may be treated by muscarinic receptor
agonists , which cause rapid miosis and contraction of the
ciliary muscles, opening the trabecular meshwork, facilitating
drainage of the aqueous humour into the canal of Schlemm
and ultimately decreasing intraocular pressure.

50. References
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Stuttgart , Germany
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3110-3023-3024-3050

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