3rd nerve- oculomotor nerve and it's disorders.pptx

3rd cranial nerve

1. 3 RD CRANIAL NERVE – ANATOMY AND APPLIED - Dr. Amritaa Varma

2. Oculomotor Nerve Supplies all the extra-ocular muscles except lateral rectus and superior oblique Intraocular muscles such as sphincter pupillae and ciliary muscle

3. FUNCTIONAL COMPONENTS M otor in function Somatic efferent component – movements of eyeball 2. General visceral efferent – parasympathetic component – accommodation and contraction of pupil General somatic afferent component – associated with carrying proprioceptive impulses from extra-ocular muscles supplied by the s omatic efferent component

4. Oculomotor N uclear C omplex The nuclear complex of the oculomotor nerve is situated in the midbrain at the level of the superior colliculus in the ventromedial part of the central grey matter that surrounds the cerebral aqueduct It is a longitudinal column of about 10 mm in length Components Main m otor nucleus Accessary parasympathetic nucleus ( Edinger-Westphal nucleus)

5. Main motor nucleus Main motor nucleus is composed of the sub – nuclei supplying the individual extraocular muscles. Modern concept of Warwick Dorsolateral nucleus – ipsilateral inferior rectus Intermediate nucleus – ipsilateral inferior oblique Ventromedian nucleus – ipsilateral medial rectus Paramedian (scattered) nucleus – contralateral superior rectus Caudal central nucleus – bilateral levator palpabrae superioris

6. Connections of the Nucleus Cerebral cortex Motor cortex ( precentral gyrus ) of both sides through the corticonuclear tracks Visual cortex through te superior colliculus and tactobulbar tracks Nuclei of 4 th , 6 th and 8 th CN through the medial longitudinal bundle Pretectal nucleus of both sides (for light reflex) Cerebellum through the vestibular nucleus

7. Course and Distribution Fascicular part Basilar part Intracavernous part Intraorbital part

8. Fascicular part Consists of efferent fibres which pass from 3 rd nerve nucleus through the red nucleus and the medial aspect of the cerebral peduncle. They then emerge from the midbrain and pass into the interpeduncular space.

9. Basilar Part Commences as a series of 15-20 rootlets in the interpeduncular fossa. These coalesce to form a large medial and a small lateral root, which unite to form a flattened nerve The nerve is twisted bringing the inferior fibres superiorly and superior fibres inferiorly- thus the nerve becomes a rounded cord The nerve then passes between the posterior cerebral artery and the superior cerebellar artery and runs forward in the interpeduncular cistern – running lateral to the posterior communicating artery to reach the cavernous sinus.

10. Intracavernous Part The nerve enters the cavernous sinus by piercing the posterior part of the roof on he lateral side of he posterior clinoid process. It then descends to the lateral wall of the sinus, where it lies above the trochlear nerve. In the anterior part of the cavernous sinus, the nerve divides into the superior and inferior divisions which enter the orbit through the middle part of the superior orbital fissure within the annulus of Zinn . In he superior orbital fissure, the nasociliary nerve lies between the 2 divisions The abducent nerve lies infero -lateral to them.

11. Intraorbital part The smaller superior division of the 3 rd nerve supplies the superior rectus and levator palpebrae superioris The larger inferior division divides into 3 branches- Nerve to medial rectus – passes inferior to optic nerve Nere to inferior rectus – passes downwards and enter the muscle on its upper aspect Nerve to inferior oblique – longest of the 3 branches – passes in between the inferior rectus and lateral rectus to supply the inferior oblique from its posterior border It also gives a motor root to the ciliary ganglion

12. Ciliary Ganglion Peripheral parasympathetic ganglion placed in the coarse of oculomotor nerve Lies near the apex of the orbit, between the optic nerve and tendon of lateral rectus muscle aproximately 1cm in front of the annulus of Zinn , on the lateral side of ophthalmic artery

13. Roots of ciliary ganglion Sensory root – comes from the nasociliary nerve. Fibres do not relay in the ganglion, pass along the short ciliary nerves to supply the ciliary body, iris and cornea Parasympathetic root – arises from the nerve to inferior oblique muscle. It contains preganglionic fibrs that begn in the Edinger-Westphal nucleus. These fibres relay in the ganglion. Postganglionic fibres arising in the ganglion pass through the short ciliary nerves and supply the sphincter pupillae and cilary muscle.

14. There are 9-10 times more fibres associated with accommodation innervationg the ciliary muscle as there are fibres reaching the sphincter pupillae . This disparity can cause light-near-dissociation. Sympathetic root – branch from the internal carotid plexus. Contains postganglionic fibres arising from the superior cervical ganglion. They supply the blood vessels of the eyeball .

15. Applied – O culomotor nerve N uclear complex Levator subnucleus – unpaired caudal midline structure that innervates both levator muscles. Lesions confined to this will give rise to bilateral ptosis. Superior rectus subnuclei – are paired, each innervates the respective contralateral superior rectus. A nuclear third nerve palsy will spare the ipsilateral and affect the contralateral superior rectus

16. 3. Medial rectus, inferior rectus and inferior oblique subnuclei – paired, innervate their corresponding ipsilateral muscles. WEBINO – Wall eyed bilateral internuclear ophthalmoplegia Lesions confined to the nuclear complex are relatively uncommon – namely, vascular diseases, primary tumor or metastasis, ischemia, usually from embolic or thrombotic occlusion, hemorrhage, inflammation, and brain stem compression. Lesions involving the entire nucleus is associated with involvement of adjacent and caudal 4 th nerve nucleus.

17. Nuclear Oculomotor Nerve Palsy

18. Fasciculus Nuclear and fascicular lesions have similar causes. Demyelination affects the fasciculus The fasciculus consists of efferent fibres that pass from 3 rd nerve nucleus throught the red nucleus and medial part of cerebral peduncle. They then emerge from the midbrain and pass into the interpeduncular space.

19. Benedikt Syndrome Red nucleus Ipsilateral 3 rd nerve palsy Contralateral extrapyramidal signs – hemi-tremor Weber syndrome Cerebral peduncle Ipsilateral 3 rd nerve palsy Contralateral hemiparesis Nothnagel syndrome Involves fasciculus and superior cerebral peduncle Ipsilateral 3 rd nerve palsy Cerebellar ataxia Claude syndrome Red nucleus Cerebral peduncle Combination benedikt and Nothnagel syndrome

20. WEBERS SYNDROME

21. Basilar Basilar part starts as a series of rootlets that leave the midbrain on the medial aspect of the cerebral peduncle, before coalescing to form the main trunk. The nerve then passes between the posterior cerebral and superior cerebral arteries, running lateral to and parallel with the posterior communicationg artery. As the nerve transverses the base of skull along its subarachnoid course unaccompanied by any other cranial nerve, an isolated 3 rd nerve palsy is common.

22. Causes of isolated 3 rd Nerve palsy Aneurysm – posterior communicating artery at its junction with the internal carotid artery typically presents acutely as a pupil-involving painful third nerve palsy.

23. Head trauma, resulting in extradural or subdural haematoma , may cause a tentorial pressure cone with downward herniation of the temporal lobe. This compresses the third nerve as it passes over the tentorial edge resulting in complete third nerve palsy.

24. Intra-cavernous The third nerve then enters the cavernous sinus by piercing the dura just lateral to the posterior clinoid process. Within the sinus, the third nerve runs in the lateral wall above the fourth nerve. In the anterior part of the cavernous sinus, the nerve divides into superior and inferior branches that enter the orbit through the superior orbital fissure within the annulus of Zinn . potential causes of intracavernous third nerve palsy: Diabetes. 2. Pituitary apoplexy (see above). Miscellaneous pathology such as aneurysm, meningioma,carotid -cavernous fistula and granulomatous inflammation ( Tolosa –Hunt syndrome). Because of its close proximity to other cranial nerves, intracavernous third nerve lesions are likely to be associated with involvement of the fourth and sixth nerves and the first division of the fifth nerve.

25. Intraorbita l Superior division innervates the levator and superior rectus muscles. Inferior division innervates the medial rectus, the inferior rectus and the inferior oblique muscles. The branch to the inferior oblique also contains preganglionic parasympathetic fibres from the Edinger – Westphal subnucleus , which innervate the sphincter pupillae and the ciliary muscle. S uperior and inferior division palsies are commonly traumatic or vascular.

26. Pupillomotor fibres Between the brainstem and the cavernous sinus, the pupillomotor parasympathetic fibres are located superficially in the superomedial part of the third nerve . T hey derive their blood supply from the pial blood vessels, whereas the main interior trunk of the nerve is supplied by the vasa nervorum . Involvement or sparing of the pupil is important, as it frequently differentiates a ‘surgical’ from a ‘medical’ lesion

27. ‘Surgical’ lesions such as aneurysms, trauma and herniation characteristically involve the pupil by compressing the pial blood vessels and the superficially located pupillary fibres . ‘Medical’ lesions such as occur in hypertension and diabetes usually spare the pupil.This is because the microangiopathy associated with medical lesions involves the vasa nervorum , causing ischaemia of the main trunk of the nerve, leaving the superficial pupillary fibres intact. These principles are not infallible

28. Signs of third nerve palsy Profound ptosis due to weakness of the levator muscle Abduction and depression in the primary position due to unopposed action of the lateral rectus and superior oblique muscles. The intact superior oblique muscle also causes intorsion of the eye at rest Limited adduction due to medial rectus weakness Normal abduction as the lateral rectus is intact Limited elevation due to weakness of the superior rectus and inferior oblique Limited depression due to weakness of the inferior rectus Dilated pupil and defective accommodation due to parasympathetic palsy

29. Isolated 3 rd nerve palsy Microvascular disease associated with systemic risk factors such as hypertension and diabetes are the most common cause of third nerve palsy, accounting for about 40% of cases. Marked periorbital pain is often associated, which is therefore not helpful in distinguishing an aneurysmal cause. In diabetes-related paresis, motility disturbance is typically profound, but there is usually (80%) relative or complete pupil sparing and when pupillary involvement does occur some degree of reaction to light is almost always preserved. As a general rule, where there is a complete third nerve palsy and a normally responsive pupil the cause is significantly more likely to be microvascular than secondary to an aneurysm. Aneurysm of the posterior communicating artery at its junction with the internal carotid is a very important cause of isolated third nerve palsy with involvement of the pupil. Pain is often present and the extent of pupillary involvement characteristically exceeds the severity of motility dysfunction. An aneurysm of the internal carotid within the cavernous sinus tends to also involve other cranial nerves.

30. 3. Trauma, both direct and secondary to subdural hematoma with herniation. However, the development of third nerve palsy following relatively trivial head trauma should alert the clinician to the possibility of an underlying aneurysm or tumour . 4. Miscellaneous uncommon causes include tumour , inflammatory disease such as syphilis, Lyme disease and sarcoidosis , GCA and vasculitis associated with collagen vascular disorders. 5. Episodic - Brief episodes of third nerve dysfunction with spontaneous recovery may be idiopathic or occur with migraine,compression , ischaemia and alterations in intracranial pressure. Myasthenia gravis may mimic intermittent pupil-sparing third nerve paresis.

31. Congenital 3 rd nerve palsy Congenital oculomotor nerve palsies constitute nearly half of the oculomotor nerve pareses seen in children. Most cases are unilateral. Patients with congenital oculomotor nerve palsies have no other neurologic or systemic abnormalities. Amblyopia is present

32. Associated Syndromes C ongenital adduction palsy with synergistic divergence Patients with this syndrome have congenital unilateral paralysis of adduction associated with simultaneous bilateral abduction on attempted gaze into the field of action of the paretic medial rectus muscle Atypical vertical retraction syndrome The main clinical feature of the vertical retraction syndrome is limitation of movement of the afected eye on elevation or depression, associated with a retraction of the globe and narrowing of the palpebral fissure. Cyclic oculomotor nerve paresis with cyclic spasm. About every 2 minutes, the ptotic eyelid elevates, the globe begins to adduct, the pupil constricts, and accommodation increases. These spasms last 10 to 30 seconds and then give way to the paretic phase. Cyclic oculomotor palsy usually continues throughout life.

33. Acquired Oculomotor Synkinesis Peripheral motor and sensory nerves, including the autonomic nerves – can regenerate. The regenerative process produces more axons than were present before the nerve was interrupted. Axons sprout from the proximal end of the severed nerve and from collateral nerves that have not been severely damaged. In peripheral nerves that innervate more than one muscle, misdirection of regenerating nerve fibers may occur. Thus, regenerating fibres sprouts from axons that previously innervated one muscle group may ultimately innervate a different muscle group with a different function. Following injury to the oculomotor nerve at any point along its pathway from the brain stem to the orbit, a syndrome of oculomotor nerve synkinesis may occur. In adults, evidence of synkinesis first appears about 9 weeks after injury W hereas in infants with oculomotor nerve palsy from birth trauma, such signs may be observed from 1 to 6 weeks following birth.

34. Aberrant regeneration may follow acute traumatic and compressive, but not vascular, third nerve palsies. This is because the endoneural nerve sheaths, which may be breached in traumatic and compressive lesions, remain intact with vascular lesions. As a general rule, synkinetic movements do not occur after ischemic insults to the nerve. The release of neurotrophic factors guiding collateral sprouting of axons generally occurs in response to a degree of crush injury. Thus, in a patient suspected of having an ischemic oculomotor nerve palsy, particularly if there have been no previous episodes, the development of oculomotor synkinesis should suggest an alternative etiology, such as compression or aggressive inflammation.

35. Muscle to Muscle: Adduction of the involved eye on attempted elevation or depression (SR or IR to MR). Conversely, elevation of the eye on attempted adduction (MR to SR or IO) Muscle to Eyelid: Pseudo- Graefe sign retraction and elevation of the eyelid on attempted downward gaze. Elevation of the eyelid on attempted adduction can also occur. Muscle to Pupil: Pseudo-Argyll Robertson pupil the involved pupil does not react or reacts poorly and irregularly to light stimulation but does constrict on adduction during conjugate gaze .

36. Treatment Observation is usually appropriate in presumed microvascular cases; the majority will resolve over weeks or months. Temporary (e.g. Fresnel stick-on) prisms may be useful if the angle of deviation is small. U niocular occlusion may be necessary to avoid diplopia if the ptosis component is partialor recovering. Botulinum toxin injection into the uninvolved lateral rectus muscle is sometimes used to prevent its contracture when recovery time is prolonged. Surgical treatment of the ocular motility element and ptosis should be contemplated only after spontaneous improvement has ceased, usually not earlier than 6–12 months from onset. Numerous innovative surgical techniques have been described.

37. R eferences Wolff’s Anatomy of the eye and orbit Kanski’s Clinical Ophthalmology Neuro -ophthalmology – AK Khurana (MSO series) Walsh and Hoyt’s clinical Neuro -ophthalmology Post-graduate Ophthalmology – Zia Chaudhuri

38. Thank You