AUTONOMIC NERVOUS SYSTEM of the eye

ATTO GLADYS

components of the autonomic nervous system:

(1) The sympathetic system, which when stimulated prepares the body to face an emergency.

(2) The parasympathetic system, which maintains and restores the resting state.

Balance is maintained between these two systems .

Ocular structures supplied by the sympathetic system

• the iris dilator

• ciliary muscle

• smooth muscle of the lids • lacrimal gland

• choroidal and conjunctival blood vessels.

• Sweat glands and piloerector muscles of the facial skin.

Ocular structures supplied by the parasympathetic system

• the iris sphincter

• ciliary muscle

• lacrimal gland

• Choroidal and conjunctival blood vessels.

The sympathetic pathway

FIRST ORDER NEURON:• This originates in the posterior hypothalamus

and descends uncrossed down the brainstem and terminates in the ciliospinal centre of Budge which is located at the level of C8-T2 in the spinal column.

• Fibres to the eye are mainly but not invariably from the first thoracic segment (T1).

SECOND ORDER NEURON

• The preganglionic fibres leave the spinal cord via the ventral root and enters the sympathetic ganglion chain.

• It then travels over the apex of the lung to synapse in the superior cervical ganglion in the neck.

• This is a relatively long course of the neuron and due to its

proximity to the apical pleura of the lung it can be damaged by tumours such as Pancoast's tumour as well as by surgery to the neck area.

• This will lead to Horner's syndrome which will be discussed later and is the reason one should refer a patient with Horner's syndrome for a chest XRAY.

THIRD ORDER NEURON• The postganglionic fibres (third order neurons)leave

the superior cervical ganglion, to form the carotid plexus around the internal carotid artery.

• The fibres then travels upward with the internal carotid artery and enters the cavernous sinus.

• From here it joins up with the ophthalmic division

of the trigeminal nerve (5th Nerve) and travels with the nasociliary and long ciliary nerves to the dilator pupillae and the ciliary body.

Cont..• Other fibres from the carotid plexus follow this

same route to the nasociliary nerve and then branch to the ciliary ganglion as the sympathetic root;

• They enter the globe as the short ciliary nerves to

innervate the choroidal and conjunctival blood vessels.

• The pathway to the conjunctival vasculature may be through either the long or the short ciliary nerves.

Cont..

• Alternately, the sympathetic root to the ciliary ganglion may emanate directly from the internal carotid plexus.

• A sympathetic nerve network accompanies the ophthalmic artery and, its branches could have a role in the control of blood flow to ocular structures.

Cont..

• Other fibres from the carotid plexus join the superior division of oculomotor nerve and travel with it into the orbit to innervate the smooth muscle of the upper eyelid(superior tarsal/Muller’s muscle)

• These fibres follow the same path as the

superior division of the oculomotor nerve as it supplies the levator muscle.

Effects of sympathetic stimulation

• activates the iris dilator, causing pupillary dilation and thereby increasing retinal illumination.

• It also causes vasoconstriction of the choroidal and conjunctival vessels.

• widening of the palpebral fissure by stimulating the smooth muscle of the eyelids (superior tarsal).

• The sympathetic nerves also exhibit a small inhibitory effect on the ciliary muscle.

The parasympathetic pathway

• parasympathetic innervation of ocular structures originates in the midbrain and pons.

• It consists of 2 neurons • The cell body of the preganglionic neuron, is

located in the brain or spinal cord, whereas the cell body of the postganglionic neuron is in a ganglion outside the central nervous system.

Cont..• The midbrain preganglionic nerve fibres to the ciliary ganglion

arises in neurons of the accessory oculomotor nuclei , the Edinger-Westphal nucleus.

• From here, the fibres reach the anterior end of the cavernous sinus where the oculomotor nerve divides into superior and inferior divisions.

• The preganglionic fibres which are myelinated follow the inferior

division of that nerve into the orbit. • The fibres then leave the inferior division and through the branch

to the inferior oblique, synapse in the ciliary ganglion as the parasympathetic root.

Cont..• The ciliary ganglion is a small, somewhat flat structure,

2 mm long and 1 mm high, located within the muscle cone between the lateral rectus muscle and the optic nerve, approximately 1 cm anterior to the optic canal.

Three roots are located at the posterior edge of the ciliary ganglion: • the parasympathetic root, mentioned previously; • the sensory root, which carries sensory fibres from the

globe and joins with the nasociliary nerve; and • the sympathetic root, which supplies the blood vessels.

Roots in the ciliary ganglion

Cont..

• Only the parasympathetic fibres synapse in the ciliary ganglion; the sensory and sympathetic fibres pass through without synapsing

Cont..• The postganglionic parasympathetic fibres,

which are unmyelinated, exit the ciliary ganglion in the short ciliary nerves.

• Enter the globe, and travel to the anterior segment of the eye to innervate the iris sphincter and ciliary muscles.

NB: Most of the fibres innervate the ciliary body; only approximately 3% supply the iris sphincter

AUTONOMIC INNERVATIONTO LACRIMAL GLAND

• Fibres originate in the pons in an area within the nucleus for cranial nerve VII called as the superior salivatory nucleus/lacrimal nucleus.

• Secretomotor fibres to salivary gland and lacrimal gland leave the brain stem (pons) as one of the components of the nervus intermedius of the facial nerve, lying btn the facial nerve and the eighth nerve and enters the internal auditory meatus and canal up to the geniculate ganglion.

• Secretomotor fibres to salivary gland then leave the nervus

intermedius of facial nerve at the geniculate ganglion to join the chorda tympani and synapse in the submandibular ganglion for relay to the salivary glands.

Cont..• While the orbital fibres leave as the greater petrosal nerve

pass through the geniculate ganglion of the facial nerve in the facial canal in the petrous portion of the temporal bone without synapsing, enter the middle cranial fossa, pass under the trigeminal ganglion to reach the foramen lacerum.

• In the foramen lacerum, the greater petrosal nerve is joined by the deep petrosal nerve, carrying sympathetic postganglionic fibres from the carotid plexus to form the vidian nerve (nerve of the pterygoid canal)

Cont..• The vidian nerve enters the pterygopalatine

ganglion, (also called the sphenopalatine ganglion) where the parasympathetic fibres synapse while the sympathetic fibres don’t.

• The autonomic fibres (all of which are now postganglionic) leave the ganglion, join with the maxillary division of the trigeminal nerve, pass into the zygomatic nerve, and then form a communicating branch to the lacrimal nerve.

Cont..• An alternate pathway bypasses the zygomatic nerve and travels

from the ganglion directly to the lacrimal gland. • The parasympathetic fibres that innervate the lacrimal gland are

of the secretomotor type and thus cause increased secretion.

• Parasympathetic stimulation therefore causes increased lacrimation.

• The sympathetic fibres innervate the blood vessels of the gland

and might indirectly cause decreased production of lacrimal gland secretion by restricting blood flow.

Cont..

• Sympathetic fibres from the zygomatic nerve also branch into the lower eyelid to innervate Müller’s muscle of the lower lid.

• Irritation of any branch of the trigeminal nerve activates a reflex afferent pathway, precipitating increased lacrimation.

Effects of Parasympathetic stimulation

• causes pupillary constriction, thus decreasing retinal illumination and reducing chromatic and spherical aberrations.

• It also causes contraction of the ciliary muscle,

enabling the eye to focus on near objects in accommodation.

• Parasympathetic activation presumably causes

vasodilation, which might raise intraocular pressure.

Lesion in the parasympathetic pathway

• A lesion in the efferent pathway will cause the eye to show poor direct and consensual pupillary responses and a poor near response.

• The pupil appears dilated on clinical presentation, and other ocular structures may be involved.

• Damage in the oculomotor nucleus or nerve could also involve

the superior rectus, medial rectus, inferior rectus, inferior oblique, or levator muscle, and the patient should be examined for related ocular motility impairment.

Cont..

• The parasympathetic fibres in the oculomotor nerve are often spared in ischemic lesions, as from diabetes, but are especially vulnerable to compression because the fibres are superficial as the nerve emerges from the midbrain.

• Third nerve involvement that includes a dilated pupil is highly suspicious of a compressive intracranial lesion.

Adie’s tonic pupil.• If the cause of the tonic pupil is not apparent, the syndrome is called Adie’s tonic pupil. • The typical patient with Adie’s pupil is a woman 20 to 40 years of age; 90% of these

patients also have diminished tendon reflexes.

• If pupillary constriction in early Adie’s pupil is examined with the biomicroscope, segmental constriction affecting only a section of the iris may be evident.

• An Adie’s pupil that has been tonic for years eventually becomes smaller and does not dilate well in the dark; thus it is the larger pupil in light and the smaller one in darkness.

• In the differential diagnosis of Adie’s pupil, a very mild, direct- acting cholinergic agonist can be used because the sphincter muscle is supersensitive.

• A dilute concentration of pilocarpine (0.125%) has minimal effect on a normal sphincter but will cause significant clinical miosis in a supersensitive sphincter.

• With one drop instilled in each eye, the Adie’s pupil should show a much greater constriction than the normal pupil.

Characteristics• Poor or absent pupillary light response and loss of accommodation due to deficient

reinnervation of the sphincter by pupillary fibres subserving the light reflex.

• Decreased corneal sensitivity often occurs because some afferent sensory fibres from the cornea pass through the short ciliary nerves and the ganglion.

• The pupillary contraction to near is asymmetrical due to asymmetry of reinnervation.

• The affected muscle may exhibit cholinergic denervation supersensitivity, a physiologic phenomenon resulting from injury to the fibres directly innervating muscles.

• The near response is retained, but it is delayed and slow, due to aberrant reinnervation of the sphincter by fibres previously predestined for the ciliary body (near- accommodation fibres) and the pupil redilates sluggishly because the partially denervated sphincter muscle is supersensitive to its cholinergic stimulus so contraction persists.

DISRUPTION IN THE SYMPATHETICPATHWAY

• An interruption in the sympathetic pathway causes miosis.

• Anisocoria (a difference in pupil size) is present under normal room light conditions but is more pronounced in dim light, with the normal eye having the larger pupil.

• The pupil responds briskly to light, but with slow and incomplete dilation in the dark.

• If the anisocoria decreases in bright lights and the pupils react

normally to a light stimulus, the disruption is likely a sympathetic interruption to the dilator muscle or benign anisocoria.

Horner’s syndrome• Damage in the sympathetic pathway to the head can cause

Horner’s syndrome, which consists of;• Partial ptosis, due to paresis of Muller's portion of the levator.• Ipsilateral miosis, due to dilator paresis and • facial anhidrosis (absence of sweat secretion) due to loss of

sweat gland stimulation.• Anhidrosis will occur with central lesions and preganglionic

lesions below the skull base and the origin of the fibres running with the external carotid artery which supply the facial skin.

• Loss of innervation to the smooth muscle of the upper eyelid causes ptosis, whereas loss of innervation to the lower eyelid causes it to rise slightly such that the palpebral fissure appears narrow, simulating enophthalmos.

Cont..

• Painful Horner’s syndrome is a classical symptom of carotid artery dissection and should be treated as an emergent situation.

• Damage along the rest of the postganglionic neuron can involve the nasociliary or long ciliary nerves.

Central lesions• May be caused by occlusion of the posterior inferior cerebellar

artery (Wallenberg’s lateral medullary syndrome) whose features reflect the territory of supply of this artery thus;

• Ipsilateral Horner’s syndrome (central fibres)

• Dysphagia (laryngeal and pharyngeal paralysis IX and X)

• Ipsilateral facial analgesia (spinal tract and nucleus of trigeminal nerve)

• Contralateral analgesia of the trunk and extremities (ascending spinothalamic tract)

• Ipsilateral cerebellar ataxia and rotary nystagmus.

Cont..

Central lesions in the cervical cord may be caused by;• tumour, • trauma, • demyelination, and • syringomyelia.

Preganglionic lesions• A root affecting the brachial plexus (and preganglionic

fibres) may occur with birth trauma and be associated with Klumpke’s paralysis of the ipsilateral arm.

• Tumours of the chest apex or superior mediastinum may also damage preganglionic fibres in the T1 root (pancoast’s syndrome) or as they enter the sympathetic chain.

• In the neck, preganglionic fibres may be damaged in relation to the carotid sheath by tumour, inflammation, enlarged lymph nodes and trauma including surgery and percutaneous carotid angiography.

Postganglionic lesions• Lesions within the cranial cavity affect postganglionic fibres, which

are not distributed to facial sweat glands.

• In some individuals, however, sweat glands on the forehead may be innervated by postganglionic fibres running in the internal carotid plexus and in the supraorbital branch of ophthalmic artery.

• Complete third neuron section will supersensitize the pupil dilator muscle to topical 1: 1000 adrenaline or 1% phenylephrine;

• Also hydroxyamphetamine 1% will fail to release catecholamine from the degenerate nerve endings and the pupil fails to dilate

Cont..

• With a complete second neuron section, the dilator is not supersensitive but hydroxyamphetamine will cause pupil dilatation by releasing transmitter from intact postganglionic fibres.

Pharmacological tests to differentiate preganglionic from postganglionic lesions

Cocaine 4%is in stilled into both eyes.• Result: the normal pupil will dilate but the Horner pupil will not.• Rationale: noradrenaline (NA) released at the postganglionic sympathetic nerve endings is reuptaken by the nerve endings, thus terminating its action. Cocaine blocks this uptake. NA therefore accumulates and causes pupillary dilatation. In Horner syndrome, there is no NA being secreted in the first place: therefore cocaine has no effect. Cocaine thus confirms the diagnosis of Horner syndrome.

Cont..Hydroxyamphetamine I% is instilled into both eyes.• Result: in a preganglionic lesion both pupils will dilate whereas in a postganglionic lesion the Horner pupil will not. (This needs to be performed the following day after the effects of cocaine have worn off.)• Rationale: hydroxyamphetamine potentiates the release of NA from post ganglionic nerve endings. If this neurone is intact (a lesion of the first - or second-order neurone and also the normal eye), NA will be released and the pupil will dilate. In a lesion of the third-order (postganglionic) neurone there can be no dilatation since the neurone is destroyed.

Cont..Adrenaline I: I000 is in stilled into both eyes.• Result : in a preganglionic lesion neither pupil will dilate because adrenaline is rapidly destroyed by monoamine oxidase: In a postganglionic lesion, the Horner pupil will dilate and ptosis may be temporarily relieved because adrenaline is not broken down due to the absence of monoamine oxidase.• Rationale: a muscle deprived of its motor supply manifests heightened sensitivity to the excitatory neurotransmitter secreted by its motor nerve. In Horner syndrome the dilator pupillae muscle similarly manifests denervation hypersensitivity to adrenergic neurotransmitters.

Therefore Adrenaline even in minute concentrations, produces marked dilatation of the Horner pupil.

Corneal reflexCorneal touch initiates the three-part corneal reflex:• lacrimation• miosis • protective blink .

• The pain sensation elicited by the touch travels to the trigeminal ganglion and then into the pons as the trigeminal nerve.

• Communication from the trigeminal nucleus to the Edinger-Westphal nucleus causes activation of the iris sphincter muscle (this communication btn two nuclei is called supranuclei control).

• Communication to the facial nerve nucleus activates the motor pathway to the

orbicularis muscle, causing the blink, and

• communication to the lacrimal nucleus and the parasympathetic pathway to the lacrimal gland stimulates increased lacrimation.

The iris equilibrium• The parasympathetic and sympathetic nerves

are in some state of balance in the normal, healthy, awake individual, and the size of the pupil changes constantly and rhythmically, reflecting this balance.

• This physiologic pupillary unrest is called hippus and is independent of changes in illumination.

• During sleep the pupils are small because the sympathetic system shuts down and the parasympathetic system predominates.

OCULOMOTOR NERVE

Presenter: Dr Guy KINTOKITutor: Dr JOHN ONYANGO

Oculomotor Nerve (CN III)

Embryo: Mesencephalon

Functions:Somatic motor (general somatic efferent)Visceral motor (general visceral efferent

parasympathetic).

Oculomotor Nerve (CN III)

Oculomotor nerve is entirely motor in function. Supplies:

Somatic motor:• All the Extraocular muscles except superior oblique and lateral rectusVisceral motor (parasympathetic):• Intra ocular muscles- Sphincter pupillae and

cilliary muscle

NucleusLocated in midbrain at the level of superior

colliculus, ventral (anterior) to the Sylvian aquiduct.There are two oculomotor nuclei, each serving one of

the functional components of the nerve.The somatic motor nucleus of the oculomotor nerve

is in the midbrain. The visceral motor (parasympathetic) accessory

(Edinger-Westphal) nucleus of the oculomotor nerve lies dorsal to the rostral two thirds of the somatic motor nucleus.

It is supplied by the anterior, middle and posterior branches of posterior cerebral artery

Oculomotor nuclei

Course

Can be divided into : Fascicular Basilar Intracavernous Intraorbital part

Course

Fascicular: From the nucleus the

fibers pass forwards through the red nucleus and the medial part of the substantia nigra, curving with a lateral convexity to emerge from the sulcus on the medial side of cerebral peduncle.

And through the corticospinal fibers

Major causes of fascicular lesion of 3rd nerve palsy

Vascular occlusion – Diabetes & Hypertension

Neoplastic lesions – primary tumour or metastasis

Haemorrhage

Syndromes of Fascicular lesion Benedikt syndrome- Ipsilateral 3rd nerve palsy and contralateral extrapyramidal signs.

Weber syndrome- Ipsilateral 3rd nerve palsy and contralateral hemiparesis.

Nothnagel syndrome involves the fasciculus and the superior cerebellar peduncle and is characterized by ipsilateral 3rd nerve palsy and cerebellar ataxia.

Claude syndrome is a combination of Benedikt

and Nothnagel syndrome

Course

Course

Basilar:

It exits in the interpeduncular space In the subarachnoid space, CN III passes below

the posterior cerebral artery and above the superior cerebellar artery, the 2 major branches of the basilar artery.

Course

Major causes of lesion in Basilar region

The 3rd nerve traverses the basilar part unaccompanied by any other cranial nerves.

Isolated 3rd nerve palsies are commonly basilar.

The important causes areAneurysmHead trauma-Extradural or subdural haematoma

continued

continued

Course

Intracavernous

Traversing the roof of the cavernous sinus It runs along the lateral wall of the cavernous

sinus and above CN IV and enters the orbit through the superior orbital fissure

Intracavernous portion of 3rd nerve

Major causes of Intracavernous lesion

Usually associated with involvement of 4th, 6th nerves & first and second division of 5th nerve.

Diabetes – causes pupil sparing 3rd nerve palsyPituitary apoplexy(hemorrhagic infarction of

the gland)Others – Aneurysm, Meningioma, Carotid-

cavernous fistula, granulomatous inflammation (Tolosa–Hunt syndrome).

Course

Intraorbital part:Enters the orbit through the superior orbital

fissure.CN III usually divides into superior and inferior

divisions after passing through the annulus of Zinn in the orbit.

CONT… The superior division of CN III runs forward to innervate

first the superior rectus and then the levator palpebrae muscles above.

The larger inferior division splits into 3 branches to supply the medial and inferior rectus muscles and the inferior oblique

CONT… The parasympathetic fibers wind around the periphery of

the nerve, enter the inferior division, and course through the branch that supplies the inferior oblique muscle

They join the ciliary ganglion, where they synapse and the postganglionic fibers, emerge as many short ciliary nerves

These pierce the sclera and travel through the choroid to innervate the pupillary sphincter and the ciliary muscle

The superficial location of these fibers makes them more vulnerable to compression, such as from an aneurysm: Pupillary dilation is a sensitive (commonly early) sign of compression

Intraorbital portion of 3rd nerve

Intraorbital causes of 3rd nerve palsy

Trauma

Vascular

Neoplasm

Inflammation

Causes of isolated 3rd nerve palsyIdiopathic – about 25%

Vascular – Hypertension & Diabetes (commonly pupil sparing)

Aneurysm – posterior communicating artery at its junction with internal carotid artery

Trauma – subdural haematoma with uncal herniation

Clinical features of total 3rd nerve palsy

SYMPTOMS

Drooping of eyelid

Binocular double vision

Pain (may be present)

Pupillomotor fibres• Between the brainstem and the cavernous sinus, the

pupillomotor parasympathetic fibres are located superficially in the superomedial part of the 3rd nerve .

• They derive their blood supply from the pial blood vessels, whereas the main trunk of the 3rd nerve is supplied by the vasa nervorum.

• 'Surgical’ lesions such as aneurysms, trauma and uncal herniation characteristically involve the pupil by compressing the pial blood vessels and the superficially located pupillary fibres.

• ‘Medical' lesions such as hypertension and diabetes usually spare the pupil. This is because the microangiopathy associated with medical lesions involves the vasa nervorum, causing ischemia of the main trunk of the nerve, sparing the superficial pupillary fibres.

SIGNS

A Weakness of the levator causing profound ptosis, due to which there is often no diplopia. b Unopposed action of the lateral rectus causing the eye to be abducted in the primary position.

The intact superior oblique muscle causes intorsion of the eye at rest which increases on attempted down gaze. c Normal abduction because the lateral rectus is intact. d Weakness of the medial rectus limiting adduction. e Weakness of superior rectus and inferior oblique, limiting elevation. f Weakness of inferior rectus limiting depression. g Parasympathetic palsy causing a dilated pupil associated with defective accommodation. h Partial involvement will produce milder degrees of ophthalmoplegia.

Examination

Pupillary reactions

Motility restrictions

Ptosis

Other cranial nerves

References• Dan Kirshenbaum BUSM Class of 2011 - Gross Anatomy

2007 Cranial-nerves.• Naeem Majeeb Cranial nerves Origine, pathway and Applied

anatomy.• W Marais, S Barrett 147 CME April 2013 Vol. 31 No. 4 An

overview of the third, fourth and sixth cranial nerve palsies• STANLEY MONKHOUSE Cambridge University Press,2006

CRANIAL NERVES Functional Anatomy• Lecturer Globa Lilian The State Medical and Pharmaceutical

University “Nicolae Testemitanu” Republic of Moldova The functional Anatomy of the Cranial nerves.

Thank you

Trochlea Nerve

Tutor: Dr. John OnyangoPresenter: Emmanuel Agwella

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Trochlea Nerve The fourth cranial nerve is a motor

(somatic efferent) nerve supplying superior oblique muscle

Named after fibrous loop that acts as

a pulley to the tendon of superior oblique muscle

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Unique Features of CN IV The smallest nerve in terms of number of

axons (3,400) Greatest intracranial length (75 mm) The only nerve that exits from the dorsal

aspect of the brainstem Innervates the contralateral superior oblique

muscles

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The Nucleus of CN IV Located in caudal mesencephalon (midbrain) beneath

cerebral aqueduct – immediately below the nucleus of CN III

Axons from the nucleus run dorsally crossing the midline and emerging from the posterior aspect of the brainstem

Thus unlike the other cranial nerves, lesions of the trochlea nucleus affect the contralateral eye.

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Nucleus and Course of Trochlea Nerve

Course of the Nerve The nerve emerges from the dorsal aspect of the

midbrain and passes anteriorly in the subarachnoid space and then

Passes between posterior cerebral artery and superior cerebellar artery, pierces the dura mater and

Runs in the lateral wall of the cavernous sinus, joined by

CN III, CN VI, ophthalmic and maxillary divisions of CN V

Enters the orbit through superior orbital fissure to supply superior oblique muscle

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Cranial Nerves in Relation to Cavernous Sinus

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Superior Oblique Muscle Superior oblique muscle originates from orbital apex,

above annulus of Zinn, and runs along superonasal aspect of orbit before becoming a tendinous cord

Tendon passes through trochlea and abruptly turns laterally and posteriorly inserting on the globe. Tendon passes beneath nasal border of superior rectus but fans out to form a broad insertion

Primary action is intorsion (anterior-posterior axis), secondary action being depression (transverse axis) and abduction (vertical axis)

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Examination of Trochlea Nerve Done by examining action of superior oblique muscle

Patient is asked to look down, other actions include reading newspaper and walking down a stair (convergent gaze)

Diplopia associated with above actions could be initial symptom of CN IV palsy

The Parks-Bielschowsky 3-step Test for CN IV Palsy

1. Find the side of the hypertropia (an ocular deviation with one eye higher than the other) in primary position

2. Determine if the hypertropia is greater on left or right gaze

3. Determine if the hypertropia is greater on left or right head tilt

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Clinical SignificanceVertical Diplopia Injury to the trochlear nerve leads to weakness

of downward gaze eye movement and eventually diplopia ensues

The affected eye drifts upward relative to the normal eye, due to the unopposed actions of the remaining extraocular muscles

As a compensatory mechanism, the patient tilts the head forward (tucking the chin in) in order to fuse the two images into a single visual field.

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Clinical Significance cont’d

Torsional Diplopia Weakness of intorsion leads to torsional diplopia, in

which there is tilting of image and to compensate for this, patients tilt their heads to the opposite side, in order to fuse the two images into a single visual field

The characteristic appearance of patients with fourth nerve palsies is that of head tilted to one side and chin tucked in.

Caution must be taken before in diagnosis because torticollis can present with similar appearance

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Fourth Nerve Palsy

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Trochlea Nerve Palsy

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Torticollis

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References 1. Basic and Clinical Science Course, Vol. 2 Fundamentals and

Principles of Ophthalmology. American Academy of Ophthalmology 2007-2008

2. Nafady H. Trochlea Nerve. http://www.slideshare.net/hytham_nafady/trochlear-nerve

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Thank You

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Trigeminal Nerve

By: Denise KavumaTutor: Dr Onyango J.

Introduction

• The trigeminal nerve (the fifth cranial nerve) is responsible for sensation in the face and motor functions such as biting and chewing.

• The largest of the cranial nerves

• There’s one nerve on each side of the pons and has three major branches: – the ophthalmic nerve (V1), sensory.

– the maxillary nerve (V2), sensory.

– the mandibular nerve (V3), sensory and motor functions.

Anatomy• The trigeminal nerve contains both a sensory and a motor root.

• The cell bodies of the sensory portion lie in the gasserian (or trigeminal) ganglion, located just behind the internal carotid and the posterior portion of the cavernous sinus.

• Proximally, the sensory root extends to the: – pons, where the fibers enter the main sensory nucleus, – the nucleus of the spinal tract,– the mesencephalic nucleus

• Most of the fibers from the main sensory and spinal tract nuclei cross to the contralateral side

Cont…

• The motor nucleus of the trigeminal nerve is located in the midpons

• Its fibers pass beneath the gasserian ganglion to join the mandibular branch of the fifth nerve to supply the muscles of mastication.

• The three sensory divisions of the trigeminal nerve are – the ophthalmic (V1),

– maxillary (V2),

– mandibular (V3)

• Sensory dermatomes. V1 ophthalmic division (fine stippling), V2 maxillary division (dark stippling), V3 mandibular division (intermediate stippling).

Course of Trigeminal Nerve• It emerges from the lateral portion of the ventral pons, passes over

the petrous apex, forms the trigeminal ganglion and then divides into 3 branches

• The trigeminal ganglion contains the cells of origin of all the CN V sensory axons and occupies a recess (Meckel’s cave) in the dura mater posterolateral to the cavernous sinus

• Meckel’s cave is near the apex of the petrous part of the temporal bone in the middle cranial fossa

• Medially, the trigeminal ganglion is close to the internal carotid artery and the posterior cavernous sinus

Anatomy: Ophthalmic Division• Occupies the lateral wall of the cavernous sinus

• Divides into the lacrimal, nasociliary, and frontal nerves. These branches pass through the superior orbital fissure to enter the orbit.

• The lacrimal nerve supplies the conjunctiva and the skin of the lateral portion of the upper lid. It also receives, parasympathetic facial nerve fibers from the sphenopalatine ganglion, which it transmits to the lacrimal gland.

• The frontal nerve divides into the supraorbital and supratrochlear nerves, which innervate the medial portion of the upper eyelid, forehead, scalp, frontal sinus, and bridge of the nose.

Cont…• The nasociliary nerve gives off long ciliary nerves and the

sensory root of the ciliary ganglion which are the sole sensory supply to the eye .

• Both long and short ciliary nerves transmit somatic sensory information from the iris, cornea, and ciliary muscle.

• The nasociliary nerve also forms the anterior and posterior ethmoidal nerves and the infratrochlear nerve, which innervate – the sphenoid and posterior ethmoid sinuses, – the upper eyelid, the canaliculi, and lacrimal sac– the caruncle, – the mucosa of the nasal septum and inferior and middle turbinates,

Anatomy: Maxillary Division• Runs inferiorly in the cavernous sinus and becomes the infraorbital

nerve as it enters the orbit through the infraorbital fissure.

• Branches of the maxillary nerve include the sphenopalatine, posterosuperior alveolar, and zygomatic nerves.

• The infraorbital nerve divides into inferior palpebral, lateral nasal, and superior labial nerves.

• The maxillary division supplies sensation to: – the nasopharynx, maxillary sinus, roof of the mouth, soft palate, upper

teeth, and an area of the face that extends from the upper lip to the side of the nose,

– Then to the lower eyelid, and then to the zygoma.

Anatomy: Mandibular Division• The mandibular nerve does not reach the cavernous sinus like the other

two divisions.

• The auriculotemporal, buccinator, lingual, and inferior alveolar nerves provide sensation to:– the lateral scalp, posterior cheek and temporal areas, temporomandibular

joint, anterior pinna, upper and outer walls of the external auditory canal, anterior half of the tympanum, lower lip and gums, chin, anterior two-thirds of the tongue, floor of the mouth, lower teeth, and lower half of the buccal surface.

• Motor fibers innervate eight muscles

• Postganglionic parasympathetic glossopharyngeal nerve fibers from the optic ganglion travel with the auriculotemporal nerve to the parotid gland.

PhysiologyOCULAR SENSATION• Sensitivity to pain is greatest in the center of the

cornea and decreases toward the limbus.

• Pain receptors are also found in the extraocular muscles, conjunctiva, uvea, sclera, and optic nerve sheaths.

• The retina, optic nerve, and lens, however, are devoid of pain sensitivity.

Cont…TRIGEMINAL REFLEXES• Pressure, or manipulation of, the ocular structures causes

bradycardia (oculocardiac reflex)

• The trigeminocardiac reflex: the afferent limb of the reflex is by way of a branch of the trigeminal nerve, and the efferent limb is by way of the vagus nerve. Vagal stimulation on the heart causes slowing and, rarely, asystole.

• Corneal stimulation can produce the corneolacrimal (reflex tearing), corneomandibular, and corneooculogyric reflexes.

• Nausea and vomiting may occur during an acute attack of glaucoma or certain intraorbital inflammatory processes.

Clinical assessment

• Corneal sensitivity is tested by the light touch of a cotton-tipped applicator. If local cornea disease is present, each quadrant should be assessed separately.

• The motor root is assessed by palpating the temporal and masseter muscles as the patient clenches his or her jaw, and noting pterygoid strength.

• Weakness of the pterygoids will produce a deviation of the jaw to the ipsilateral side when the patient opens their mouth.

Trigeminal Nerve Dysfunction• Trigeminal nerve disorders may present with:

– loss of function (e.g., anesthesia and paresis of mastication) – abnormal sensation (e.g., pain and paresthesias).

• In general, peripheral nerve lesions produce anesthesia on the face and inside the mouth, whereas, central lesions only involve the face.

• Lesions peripheral to the gasserian ganglion usually involve only one or two trigeminal divisions, whereas proximal lesions tend to affect the whole half of the face.

• Combined involvement of cranial nerves three, four, and six or a Horner's syndrome may localize the lesion to the cavernous sinus.

Cont…LOSS OF CORNEAL SENSATION• Corneal sensation is almost always decreased when a

lesion of the trigeminal nerve impairs cutaneous sensation in the ophthalmic division.

• Direct ocular impairment from surgery, medications, corneal dystrophy, and infection can result in isolated loss of corneal sensation.

• Neuroparalytic keratitis or widespread loss of corneal epithelium may occur in an eye that becomes denervated.

Cont…PERIPHERAL BRANCHES• Peripheral branches of the trigeminal nerve can be affected

by numerous disease processes, facial trauma and dental procedures.

• The usual presentation of trigeminal neuropathy is either anesthesia or paresthesias, but after partial regeneration of the nerve, pain may also occur.

• In Trigeminal sensory neuropathy, the second and third trigeminal divisions are affected most often, and a sensory deficit can usually be detected in the involved dermatome. This condition is only rarely bilateral.

Cont…CAVERNOUS SINUS• Inflammation in the superior orbital fissure or cavernous sinus may

affect the ophthalmic and maxillary divisions of the trigeminal nerve as well as the oculomotor, trochlear, abducens, and sympathetic nerves.

• Inflammation in the cavernous sinus has been called the Tolosa-Hunt syndrome. Pain is a prominent feature and may precede signs of involvement of the other nerves.

• Cranial polyneuropathy is a condition of multiple cranial nerve palsies. – Causes include the Guillain-Barre syndrome, infections, tumors,

carcinomatous meningitis, sarcoidosis, collagen vascular disease, and idiopathic causes

Cont…• Cluster headache (CH) is a neurological disorder characterized by

recurrent, severe headaches on one side of the head, typically around the eye.

• Has eye watering, nasal congestion and swelling around the eye, typically confined to the side of the head with the pain.

• Cluster headache belongs to a group of primary headache disorders, classified as the trigeminal autonomic cephalalgias or (TACs).

• It has been proposed that intense pain was caused by dilation of blood vessels which in turn, was thought to create pressure on the trigeminal nerve.

Cont…• Trigeminal neuralgia is a neuropathic chronic pain disorder

affecting the trigeminal nerve.

• Evidence indicates that TN is caused by demyelination of the sensory fibers within the trigeminal nerve itself.

• The classic presentation is characterized by episodes of sudden, explosive severe pain along the trigeminal nerve, with periods of pain-free remission between attacks

• Trigeminal neuralgia most commonly involves the middle branch (the maxillary nerve or V2) and lower branch (mandibular nerve or V3) of the trigeminal nerve

Thank You

OLFACTORY NERVE

PRESENTER :SERAPHINE NTIZAHUVYETUTOR : JOHN ONYANGO

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OLFACTORY NERVE

• The cranial nerve I originates from small olfactory receptors in the mucous membrane of the nose.

• It is purely sensory• Unmyelinated CN I fibers pass from olfactory

receptors in the nasal cavity through the cribriform plate of the ethmoid bone and,

• they enter the ventral surface of the olfactory bulb, where they form the nerve

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OLFACTORY BULB

• It is a structure organised in several distinct layers • From outside toward the centre of the bulb, the

layers are differentiated as follows• Glomerular layer• External plexiform layer• Mitral cell layer• Internal plexiform layer• Granule cell layer

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OLFACTORY BULB

• in the cranial cavity, the fibres enter the olfactory bulb, which lies in the olfactory groove, within the anterior cranial fossa.

• The olfactory bulb contains specialised neurones, called mitral cells.

• The olfactory nerve fibres synapse with the mitral cells, forming collections known as synaptic glomeruli.

• From the glomeruli, second order nerves then pass posteriorly into the olfactory tract.

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ALFACTORY TRACT• The olfactory tract runs inferiorly to the frontal lobe. • As the tract reaches the anterior perforated substance, it

divides into medial and lateral stria:• The lateral stria carries the axons to the olfactory area of the

cerebral cortex (also known as the primary olfactory cortex).• The medial stria carry the axons across the medial plane of

the anterior commissure where they meet the olfactory bulb of the opposite side

• The primary olfactory cortex sends nerve fibres to many other areas of the brain, notably the piriform cortex, the amygdala, olfactory tubercle and the secondary olfactory cortex.

• These areas are involved in the memory and appreciation of olfactory sensations

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• Fibers runs through the olfactory bulb and terminate in the primary cortex

• Functions solely by carrying afferent impulses for the sense of smell

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Central Projections

• The pyriform lobe includes the olfactory tract, the uncus , and the anterior part of the hippocampal gyrus .

• The prepyriform and the periamygdaloid areas of the temporal lobe represent the primary olfactory cortex.

• The entorhinal area is known as the secondary olfactory cortex and is included in the pyriform lobe.

• The olfactory system is the only sensory system that has direct cortical projections without a thalamic relay nucleus.

ABDCENS NERVE (CNVI)

• The abducens nerve arises from the abducens nucleus in the pons of the brain, and exits the brainstem at the junction of the pons and the medulla.

• It then enters the subarachnoid space and pierces the dura mater to run in a space known as Dorello’s canal.

• The nerve travels through the cavernous sinus at the tip of the petrous temporal bone, before entering the orbit of the eye through the superior orbital fissure.

• Within the bony orbit, the abducens nerve terminates by innervating the lateral rectus muscle.

NUCLEI

• The abducens nucleus is located in the pons, on the just beneath the fourth ventricle

• the abducens nucleus is surrounded by the looping fibers of the facial nerve (genu) and is adjacent to the pontine paramedian reticular formation and the medial longitudinal fasciculus

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COURSE OF CRANIAL NERVE VI

• The fascicular portion of the nerve runs ventrally through the paramedian pontine reticular formation and the pyramidal tract and leaves the brain stem in the pontomedullary junction

• CN VI takes a vertical course along the ventral face of the pons and is crossed by the anterior inferior cerebellar artery .

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• It ascends farther through the subarachnoid space along the surface of the clivus, surrounded by Batson's venous plexus, to perforate the dura mater below the crest of the petrous portion of the temporal bone approximately 2 cm below the posterior clinoid process

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• It then passes intradurally through the inferior petrosal sinus and beneath the petroclinoid (Gruber) ligament (which connects the petrous pyramid to the posterior clinoid ) through Dorello's canal,

• where it enters the cavernous sinus

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• In the cavernous sinus, CN VI runs below and laterals to the carotid artery and may transiently carry sympathetic fibers from the carotid plexus

• It passes through the superior orbital fissure within the annulus of Zinn and innervates the lateral rectus muscle .

• it has a long course within the cranial cavity , so the increase intracranial tension can domage the nerve

• in abducens neuropathy, affected eye will not abduct

• Thank you

FACIAL NERVE

TUTOR: Dr JOHN ONYANGOPRESENTER: BYAMUNGU SAKANO

FACIAL NERVEANATOMY

FACIAL NERVE PALSY

ANATOMYFacial nerve is a mixed nerve, having a motor root and a

sensory root.

Motor root supplies all the mimetic muscles of the face which develop from the 2nd brachial arch.

Sensory root “nerve of Wrisberg” carries taste fibers from the anterior 2/3 of the tongue and general sensation from the concha and retroauricular skin.

Also it carries secretomotor fibers to the lacrimal, submandibular and sublingual glands as well as those in the nose and palate.

ANATOMY

Structure of the nerve

From inside outward:

AxonMyelin sheathNeurolimma Endoneurium Perineurium Epineurium

ANATOMY

Function

The facial nerve is responsible for:

Contraction of the muscles of the faceProduction of tears from the lacrimal glandConveying the sense of taste from the front part of the

tongue (via the Chorda tympani nerve)The sense of touch at auricular conchae

ANATOMY BRANCHIAL MOTOR

ANATOMY BRANCHIAL MOTOR

ANATOMY PARASYMPATHYTIC FIBERS

ANATOMY VISCERAL SENSATION

FACIAL NERVE PALSYClassification of facial nerve palsy

1. Upper motor neuron (supranuclear causes)

2. Lower motor neuron (nuclear and infranuclear causes)

Stroke (different stroke syndromes) Tumors

Idiopathic(Bell’s palsy: Most common cause of lower motor neuron VII CN palsy)

Infectious: Herpes zoster, others(syphilis,meningitis)

Tumors: Parotid gland tumors, Cerebellopontine angle tumors)

Trauma: Temporal bone fracture, Facial trauma

Vascular: Pontine stroke

Metabolic: DM

FACIAL NERVE PALSY

Clinical approach

Hyperacusis (paralysis of the stapedius muscle)

Symptoms

Otalgia (irritation of the sensory fibers)

Gustatory disturbances

Disturbances of lacrimation (dryness, crocodile tears = gustatory lacrimation due to faulty neural regulation)

Facial muscles paresis or paralysis (Motor paralysis is the most important and by far the most common symptom of facial nerve pathology.)

FACIAL NERVE PALSY

Management of facial nerve palsy

1.Temporary treatment required for acute corneal symptoms

Artificial tears and ointmentsTaping of lids at night

a.Conservative

b.Surgical: tarsorrhaphy

2.Permanent treatment required

Medial canthoplastyLateral canthoplasty

THANK YOU