Trochlear nerve

7,409 views 49 slides Jun 23, 2019
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About This Presentation

anatomy, physiology and clinical aspects of trochlear nerve


Slide Content

TROCHLEAR NERVE Dr Kumar Siddharth MBBS, 2 nd Year PG MS Ophthalmology SCBMCH, Cuttack

INTRODUCTION Purely motor nerve, supplies only superior oblique muscle of the eye The nerve is named after trochlea, the fibrous pulley through which the tendon of the superior oblique muscle passes Only cranial nerve to arise from the dorsal aspect of the brain Trochlear nerve contains fewer number of axons compared to other cranial nerves

introduction Only cranial nerve to cross completely to the other side (arises from the contralateral nucleus) Longest intracranial course (7.5cm) and thinnest of all cranial nerves Unprotected intracranial course of trochlear nerve is responsible for frequent involvement in intracranial lesions Superior oblique palsy is the most common type of paralytic squint

FUNCTIONAL COMPONENTS Somatic efferent – movement of eyeball through Superior oblique General somatic afferent Proprioceptive signals from Superior oblique These impulses are relayed to mesencephalic nucleus of Trigeminal nerve

NUCLEUS Located in the Tegmentum of the midbrain It is caudal to and continuous with the third nerve nuclear complex It belongs to somatic efferent column of nuclei

Relations of the nucleus Ventrolateral to the Cerebral Aqueduct At the level of superior border of inferior colliculus Dorsal to Medial longitudinal bundle

CONNECTIONS OF NUCLEUS Cerebral cortex Motor cortex (precentral gyrus) On both sides through Corticonuclear tracts Visual cortex Through Superior colliculus Frontal eye fields

CONNECTIONS OF NUCLEUS Nuclei of 3 rd , 6 th and 8 th cranial nerve Through medial longitudinal bundle Superior colliculi Tectobulbar tract Tectospinal tract Vertical and torsional gaze centres Cerebellum Through the vestibular nuclei

FASCICULAR PART Efferent fibres after leaving the nucleus, pass posteriorly around the Aqueduct in the central grey matter Decussate completely in the anterior medullary vellum

PRECAVERNOUS PART Emerges from the anterior medullary vellum just below inferior colliculus, on the dorsal aspect of midbrain It winds around Superior cerebellar peduncle and Cerebral peduncle just above the Pons It runs beneath the free edge of Tentorium

Passes between Posterior cerebral and Superior cerebellar arteries Pierces Arachnoid on the posterior corner of the roof of Cavernous sinus to enter the Subdural space

INTRACAVERNOUS PART Runs forward in the lateral wall Lies below the oculomotor nerve Lies above the 1 st division of 5 th cranial nerve

In anterior part of the Cavernous sinus, it rises and crosses over the 3 rd nerve Leaves sinus to pass through the lateral part of Superior orbital fissure Lies superolateral to the Annulus of Zinn and medial to the Frontal nerve

INTRAORBITAL Nerve passes medially above the origin of Levator palpebrae superioris Fans out in 3-4 branches which end up supplying Superior oblique muscle on the Orbital surface Number of fibres in the Intraorbital part is greater than the Intracranial part, extra General somatic afferent fibres

BLOOD SUPPLY INTRACRANIAL Superior cerebellar artery - Vermian and Paravermian artery Posterior cerebral artery - Collicular artery Internal carotid artery - Inferolateral trunk and Meningohypophyseal trunk EXTRACRANIAL Internal carotid artery branches Intrasinusoidal branches Ophthalmic artery Posterior ethmoidal artery

CAUSES OF 4 TH NERVE PARALYSIS Congenital paralysis Trauma Idiopathic Vascular and neurogenic

Congenital paralysis 40% cases Usually symptoms do not develop until decompensation occurs in adult life A compensatory head tilt to the contralateral side is seen in order to compensate for underacting superior oblique muscle Examination of old photographs maybe helpful

Trauma 34% cases It usually causes Bilateral 4 th nerve palsy due to impact in the area of Anterior medullary velum, where two nerves decussate

Idiopathic 20% cases

Vascular and neurogenic causes 3 - 5% In older individuals micro vasculopathy secondary to Diabetes, Hypertension, Atherosclerosis is common Aneurysms rarely affect Trochlear nerve Other causes can be intracranial space occupying lesions

CLINICAL FEATURES Supranuclear lesion Nuclear lesion Features of 4 th nerve palsy

SUPRANUCLEAR LESION Loss of conjugate movements of the eyeball

NUCLEAR LESIONS Lesions involving the nucleus in the midbrain before the decussation leads to paralysis of contralateral Superior oblique Most often due to stroke, less often neoplasm Other causes include demyelinative disease and trauma Nuclear lesions are never isolated

FEATURES OF 4 TH NERVE PALSY Hyper deviation Ocular movement disorder Diplopia Abnormal head posture

Hyper deviation Due to weakness of the superior oblique muscle More obvious when head is tilted to the ipsilateral shoulder (Bielchowsky’s sign)

Ocular movements Depression is limited in adduction Intorsion is also limited

Diplopia Homonymous vertical diplopia occurs on looking downwards Vision is single as long as eyes look above the horizontal plane Usually noticed when patient is coming downstairs Torsional diplopia

Abnormal head posture To avoid diplopia head takes posture towards the action of Superior oblique muscle Head tilted towards the opposite shoulder, face tilted to the opposite side with chin depressed

SYNDROMES ASSOCIATED WITH 4 TH NERVE PALSY Nuclear fascicular syndrome Subarachnoid space syndrome Cavernous sinus syndrome Orbital syndrome Isolated 4 th nerve palsy

NUCLEAR FASCICULAR SYNDROME Distinguishing between nuclear and fascicular lesion is virtually impossible due to short course of fascicles in the midbrain May get contralateral Horner’s syndrome Because of close proximity of the descending ocular sympathetic tract to the Trochlear nerve nucleus Causes Haemorrhage Infarction Demyelination Trauma

SUBARACHNOID SPACE SYNDROME Causes Trauma Basal meningitis Neoplasia like Pinealomas, Tentorial meningiomas, aneurysms Post lumbar puncture or post spinal anaesthesia

CAVERNOUS SINUS SYNDROME Associated with other cranial nerve palsies like 3 rd , 5 th , 6 th and ocular sympathetic paralysis Causes - to cavernous sinus disease Inflammation Infection Neoplasm (lymphoproliferative, meningioma, pituitary macroadenoma) Vascular anomalies like fistula or aneurysm

ORBITAL SYNDROME Seen in association with other cranial nerve palsies (3 rd , 5 th and 6 th ) Associated orbital signs are proptosis, chemosis and conjunctival injection Causes Trauma Inflammation Tumours like rhabdomyosarcoma

ISOLATED 4 TH NERVE PALSY Congenital Symptoms usually do not appear till decompensation occurs in adult life Diplopia Large vertical fusion amplitude (10 -15 prism dioptres) In patients presenting at older age Family album tomography scan Acquired Trauma Ischaemic conditions Diabetes mellitus, hypertension Herpes zoster Nuclear, cavernous and orbital Trochlear palsy are rarely isolated and usually involve 3 rd , 5 and 6 th cranial nerve

evaluation Initial observations Hypertropia and exotropia Head tilt to the other side Facial asymmetry Ocular history Diplopia, whether vertical or horizontal, worsening of diplopia on reading or climbing stairs Head posture in childhood. Systemic history Diabetes, Hypertension, Myasthenia gravis, ICSOL, Trauma Family history To be ruled out in congenital Trochlear nerve palsy

diagnosis Park - Bielschowsky three step test Double Maddox rod test

PARK-BIELSCHOWSKY test STEP 1 Aim - To assess which eye is hypertropic in the primary gaze In case of vertical strabismus, the following four muscles could be involved 1) Depressors of the right eye - superior oblique and inferior rectus. 2) Elevators of the left eye - the superior rectus and inferior oblique. In 4 th nerve palsy the involved eye is always higher

PARK-BIELSCHOWSKY test Step 2 Aim - which lateral direction has worse hypertropia If the right hypertropia increases on left gaze implicates a right superior oblique or left superior rectus involvement Increase in the right gaze implicates that either the left inferior oblique or right inferior rectus are involved. In 4 nerve palsy the deviation is worse on opposite gaze

PARK-BIELSCHOWSKY test Step 3 Aim - in which head tilt direction is the hypertropia worse The head tilt test is performed with the patient fixating at a straight ahead target at 3 mts. Increase in right hypertropia on right head tilt implies the right superior oblique is involved Increase in left hypertropia on right head tilt indicates the left inferior rectus is involved. In 4 nerve palsy the deviation is better on opposite tilt

DOUBLE MADDOX ROD TEST Unilateral 4 th nerve palsy is characterized by less than 10 prism diopter of excyclodeviation Bilateral palsy will have more than 10 prism dioptre of excyclodeviation A Maddox rod is positioned in front of each eye The patient or examiner rotates the axes of the rods until the lines are perceived to be parallel. The degrees of deviation (excyclodeviation) can be determined by the angle of rotation that causes the line images to appear horizontal and parallel.

UNILATERAL VS BILATERAL SUPERIOR OBLIQUE PASLY Bilateral Superior oblique palsy is always suspected until proven otherwise Most common cause of bilateral Trochlear nerve palsy is injury to the anterior medullary velum Esotropia on downgaze is usually little in unilateral palsy, whereas in bilateral palsy there is V pattern esotropia On double Maddox rod it shows Excyclodeviation of less than 10 degrees in unilateral cases and of more than 10 degrees in bilateral cases Ductions of Superior oblique muscle are usually diminished on both sides in bilateral cases Head tilt test Positive in unilateral palsy whereas in bilateral palsy tilting on either side will increase the hypertropia

Checking for 4 th nerve in 3 rd nerve palsy Vertical actions cannot be tested as there is 3 rd nerve palsy Eye is abducted Note a limbal or conjunctival landmark Patient is asked to look down Patient will not be able to look down in 3 rd nerve palsy in abducted eye (IR weakness) Check for intorsion of the eye by observing the limbal/conjunctival landmark If the conjunctival landmark is moving, the eye is intorting then the 4 CN is intact.

DIFFERENTIAL DIAGNOSIS OF VERTICAL DIPLOPIA Skew deviation Myasthenia gravis Thyroid ophthalmopathy

SKEW DEVIATION Vertical misalignment of visual axis It maybe transient/constant Due to imbalance of supranuclear inputs Associated with brainstem and cerebellar signs and symptoms Not associated with torsional diplopia or cyclodeviation

MYASTHENIA GRAVIS Can involve isolated Superior oblique and mimic 4 th nerve palsy Shows diurnal variation Can involve other extraocular muscles Tensilon test positive Acetyl choline receptor antibodies positive

THYROID OPHTHALMOPATHY Other signs of hyperthyroidism maybe present T3, T4 levels are suggestive In Superior oblique palsy, hypertropia is worse on downgaze while in thyroid ophthalmopathy it is worse in up gaze

INVESTIGATIONS IN 3 RD NERVE PALSY Basic investigations Blood sugar Blood pressure Lipid profile ESR Thyroid profile MRI brain Cerebral angiography Lumbar puncture Blood in CSF Inflammation Neoplasia Infection Meningeal carcinomatosis or lymphomatous/leukemic infiltration

treatment Congenital decompensated and microvascular palsies commonly resolve spontaneously Strabismus surgery is not frequently required for traumatic cases because of troublesome diplopia and childhood cases because of substantial compensatory head posture Small hypertropia - <15 prism dioptres is usually treated by either Inferior oblique weakening or by Superior oblique tucking Moderate to large deviation - ipsilateral Inferior oblique weakening combined with ipsilateral Superior rectus weakening and contralateral Inferior rectus weakening (defective elevation is potential complication) Excyclodeviation – Harada Ito procedure, splitting of anterolateral transposition of lateral half of Superior oblique tendon

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