This document provides an overview of the trochlear nerve (cranial nerve IV), which innervates the superior oblique eye muscle. It discusses the anatomy and course of the nerve from its nucleus in the midbrain through the skull and orbit. Key points include that the trochlear nerve is the only cranial nerve to decussate and has the longest intracranial course. Causes of trochlear nerve palsy include congenital issues, trauma, vascular problems, and tumors. Clinical features of trochlear nerve palsy are hyperdeviation of the eye, limited eye movements, diplopia, and abnormal head posture. The document also outlines tests to diagnose trochlear nerve pals

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

2. 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

3. 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

4. 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

5. 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

6. RELATIONS OF THE NUCLEUS
Ventrolateral to the Cerebral
Aqueduct
At the level of superior border of
inferior colliculus
Dorsal to Medial longitudinal
bundle

7. CONNECTIONS OF NUCLEUS
Cerebral cortex
1. Motor cortex (precentral gyrus)
 On both sides through Corticonuclear tracts
2. Visual cortex
 Through Superior colliculus
3. Frontal eye fields

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

9. 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

10. 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

11. 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

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

13. In anterior part of the Cavernous
sinus, it rises and crosses over the 3rd
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

14. 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

15. 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

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

17. 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

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

19. IDIOPATHIC
20% cases

20. 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

21. CLINICAL FEATURES
1. Supranuclear lesion
2. Nuclear lesion
3. Features of 4th nerve palsy

22. SUPRANUCLEAR LESION
Loss of conjugate movements
of the eyeball

23. 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

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

25. HYPER DEVIATION
Due to weakness of the
superior oblique muscle
More obvious when head is
tilted to the ipsilateral
shoulder (Bielchowsky’s sign)

26. OCULAR MOVEMENTS
Depression is limited in adduction
Intorsion is also limited

27. 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

28. 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

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

30. 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

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

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

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

34. ISOLATED 4TH 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 3rd, 5 and 6th cranial nerve

35. 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

36. DIAGNOSIS
Park - Bielschowsky three step test
Double Maddox rod test

37. 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 4th nerve palsy the involved eye is always
higher

38. 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

39. 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

40. DOUBLE MADDOX ROD TEST
Unilateral 4th 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.

41. 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

42. CHECKING FOR 4TH NERVE IN 3RD
NERVE PALSY
Vertical actions cannot be tested as there is 3rd 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 3rd 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.

43. DIFFERENTIAL DIAGNOSIS OF
VERTICAL DIPLOPIA
Skew deviation
Myasthenia gravis
Thyroid ophthalmopathy

44. 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

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

46. 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

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

48. 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

49. THANK YOU