The document discusses the anatomy and clinical significance of the fourth cranial nerve (trochlear nerve). It describes the functional components and course of the nerve from the brainstem through the cavernous sinus and orbit. The trochlear nerve is unique as the only cranial nerve to emerge from the dorsal aspect of the brainstem and the only crossed nerve. Clinical features of trochlear nerve palsy include double vision, difficulty going downstairs, and head tilt. Special tests like Parks three step test and double Maddox rod test can help in diagnosis. Treatment depends on severity and may involve weakening other extraocular muscles.

1. ANATOMY & CLINICAL
SIGNIFICANCE OF 4TH
CRANIAL NERVE
Dr.Ashok Kumar
Valuroutu

2. TROCHLEAR NERVE
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3. FUNCTIONAL COMPONENTS
• SOMATIC EFFERENT-concerned with
movement of eye ball through SO.
• GENERAL SOMATIC AFFERENT-carries
proprioceptive impulses from SO which are
relayed in the mesencephalic nucleus of 5th
nerve.
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4. COURSE AND DISTRIBUTION
1)Fascicular part
2)Pre cavernous part
3)Intra cavernous part
4)Intra orbital part
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5. • SITUATION: at the level of inferior colliculus
in the ventromedial part of central gray
metter of midbrain dorsal to medial
longitudinal bundle.
• Caudal & continous with 3rd nucleus
complex.
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8. FASCICULAR PART:
• axons leave the nucleus
• curve posteriorly around the aquiduct in the
central greymatter
• decussate in the anterior medullary velum.
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10. PRECAVERNOUS PART:
leaves the brainstem on the dorsal surface
just caudal to inferior colliculus
winds around brainstem
runs forwards beneath the free edge of
tentorium
pierces the dura on the posterior corner of
the roof of cavernous sinus to enter in to it.
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11. INTRACAVERNOUS PART:
Runs forwards in the lateral wall of the
sinus,lying below 3rd nerve and above the 1st
division of 5th nerve.
In the anterior part of the sinus, it rises,
crosses over the 3rd nerve
passes through the superior orbital fissure,
above and lateral to annulus of zinn.
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13. INTRA ORBITITAL PART:
• Enters the orbit through lateral part of SOF
• Frontal & lacrimal nerves laterally,
ophthalmic vein inferiorly.
• Divides in to fan shaped manner into 3 or 4
branches
• Ends by supplying SO on its orbital surface
near lateral border.
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17. CONNECTIONS:
1)Cerebral cortex
Motor cortex - cortico nuclear tracts
Visual cortex - supeior colliculus & tactobulbar
Frontal eye field. tracts.
2)Nuclei of 3rd ,6th&8th -MLF
3)Superior colliculi -descending predorsal bundle
4)Vertical & torsional gaze centres
5)Cerebellum - vestibular nuclei.
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18. UNIQUE CHARACTERS
• Only cranial nerve to emerge from dorsal
aspect of brain.
• Only crossed cranial nerve
• Longest Intra cranial course(about 75 mm)&
thinnest of all cranial nerves
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19. CLINICAL FEATURES
SYMPTOMS:
• Ac.onset of double vision,
• Difficulty in going downstairs,
• Vertigo
SIGNS:
• Hyperdeviation ,limitation of depression in adduction,
• Extorsion, vertical diplopia,
• Hypertropia on opposite gaze
• Charecteristic head posture-head
tilted to opposite side
face turned towards opposite side
chin depressed
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21. SPECIAL TESTS
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22. PARK’S 3 STEP TEST:
STEP 1: Identify the HYPERTROPIC EYE in
primary position.
depressors of hypertropic eye- SO,IR.
elevators of hypotropic eye-SR,IO.
STEP 2: Determine whether hypertropia is
greater in Rt or Lt gaze.
on Lt gaze Lt SR, Rt.SO
on Rt gaze Rt IR, Lt IO
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23. STEP 3: Tilt the head towards each shoulder,
look for vertical sqint.
BEILSCHOWSKY HEAD TILT TEST:
same principle as the 3rd step of PARK TEST
Pt fixates, head tilted Rt &Lt
of Lt hypertropia on Lt head tilt- Lt SO
of Lt hypertropia on Rt head tilt- Lt IR
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25. DOUBLE MADDOX ROD TEST :
For measuring the degree of cyclodeviation.
In unilateral palsy – cyclodeviation <10 deg
In bilateral palsy – cyclodeviation >10 deg
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27. Differential Diagnosis of Vertical
Binocular Diplopia
• Superior Oblique Palsy
• Thyroid Ophthalmopathy
• Myasthenia Gravis
• Brown Syndrome
• Orbital fracture with entrapment
• Cyclovertical paresis or overaction
• Skew Deviation/Ocular Tilt
• Dissociated Vertical Deviation
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28. Isolated Superior Oblique Palsy
• Most common etiologies are congenital and
traumatic
• Also vascular; less commonly tumor,
demyelinating
• In absence of other neurological symptoms
and presence of vascular risk factors,
reasonable to observe
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29. TREATMENT
• CONGENITAL:large hypertropia in PP treated by
SO tucking
• ACQUIRED:
SMALL- ipsilateral IO weakening.
MODERATE- ipsilateral IO weakening with
ipsilateral SR weakening .
PURE EXCYCLOTROPIA: without hypertropia –
HARADA- Ito procedure
Splitting & ALT OF lateral half of SO tendon.
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