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DR. N.VASANTHAKUMAR
MODERATORS:
PROF DR.K.SRIKANTH
DR.N.SWATHI(ASSOC)
OCULAR MOTOR NERVES
CONTENTS
 OCULOMOTOR NERVE
 TROCHLEAR NERVE
 ABDUCENT NERVE
OCULOMOTOR NERVE (3rd NERVE)
 It consists of 5 components.
 NUCLEAR COMPLEX
 FASCICULUS PART
 BASILAR PART
 INTRACAVERNOUS PART
 INTRAORBITAL PART
NUCLEAR COMPLEX
 It is situated in the MIDBRAIN AT THE LEVEL OF
SUPERIOR COLLICULUS, VENTRAL TO
SLYVIAN AQUEDUCT.
 Five MAIN MOTOR subnuclei are present.
 Levator
 Superior rectus
 Medial rectus
 Inferior rectus
 Inferior oblique
SUBNUCLEI
 LEVATOR SUBNUCLEUS :
Unpaired caudal midline structure, innervates both
levator muscles.
 SUPERIOR RECTUS :
Paired, each innervates contralateral superior
rectus.
SUBNUCLEI
 MEDIAL RECTUS :
Paired ventromedial nucleus, each innervates
ipsilateral medial rectus.
 INFERIOR RECTUS :
Paired dorsolateral nucleus, each innervates
ipsilateral inferior rectus.
 INFERIOR OBLIQUE :
Paired intermedial nucleus, each innervates
ipsilateral inferior oblique.
ACCESSORY MOTOR NUCLEUS
 EDINGER-WESTPHAL NUCLEUS :
- Sends pre ganglionic parasympathetic fibres along
other oculomotor nerve fibres.
- Situated posterior to the main occulomotor
nuclear complex.
COURSE OF 3rd NERVE
 FASCICULAR PART :
- Consist of efferent fibres which pass from the 3rd
nerve nucleus through red nucleus & medial aspect
of the cerebral peduncle.
- From there they emerge from the midbrain & pass
into the interpeduncular space.
COURSE contd...
 BASILAR PART :
- Series of rootlets which have midbrain on the
medial aspect of cerebral peduncle, before coalescing
to form the main trunk.
- Then it passes between posterior cerebral &
superior cerebellar artery, running parallel &
laterally to the posterior communicating artery.
COURSE contd....
 INTRACAVERNOUS PART:
- Enters the cavernous sinus by piercing the dura
just lateral to posterior clinoid process.
- Within the cavernous sinus, it runs in lateral wall
above the trochlear nerve.
- In the anterior part, it divides into superior &
inferior branches which enter the orbit through
superior orbital fissure within the annulus of Zinn.
COURSE contd...
 INTRA ORBITAL PART :
- Superior division innervates levator palpabre
superioris and superior rectus muscle.
- Inferior division innervates medial rectus, inferior
rectus and inferior oblique.
- Branch to inferior oblique contains the
preganglionic parasympathetic fibres from the
Edinger-Westphal nucleus which innervates the
sphincter pupillae ciliary muscle.
PUPILLOMOTOR FIBRES
 Between brainstem & cavernous sinus, the fibres are
located superficially in the superomedial part of the
oculomotor nerve.
 Blood supply : Pial vessels.
 Main trunk receives its supply from vasa nervorum.
APPLIED ANATOMY
 A. Lesions at Oculomotor Nucleus (Midbain)
 B. Lesions at Oculomotor Nerve Fascicles (Leaving
the 3rd nerve nucleus)
 C. Lesions in the Subarachnoid space
 D. Lesions within the Cavernous Sinus and Superior
Orbital Fissure
 E. Lesions within the Orbit
A. Lesions at Oculomotor Nucleus (Midbain)
 Produces bilateral defects.
 It is divided in subnuclei according to the innervated
area. Each superior recti are innervated by
contralateral CN III subnucleus, so a nuclear CN III
palsy would produce paralysis of the contralateral
superior rectus.
 Both levator palpebrae superioris are innervated by
the one subnuclei (central caudal nucleus), so a
nuclear palsy would produce bilateral ptosis.
B. Lesions at Oculomotor Nerve Fascicles
(Leaving the 3rd nerve nucleus)
 Lesions at this level can produce complete or
incomplete palsies.
 Often it cannot be differentiated from lesion outside
of the midbrain.
 When the lesion is adjacent to CN III nucleus
(midbrain) it can produce several manifestations:
 Nothnagel’s Syndrome :Lesion at the superior
cerebellar peduncle presents with ipsilateral 3rd
nerve palsy and cerebellar ataxia.
Contd..
 Benedikt's Syndrome :Lesions at the Red
Nucleus are characterized by ipsilateral 3rd nerve
palsy and contralateral involuntary movement.
 Weber’s Syndrome :Lesion at the cerebral
peduncle produces ipsilateral 3rd nerve palsy and
contralateral hemiplegia.
 Claude Syndrome : Combination of Benedikt's
and Nothnagel's syndromes.
 Lesions can present with combination of these
findings depending on the degree of the insult.
Weber’s
Benedi
kt’s
Claud
’s
Nothn
agel’s
Contd..
 It is known that CN III separates in superior and
inferior divisions at the superior orbital fissure,
sometimes lesions at the fascicles can produce
isolated dysfunction of either the superior or inferior
division.
 Most common causes are ischemic, haemorrhagic,
compressive, traumatic.
 Rare cause is infiltrative.
C. Lesions in the Subarachnoid space
 It is the area where 3rd nerve passes between ventral
surface of midbrain to entrance of cavernous sinus
(Interpeduncular fossa).
 Damage in this area can produce various presentations.
 CN III palsy with fixed dilated pupil, it is important
to know that pupillary fibres occupy a peripheral location
and receive more collateral blood supply than the main
trunk of the nerve making it susceptible to compression
(e.g. aneurysm). The most common known etiology is a
posterior communicating artery aneurysm. This is a
medical emergency.
Contd..
 CN III palsy without pupil involvement : Most common
causes are diabetes mellitus, systemic hypertension,
atherosclerosis and in some cases migraine.
 Also compressive masses or aneurysm can cause it.
 On the course to the cavernous sinus the CN III rest on the
edge of the tentorium cerebelli. The edge of the uncal portion
overlies the tentorium, so in case of raised intracranial
pressure this section can herniate producing displacement of
the midbrain compressing the ipsilateral oculomotor nerve.
 This causes ipsilateral ophthalmoplegia and mydriasis. The
most common cause of uncal herniation is intracranial
hemorrhages.
D. Lesions within the Cavernous Sinus and
Superior Orbital Fissure
 Lesion at these zones can produce isolated CN III palsy,
but it is most commonly associated with other cranial
nerves dysfunctions.
 Differentiating between lesions at the cavernous sinus
versus the superior orbital fissure can be challenging and
sometimes the it is called as sphenocavernous syndrome.
 It presents as paresis of oculomotor, trochlear and
abducent nerves associated with maxillary division of
trigeminal nerve, producing pain.
 This can be caused by primary (direct invasion) or
secondary (intracranial/intra orbital lesion compressing
these areas) lesions.
Contd..
 Most common causes are tumour (e.g.
meningiomas).
 Another cause within the cavernous sinus and
superior orbital fissure that presents with painful
ophthalmoplegia known as Tolosa Hunt Syndrome.
 It is described as an idiopathic granulomatous
inflammation. This is a diagnosis of exclusion,
therefore tumors, metastasis or aneurysm must be
ruled out with neuroimaging.
Contd..
 Although tumours are the most common causes of
lesions at this zone, vascular processes can also
produce damages to the structures present in it.
Cavernous sinus thrombosis, carotid cavernous
fistulas, syphilis, vasculitis, and/or autoimmune
connective tissue diseases (e.g. systemic lupus
erythematosus) can produce painful ophthalmolegias
typical of cavernous sinus syndrome.
E. Lesions within the Orbit
 Lesions within the orbit are associated with visual
loss, ophthalmoplegia and proptosis.
 3rd nerve ophthalmoplegia can be associated with
trochlear and abducent nerves palsies.
 It is known that at the orbit the oculomotor nerve
divides into superior and inferior division. This can
cause partial oculomotor nerve palsies.
 Most common etiologies : trauma, masses,
inflammation, and/or infiltrative processes.
ABERRANT REGENERATION
 It usually occurs following traumatic and
compressive lesions where endoneural sheaths are
breached but not seen in vascular lesion where they
remain intact.
 Pseudo-von Graefe phenomenon:
Elevation of upper eyelid on attempted adduction
or depression caused by misdirected regenerating
axons that re-innervate the incorrect extraocular
muscle.
 Pupil may also be involved.
CAUSES OF ISOLATED 3rd NERVE PALSY
 Microvascular : Diabetes and Hypertension.
 Aneurysm of : PCA & ICA.
 Trauma : Subdural haematoma or underlying
aneurysm.
 Miscellaneous uncommon causes: Syphilis, Lyme’s
disease, Sarcoidosis, Giant cell arteritis & vasculitis
associated with collagen vascular disorders.
 Episodic: Idiopathic, migraine, compressions,
ischemia, alterations in ICP.
 Myasthenia may mimic intermittent pupil-sparing 3rd
nerve paresis.
INVESTIGATIONS
 Vascular risk factor : This may involve LP.
 CT angiography for aneurysm if there is marked
pupillary involvement with partial ptosis and
motility dysfunction.
 MRI brain and orbits with venography for
brainstem tumour, cavernous sinus or orbital apex
lesion.
 Conventional cerebral angiography is
occasionally used.
TREATMENT
 MEDICAL :
 Observation in cases of micro vascular causes
majority of which will resolve over weeks or months.
 Fresnel prism if angle of deviation is small.
 Uniocular occlusion to avoid diplopia if ptosis is
partial or recovering.
 Botulinum toxin injection in uninvolved lateral
rectus is used sometimes to prevent contracture
when recovery is prolonged
Contd..
 SURGICAL :
 Only if spontaneous recovery has ceased, usually not
earlier than 6-12 months from onset.
NUCLEUS OF TROCHEAR NERVE
 It is located at the level of INFERIOR COLLICULI
VENTRAL TO THE SYLVIAN AQUEDUCT.
 It is caudal to, and continuous with the third nerve
nucleus.
 COMPONENTS :
 Nucleus
 Fascicular
 Trunk
 Intracavernous part
 Intraorbital part
TROCHLEAR NERVE (4th NERVE)
KEY FEATURES :
 Only cranial nerve to emerge from the dorsal aspect
of the brain.
 It is a slender nerve which has the longest
intracranial course.
 Only decussated (crossed) cranial nerve other than
optic nerve innervating contralateral superior
oblique.
 It has the fewest axons among all cranial nerves.
FASCICULAR PART
 Consists of axons that curve posteriorly around the
aqueduct & deccusate completely in the anterior
medullary velum.
TRUNK
 Leaves the brainstem on dorsal surface, just caudal
to inferior collilculus.
 Then curves laterally around the brainstem, runs
forward beneath the free edge of the tentorium and
like the third nerve passes between the posterior
cerebral artery and the superior cerebellar artery.
 Pierces the dura and enters the cavernous sinus.
INTRACAVERNOUS PART
 Runs in the lateral wall of the sinus, inferior to 3rd
nerve and above the 1st division of the 5th nerve.
 In the anterior part of the cavernous sinus it rises
and passes through the superior orbital fissure above
and lateral to the annulus of Zinn.
 INTRA ORBITAL PART :
- Innervates the superior oblique muscle.
CAUSES OF ISOLATED 4th NERVE PALSY
 Idiopathic: More common, often congenital.
 Patient may be asymptomatic until decompensation
occurs in adult life due to reduced fusional ability.
 Unlike in acquired lesions, patient may not be aware
of the torsional aspect till he develops vertical
diplopia.
 Compensatory head posture may be useful in
clinching the diagnosis.
Contd...
 Trauma : Usually causes bilateral 4th nerve palsy.
- long and slender nerve more vulnerable in anterior
medullary velum through tentorial edge.
- Important to not mistake a bilateral palsy for a
unilateral lesion.
 Microvascular : more common when systemic risk
factors are present in absence of congenital defect.
 Aneurysms & tumours are rare.
TREATMENT
 Congenital decompensated and microvascular
palsies resolve spontaneously.
 Strabismus surgery is not useful in traumatic cases
due to diplopia and in childhood cases due to
substantial compensatory head posture.
 A Small hypertropia under 15 prism dioptres is
usually treated by inferior oblique weakening or by
superior oblique tucking.
Contd..
 A moderate-large deviation may be treated by
ipsilateral inferior oblique weakening with or
followed by ipsilateral superior rectus weakening and
or contralateral inferior rectus weakening if
required.
 Defective elevation is a potential complication.
Contd..
 Excyclotorsion in case of bilateral cases; the
Harada-Ito procedure involves splitting and
anterolateral transposition of the lateral half of the
superior oblique tendon.
ABDUCENT NERVE (6th NERVE)
 NUCLEUS : It lies at the MID-LEVEL OF PONS,
VENTRAL TO THE FLOOR OF THE FOURTH
VENTRICLE.
 The fibres leaves the brainstem ventrally at the
pontomedullary junction.
COURSE OF 6th NERVE
 It has 4 components.
 Nuclear part
 Basilar part
 Intracavernous part
 Intraorbital part
BASILAR PART
 Enters the prepontine basilar cistern passes upwards
close to the base of the skull and is crossed by the
anterior inferior cerebellar artery.
 It pierces the dura below the posterior clinoids & and
angles forward over the tip of the petrous bone,
passing through or around the inferior petrosal
sinus, through the Dorello canal ( underneath the
petroclinoid ligament ) to enter the cavernous sinus.
INTRACAVERNOUS PART
 Intracavernous part runs below the 3rd , 4th & 1st
division of 5th nerves.
 6th nerve is the most medially situated & runs in
close relation to the internal carotid artery through
the middle of the sinus.
INTRA ORBITAL PART
 Enters the orbit through the superior orbital fissure
within the annulus of Zinn to innervate the lateral
rectus.
APPLIED ANATOMY
 Nuclear Lesion:
- Failure of horizontal gaze towards the side of
the damage due to involvement of the adjacent
horizontal gaze centre (paramedian pontine
reticular formation).
-Facial nerve wrap around the 6th nerve nucleus,
so ipsilateral LMN facial nerve palsy is also
common.
-Isolated 6th nerve palsy is never nuclear in
origin.
FOVILLE
SYNDROME
MILLARD GUBLER
SYNDROME
Contd...
Foville (Inferior medial pontine) Syndrome:
- Most often caused by vascular disease or tumours
involving the dorsal pons.
-Ipsilateral involvement of 5th – 8th cranial nerves,
central sympathetic fibres (HORNERS syndrome)
and horizontal gaze palsy.
Contd..
Millard – Gubler (Ventral pontine)
Syndrome:
- Involves fasciculus as it passes through pyramidal
tract
- With Ipsilateral 6th nerve palsy, there is
contralateral hemiplegia and ipsilateral LMN
facial nerve palsy.
BASILAR PART
 Acoustic Neuroma:
-1st Symptom : Hearing loss
-1st sign : decreased corneal sensitivity
- corneal sensation should be checked in all patients with 6th
nerve palsy
Nasopharyngeal Tumours:
-Damages the nerve during its basilar course
Raised intra-cranial pressure:
-Downward displacement of brain stem
- Stretches one of both 6th nerves over the petrous tip, when
paresis is a false localizing sign.
Contd..
 Basal Skull Fracture:
- Unilateral or Bilateral palsy.
Gradenigo Syndrome:
-Mastoiditis or acute petrositis may damage the 6th
nerve at the petrous tip.
-Latter is often accompanied by facial weakness,
pain and hearing difficulties.
Contd..
 INTRA CAVERNOUS PART:
-Intra cavernous 6th nerve palsy is followed by post
ganglionic Horner syndrome (Parkinson
syndrome) due to damage of paracarotid
sympathetic plexus.
-Causes of palsy in this region is similar to that of 3rd
nerve palsy.
TREATMENT
 Observation:
-Mono occular occlusion or prismatic.
-90% will recover spontaneously over weeks to
several months.
-Young children should be treated with alternate
patching to prevent ambylopia.
Botulinum Toxin:
-Ipsilateral medial rectus may be used to prevent
contracture, asess residual function and rarely to
facilitate prismatic correction with large deviation
-Rarely curative.
Contd...
 Surgery:
- only after cessation of maximal spontaneous
improvement typically after 6-12 months from
onset.
- Partial palsy (Paresis) treated by medial rectus
recession and lateral rectal resection in affected eye
for small exophoria in the primary position to
maximise the field of binocular single vision.
- Complete palsy treated by transposition of superior
and inferior recti to positions above and below the
affected lateral rectus muscle + Weakening of
ipsilateral medial rectus.
 -Three rectus muscles should not be detached from
the globe at the same procedure because at the risk
of anterior segment ischemia.
Permanent Prism:
-Troublesome but mild residual deviation may be
treated with a prism incorporated into specticales
as an alternative to surgery.
Ocular motor nerves

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Ocular motor nerves

  • 2. CONTENTS  OCULOMOTOR NERVE  TROCHLEAR NERVE  ABDUCENT NERVE
  • 3. OCULOMOTOR NERVE (3rd NERVE)  It consists of 5 components.  NUCLEAR COMPLEX  FASCICULUS PART  BASILAR PART  INTRACAVERNOUS PART  INTRAORBITAL PART
  • 4. NUCLEAR COMPLEX  It is situated in the MIDBRAIN AT THE LEVEL OF SUPERIOR COLLICULUS, VENTRAL TO SLYVIAN AQUEDUCT.  Five MAIN MOTOR subnuclei are present.  Levator  Superior rectus  Medial rectus  Inferior rectus  Inferior oblique
  • 5.
  • 6. SUBNUCLEI  LEVATOR SUBNUCLEUS : Unpaired caudal midline structure, innervates both levator muscles.  SUPERIOR RECTUS : Paired, each innervates contralateral superior rectus.
  • 7. SUBNUCLEI  MEDIAL RECTUS : Paired ventromedial nucleus, each innervates ipsilateral medial rectus.  INFERIOR RECTUS : Paired dorsolateral nucleus, each innervates ipsilateral inferior rectus.  INFERIOR OBLIQUE : Paired intermedial nucleus, each innervates ipsilateral inferior oblique.
  • 8. ACCESSORY MOTOR NUCLEUS  EDINGER-WESTPHAL NUCLEUS : - Sends pre ganglionic parasympathetic fibres along other oculomotor nerve fibres. - Situated posterior to the main occulomotor nuclear complex.
  • 9.
  • 10.
  • 11.
  • 12. COURSE OF 3rd NERVE  FASCICULAR PART : - Consist of efferent fibres which pass from the 3rd nerve nucleus through red nucleus & medial aspect of the cerebral peduncle. - From there they emerge from the midbrain & pass into the interpeduncular space.
  • 13. COURSE contd...  BASILAR PART : - Series of rootlets which have midbrain on the medial aspect of cerebral peduncle, before coalescing to form the main trunk. - Then it passes between posterior cerebral & superior cerebellar artery, running parallel & laterally to the posterior communicating artery.
  • 14. COURSE contd....  INTRACAVERNOUS PART: - Enters the cavernous sinus by piercing the dura just lateral to posterior clinoid process. - Within the cavernous sinus, it runs in lateral wall above the trochlear nerve. - In the anterior part, it divides into superior & inferior branches which enter the orbit through superior orbital fissure within the annulus of Zinn.
  • 15. COURSE contd...  INTRA ORBITAL PART : - Superior division innervates levator palpabre superioris and superior rectus muscle. - Inferior division innervates medial rectus, inferior rectus and inferior oblique. - Branch to inferior oblique contains the preganglionic parasympathetic fibres from the Edinger-Westphal nucleus which innervates the sphincter pupillae ciliary muscle.
  • 16. PUPILLOMOTOR FIBRES  Between brainstem & cavernous sinus, the fibres are located superficially in the superomedial part of the oculomotor nerve.  Blood supply : Pial vessels.  Main trunk receives its supply from vasa nervorum.
  • 17.
  • 18. APPLIED ANATOMY  A. Lesions at Oculomotor Nucleus (Midbain)  B. Lesions at Oculomotor Nerve Fascicles (Leaving the 3rd nerve nucleus)  C. Lesions in the Subarachnoid space  D. Lesions within the Cavernous Sinus and Superior Orbital Fissure  E. Lesions within the Orbit
  • 19. A. Lesions at Oculomotor Nucleus (Midbain)  Produces bilateral defects.  It is divided in subnuclei according to the innervated area. Each superior recti are innervated by contralateral CN III subnucleus, so a nuclear CN III palsy would produce paralysis of the contralateral superior rectus.  Both levator palpebrae superioris are innervated by the one subnuclei (central caudal nucleus), so a nuclear palsy would produce bilateral ptosis.
  • 20. B. Lesions at Oculomotor Nerve Fascicles (Leaving the 3rd nerve nucleus)  Lesions at this level can produce complete or incomplete palsies.  Often it cannot be differentiated from lesion outside of the midbrain.  When the lesion is adjacent to CN III nucleus (midbrain) it can produce several manifestations:  Nothnagel’s Syndrome :Lesion at the superior cerebellar peduncle presents with ipsilateral 3rd nerve palsy and cerebellar ataxia.
  • 21. Contd..  Benedikt's Syndrome :Lesions at the Red Nucleus are characterized by ipsilateral 3rd nerve palsy and contralateral involuntary movement.  Weber’s Syndrome :Lesion at the cerebral peduncle produces ipsilateral 3rd nerve palsy and contralateral hemiplegia.  Claude Syndrome : Combination of Benedikt's and Nothnagel's syndromes.  Lesions can present with combination of these findings depending on the degree of the insult.
  • 23. Contd..  It is known that CN III separates in superior and inferior divisions at the superior orbital fissure, sometimes lesions at the fascicles can produce isolated dysfunction of either the superior or inferior division.  Most common causes are ischemic, haemorrhagic, compressive, traumatic.  Rare cause is infiltrative.
  • 24. C. Lesions in the Subarachnoid space  It is the area where 3rd nerve passes between ventral surface of midbrain to entrance of cavernous sinus (Interpeduncular fossa).  Damage in this area can produce various presentations.  CN III palsy with fixed dilated pupil, it is important to know that pupillary fibres occupy a peripheral location and receive more collateral blood supply than the main trunk of the nerve making it susceptible to compression (e.g. aneurysm). The most common known etiology is a posterior communicating artery aneurysm. This is a medical emergency.
  • 25.
  • 26. Contd..  CN III palsy without pupil involvement : Most common causes are diabetes mellitus, systemic hypertension, atherosclerosis and in some cases migraine.  Also compressive masses or aneurysm can cause it.  On the course to the cavernous sinus the CN III rest on the edge of the tentorium cerebelli. The edge of the uncal portion overlies the tentorium, so in case of raised intracranial pressure this section can herniate producing displacement of the midbrain compressing the ipsilateral oculomotor nerve.  This causes ipsilateral ophthalmoplegia and mydriasis. The most common cause of uncal herniation is intracranial hemorrhages.
  • 27.
  • 28.
  • 29. D. Lesions within the Cavernous Sinus and Superior Orbital Fissure  Lesion at these zones can produce isolated CN III palsy, but it is most commonly associated with other cranial nerves dysfunctions.  Differentiating between lesions at the cavernous sinus versus the superior orbital fissure can be challenging and sometimes the it is called as sphenocavernous syndrome.  It presents as paresis of oculomotor, trochlear and abducent nerves associated with maxillary division of trigeminal nerve, producing pain.  This can be caused by primary (direct invasion) or secondary (intracranial/intra orbital lesion compressing these areas) lesions.
  • 30. Contd..  Most common causes are tumour (e.g. meningiomas).  Another cause within the cavernous sinus and superior orbital fissure that presents with painful ophthalmoplegia known as Tolosa Hunt Syndrome.  It is described as an idiopathic granulomatous inflammation. This is a diagnosis of exclusion, therefore tumors, metastasis or aneurysm must be ruled out with neuroimaging.
  • 31. Contd..  Although tumours are the most common causes of lesions at this zone, vascular processes can also produce damages to the structures present in it. Cavernous sinus thrombosis, carotid cavernous fistulas, syphilis, vasculitis, and/or autoimmune connective tissue diseases (e.g. systemic lupus erythematosus) can produce painful ophthalmolegias typical of cavernous sinus syndrome.
  • 32. E. Lesions within the Orbit  Lesions within the orbit are associated with visual loss, ophthalmoplegia and proptosis.  3rd nerve ophthalmoplegia can be associated with trochlear and abducent nerves palsies.  It is known that at the orbit the oculomotor nerve divides into superior and inferior division. This can cause partial oculomotor nerve palsies.  Most common etiologies : trauma, masses, inflammation, and/or infiltrative processes.
  • 33.
  • 34. ABERRANT REGENERATION  It usually occurs following traumatic and compressive lesions where endoneural sheaths are breached but not seen in vascular lesion where they remain intact.  Pseudo-von Graefe phenomenon: Elevation of upper eyelid on attempted adduction or depression caused by misdirected regenerating axons that re-innervate the incorrect extraocular muscle.  Pupil may also be involved.
  • 35. CAUSES OF ISOLATED 3rd NERVE PALSY  Microvascular : Diabetes and Hypertension.  Aneurysm of : PCA & ICA.  Trauma : Subdural haematoma or underlying aneurysm.  Miscellaneous uncommon causes: Syphilis, Lyme’s disease, Sarcoidosis, Giant cell arteritis & vasculitis associated with collagen vascular disorders.  Episodic: Idiopathic, migraine, compressions, ischemia, alterations in ICP.  Myasthenia may mimic intermittent pupil-sparing 3rd nerve paresis.
  • 36. INVESTIGATIONS  Vascular risk factor : This may involve LP.  CT angiography for aneurysm if there is marked pupillary involvement with partial ptosis and motility dysfunction.  MRI brain and orbits with venography for brainstem tumour, cavernous sinus or orbital apex lesion.  Conventional cerebral angiography is occasionally used.
  • 37. TREATMENT  MEDICAL :  Observation in cases of micro vascular causes majority of which will resolve over weeks or months.  Fresnel prism if angle of deviation is small.  Uniocular occlusion to avoid diplopia if ptosis is partial or recovering.  Botulinum toxin injection in uninvolved lateral rectus is used sometimes to prevent contracture when recovery is prolonged
  • 38. Contd..  SURGICAL :  Only if spontaneous recovery has ceased, usually not earlier than 6-12 months from onset.
  • 39. NUCLEUS OF TROCHEAR NERVE  It is located at the level of INFERIOR COLLICULI VENTRAL TO THE SYLVIAN AQUEDUCT.  It is caudal to, and continuous with the third nerve nucleus.  COMPONENTS :  Nucleus  Fascicular  Trunk  Intracavernous part  Intraorbital part
  • 40. TROCHLEAR NERVE (4th NERVE) KEY FEATURES :  Only cranial nerve to emerge from the dorsal aspect of the brain.  It is a slender nerve which has the longest intracranial course.  Only decussated (crossed) cranial nerve other than optic nerve innervating contralateral superior oblique.  It has the fewest axons among all cranial nerves.
  • 41.
  • 42. FASCICULAR PART  Consists of axons that curve posteriorly around the aqueduct & deccusate completely in the anterior medullary velum.
  • 43. TRUNK  Leaves the brainstem on dorsal surface, just caudal to inferior collilculus.  Then curves laterally around the brainstem, runs forward beneath the free edge of the tentorium and like the third nerve passes between the posterior cerebral artery and the superior cerebellar artery.  Pierces the dura and enters the cavernous sinus.
  • 44. INTRACAVERNOUS PART  Runs in the lateral wall of the sinus, inferior to 3rd nerve and above the 1st division of the 5th nerve.  In the anterior part of the cavernous sinus it rises and passes through the superior orbital fissure above and lateral to the annulus of Zinn.  INTRA ORBITAL PART : - Innervates the superior oblique muscle.
  • 45.
  • 46. CAUSES OF ISOLATED 4th NERVE PALSY  Idiopathic: More common, often congenital.  Patient may be asymptomatic until decompensation occurs in adult life due to reduced fusional ability.  Unlike in acquired lesions, patient may not be aware of the torsional aspect till he develops vertical diplopia.  Compensatory head posture may be useful in clinching the diagnosis.
  • 47. Contd...  Trauma : Usually causes bilateral 4th nerve palsy. - long and slender nerve more vulnerable in anterior medullary velum through tentorial edge. - Important to not mistake a bilateral palsy for a unilateral lesion.  Microvascular : more common when systemic risk factors are present in absence of congenital defect.  Aneurysms & tumours are rare.
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 53. TREATMENT  Congenital decompensated and microvascular palsies resolve spontaneously.  Strabismus surgery is not useful in traumatic cases due to diplopia and in childhood cases due to substantial compensatory head posture.  A Small hypertropia under 15 prism dioptres is usually treated by inferior oblique weakening or by superior oblique tucking.
  • 54. Contd..  A moderate-large deviation may be treated by ipsilateral inferior oblique weakening with or followed by ipsilateral superior rectus weakening and or contralateral inferior rectus weakening if required.  Defective elevation is a potential complication.
  • 55. Contd..  Excyclotorsion in case of bilateral cases; the Harada-Ito procedure involves splitting and anterolateral transposition of the lateral half of the superior oblique tendon.
  • 56. ABDUCENT NERVE (6th NERVE)  NUCLEUS : It lies at the MID-LEVEL OF PONS, VENTRAL TO THE FLOOR OF THE FOURTH VENTRICLE.  The fibres leaves the brainstem ventrally at the pontomedullary junction.
  • 57. COURSE OF 6th NERVE  It has 4 components.  Nuclear part  Basilar part  Intracavernous part  Intraorbital part
  • 58.
  • 59.
  • 60. BASILAR PART  Enters the prepontine basilar cistern passes upwards close to the base of the skull and is crossed by the anterior inferior cerebellar artery.  It pierces the dura below the posterior clinoids & and angles forward over the tip of the petrous bone, passing through or around the inferior petrosal sinus, through the Dorello canal ( underneath the petroclinoid ligament ) to enter the cavernous sinus.
  • 61. INTRACAVERNOUS PART  Intracavernous part runs below the 3rd , 4th & 1st division of 5th nerves.  6th nerve is the most medially situated & runs in close relation to the internal carotid artery through the middle of the sinus.
  • 62. INTRA ORBITAL PART  Enters the orbit through the superior orbital fissure within the annulus of Zinn to innervate the lateral rectus.
  • 63. APPLIED ANATOMY  Nuclear Lesion: - Failure of horizontal gaze towards the side of the damage due to involvement of the adjacent horizontal gaze centre (paramedian pontine reticular formation). -Facial nerve wrap around the 6th nerve nucleus, so ipsilateral LMN facial nerve palsy is also common. -Isolated 6th nerve palsy is never nuclear in origin.
  • 65. Contd... Foville (Inferior medial pontine) Syndrome: - Most often caused by vascular disease or tumours involving the dorsal pons. -Ipsilateral involvement of 5th – 8th cranial nerves, central sympathetic fibres (HORNERS syndrome) and horizontal gaze palsy.
  • 66. Contd.. Millard – Gubler (Ventral pontine) Syndrome: - Involves fasciculus as it passes through pyramidal tract - With Ipsilateral 6th nerve palsy, there is contralateral hemiplegia and ipsilateral LMN facial nerve palsy.
  • 67. BASILAR PART  Acoustic Neuroma: -1st Symptom : Hearing loss -1st sign : decreased corneal sensitivity - corneal sensation should be checked in all patients with 6th nerve palsy Nasopharyngeal Tumours: -Damages the nerve during its basilar course Raised intra-cranial pressure: -Downward displacement of brain stem - Stretches one of both 6th nerves over the petrous tip, when paresis is a false localizing sign.
  • 68. Contd..  Basal Skull Fracture: - Unilateral or Bilateral palsy. Gradenigo Syndrome: -Mastoiditis or acute petrositis may damage the 6th nerve at the petrous tip. -Latter is often accompanied by facial weakness, pain and hearing difficulties.
  • 69. Contd..  INTRA CAVERNOUS PART: -Intra cavernous 6th nerve palsy is followed by post ganglionic Horner syndrome (Parkinson syndrome) due to damage of paracarotid sympathetic plexus. -Causes of palsy in this region is similar to that of 3rd nerve palsy.
  • 70.
  • 71.
  • 72. TREATMENT  Observation: -Mono occular occlusion or prismatic. -90% will recover spontaneously over weeks to several months. -Young children should be treated with alternate patching to prevent ambylopia. Botulinum Toxin: -Ipsilateral medial rectus may be used to prevent contracture, asess residual function and rarely to facilitate prismatic correction with large deviation -Rarely curative.
  • 73. Contd...  Surgery: - only after cessation of maximal spontaneous improvement typically after 6-12 months from onset. - Partial palsy (Paresis) treated by medial rectus recession and lateral rectal resection in affected eye for small exophoria in the primary position to maximise the field of binocular single vision. - Complete palsy treated by transposition of superior and inferior recti to positions above and below the affected lateral rectus muscle + Weakening of ipsilateral medial rectus.
  • 74.  -Three rectus muscles should not be detached from the globe at the same procedure because at the risk of anterior segment ischemia. Permanent Prism: -Troublesome but mild residual deviation may be treated with a prism incorporated into specticales as an alternative to surgery.

Notas del editor

  1. Bilateral superior oblique palsy