Sridevi Rajeeve

2008 batch

1

Oculomotor nerve innervations:

Superior rectus Inferior rectus Medial rectus, Inferior oblique Levator palpebrae superioris Ciliary muscle Iris sphincter (Constrictor pupillae)

The anatomy and its relations of the various

portions of the third cranial nerve accounts for the clinical features of third cranial nerve palsy.

1)Nuclear portion: situated in the midbrain. 2)Fascicular portion : situated ventrally to the mid brain 3)Fascicular subarachnoid portion: situated anterior to the

midbrain and in close proximity to the posterior communicating artery.

4)Fascicular cavernous sinus portion: Runs through the lateral wall of the cavernous sinus and enters the cavernous sinus

5)Fascicular orbital portion: situated in the posterior part of the orbit

oIII portion: Fascicular subarachnoid portion: Clinical significance: Berry aneurysm at the junction between the posterior communicating artery and the internal carotid artery.

oIV Portion: Fascicular cavernous sinus portion: Clinical significance: Masses invading the cavernous sinus are likely to cause third cranial nerve dysfunction

1. direct trauma,2. demyelinating diseases (e.g., multiple sclerosis)3. increased intracranial pressure (leading to uncal herniation)

1. due to a space-occupying lesion (e.g., brain cancer) or a2. spontaneous subarachnoid haemorrhage (e.g.,

berry aneurysm), and4. microvascular disease, e.g., diabetes.

Symptoms :

1) Diplopia from misalignment of the visual axes 2) Symptomatic Glare in bright light (if the ptotic lid does not cover the pupil)

Findings:

1) Involved eye usually is deviated down and out

(infraducted, abducted) 2) Ptosis (differentiated from myasthenia gravis by

TENSILLON TEST) 3) Pupillary Dilatation 4) Paralysis of Accommodation causes blurred

vision for near objects

Treatment

1) Symptomatic cases can be treated with Strabismus surgery, 2) Surgical correction of Ptosis: Ptosis surgery

Innervation:Innervation: the Superior oblique muscle

Physiological ActionsPhysiological Actions: 1) Primarily Intort the eye (such that the top of the eye rolls toward the nose),

2)Secondary actions of depression (down gaze) and abduction (looking away from the nose).

Clinical features in PalsyClinical features in Palsy: 1) The affected eye Extorts, 2) Deviate Upwards (Hypertropia), 3) Drift Inward.

Aetiologyof IV Cranial Nerve Palsy:

1) Usually neurogenic 2) Dysgenesis of the IV CN nucleus or nerve, 3) Clinically similar palsy may result from absence or mechanical dysfunction (e.g., abnormal laxity) of the superior oblique tendon

Congenital IV cranial nerve palsy:

1) It may not become symptomatic until later childhood or adulthood. 2) Young children adopt a compensatory position head tilt (Torticollis) in order to compensate for the underacting superior oblique muscle (towards contralateral side) 3) Facial asymmetry due to chronic head tilt. 4) Vertical diplopia

1) Lack of subjective symptoms of torsion (Torsion -rotation of vertical corneal meridians)

2) Diplopia - following Cataract surgery

- manifest transiently during pregnancy 3) Neck Pain after years of head tilting.

Treatment

1.Symptomatic cases can be treated with Strabismus surgery2.Prism lenses set to make minor optical changes in the vertical alignment may be prescribed instead of or after surgery to fine-tune the correction.

Innervation: Lateral rectus muscle

Physiological action: Abduction

Palsy causes: 1.Horizontal double vision 2. Convergent Strabismus

(Esotropia)

Increased intra-cranial tension Diabetes mellitus Trauma Brain stem hemorrhage/infarction Tumour Meningitis Aneurysms(basilar artery) Cerebello-Pontine angle tumour Orbital tumour Gradenigo’s syndrome (otorrhoea–diplopia-

retroorbital pain)

1. BrainstemIsolated lesions of the VI nerve nucleus will not give rise to an isolated VIth neve palsy because paramedian pontine reticular formation fibers pass through the nucleus to the opposite IIIrd nerve nucleus. Thus, a nuclear lesion will give rise to an ipsilateral gaze palsy. In addition, fibers of the seventh cranial nerve wrap around the VIth nerve nucleus, and, if this is also affected, a VIth nerve palsy with ipsilateral facial palsy will result. In Millard Gubler syndrome, a unilateral softening of the brain tissue arising from obstruction of the blood vessels of the pons involving sixth and seventh cranial nerves and the corticospinal tract, the VIth nerve palsy and ipsilateral facial paresis occur with a contralateral hemiparesis.[4]. Foville's syndrome can also arise as a result of brainstem lesions which affect Vth, VIth and VIIth cranial nerves.

2. Sub arachnoid spaceAs the VIth nerve passes through this space it lies adjacent to anterior inferior and posterior inferior cerebellar and basilar arteries and is therefore vulnerable to compression against the clivus. Typically palsies caused in this way will be associated with signs and symptoms of headache and/or a rise in ICP.

3. Petrous ApexThe nerve passes adjacent to the mastoid sinus and is vulnerable to mastoiditis, leading to inflammation of the meninges, which can give rise to Gradenigo's syndrome. This condition results in a VIth nerve palsy with an associated reduction in hearing ipsilaterally, plus facial pain and paralysis, and photophobia. Similar symptoms can also occur secondary to petrous fractures or to nasopharyngeal tumours.

4. Cavernous sinus/Superior orbital fissureThe nerve runs in the sinus body adjacent to the internal carotid artery and oculo-sympathetic fibres responsible for pupil control, thus, lesions here might be associated with pupillary dysfunctions such as Horner's syndrome. In addition, III, IV, V1, and V2 involvement might also indicate a sinus lesion as all run toward the orbit in the sinus wall. Lesions in this area can arise as a result of vascular problems, inflammation, metastatic carcinomas and primary meningiomas.

5. OrbitThe VIth nerve's course is short and lesions in the orbit rarely give rise to isolated VIth nerve palsies, but more typically involve one or more of the other extraocular muscle groups.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development.

Thereafter, a period of observation of around 9 to 12 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

Fresnel prisms: : slim flexible plastic prisms can be attached to the patient's glasses, or to plano glasses if the patient has no refractive error, and serve to compensate for the inward misalignment of the affected eye.

Use of Botulinum toxin◦ helps to prevent the contracture of the medial rectus which

might result from its acting unopposed for a long period. ◦ reduces the size of the deviation temporarily it might allow

prismatic correction to be used where this was not previously possible

◦ removes the pull of the medial rectus it may serve to reveal whether the palsy is partial or complete by allowing any residual movement capability of the lateral rectus to operate

Vertical muscle transposition procedures such as Jensen's, Hummelheim's or whole muscle transposition

III NERVE: Eye Movements , Eyelid Movements, Pupil: Size, Symmetry, Reactions.

IV and VI NERVE: Eye Movements

V NERVE:Sensation to faceCorneal reflex

Jaw movements