Cranial nerves pathology Dr. Massud Wasel MD DO ND BSc (Hons) P.G.C.A.P Fellow of Higher Education Academy.

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Presentation transcript:

Cranial nerves pathology Dr. Massud Wasel MD DO ND BSc (Hons) P.G.C.A.P Fellow of Higher Education Academy

Acoustic schwannoma Nerve sheet tumours 6% of all primary intracranial tumours Middle age years More frequent in female Benign, slow growing

Arises from the vestibular portion of the VIII CN Expand at an average rate of 2mm/year

Clinical features Occipital pain on the side of tumour Gradually progressive sensorineural deafness over many month or year Vertigo Tinnitus V nerve damage can occur with tumour >2 cm and causes facial pain

Could cause parasthesia, numbness Depression of the corneal reflex is an important early sign

Compression of the aqueduct and the 4 th ventricle result in hydrocephalus with sy and si of raised ICP Facial weakness is uncommon despite marked VII nerve compression

IX,X and XI nerve damage seldom occurs but occasionally large tumours cause swallowing difficulty, voice change and palatal weakness

Tumours> 4 cm may compress the cerebellum-causing ataxia, ipsilateral incoordination and nystagmus Pontine damage produces a contralateral hemiparesis

Investigations Neuro-otological tests CT scan MRI

Management Tumour removal with minimal risk Preservation of facial nerve function Retention of useful hearing unless this is already lost

Trigeminal neuralgia ( tic douloureux ) Paroxysmal attacks of severe, short, sharp, stabbing pain affecting one or more divisions of the CN V The pain involves the 2 nd and 3 rd more then 1 st It rarely occurs bilaterally and never simultaneously on each side

Occasionally more than one division is involved Attacks last for several days or weeks When the attacks settle the patient may remain pain free for many months

Chewing, speaking, washing the face, tooth-brushing, cold winds or touching a specific' trigger spot ’, e.g. upper lip or gum, may all precipitate an attack of pain More common in female and patients over 50 years of age

Aetiology Root or root entry zone compression: Arterial vessels Tumours of the cerebellopontine angle lying against the V nerve roots, e.g. meningioma, epidermoid cyst Demyelination such a lesion in the pons--- in young person

Investigations CT MR scan to exclude a cerebello- pontine angle lesion or demyelination

Management Drug therapy: Carbamazepine Baclofen Lamotrigine Gabapentin Phenyton

Operative therapy: Nerve block with alcohol provides temporary relief Avulsion of the supera or infraorbital nerves gives more prolonged pain relief

Radiosurgical lesion of CNV Trigeminal root section Microvascular decompression Radiofrequency thermocoagulation

BLINDNESS

Sudden painless loss of vision Amaurosis fugax: is temporary loss of vision ‘like a curtain descending’ It may precede permanent visual loss(in embolism or giant cell arteritis) Transient visual loss lasting sec in papilloedema(ICP)

Ischemic optic neuropathy:the optic nerve is damaged If the posterior ciliary arteries are occluded by inflammation or arterioslerosis Fundoscopy shows a pale, swollen optic disc

Temporal arteritis/GCA: Symptoms: malaise, jaw claudication and a tender scalp/temporal arteries Association: polymyalgia rheumatica ESR>40 Temporal artery biopsy

Arteriosclerotic ischemic optic neuropathy: hypertension, lipid disorders and diabetes may predispose younger patients to this Treat these conditions to protect vision

Occlusion of a central retinal artery: dramatic visual loss Vitreous haemorrhage: this a particularly common cause of visual loss in DM with new vessel formation Also may occur in bleeding disorders May be need operation to remove the blood (vitrectomy)

Subacute loss of vision optic neuritis: Unilateral Reduces acuity over hours or days Discrimination of colours is affected Reds appear less red The optic disc may be swollen(papillitis) Recovery is usual over 2-6 weeks

45-80% develop MS Other causes-neurosyphilis,DM and vitamin deficiency Treatment:prednisolon