Cranial Nerve Palsy

Cranial Nerve PalsyMohammad haziq bin jammuri1217439IntroductionThe extraocular muscles are innervated by the third, fourth, and sixth cranial nerves. Extraocular muscle paralysis resulting from destructive lesions in one or more of these cranial nerves results in failure of one or both eyes to rotate in concert with the other eye.The primary symptom isdiplopiafrom misalignment of the visual axes

Oculomotor Nerve PalsyOculomotor NerveOrigin

Peripheral Distribution

FunctionOculomotor nucleusMedial, superior , inferior recti, inferior oblique musclesEye movementsOculomotor nucleus

Superior palpebral levatorElevation of eyelidEdinger-Westphal nucleusCiliary ganglion, postganglionics to sphincter of pupil and ciliary musclesPupillary constriction and accomodation

EtiologyNucleus partFasciculus partBasilar partIntracavernous partIntraorbital part

Isolated 3rd Nerve PalsyIdiopathic 25%Vascular diseasesystemic risk factors such as hypertension and diabetes are the most common causeTraumaAneurysmaneurysm of the posterior communicating artery at its junction with the internal carotidMiscellanoustumour, inflammatory disease such as syphilis, Lyme disease and sarcoidosis, giant cell arteritis and vasculitis associated with collagen vascular disorders.Episodicbrief episodes of third nerve dysfunction with spontaneous recovery may be idiopathic or occur with migraine, compression, ischaemia and alterations in intracranial pressure

Clinical FeaturesProfound ptosis due to weakness of the levator muscle Abduction and depression in the primary position (down and out) due to unopposed action of the lateral rectus and superior oblique musclesNormal abduction as the lateral rectus is intact Limited adduction due to medial rectus weakness Limited elevation due to weakness of the superior rectus and inferior oblique Limited depression due to weakness of the inferior rectusDilated pupil and defective accommodation due to parasympathetic palsy.

InvestigationVascular risk factorCT angiographyMRI brain and orbits with venographyTreatmentObservationMicrovascular cases - the majority will resolve over weeks or months.Temporary (e.g. Fresnel stick-on) prisms may be useful if the angle of deviation is small.Surgical treatment of the ocular motility element and ptosis should be contemplated only after spontaneous improvement has ceased, usually not earlier than 612 months from onsetTrochlear Nerve PalsyTrochlear Nerve OriginPeripheral DistributionFunctionTrochlear nucleusSuperior oblique muscleEye movements

EtiologyIdiopathic lesions are common, and many of these are thought to be congenital.Trauma frequently causes bilateral fourth nerve palsy. The long and slender nerves are particularly vulnerable as they decussate in the anterior medullary velum, through impact with the tentorial edge. Microvascular lesions are relatively commonAneurysms and tumours are extremely rare.Clinical FeaturesAcute onset of vertical diplopia in the absence of ptosisLoss of the main actions of the superior oblique are intorsion (incyclotorsion), and depression in adductionFor example in left paresis:Limitation of left depression, most marked in adduction Left extorsion, greatest in abduction.Normal abduction of the left eye Normal elevation of the left eye A compensatory head posture avoids diplopia: vertical, torsional and worse on downgaze. To compensate for weakness of intorsion there is contralateral head tilt to the right. To alleviate the weakened depression of the eye the chin is slightly depressed; as this is most marked in adduction

Special Test - Parks Three-Step Test

TreatmentCongenital decompensated and presumed microvascular palsies commonly resolve spontaneously.Strabismus surgery is not infrequently required for traumatic and childhood casesA small hypertropia under 15 prism dioptres can usually be treated either by inferior oblique weakening or by superior oblique tuckingA moderatelarge deviation may be treated by ipsilateralinferior oblique weakening combined with, or followed by, ipsilateral superior rectus weakening and/or contralateral inferior rectus weakening if requiredHaradaIto procedure - splitting and anterolateral transposition of the lateral half of the superior oblique tendon

Abducens Nerve PalsyAbducens NerveOriginPeripheral Distribution

FunctionAbducens nucleusLateral rectus muscleEye movements

EtiologyElevated intracranial pressure can result in downward displacement of the brainstem, causing stretching of the sixth nerve secondary to its anatomic location within the Dorello canal Subarachnoid space lesions can be causes of abducens nerve palsy (eg, hemorrhage, infection, inflammation, space-occupying tumor, cavernous sinus mass). Inflammatory (eg, postviral, demyelinating, sarcoid, giant cell arteritis)VascularNeoplasm (children) - Pontine gliomaInfectious (eg, Lyme disease, syphilis)Congenital absence of the sixth nerve (eg, Duane syndrome)Trauma, particularly if it results in a torsional head motion

Clinical FeaturesSymptoms. Double vision is characteristically worse for a distant target and less or absent for near fixation.Esotropia in the primary position due to relativelyunopposed action of the medial rectus Limitation of abduction on the side of the lesion Normal adduction of the affected eye A compensatory face turn is towards the side of theparalysed muscle in unilateral palsy.

TreatmentObservation with monocular occlusion or prismatic correction of diplopia is appropriate in idiopathic and presumed microvascular lesions; up to 90% will recover spontaneously, usually over weeks to several months. Surgery should be considered only when adequate time has been allowed for maximal spontaneous improvement, typically at least 612 months from onset.Partial palsy (paresis) is treated by adjustable medial rectus recession and lateral rectus resection in the affected eye, Complete palsy is treated by transposition of the superior and inferior recti to positions above and below the affected lateral rectus muscle (see Fig. 18.70), coupled with weakening of the ipsilateral medial rectus (sometimes with injection of botulinum toxin toxin transposition)