The Abducens nerve

Welcome to the Clinical Neurology with KD Podcast Season 2. After the overwhelming response to Season 1, which focused on neurological localization for medical students, we are back with a brand new season dedicated to an exciting and often challenging topic of neurophthalmology. If you haven't listened to Season 1, I highly recommend doing so. It will help you understand the fundamentals of neurological localization, which forms the foundation for this season. The podcast aims to help medical students enjoy the process of learning neurology by teaching it from a clinical perspective. This season, we'll benefit medical students, medicine, ophthalmology, neurology residents and consultants. Each episode starts with the pretest of multiple choice questions based on the topic discussed. The answers will be provided at the end of the episode. Study materials, illustrations and clinical resources for the podcast are available in the description and on the neurology teaching club.com website and its Instagram page. I'm your host, Dr. Peshadhas N.C. and let's get started. In this session, we will discuss the abducine now. As usual, we will begin with the pretest multiple choice questions. Question 1. What structure forms the roof of the Dorillow's canal? A. pretest temporal bone, B. posterior clientoid process, C. Gruber's ligament, D. Paltzerbite. 2. Which syndrome features abducine palsy, facial pain and ear discharge? A. Fowell's syndrome, B. Gradinigo's syndrome, C. Miller's Googler's syndrome, D. Godfret's syndrome. Question 3. Elysian in which location is most likely to cause bilateral six nerve palsy with twelfth cranial nerve involvement? Choice A, Covenous Sinus, B. Clivus, C. Midbrain, D. Orbit. Question 4. In a patient with six nerve palsy with thornous syndrome, which feature best differentiates a Covenous Sinus lesion from a pontine lesion? Choice A. presence of abduction deficit, B. distribution of facial sweating, C. involvement of the medial rectus, D. conjugate gase palsy. But question 5. Which clinical scenario strongly suggests divergence in sufficiency rather than an isolated six nerve palsy? Choice A, esotropia at near and distance? B, adduction deficit on dexantesting? C, full dexions with esotropia only at a distance? D, sudden onset deplopia with medial rectus overaction? The abducinear supplies a single muscle, the epsyllateral lateral rectus, which abducts the eye. The abducine nucleus is situated in the mid to lower dorsal pontine tecmentum, separated from the fourth ventricle by the genu of the facial nerve, which forms the facial coliculus. The nucleus consists of somatic motor neurons. The sixth cranial nerve nucleus contains motor neurons that give rise to the sixth nerve vesicle and inner neurons that give rise to the axons in the contralateral medial longitudinal vesicles that innervites the contralateral medial rectus subnoclas of the third cranial nerve. Thus, the sixth cranial nerve nucleus mediates the epsyllateral conjugate horizontal eye moments as well. The physical of the abducinear moves forward through the pontine tecmentum, close to the para-pontine reticular formation after exiting the nucleus. It lies medial to the facial nerve vesicles and adjacent to the medial limitiscus and the corticospinal tract. The abducinear leaves the brainstem in the horizontal sulcus between the ponds and the middella, latter to the corticospinal bundle. In the subarachnoid space, the abducinear crosses the internal auditory artery and ascends the clavus in the pre-pondane system to reach the pitrose epics. Then it pierces the dura at the dorsum cellar and traverses the Dorilo's canal between the posterior clinoid process and the pitrose epics. Dorilo's canal is the invagination of the dura in the pitroclival region from the pitroclival entrance point to the posterior end of the kevanas sinus. The pitrose-phenoidal ligament, otherwise known as grubers ligament, forms the roof of the canal. The pitrose temporal bone forms the floor of the canal. The Dorilo's canal is a passageway for abducinear from the brainstem to the kevanas sinus. It is a potential site of abducinear entrapment during trauma and raised intra-cranial pressure. In the kevanas sinus, the abducinear lies lateral to the internal carotid artery and medial to the ophthalmic division of the trigeminal nerve. The nerve lies below and medial to the oculomotor nerve. The abducinear is the only nerve that lies in the lumen of the kevanas sinus. Others are in the world of the sinus. The pupal sympathetic fibers, from their cores from pericarotid plexus to the ophthalmic division of the trigeminal, will travel a few millimeters through the abducinear in the kevanas sinus. The abducinear enters the orbit through the superior orbiter fissure and the annulus of sin and supplies the lateral rectus. Medical features Patients with abducinear palsy will have binocular diplopia with horizontally separated images, more when looking at a distance and in the direction of the weak muscle. There will be limited abduction in the eye of the involved side and the resting eye will be in addicted position. This esotropia will increase when looking at the side of the lesion. In patients with mild abducine weakness, the esophoria detected by a cover and cover test on looking to the peritic side may be the only sign of abducinear palsy as the range of moments may be normal. In these patients, the misalignment is concealed by the brain's fusional mechanism and becomes apparent only when binocular vision is disrupted. Localization of the sixth cranial nerve palsy. Nuclear lesion A nuclear sixth nerve palsy produces a horizontal gaze palsy to the same side rather than an isolated lateral rectus palsy as the nucleus contains interneurons that supply the opposite medial rectus through the medial longitudinal vesicles. The abducinear nucleus lesion in early life will result in mobius syndrome and duane retraction syndrome. Mobius syndrome Most patients have bilateral nuclear sixth nerve palsy. The most common ocular motor abnormality is bilateral horizontal gaze palsy. They may also have additional bilateral facial dipletia and other cranial nerve palsies including 9/10/12. The long tracts can also get involved, producing general motor disability and incordination. It is a disorder of romensophalic maldevelopment. Duane retraction syndrome Duane retraction syndrome is characterized by the narrowing of palpable fissure and retraction of the globe on adduction. There are three types. Type 1 abduction is limited while adduction is normal. Type 2 imbade adduction with normal abduction. Type 3 abduction and adduction are both imbade. The abducinear is absent in type 1 and in some cases in type 3. It is congenital caused by the anomalous innervation of the lateral rectus by the inferior division of the ocular motor nerve. This results in simultaneous contraction of the medial and lateral rectus on attempted adduction, resulting in globes retraction. The patients often don't have deplopia or esotropia in primary gaze. They also usually don't develop amblyopia. All types shows vertical deviation of the adducting eye through upshoots or downshoots during horizontal gaze. It is more common in females and affects the left eye more than the right eye, but it can be bilateral. It can rarely occur with acquired causes like pontine glauoma and following surgery for orbital cavernous hemangiooma. When infecting the angira-inferior cerebellar artery can lead to four-village syndrome which affects the dorsal pontine tegmentum. This syndrome features epsyllatal horizontal gaze palsy resulting from involvement of the abducine nucleus, facial palsy due to damage of the physical of the seventh cranial nerve and contralatal hemiparesis. Physical Arleation An angira-pontine paramedian lesion can spare the abducine nucleus and involves the vesiculus. Discommonly associated with the epsyllatal facial nerve and contralatal hemiparesis, a condition known as millet gobler syndrome. Sometimes a small lesion in the ponds can involve the abducine vesicle alone resulting in isolated six cranial nerve palsy. Nuclear and vesicular lesions can have associated long track signs like ataxia, hornocindrom and hemiparesis. The fifth, seventh and eighth cranial nerve can also get involved in these cases. Similar and vesicular lesions may be due to infarction, hemorrhage, tumor, infection, inflammation or trauma. An imaging ideally an MRI of the brain will confirm the lesion. Sub-arachnode space Lesions affecting the abducine nerve in the pre-pondine system may compress the epsyllatal corticospinal bundles leading to contralatal hemiparesis and epsyllatal six nerve palsy. Compressions of the trigonal nerve can cause epsyllatal facial pain. Reminds in the sub-arachnode space can cause unilateral or bilateral six cranial nerve palsy. Any cause of raised intra cranial pressure can cause abducine palsy. Cranial nerve six palsies are most common and classic force-localizing signs. They are non-specific and do not necessarily relate anatomically to the central nervous system pathology that produces them. For example, a frontal lobe mass lesion may be the cause of raised ICT that causes the sixth nerve palsy. We assume that the pathology is somewhere in the cause of the sixth cranial nerve when it is in the frontal lobe, over near the sixth cranial nerve. That is why it is called a force-localizing sign. Both idiopathy-indra cranial hypertension and hypotension can cause sixth cranial nerve palsy. All cases requires imaging, ideally a contrast in hand's MRI and CSO study if the imaging is normal. Sub-arachnodes can involve the abducine nerve. Clivus. Combined sixth and 12th cranial nerve palsy usually suggest a cleivus lesion. Discalled godfretsin syndrome and the theology is usually ominous like an esopharyngeal carcinoma or cleival metastasis. Rarely sub-arachnod pathologies can also produce this syndrome. Both sixth nerve lies very close to each other at the cleivus. Lesions here can also cause bilateral sixth nerve palsy. Petrocepics and Dorilo's canal. Based on neurological findings alone, it may be challenging to determine whether the nerve has been injured within sub-arachnod space or in its petrocepotion in the Dorilo's canal. Associated trigonal nerve involvement is more likely if the lesion is in the petrocepotion. Other clinical findings may point to disease in the petroce bone such as ear discharge from chronic otitis media or mastoditis and deafness. An infectious or neoplastic process that spread to the tip of the petroce bone can lead to gradinego syndrome. These syndrome features the triad of abducent nerve paralysis, facial pain and ear discomfort or discharge. Additionally, trauma, inferior petrocell sinus thrombosis, vascular malformations, aneurysms and tumors may also produce injury to the nerve at this location. Increased intra-cranial pressure often leads to dysfunction of the abducent nerve due to stretching of the nerve over the petro-stip, as the highest end pressure pushes the brain stem attachments inferiorly. Abducent sinus and superior orbital fissure. The involvement of the other ocular motor nerves, retroorbital pain and honours syndrome suggest a kevana sinus lesion. Without honours syndrome, it is impossible to clinically differentiate a kevana's lesion from a superior orbital fissure lesion. The sympathetic fibers travel with abducent nerve for a short distance in the kevana sinus. Unilateral abducent nerve palsy with honours syndrome localizes to the kevana sinus called Parkinson's syndrome. A pontein lesion can also produce sixth nerve palsy with honours syndrome. However, the kevana's lesion causes a post-ganglionic honours syndrome with the absence of sweating confined to the forehead. In contrast, in central honours syndrome due to pontein lesion, sweating is affected over the end-air phase. Tricinaminal nerve sensory loss in V2 distribution with abducent palsy can occur due to nasopharyngeal carcinoma arising in the force of rosenmulla and extending into the foramen lesira. The théories of the kevana's and the superior orbital fissure lesions are the same, and it eludes infective inflammatory and neoplastic causes. Orbit. The sixth cranial nerve can be damaged inside the orbital cavity to produce lateral rectus palsy. Proptosis, chemosis, and optic nerve involvement may also be present, along with other ocular motor nerve involvement. Trauma, tumors, and inflammatory process can cause abducent weakness in the orbit. Ischemic abducent palsy. Vasculopathy is the most common cause of isolated sixth cranial nerve palsy. The nerve can be involved anywhere along its course. Along with diabetes, patients can have other vascular risk factors like hypertension, dyslipidemia, etc. The sixth nerve palsy can evolve over one week and usually recovers spontaneously over three to six months. Recurrence is not uncommon. Older people with headaches should undergo evaluation for giant cell arthritis. Older causes of abduction environment. Convergence Palsum Convergence Palsum causes esotropia on lateral gaze and can be mistaken for sixth cranial nerve palsy. It is a functional disorder caused by voluntary convergence interrupting the lateral gaze. When the patient looks laterally, the sudden convergence top the abducting eye midway, giving a feeling of lateral rectus palsy. The associated pupillary constriction is the clue that differentiates a convergence palsum from lateral rectus palsy. It can be rarely caused by mid-brain compression. Divergence Insurficiency These patients have impaired abduction and esotropia when looking at a distance. They, however, have full abduction on-duction testing. Patients have a horizontal comitant uncrossed diplopia at far while near vision is normal. It can develop as an isolated entity in another ways healthy person. Talamic esotropia Acute esotropia can occur in patients with contralateral talamic infact. Acute talamic hemorrhage can cause bilateral asymmetric esotropia with severity more on the contralateral side. The esotropia is due to supranuclear disinhibition of the convergence pathway. Other causes of abduction environment include medial rectus entrapment in orbital fractures, myastenia gravies, orbital pseudo tumor and thyroid of telmopadi. Acute esotropia can occur in initial manifestation of cerebellar disease. Hypophosphatemia is often under-recognized, but the downstream consequences such as osteomalacia, fractures and functional decline can be substantial. To our listeners a single most important actionable message today is to check a phosphate. It's not on the typical campaign, also you have to order it when the story fits. Multiple ocular motor no-palsy Multiple ocular motor no-palsy can occur in lesions involving the brainstem, sub-recognized space, cavernous sinus, superior orbital fissure or orbit. Lesions involving the neuromuscular junction like ocular myastenia and muscle disease like progressive external of telmoplicia can also affect the extrocular muscles. We'll discuss a few common disorders involving multiple extrocular nerves. Miller fissure syndrome is a variant of gillenberry syndrome characterized by a refluxia of telmoplicia and a texia. Most of these patients show anti-GQ1B ganglocyte positivity. The third, fourth and sixth cranial nerve contains a higher concentration of GQ1B in their ganglocyte composition, making them vulnerable. This can have complete external of telmoplicia in loading bilateral toses. Puebular involvement is rare. In new conduction study reveals demilinating neuropathy and the cerebrospinal fluid will show albuminocytological dissociation. Patients response well to IVIG or plasma exchange. Vernicus encephalopathy Vernicus encephalopathy is characterized by the triad of confusion of telmoplicia and a texia and is due to thiamine deficiency. Alcoholics, hypermysis gravitarium, dialysis patients, cancer patients and mild nutrition due to any cause can produce this syndrome. Ocular findings can range from gaseous oakness tagmas to total of telmoplicia. The ocular motor deficits in vernicus encephalopathy arise from selective neurotoxic damage to brain stem nuclei and cerebellar pathways critical for gase control, driven by thiamine-dependent metabolic failure. Drompt intravenous thiamine replacement reverses ocular motor deficits within hours to days. Delay treatment risks progression to cause a cause syndrome characterized by irreversible memory impairment. Of telmoplicic migraine Of telmoplicic migraine causes painful of telmoplicia, which usually starts in the first decade of life. The ocular motor now is commonly involved, though isolated trochlear or multiple ocular motor nows can also get involved. Students will have a history of typical migraine attacks. The third no-palsy reaches maximum as their digs subsides and can last for one to four weeks. Some patients can have partial third no-palsy. It is a diagnosis of exclusion and a detailed evaluation is necessary to roll out other causes. Patients are usually asymptomatic between attacks. MRI of the brain may show enhancement of the cranial nose. Stirodes are the mainstay in the treatment. Also a hundred syndrome causes recurrent painful of telmoplicia due to idiopathy granulomate as inflammation of the kevana sinus, superior orbital fissure, or the orbit. The cardinal feature is retroorbital pain, accommodated by the palsy of 3rd, 4th and 6th cranial nose. Other cranial nose including the 5th and 7th can be involved rarely. MRI of the brain shows focal enhancement of the kevana sinus. The differentials include infection, vasculitis and neoplasm. Serbospinal fluid study and contrast imaging should be done in all cases to rule out alternate diagnosis. Stirodes are the first line of treatment and pain usually responds within 72 hours, which also supports the diagnosis. The telmoplicia improves over weeks. Around 40% of the cases can have recurrence. Refractory cases need immunosuppression and radiation. Correlated cavernous fistula is an abnormal vascular connection between the internal carotid artery, external carotid artery or their branches and the kevana sinus. They are classified as direct or high flow CCF if they arise from direct connection between the intra-cavernous carotid artery and the kevana sinus. They are called indirect low flow or dual CCF if they result from indirect communication between the kevana sinus and branches of the internal or external carotid artery within the adjacent duro. Traumatic CCF accounts for 70% of the cases. Spondyne's CCF accounts for 30% of the cases and is usually due to rupture of the internal carotid aneurysm. Clinical manifestations include pulse cell tinnitus, connective injection, proptosis and of telmoplicia due to cranial nose 3, 4 and 6 compression. We shouldn't know smoker from ocular ischemia or glaucoma. This requires neuroimaging, CT or MRI detects proptosis superior of telmic vein enlargement and kevana sinus abdominal disease while digital subtraction angiography confirms fistula anatomy and flow dynamics. Treatment is endovascular embolization via trans arterial or transvenous roots to occlude the fistula, preserving internal carotid artery patency, corticosteroids may elevate inflammation pre-intervention. Treated CCF search risk vision loss, cerebral ischemia or hemorrhage from cortical venus surfflux. Now let's see the answers for the pre-test multiple choice questions. Question 1. What structure forms the roots of the doorillow's canal? A. Petra's temporal bone. B. Posteroclineoid process. C. Gruber's ligament. D. Fax cerebride. Answer is C. Gruber's ligament. Gruber's ligament also known as pittrosvenoidal ligament forms the root of doorillow's canal through which the abducent nerve passes. Question 2. Which syndrome features abducent palsy facial pain and DR discharge? A. Fowell's syndrome. B. Gradinigo syndrome. C. Millard-Gobler. D. Görtret's syndrome. Answer is B. Gradinigo syndrome. Gradinigo syndrome is classically a triad of abducent nerve palsy, facial pain and ear discharges usually due to pittros' epics pathology. Question 3. Question in which location is most likely to cause bilateral succino palsy with 12 cranial nerve involvement? Choice a cavernous sinus b-clivus, c-mid-brain d-orbid, answer is box. Clivus. A clival lesion may involve both abducent nerves as they run near to each other in the clivus and hypoglossal nerve causing Görtret's syndrome. Question 4. In a patient with succino palsy with thornous syndrome, which features best differentiated cavernous sinus lesion from a pontine lesion. Choice a presence of abduction deficit, b-distribution of facial sweating, c-involmetement of the medial rectus, d-conjugate gaze palsy, answer is box, distribution of facial sweating. Cavernous sinus lesion causes post-ganglionic honours syndrome with sweating's priored expect for the forehead while pontine lesion affect entire facial sweating. Question 5. Which clinical scenarios strongly suggest divergence in sufficiency rather than an isolated 6th nerve palsy? Choice a esotropia at near and distance, b-attection deficit on-dexion testing, c-full dexions with esotropia only at a distance, d- sudden onset deplopia with medial rectus over action, answer is c-full dexions with esotropia only at a distance. In a divergence in sufficiency, ocular mortality is normal on-dexion, but esotropia is present only when viewing distant objects, not near. This helps to differentiate it from true lateral rectus palsy. Please note that the podcast and online content are meant for medical education only and should not be used to guide clinical decision making or treatment. You can find more episodes on Apple Podcasts, Spotify, Amazon Music or wherever you enjoy podcasts. This is KD Signing off, until next time, spread knowledge. [BLANK_AUDIO]