DOCSLIB.ORG

An Overview of the Third, Fourth and Sixth Cranial Nerve Palsies Palsies of the Third, Fourth and Sixth Cranial Nerves Have Ophthalmological Consequences

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
An Overview of the Third, Fourth and Sixth Cranial Nerve Palsies Palsies of the Third, Fourth and Sixth Cranial Nerves Have Ophthalmological Consequences An overview of the third, fourth and sixth cranial nerve palsies Palsies of the third, fourth and sixth cranial nerves have ophthalmological consequences. W Marais, MB ChB, MMed (Ophth); S Barrett, MB ChB, MMed (Ophth) Consultants, Department of Ophthalmology, University of the Free State, Bloemfontein, South Africa Correspondence to: W Marais ([email protected]) Third nerve (oculomotor • nuclear third nerve palsy will spare the Basilar part of CN III[2] nerve) ipsilateral, and aect the contralateral, e basilar part of CN III Cranial nerve III (CN III) innervates the superior rectus. • starts as a series of ‘rootlets’ superior, inferior, medial recti and the • Medial rectus, inferior rectus and • leaves the midbrain on the medial aspect inferior oblique muscles. It also innervates inferior oblique subnuclei of the cerebral peduncle, before coalescing the levator palpebrae superioris and carries • paired to form the main trunk with it the parasympathetic innervations • innervate their corresponding ipsi- • then passes between the posterior to the pupil. Involvement of CN III will lateral muscles cerebral and superior cerebellar arteries produce a symptom complex that involves • lesions conned to the nuclear com- • runs lateral to and parallel with the one or several of these muscles and usually plex are relatively uncommon posterior communicating artery results in double vision.[1] • most frequent cause of palsy are vascular • is unaccompanied by other cranial disease, primary tumours and metastases nerves, therefore isolated CN III is Components of CN III • involvement of the paired medial commonly basilar (Fig. 1). • nuclear complex rectus subnuclei causes a wall-eyed • fasciculus bilateral internuclear ophthalmoplegia Important causes of basilar CN III • basilar (WEBINO), characterised by exo- palsy • intracavernous tropia, and defective convergence Aneurysm • intraorbital and adduction. Lesions involving the Aneurysm of the posterior communicating • pupillomotor bres. entire nucleus are oen associated with artery at its junction with the internal involvement of the adjacent and caudal carotid artery typically presents as acute, Nuclear complex[2] fourth nerve nucleus. painful third nerve palsy with pupil • situated in the midbrain • Fasciculus[2] involvement. • at the level of the superior colliculus • consists of eerent bres which pass • ventral to the Sylvian aqueduct. from the third nerve nucleus through Head trauma the red nucleus and the medial aspect Head trauma resulting in extradural/ e nuclear complex is composed of the of the cerebral peduncle subdural haematoma (Fig. 2) causes a following paired and unpaired subnuclei:[2] • emerges from the midbrain and passes tentorial pressure cone with downward • Levator subnucleus into the interpeduncular space herniation of the temporal lobe and • unpaired caudal midline structure • causes of nuclear and fascicular lesions compresses the CN III as it passes over the • innervates both levator muscles are similar, except that demyelination tentorial edge, initially causing irritative • lesions conned in this area will may aect the fasciculus.[2] miosis followed by mydriasis and total CN therefore give rise to bilateral ptosis. III palsy. • Superior rectus subnuclei Midbrain fascicular third cranial • paired nerve palsies Intracavernous part of CN III[2] • innervates the respective contralateral Table 1 describes midbrain fascicular third e intracavernous part of CN III enters superior rectus cranial nerve palsies.[1,2] the cavernous sinus by piercing the dura Table 1. Midbrain fascicular third cranial nerve palsies Syndrome Signs/characteristics Location of lesion Benedikt Ipsilateral CN III palsy Red nucleus Contralateral extrapyramidal signs Hemitremor/involuntary movements Nothnagel Ipsilateral CN III palsy Fasciculus Cerebellar ataxia Superior cerebellar peduncle Claude Combination of Benedikt and Nothnagel syndromes Weber Ipsilateral CN III palsy Cerebral peduncle Contralateral hemiparesis 147 CME April 2013 Vol. 31 No. 4 Cranial nerve palsies lateral to the posterior clinoid process Intracavernous CN III palsy is usually onset of diplopia as an aneurysm expands. (Fig. 3). Within the cavernous sinus the associated with Pupillary involvement may be the only sign CN III runs in the lateral wall above CN • CN IV of CN III palsy. IV. Anteriorly in the cavernous sinus it • CN VI divides into superior and inferior branches, • rst division of CN V. Signs of right CN III palsy[2] entering the orbit through the superior • weakness of the levator with ptosis orbital ssure within the annulus of Zinn. The intra-orbital part of CN III[2] • eye abducted in primary position due to e superior division innervates the unopposed action of the lateral rectus Important causes of intracavernous CN • levator muscle III palsy • superior rectus. • normal abduction • Diabetes – causes a vascular palsy usually • intorsion of the eye which increases sparing the pupil. e inferior division innervates the on down gaze due to intact function of • Pituitary apoplexy (haemorrhagic in- • medial rectus superior oblique muscle farction) may cause a CN III palsy if the • inferior rectus – the branch to the inferior • limited adduction due to weakness of gland swells laterally and impinges on oblique also contains parasympathetic medial rectus muscle the cavernous sinus. preganglionic bres from the Edinge- • limited supraduction due to weakness • Intracavernous pathology such as Westphal subnucleus of superior rectus and inferior oblique • aneurysm • sphincter pupillae. muscles • meningioma • limited infraduction due to weakness of • carotid-cavernous stula Lesions to the inferior division are inferior rectus muscle • granulomatous inammation (Tolosa- characterised by • dilated pupil with defective accom- Hunt syndrome). • limited abduction modation due to parasympathetic palsy. • limited infraduction • dilated pupil. Aberrant regeneration[1,2] • may follow acute traumatic and Superior and inferior palsies are commonly compressive (but not vascular) third traumatic or vascular. nerve palsies • the endoneural nerve sheaths remain Pupillomotor fibres[2] intact in vascular pathology, may be These fibres are located superficially in the breached in traumatic and compressive superomedial part of CN III. Their blood lesions supply comes from the pial blood vessels. • bizarre defects in ocular motility Fig. 1. Dorsal view of the course of the third The main trunk of CN III is supplied by • elevation of the upper eyelid on nerve. the vasa nervorum. Involvement of the attempted abduction or infraduction pupil is of great importance because it • caused by misdirection of regenerating differentiates a ‘surgical’ from a ‘medical’ axons which reinervate the wrong lesion. extraocular muscle • pupil may also be involved. Surgical CN III lesions[2] Causes include Causes of isolated CN III palsy[2,3] • trauma 1. Idiopathic – 25 % • aneurysms 2. Vascular disease • uncal herniation. • diabetes • hypertension ese lesions characteristically involve the • most common cause of pupil-sparing Fig. 2. Mechanism of third nerve palsy by pupil by compressing the pial blood vessels CN III extradural haematoma. and the supercially located pupillary • spontaneous recovery in 3 months bres. • diabetic CN III palsy may be associated with periorbital pain Medical CN III lesions[2] • occasionally the presenting feature of • causes include hypertension and diabetes diabetes • characteristically spare the pupil • pain is therefore not helpful in • the microangiopathy involves the vasa dierentiating aneurismal and diabetic nervorum, causing ischaemia of the main CN III nerve palsy trunk. 3. Aneurysm • the posterior communicating artery at its Fig. 3. Location of cranial nerves in the ese principles are not infallible. Pupillary junction with the internal carotid artery cavernous sinus viewed from behind. involvement may develop a few days aer • pupil involvement 148 CME April 2013 Vol. 31 No. 4 Cranial nerve palsies 4. Trauma Fourth nerve (trochlear nerve) superior orbital ssure above and lateral • direct and secondary to subdural Anatomy of CN IV[2,3] to the annulus of Zinn. haematoma with uncal herniation Important features of CN IV • trivial head trauma not associated with • only cranial nerve to emerge from the Intraorbital part of CN IV loss of consciousness should alert one dorsal aspect of the brain (Fig. 4) • innervates the superior oblique. of a basal intracranial tumour causing • crossed cranial nerve – it means the nerve trunk to be stretched and that nerve nucleus innervates the Symptoms and signs of CN IV tethered contralateral superior oblique muscles palsy[5] 5. Miscellaneous (uncommon) • very long and slender nerve. A fourth nerve palsy typically causes • tumours diplopia that is worse in down gaze. Hence, • syphillis Components of CN IV patients almost always report diplopia (or • meningeal inammation • nucleus tendency to close one eye) while reading. • giant cell arteritis • fasciculus • vasculitis associated with collagen • trunk Signs of CN IV palsy[2] vascular disorders • intracavernous • acute onset of vertical diplopia in the • ophthalmoplegic migraine • intraorbital. absence of ptosis • internal carotid artery dissection • characterised by a head posture • myasthenia may also mimic intermittent Nucleus • features of nuclear, fascicular and pupil-sparing CN III palsy • located at level of the inferior colliculus peripheral CN IV are clinically identical • chemotherapeutic toxicity. ventral to the Sylvian aqueduct •
Load more

Recommended publications
  • MR Imaging of the Orbital Apex
    J Korean Radiol Soc 2000;4 :26 9-0 6 1 6 MR Imaging of the Orbital Apex: An a to m y and Pat h o l o g y 1 Ho Kyu Lee, M.D., Chang Jin Kim, M.D.2, Hyosook Ahn, M.D.3, Ji Hoon Shin, M.D., Choong Gon Choi, M.D., Dae Chul Suh, M.D. The apex of the orbit is basically formed by the optic canal, the superior orbital fis- su r e , and their contents. Space-occupying lesions in this area can result in clinical d- eficits caused by compression of the optic nerve or extraocular muscles. Even vas c u l a r changes in the cavernous sinus can produce a direct mass effect and affect the orbit ap e x. When pathologic changes in this region is suspected, contrast-enhanced MR imaging with fat saturation is very useful. According to the anatomic regions from which the lesions arise, they can be classi- fied as belonging to one of five groups; lesions of the optic nerve-sheath complex, of the conal and intraconal spaces, of the extraconal space and bony orbit, of the cav- ernous sinus or diffuse. The characteristic MR findings of various orbital lesions will be described in this paper. Index words : Orbit, diseases Orbit, MR The apex of the orbit is a complex region which con- tains many nerves, vessels, soft tissues, and bony struc- Anatomy of the orbital apex tures such as the superior orbital fissure and the optic canal (1-3), and is likely to be involved in various dis- The orbital apex region consists of the optic nerve- eases (3).
    [Show full text]
  • Extraocular Muscles Orbital Muscles
    EXTRAOCULAR MUSCLES ORBITAL MUSCLES INTRA- EXTRA- OCULAR OCULAR CILIARY MUSCLES INVOLUNTARY VOLUNTARY 1.Superior tarsal muscle. 1.Levator Palpebrae Superioris 2.Inferior tarsal muscle 2.Superior rectus 3.Inferior rectus 4.Medial rectus 5.Lateral rectus 6.Superior oblique 7.Inferior oblique LEVATOR PALPEBRAE SUPERIORIOS Origin- Inferior surface of lesser wing of sphenoid. Insertion- Upper lamina (Voluntary) - Anterior surface of superior tarsus & skin of upper eyelid. Middle lamina (Involuntary) - Superior margin of superior tarsus. (Superior Tarsus Muscle / Muller muscle) Lower lamina (Involuntary) - Superior conjunctival fornix Nerve Supply :- Voluntary part – Oculomotor Nerve Involuntary part – Sympathetic ACTION :- Elevation of upper eye lid C/S :- Drooping of upper eyelid. Congenital ptosis due to localized myogenic dysgenesis Complete ptosis - Injury to occulomotor nerve. Partial ptosis - disruption of postganglionic sympathetic fibres from superior cervical sympathetic ganglion. Extra ocular Muscles : Origin Levator palpebrae superioris Superior Oblique Superior Rectus Lateral Rectus Medial Rectus Inferior Oblique Inferior Rectus RECTUS MUSCLES : ORIGIN • Arises from a common tendinous ring knows as ANNULUS OF ZINN • Common ring of connective tissue • Anterior to optic foramen • Forms a muscle cone Clinical Significance Retrobulbar neuritis ○ Origin of SUPERIOR AND MEDIAL RECTUS are closely attached to the dural sheath of the optic nerve, which leads to pain during upward & inward movements of the globe. Thyroid orbitopathy ○ Medial & Inf.rectus thicken. especially near the orbital apex - compression of the optic nerve as it enters the optic canal adjacent to the body of the sphenoid bone. Ophthalmoplegia ○ Proptosis occur due to muscle laxity. Medial Rectus Superior Rectus Origin :- Superior limb of the tendonous ring, and optic nerve sheath.
    [Show full text]
  • Cranial Nerve Palsy
    Cranial Nerve Palsy What is a cranial nerve? Cranial nerves are nerves that lead directly from the brain to parts of our head, face, and trunk. There are 12 pairs of cranial nerves and some are involved in special senses (sight, smell, hearing, taste, feeling) while others control muscles and glands. Which cranial nerves pertain to the eyes? The second cranial nerve is called the optic nerve. It sends visual information from the eye to the brain. The third cranial nerve is called the oculomotor nerve. It is involved with eye movement, eyelid movement, and the function of the pupil and lens inside the eye. The fourth cranial nerve is called the trochlear nerve and the sixth cranial nerve is called the abducens nerve. They each innervate an eye muscle involved in eye movement. The fifth cranial nerve is called the trigeminal nerve. It provides facial touch sensation (including sensation on the eye). What is a cranial nerve palsy? A palsy is a lack of function of a nerve. A cranial nerve palsy may cause a complete or partial weakness or paralysis of the areas served by the affected nerve. In the case of a cranial nerve that has multiple functions (such as the oculomotor nerve), it is possible for a palsy to affect all of the various functions or only some of the functions of that nerve. What are some causes of a cranial nerve palsy? A cranial nerve palsy can occur due to a variety of causes. It can be congenital (present at birth), traumatic, or due to blood vessel disease (hypertension, diabetes, strokes, aneurysms, etc).
    [Show full text]
  • Periorbital Sinuses the Periorbital Sinuses Have a Close Anatomical Relationship with the Orbits (Fig 1-8)
    12 ● Fundamentals and Principles of Ophthalmology Lacrimal nerve Frontal nerve Trochlear nerve (CN IV) Superior ophthalmic vein Superior division Ophthalmic artery of CN III Nasociliary nerve Abducens nerve (CN VI) Inferior division of CN III Inferior ophthalmic vein A Figure 1-7 A, Anterior view of the right orbital apex showing the distribution of the nerves as they enter through the superior orbital fissure and optic canal. This view also shows the annu- lus of Zinn, the fibrous ring formed by the origin of the 4 rectus muscles. (Continued) The course of the inferior ophthalmic vein is variable, and it can travel within or below the ring as it exits the orbit. The inferior orbital fissure lies just below the superior fissure, between the lateral wall and the floor of the orbit, providing access to the pterygopalatine and inferotemporal fos- sae (see Fig 1-1). Therefore, it is close to the foramen rotundum and the pterygoid canal. The inferior orbital fissure transmits the infraorbital and zygomatic branches of CN V2, an orbital nerve from the pterygopalatine ganglion, and the inferior ophthalmic vein. The inferior ophthalmic vein connects with the pterygoid plexus before draining into the cav- ernous sinus. Periorbital Sinuses The periorbital sinuses have a close anatomical relationship with the orbits (Fig 1-8). The medial walls of the orbits, which border the nasal cavity anteriorly and the ethmoid sinus and sphenoid sinus posteriorly, are almost parallel. In adults, the lateral wall of each orbit forms an angle of approximately 45° with the medial plane. The lateral walls border the middle cranial, temporal, and pterygopalatine fossae.
    [Show full text]
  • Complex Strabismus and Syndromes
    Complex Strabismus & Syndromes Some patients exhibit complex combinations of vertical, horizontal, and torsional strabismus. Dr. Shin treats patients with complex strabismus arising from, but not limited to, thyroid-related eye disease, stroke, or brain tumors as well as strabismic disorders following severe orbital and head trauma. The following paragraphs describe specific ocular conditions marked by complex strabismus. Duane Syndrome Duane syndrome represents a constellation of eye findings present at birth that results from an absent 6th cranial nerve nucleus and an aberrant branch of the 3rd cranial nerve that innervates the lateral rectus muscle. Duane syndrome most commonly affects the left eye of otherwise healthy females. Duane syndrome includes several variants of eye movement abnormalities. In the most common variant, Type I, the eye is unable to turn outward to varying degrees from the normal straight ahead position. In addition, when the patient tries to look straight ahead, the eyes may cross. This may lead a person with Duane syndrome to turn his/her head toward one side while viewing objects in front of them in order to better align the eyes. When the involved eye moves toward the nose, the eye retracts slightly back into the eye socket causing a narrowing of the opening between the eyelids. In Type II, the affected eye possesses limited ability to turn inward and is generally outwardly turning. In Type III, the eye has limited inward and outward movement. All three types are characterized by anomalous co-contraction of the medial and lateral rectus muscles, so when the involved eye moves towards the nose, the globe pulls back into the orbit and the vertical space between the eyelids narrows.
    [Show full text]
  • MR Imaging of Primary Trochlear Nerve Neoplasms
    707 MR Imaging of Primary Trochlear Nerve Neoplasms Lindell R. Gentry 1 We present the clinical, anatomic, and MR imaging findings in six patients with seven Rahul C. Mehta 1 primary trochlear nerve neoplasms, as well as the MR and clinical criteria that serve to Richard E. Appen2 establish the diagnosis of these rare cranial nerve neoplasms. Three patients had a Joel M. Weinstein2 history of neurofibromatosis and five patients had clinical evidence of a trochlear nerve palsy. Six of seven neoplasms produced localized, fusiform enlargement of the proximal cisternal segments of the trochlear nerves. The lesions that were visible on noncontrast MR scans (T1-, T2-, and proton density-weighted) had signal intensities that were virtually identical to normal brain parenchyma. All lesions showed intense, homogeneous enhancement on contrast-enhanced scans. Contrast-enhanced imaging was necessary for the detection of five of seven lesions and greatly increased the value of the MR study in all six patients. AJNR 12:707-713, July/August 1991; AJR 157: September 1991 Primary neoplasms arising from pure motor cranial nerves such as the trochlear nerve are rare. To our knowledge just nine primary trochlear nerve neoplasms have been reported in the literature [1-7), only one of which was imaged with MR [1). Over the last 6 years, since we began to use MR as the primary imaging method for evaluating patients with cranial nerve palsies , we have noticed a striking increase in the number of primary trochlear nerve neoplasms over those encountered during the CT era. We believe this is due to a much greater sensitivity of MR in detecting these typically small lesions.
    [Show full text]
  • Canine Red Eye Elizabeth Barfield Laminack, DVM; Kathern Myrna, DVM, MS; and Phillip Anthony Moore, DVM, Diplomate ACVO
    PEER REVIEWED Clinical Approach to the CANINE RED EYE Elizabeth Barfield Laminack, DVM; Kathern Myrna, DVM, MS; and Phillip Anthony Moore, DVM, Diplomate ACVO he acute red eye is a common clinical challenge for tion of the deep episcleral vessels, and is characterized general practitioners. Redness is the hallmark of by straight and immobile episcleral vessels, which run Tocular inflammation; it is a nonspecific sign related 90° to the limbus. Episcleral injection is an external to a number of underlying diseases and degree of redness sign of intraocular disease, such as anterior uveitis and may not reflect the severity of the ocular problem. glaucoma (Figures 3 and 4). Occasionally, episcleral Proper evaluation of the red eye depends on effective injection may occur in diseases of the sclera, such as and efficient diagnosis of the underlying ocular disease in episcleritis or scleritis.1 order to save the eye’s vision and the eye itself.1,2 • Corneal Neovascularization » Superficial: Long, branching corneal vessels; may be SOURCE OF REDNESS seen with superficial ulcerative (Figure 5) or nonul- The conjunctiva has small, fine, tortuous and movable vessels cerative keratitis (Figure 6) that help distinguish conjunctival inflammation from deeper » Focal deep: Straight, nonbranching corneal vessels; inflammation (see Ocular Redness algorithm, page 16). indicates a deep corneal keratitis • Conjunctival hyperemia presents with redness and » 360° deep: Corneal vessels in a 360° pattern around congestion of the conjunctival blood vessels, making the limbus; should arouse concern that glaucoma or them appear more prominent, and is associated with uveitis (Figure 4) is present1,2 extraocular disease, such as conjunctivitis (Figure 1).
    [Show full text]
  • 98796-Anatomy of the Orbit
    Anatomy of the orbit Prof. Pia C Sundgren MD, PhD Department of Diagnostic Radiology, Clinical Sciences, Lund University, Sweden Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Lay-out • brief overview of the basic anatomy of the orbit and its structures • the orbit is a complicated structure due to its embryological composition • high number of entities, and diseases due to its composition of ectoderm, surface ectoderm and mesoderm Recommend you to read for more details Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 3 x 3 Imaging technique 3 layers: - neuroectoderm (retina, iris, optic nerve) - surface ectoderm (lens) • CT and / or MR - mesoderm (vascular structures, sclera, choroid) •IOM plane 3 spaces: - pre-septal •thin slices extraconal - post-septal • axial and coronal projections intraconal • CT: soft tissue and bone windows 3 motor nerves: - occulomotor (III) • MR: T1 pre and post, T2, STIR, fat suppression, DWI (?) - trochlear (IV) - abducens (VI) Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Superior orbital fissure • cranial nerves (CN) III, IV, and VI • lacrimal nerve • frontal nerve • nasociliary nerve • orbital branch of middle meningeal artery • recurrent branch of lacrimal artery • superior orbital vein • superior ophthalmic vein Lund University / Faculty of Medicine / Inst. Clinical Sciences / Radiology / ECNR Dubrovnik / Oct 2018 Lund University / Faculty of Medicine / Inst.
    [Show full text]
  • Eleventh Edition
    SUPPLEMENT TO April 15, 2009 A JOBSON PUBLICATION www.revoptom.com Eleventh Edition Joseph W. Sowka, O.D., FAAO, Dipl. Andrew S. Gurwood, O.D., FAAO, Dipl. Alan G. Kabat, O.D., FAAO Supported by an unrestricted grant from Alcon, Inc. 001_ro0409_handbook 4/2/09 9:42 AM Page 4 TABLE OF CONTENTS Eyelids & Adnexa Conjunctiva & Sclera Cornea Uvea & Glaucoma Viitreous & Retiina Neuro-Ophthalmic Disease Oculosystemic Disease EYELIDS & ADNEXA VITREOUS & RETINA Blow-Out Fracture................................................ 6 Asteroid Hyalosis ................................................33 Acquired Ptosis ................................................... 7 Retinal Arterial Macroaneurysm............................34 Acquired Entropion ............................................. 9 Retinal Emboli.....................................................36 Verruca & Papilloma............................................11 Hypertensive Retinopathy.....................................37 Idiopathic Juxtafoveal Retinal Telangiectasia...........39 CONJUNCTIVA & SCLERA Ocular Ischemic Syndrome...................................40 Scleral Melt ........................................................13 Retinal Artery Occlusion ......................................42 Giant Papillary Conjunctivitis................................14 Conjunctival Lymphoma .......................................15 NEURO-OPHTHALMIC DISEASE Blue Sclera .........................................................17 Dorsal Midbrain Syndrome ..................................45
    [Show full text]
  • 2002 Samel 10 Most Common Systemic Health Conditions with A
    Avanti Samel / March 15, 2002 10 Most Common Systemic Health Conditions with a Listing of Frequently Prescribed Medications and their Ocular Side Effects HYPERTENSION ACE Inhibitors: Captopril (Capoten}- blurred vision Enalapril (Vasotec) - Blurred vision, conjunctivitis, dry eyes, tearing Quinipril (Accupril)- amblyopia Benazepril (Lotensin)- N/A Lisinopril (Zestril) - Visual loss, diplopia, blurred vision, photophobia Beta-Blockers: Propranolol (Inderal)- visual disturbances, dry eyes Atenolol (Tenormin)- blurred vision, dry eyes, visual disturbances Metoprolol (Lopressor) - blurred vision, dry eyes calcium Channel Blockers: Diltiazem (Cardizem)- Amblyopia, eye irritation Amlodipine (Norvasc)- abnormal vision, conjunctivitis, diplopia, eye pain Verapamil (Calan)- Blurred vision Nifedipine (Procardia) - blurred vision, Transient blindness at the peak of plasma level · Diuretics: Thiazides: Chlorothiazide (Diuril) - Transient blurred vision, xanthopsia Loop: Furosemide (Lasix) - Blurred vision, Xanthopsia Potassium Sparing: Amiloride (Midamor) - Visual disturbances, Increased lOP Triamterene (Dyrenium)- N/A HYPERLIPIDEMIA Statins: Lovastatin (Mevacor) - Blurred vision, Eye irritation Simvastatin (Zocor)- Cataracts Atorvastatin (Lipitor)- Amblyopia, dry eyes, refraction disorder, eye hemorrhage, glaucoma Resins: Cholestyramine (Questran)- Uveitis Fibrates: Gemfibrozil (Lopid)- Blurred vision Niacin: Niacin (Niacor) - Toxic amblyopia, cystoid macular edema ASTHMA ( ) Beta 2 Agonists: Albuterol (Proventil) - N/A ( Salmeterol (Serevent)-
    [Show full text]
  • Ocular Torticollis
    FOCUS | CLINICAL Ocular torticollis A tilt in perspective Helen Dooley, Morgan Berman, (Figure 2). No pain was present on eye QUESTION 4 Chido Mwaturura movements. How does SOP present and how is it Ophthalmological review concluded diagnosed? that the head tilt was due to left congenital CASE fourth cranial nerve palsy, causing weakness QUESTION 5 On a home visit, a woman aged 95 years of the left superior oblique. No intervention What is the management of SOP? was observed to have a right-sided head was recommended given the patient’s age tilt. The patient recalled that her head and lifelong adaptation. Examination of ANSWER 1 tilt had been present for the majority of each eye (when covering the other eye) The differential diagnosis of irreversible her life. Early childhood photographs did not show diplopia in either eye. torticollis includes the following conditions: confirmed this. At rest, the patient • Congenital muscular torticollis is the adopted a head tilt towards the right most common cause of torticollis. It can (Figure 1). In this position, she did not QUESTION 1 be due to birth trauma or intrauterine have any diplopia. There was facial What is the differential diagnosis of malpositioning.1 asymmetry, with hypoplasia of the irreversible torticollis? • Ocular torticollis. Superior oblique right face. palsy (SOP) is the most common type Examination of extraocular muscles QUESTION 2 of ocular torticollis.1 found that the patient had vertical What is the aetiology of superior oblique • Other rarer forms of non-paroxysmal diplopia. This was marked on upward palsy (SOP)? torticollis are osseous torticollis, gaze and to the right, when her left eye peripheral or central nervous system was observed to show limited adduction QUESTION 3 torticollis and non-muscular soft tissue and elevation with vertical strabismus What is the incidence of SOP? torticollis.1 Figure 1.
    [Show full text]
  • GAZE and AUTONOMIC INNERVATION DISORDERS Eye64 (1)
    GAZE AND AUTONOMIC INNERVATION DISORDERS Eye64 (1) Gaze and Autonomic Innervation Disorders Last updated: May 9, 2019 PUPILLARY SYNDROMES ......................................................................................................................... 1 ANISOCORIA .......................................................................................................................................... 1 Benign / Non-neurologic Anisocoria ............................................................................................... 1 Ocular Parasympathetic Syndrome, Preganglionic .......................................................................... 1 Ocular Parasympathetic Syndrome, Postganglionic ........................................................................ 2 Horner Syndrome ............................................................................................................................. 2 Etiology of Horner syndrome ................................................................................................ 2 Localizing Tests .................................................................................................................... 2 Diagnosis ............................................................................................................................... 3 Flow diagram for workup of anisocoria ........................................................................................... 3 LIGHT-NEAR DISSOCIATION .................................................................................................................
    [Show full text]