DOCSLIB.ORG

Pupillary Disorders LAURA J

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

13 Pupillary Disorders LAURA J. BALCER Pupillary disorders usually fall into one of three major cat- cortex generally do not affect pupillary size or reactivity. egories: (1) abnormally shaped pupils, (2) abnormal pupillary Efferent parasympathetic fibers, arising from the Edinger– reaction to light, or (3) unequally sized pupils (anisocoria). Westphal nucleus, exit the midbrain within the third nerve Occasionally pupillary abnormalities are isolated findings, (efferent arc). Within the subarachnoid portion of the third but in many cases they are manifestations of more serious nerve, pupillary fibers tend to run on the external surface, intracranial pathology. making them more vulnerable to compression or infiltration The pupillary examination is discussed in detail in and less susceptible to vascular insult. Within the anterior Chapter 2. Pupillary neuroanatomy and physiology are cavernous sinus, the third nerve divides into two portions. reviewed here, and then the various pupillary disorders, The pupillary fibers follow the inferior division into the orbit, grouped roughly into one of the three listed categories, are where they then synapse at the ciliary ganglion, which lies discussed. in the posterior part of the orbit between the optic nerve and lateral rectus muscle (Fig. 13.3). The ciliary ganglion issues postganglionic cholinergic short ciliary nerves, which Neuroanatomy and Physiology initially travel to the globe with the nerve to the inferior oblique muscle, then between the sclera and choroid, to The major functions of the pupil are to vary the quantity of innervate the ciliary body and iris sphincter muscle. Fibers light reaching the retina, to minimize the spherical aberra- to the ciliary body outnumber those to the iris sphincter tions of the peripheral cornea and lens, and to increase the muscle by 30 : 1. depth of field (the depth within which objects will appear The near response consists of pupillary constriction, accom- sharp). In most individuals the two pupils are equal in size, modation (change in the shape of the lens), and convergence and each is situated slightly nasal and inferior to the center of the eyes (see Chapter 2). Although the pathways are of the cornea and iris (Fig. 13.1). uncertain, the supranuclear control for the near response The iris contains the two muscles that control the size of likely arises from diffuse cortical locations. Stimulation of the pupil. Contraction of the dilator muscle leads to pupillary the peristriate cortex (areas 19 and 22) in primates can evoke enlargement (mydriasis), while sphincter muscle contraction a near response,5 but more recent evidence suggests the causes pupillary constriction (miosis). The sphincter muscle lateral suprasylvian area is also related to the control of lens wraps 360 degrees around the pupillary margin, and the accommodation.6 The signals converge in the rostral superior dilator muscle similarly encircles the pupil but is more periph- colliculus, near which a group of midbrain near-response erally located. neurons coordinates the pretectum for accommodation and Normally, light directed at either eye leads to bilateral miosis, the mesencephalic reticular formation for accom- pupillary constriction, and this pupillary light reflex is medi- modation and vergence, and the raphe interpositus for visual ated by a parasympathetic pathway (see Fig. 13.2 for details). fixation.6,7 The final signal for pupillary miosis during near Light entering the eye causes retinal photoreceptors to hyper- viewing is still mediated by the Edinger–Westphal nuclei. polarize, in turn causing activation of retinal interneurons Pupillary dilation is the function of the oculosympathetic and ultimately the retinal ganglion cells. Additionally, intrin- system (the ocular part of the sympathetic nervous system), sically photosensitive retinal ganglion cells (ipRGCs) contain- which consists of three neurons beginning in the postero- ing melanopsin, a photopigment, can be activated by light lateral hypothalamus and ending at the iris and eyelids (see without photoreceptor input.1,2 The ipRGCs are most sensitive Fig. 13.4 for details). The first-order neuron projects from to blue light, and the preservation of circadian rhythms and the hypothalamus through ill-defined brainstem pathways the pupillary light reflexes in patients with severe photore- to synapse on the intermediolateral cell column in the spinal ceptor diseases and Leber’s hereditary optic neuropathy can cord at C8–T2 (ciliospinal center of Budge). The second-order be explained by intact ipRGC function.3,4 neuron (preganglionic) leaves the spinal cord and travels Retinal ganglion cell axons activated by photoreceptors over the apex of the lung before ascending with the internal and ipRGCs together mediate the pupillary light reflex and carotid artery to synapse at the superior cervical ganglion. travel through the optic nerve, chiasm, and optic tract to In the region of the lung apex, the sympathetic pathway lies reach the pretectal nuclei (afferent arc). Interneurons then in close proximity to the lower brachial plexus. The third- connect the pretectal nuclei to the Edinger–Westphal nuclei. order neuron (postganglionic) travels along the internal Although these connections are bilateral, the input into the carotid into the cavernous sinus, after which the sympathetic Edinger–Westphal nuclei is predominantly from the contra- pathways follow the sixth nerve, then the nasociliary nerve lateral pretectal nucleus. Since the afferent pupillary fibers (a branch of the first division of the trigeminal nerve), then leave the optic tract before the lateral geniculate nucleus, the long ciliary nerve into the orbit.8 This neuron releases isolated lesions of the geniculate, optic radiations, and visual the neurotransmitter norepinephrine at the iris dilator muscle. 417 Downloaded for Anonymous User (n/a) at The Pennsylvania State University from ClinicalKey.com by Elsevier on June 21, 2018. For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved. 418 PART 3 • Efferent Neuro-Ophthalmic Disorders SC PTN LGN E–W III OT CHI Figure 13.1. A normal left eye. Note the pupil is slightly nasal to the center of the cornea and iris. CG Pharmacologic Testing ON of the Pupils RET As will be discussed, pharmacologic testing helps confirm the clinical diagnosis of many pupillary abnormalities. Some general guidelines need to be followed in this regard. By dis- rupting the corneal epithelium, corneal reflex evaluation and applanation or pneumotonometry may alter corneal permeability of the drug and therefore should not be per- Figure 13.2. Pupillary light reflex—parasympathetic pathway. Light formed on the same day as pharmacologic testing. In general, entering one eye (straight dark arrow, bottom right) stimulates the retinal photoreceptors (RET), resulting in excitation of ganglion cells, whose the drops should be instilled in the inferior cul-de-sac, with axons travel within the optic nerve (ON), partially decussate in the chiasm care taken to use the same size drop in each eye. Drop admin- (CHI), then leave the optic tract (OT) (before the lateral geniculate nucleus istration should be repeated 1–5 minutes later. The pupil (LGN)) and pass through the brachium of the superior colliculus (SC) sizes then can be measured 30–45 minutes after instillation before synapsing at the mesencephalic pretectal nucleus (PTN). This of the last set of drops. Baseline and test pupillary sizes are structure connects bilaterally, but predominantly contralaterally, to the oculomotor nuclear complex at the Edinger–Westphal (E-W) nuclei, best measured in the same lighting conditions, and photo- which issue parasympathetic fibers that travel within the third nerve graphic documentation before and after testing can be helpful. (inferior division) and terminate at the ciliary ganglion (CG) in the orbit. Postsynaptic cells innervate the pupillary sphincter, resulting in miosis. Light in one eye causes bilateral pupillary constriction. Pupillometry: an Additional Tool Pupillometry, the computerized measurement of pupillary responses to light stimulation, can be used to characterize Box 13.1 Causes of Abnormally Shaped Pupils relative afferent pupillary defects (RAPDs) objectively in patients 9–11 with or without vision loss. In addition, pupillometry has Congenital Causes been used in the intensive care setting to document abnor- Aniridia malities in pupillary reactivity related to increases in intra- Ectopia lentis et pupillae 12,13 cranial pressure in patients with traumatic brain injury. Iris coloboma Anterior chamber cleavage anomalies Ectopic pupils Abnormally Shaped Pupils Persistent pupillary membranes Acquired Causes Irregularly shaped pupils may be congenital or acquired (Box 13.1). Congenital conditions include the following: Iritis Iridocorneal endothelial syndrome Trauma (accidental or surgical) 1. Aniridia, in which the iris is hypoplastic, creating a large Iris atrophy (e.g., diabetes, herpetic disease) pupillary opening. Associated ocular findings often Neurologic (e.g., tonic pupils, midbrain damage (corectopia), include cataracts, glaucoma, and impaired vision due to tadpole-shaped pupils) macular or optic nerve hypoplasia. Patients with aniridia, Downloaded for Anonymous User (n/a) at The Pennsylvania State University from ClinicalKey.com by Elsevier on June 21, 2018. For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved. 13 • Pupillary
Recommended publications
  • Medical Diary Official Publication for the Federation of Medical Societies of Hong Kong

    Medical Diary Official Publication for the Federation of Medical Societies of Hong Kong

    VOL.12 NO.9 SEPTEMBER 2007 ॷġ෫ġᚂġଉ THE HONG KONG MEDICAL DIARY OFFICIAL PUBLICATION FOR THE FEDERATION OF MEDICAL SOCIETIES OF HONG KONG www.fmshk.org Editorial Editorial Dr. Timothy YY Lai Medical Bulletin Management of Tearing in Adults Dr. Alan CK Ng Dr. Dylan DN Chan Ocular Allergy in Children Dr. Koon-man Lam Neuro-ophthalmology for General Practitioners: A Revision Dr.CarmenKMChan Normal Tension Glaucoma - a Sick Eye in a Sick Body Dr. Dexter YL Leung Retinal Complications of High Myopia Dr. Timothy YY Lai Amblyopia: An overview Dr. Wilson WK Yip Prof. Dorothy SP Fan Surgical Correction for Near Sightedness Dr. Arthur CK Cheng Traditional Chinese Medicine and Ophthalmology Dr. Jane CC Yeung Special Feature Rosiglitazone and Risk of Myocardial Infarction: Clear Danger or Dr. Norman Chan Media Hype? Clinical Quiz Clinical Quiz Dr. Helen KS Tung Society News Medical Diary of September Calendar of Events ISSN 1812 - 1691 ᚂᖒԙষΙড়ᒑȅᩧҕ୊ஶቆᜰЖ VOL.12 NO.9 SEPTEMBER 2007 Contents The Federation of Medical Societies of Hong Kong 4/F Duke of Windsor Social Service Building, Contents 15 Hennessy Road, Wanchai, Hong Kong Tel: 2527 8898 Fax: 2865 0345 Editorial President Dr. FONG To-sang, Dawson 方道生醫生 1st Vice- President Editorial 2 Dr. CHAN Chi-kuen 陳志權醫生 2nd Vice- President Dr. Timothy YY Lai Dr. LO Sze-ching, Susanna 盧時楨醫生 Hon. Secretary Dr. LO See-kit, Raymond 勞思傑醫生 Medical Bulletin Deputy Hon. Secretary Dr. CHAN Sai-kwing 陳世炯醫生 Management of Tearing in Adults 4 Hon. Treasurer Mr. LAM Lop-chi, Nelson 林立志先生 Dr.AlanCKNg Deputy Hon. Treasurer Dr. Dylan DN Chan Mr.
  • AD Singh1, PA Rundle1, a Berry-Brincat1, MA Parsons2 and and Accommodation Were Considered Normal

    AD Singh1, PA Rundle1, a Berry-Brincat1, MA Parsons2 and and Accommodation Were Considered Normal

    Tadpole pupil KL Koay et al 93 5 Currie ZI, Rennie IG, Talbot JF. Retinal vascular changes associated with transpupillary thermotherapy for choroidal melanomas. Retina 2000; 20: 620–626. 6 Shields CL, Cater J, Shields JA, Singh AD, Santos MCM, Carvalho C. Combination of clinical factors predictive of growth of small choroidal melanocytic tumors. Arch Ophthalmol 2000; 118: 360–364. 7 Journee-de Korver JG, Oosterhuis JA, de Wolff-Rouendaal D, Kemme H. Histopathological findings in human choroidal melanomas after transpupillary thermotherapy. Br J Ophthalmol 1997; 81: 234–239. 8 Anonymous. Histopathologic characteristics of uveal melanomas in eyes enucleated from the Collaborative Ocular Melanoma Study. COMS report no. 6. Am J Figure 1 Ophthalmol 1998; 125: 745–766. Tadpole-shaped pupil. 9 Diaz CE, Capone Jr A, Grossniklaus HE. Clinicopathologic findings in recurrent choroidal melanoma after transpupillary thermotherapy. Ophthalmology 1998; 105: 1419–1424. periocular sensation. The symptom occurred 10 Singh AD, Eagle Jr RC, Shields CL, Shields JA. Enucleation sporadically, sometimes with several weeks in between following transpupillary thermotherapy of choroidal episodes, but occasionally happening several times on melanoma :clinicopathologic correlations. Arch Ophthalmol the same day. There were no other visual symptoms and (in press). 11 Seregard S, Landau I. Transpupillary thermotherapy as an no significant past ocular history. General health was adjunct to ruthenium plaque radiotherapy for choroidal good and no regular medications were taken. melanoma. Acta Ophthalmologica Scand 2001; 79: 19–22. On examination, visual acuity was normal bilaterally. 12 Keunen JE, Journee-de Korver JG, Oosterhuis JA. There was a 1 mm right ptosis with mild anisocoria, the Transpupillary thermotherapy of choroidal melanoma with right pupil being 1 mm smaller in normal room or without brachytherapy: a dilemma.
  • Accommodation in the Holmes-Adie Syndrome by G

    Accommodation in the Holmes-Adie Syndrome by G

    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.21.4.290 on 1 November 1958. Downloaded from J. Neurol. Neurosurg. Psychiat., 1958, 21, 290. ACCOMMODATION IN THE HOLMES-ADIE SYNDROME BY G. F. M. RUSSELL From the Neurological Research Unit, the National Hospital, Queen Square, London In 1936, Bramwell suggested that the title response to near and far vision respectively. But it "Holmes-Adie syndrome" be given to the clinical has also been noted that the reaction to convergence complex of a slowly reacting pupil and absent tendon may be remarkably wide in its range, considering reflexes in recognition of the descriptions by Holmes that it often follows a stage of complete paralysis (1931) and Adie (1932). Both authors had empha- (Strasburger, 1902). Not only is the reaction to sized the chief clinical features-dilatation of the convergence well preserved when compared to the pupil, apparent loss of the reaction to light, slow reaction to light, but it may in fact be excessive constriction and relaxation in response to near and (Alajouanine and Morax, 1938; Heersema and distant vision, and partial loss of the tendon reflexes. Moersch, 1939). In assessing the degree of tonicity Although the syndrome had been recognized wholly there are, therefore, two criteria: slowness ofguest. Protected by copyright. or in part many years previously (Strasburger, 1902; pupillary movement and preservation of the range Saenger, 1902; Nonne, 1902; Markus, 1906; Weill of movement. and Reys, 1926), credit must go to Adie for stressing Adler and Scheie (1940) showed that the tonic the benign nature of the disorder and distinguishing pupil constricts after the conjunctival instillation it clearly from neurosyphilis.
  • Adie Syndrome: a Case Report

    Adie Syndrome: a Case Report

    J Am Board Fam Pract: first published as 10.3122/jabfm.10.6.439 on 1 November 1997. Downloaded from Adie Syndrome: A Case Report T. Micheal Sherrill, MD, and DavidJ Lutz In 1932 Adie 1 described a syndrome in which were roughly equal, and the right corneal reflex unilateral accommodation and pupillary contrac­ was decreased. A rapid plasma reagin was ob­ tion were abnormal. It typically was observed in tained and found to be negative. The patient was young women with no history or evidence of subsequently referred to an ophthalmologist for syphilis and involved a unilateral dilated pupil confirmation of the diagnosis and to rule out that was unresponsive to light. He noted that other abnormalities. Confirmation was per­ deep tendon reflexes were absent or markedly di­ formed using'a dilute solution of pilocarpine. minished in these patients. He concluded that it was "a benign disorder sui generis." We report a Discussion recent case of Adie syndrome. Patients with Adie syndrome have anisocoria characterized by a dilated pupil that is minimally Case Report reactive or unresponsive to light. Deep tendon A 37-year-old woman came to the office with reflexes (knees and ankles) are either diminished right pupil dilatation. It was noticed by a nurse or absent.2 This disorder is most often seen in for the first time earlier that morning and had not young women, who have an average age of onset been present previously according to the patient's in their 30s. It usually occurs in one eye, but oc­ report. The patient's only visual complaint was curs bilaterally in up to 4 percent of patients.3 mild photophobia in sunlight.
  • Taking the Mystery out of Abnormal Pupils

    Taking the Mystery out of Abnormal Pupils

    Taking the mystery out of abnormal pupils No financial disclosures Course Title: Taking the mystery out [email protected] of abnormal pupils Lecturer: Brad Sutton, OD, FAAO Clinical Professor IU School of Optometry . •Review of Anatomy Iris anatomy Iris sphincter Iris dilator Parasympathetic pathway Sympathetic pathway Parasympathetic Pathway Parasympathetic Pathway Light stimulates the retina then impulse Four neuron arc travels with the ganglion cells through the Retina to the pretectal nucleus in the chiasm into the optic tracts. 80% go to the midbrain (1) LGN , 20% to the pretectal nuclei.They Pretectal nucleus to the EW nucleus (2) then hemidecussate and terminate at the EW nucleus EW nucleus to the ciliary ganglion (3) Ciliary ganglion to the iris sphincter with short ciliary nerves (4) 1 Points of Interest Sympathetic Pathway Within the second order neuron there are Three neuron arc 30 near response fibers for every light Posterior hypothalamus to ciliospinal response fiber. This allows for light - near center of Budge ( C8 - T2 ). (1) dissociation. Center of Budge to the superior cervical The third order neuron runs with cranial ganglion in the neck (2) nerve III from the brain stem to the ciliary Superior cervical ganglion to the dilator ganglion. Superficially located prior to the muscle (3) cavernous sinus. Points of Interest Second order neuron runs along the surface of the lung, can be affected by a Pancoast tumor Third order neuron runs with the carotid artery then with the ophthalmic division of cranial nerve V 2 APD Testing testing……………….AKA……… … APD / reverse APD Direct and consensual response Which is the abnormal pupil ? Very simple rule.
  • Complete and Incomplete Forms of the Benign Disorder Characterised By

    Complete and Incomplete Forms of the Benign Disorder Characterised By

    Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932. Downloaded from THE BRITISH JOURNAL OF OPHTHALMOLOGY AUGUST, 1932 COMMUNICATIONS COMPLETE AND INCOMPLETE FORMS OF THE BENIGN DISORDER CHARACTERISED BY TONIC PUPILS AND ABSENT copyright. TENDON REFLEXES BY W. J. ADIE, M.D., F.R.C.P. PHYSICIAN, CHARING CROSS HOSPITAL AND ROYAL LONDON OPHTHALMIC HOSPITAL. OUT-PATIENT PHYSICIAN, THE NATIONAL HOSPITAL FOR NERVOUS DISEASES, QUEEN SQUARE http://bjo.bmj.com/ IN earlier papers on this subject it has been suggested that certain apparently dissimilar abnormal pupillary reactions formerly described as occurring in unrelated conditions are manifestations of the same disorder. The abnormal reactions are, on the one hand, the tonic pupillary reaction (syn. pupillotonia, myotonic reaction, tonic convergence reaction of pupils apparently inactive to light, on September 30, 2021 by guest. Protected Marcus's peculiar pupil phenomenon, non-luetic Argyll Robertson pupil, pseudo-Argyll Robertson pupil) and, on the other hand what may be called atypical phases of the tonic pupil. In the atypical phases tonic reactions are absent or difficult to detect and the state of the pupil in cases that present them is usually desig- nated by the term fixed pupil, ophthalmoplegia interna, iridoplegia or partial iridoplegia, of unknown origin. The disorder referred to, if the views expressed here are correct, may manifest itself in the following clinical forms: A. The complete form characterized by the presence in one or both eyes of the tonic convergence reaction in a pupil apparently Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932.
  • May Clinical-Sharma (Pdf 143KB)

    May Clinical-Sharma (Pdf 143KB)

    CLINICAL New-onset ptosis initially diagnosed as conjunctivitis Neil Sharma, Ju-Lee Ooi, Rebecca Davie, Palvi Bhardwaj Case Question 2 divides into superior and inferior branches, Joe, 66 years of age, was referred with What are the causes of an isolated which enter the orbit through the superior a 2-week history of a right upper eyelid oculomotor nerve palsy? orbital fissure. abnormality. He complained of associated The superior division innervates diplopia initially, but this subjectively Question 3 the levator palpebrae superioris and improved after a few days as the eye What clinical features raise the index of superior rectus, while the inferior division became more difficult to open. He had a suspicion of a compressive lesion? mild, intermittent headache for 4 weeks, relieved with oral paracetamol. There Question 4 were no other neurological symptoms. What investigation does this patient He had no other symptoms of giant cell urgently require? arteritis. His past medical history included hypercholesterolaemia for which he was Case continued taking regular statin therapy. He was an Joe was referred for an urgent CT ex-smoker with a 40 pack-year history. angiogram. This showed a large Initially, Joe’s general practitioner (GP) unruptured posterior communicating diagnosed conjunctivitis and prescribed artery aneurysm (Figure 1). He was chloramphenicol drops four times daily. admitted under the neurosurgical team. One week later the symptoms had not improved and Joe was referred to the eye Question 5 Figure 1. 3-dimensional reconstruction image clinic complaining of increasing right What are the surgical options for dealing of the CT-angiogram showing an unruptured periocular pain.
  • Towards a Chromatic Pupillometry Protocol for Assessing Melanopsin-Driven Post-Illumination Pupil Response in Basic Science and Clinical Investigations

    Towards a Chromatic Pupillometry Protocol for Assessing Melanopsin-Driven Post-Illumination Pupil Response in Basic Science and Clinical Investigations

    TOWARDS A CHROMATIC PUPILLOMETRY PROTOCOL FOR ASSESSING MELANOPSIN-DRIVEN POST-ILLUMINATION PUPIL RESPONSE IN BASIC SCIENCE AND CLINICAL INVESTIGATIONS by Shaobo Lei A thesis submitted in conformity with the requirements for the degree of Master of Science Institute of Medical Science University of Toronto © Copyright by Shaobo Lei 2016 Towards a Chromatic Pupillometry Protocol for Assessing Melanopsin-Driven Post-Illumination Pupil Response in Basic Science and Clinical Investigations Shaobo Lei Master of Science Institute of Medical Science University of Toronto 2016 Abstract The pupillary light reflex (PLR) is mediated by intrinsically photosensitive retinal ganglions cells (ipRGCs), a sub-group of retinal ganglion cells that contain photopigment melanopsin. Melanopsin activation drives a sustained pupil constriction after the offset of light stimulus, this so-called post-illumination pupil response (PIPR) is an in vivo index of melanopsin-driven ipRGC photoactivity. PIPR can be assessed by chromatic pupillometry, but consensus on a standardized PIPR testing protocol has not been reached yet. The purpose of this thesis is to develop an optimized PIPR testing methodology, and to use it to investigate clinical and basic science questions related to melanopsin and ipRGCs. Based on previous pilot work on full-field chromatic pupillometry, a new and repeatable method was developed to measure PIPR induced by hemifield, central-field and full-field light stimulation. This chromatic pupillometry system was then used to investigate a series of basic science and clinical questions related to melanopsin and ipRGCs. ii Acknowledgments I would like to take this opportunity to express my gratitude to a number of people who have helped me to see through this thesis project.
  • CN Palsy Update for the Primary Care OD 2018

    CN Palsy Update for the Primary Care OD 2018

    CN Palsy Update for the Primary Care OD 2018 Christopher Wolfe, OD, FAAO, Dipl. ABO Oculomotor Nerve Palsy (CN 3) Signs and Symptoms The primary symptom is diplopia caused by misalignment of the visual axes, the pattern of image separation (horizontal, vertical, oblique) is the key to diagnosing which particular ocular motor cranial nerve (and extraocular muscle) is involved. With a complete unilateral third cranial nerve palsy, the involved eye is deviated "down and out" with partial or complete ptosis. • Pupillary dilatation (involvement) can cause: • Anisocoria (greater in the light) • Symptomatic glare in bright light • Blurred vision for near objects – due to accommodation deficit A painful pupil-involved oculomotor nerve palsy may result from a life-threatening intracranial aneurysm. Prompt diagnosis of an oculomotor nerve palsy is critical to ensure appropriate evaluation and management. Pathophysiology The clinical features of a CN 3 palsy are due to the anatomical relationship of the various branches of the oculomotor nerve and the location of the problem causing the palsy. These anatomical sites can be broken down into: • Nuclear portion: The axons start on each side of the midbrain. Each of the axon origination within the midbrain that travel to a specific extraocular and intraocular muscle can be further classified into a subnucleus. • Fascicular intraparenchymal midbrain portion: This portion of the oculomotor nerve travels courses ventrally (forward) from the nucleus, through the red nucleus, and emerges medially from the cerebral peduncle. • Subarachnoid portion: The nerve then travels in the subarachnoid space anterior to the midbrain and near the posterior communicating artery. An aneurysm at the INTRAOCULAR junction between the posterior communicating artery and INNERVATION the internal carotid artery is one of the critical reasons to differentiate a pupil involved CN 3 palsy.
  • Congenital Oculomotor Palsy: Associated Neurological and Ophthalmological Findings

    Congenital Oculomotor Palsy: Associated Neurological and Ophthalmological Findings

    CONGENITAL OCULOMOTOR PALSY: ASSOCIATED NEUROLOGICAL AND OPHTHALMOLOGICAL FINDINGS M. D. TSALOUMAS1 and H. E. WILLSHA W2 Birmingham SUMMARY In our group of patients we found a high incidence Congenital fourth and sixth nerve palsies are rarely of neurological abnormalities, in some cases asso­ associated with other evidence of neurological ahnor­ ciated with abnormal findings on CT scanning. mality, but there have been conflicting reports in the Aberrant regeneration, preferential fixation with literature on the associations of congenital third nerve the paretic eye, amblyopia of the non-involved eye palsy. In order to clarify the situation we report a series and asymmetric nystagmus have all been reported as 1 3 7 of 14 consecutive cases presenting to a paediatric associated ophthalmic findings. - , -9 However, we tertiary referral service over the last 12 years. In this describe for the first time a phenomenon of digital lid series of children, 5 had associated neurological elevation to allow fixation with the affected eye. Two abnormalities, lending support to the view that con­ children demonstrated this phenomenon and in each genital third nerve palsy is commonly a manifestation of case the accompanying neurological defect was widespread neurological damage. We also describe for profound. the first time a phenomenon of digital lid elevation to allow fixation with the affected eye. Two children demonstrated this phenomenon and in each case the PATIENTS AND METHODS accompanying neurological defect was profound. The Fourteen children (8 boys, 6 girls) with a diagnosis of frequency and severity of associated deficits is analysed, congenital oculomotor palsy presented to our paed­ and the mechanism of fixation with the affected eye is iatric tertiary referral centre over the 12 years from discussed.
  • Multiple Sclerosis Presenting As Isolated Oculomotor Nerve Palsy Ryan J

    Multiple Sclerosis Presenting As Isolated Oculomotor Nerve Palsy Ryan J

    THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Multiple Sclerosis Presenting as Isolated Oculomotor Nerve Palsy Ryan J. Uitti and A.H. Rajput ABSTRACT: A 23-year old woman came to the emergency room with an isolated oculomotor nerve palsy (including pupillary dilatation) of rapid onset. Investigations and history revealed no cause. The subsequent course of events indicated a diagnosis of multiple sclerosis. While the third nerve has been shown to be involved during the course of multiple sclerosis, this is the first report of a case presenting as an isolated oculomotor nerve paralysis. RESUME: La paralysie isolee du nerf moteur oculaire commun commc manifestation initiale de la sclerose en plaques. Une femme agee de 23 ans se presente a la salle d'urgence avec une paralysie isolee du nerf moteur oculaire commun (incluant une dilatation pupillaire) a debut brusque. L'investigation et l'histoire sont non contributives. L'eVolution subsequente de la maladie r6vele un diagnostic de sclerose en plaques. Meme s'il a ete demontre que le troisieme nerf cranien peut etre atteint a un moment ou l'autre de revolution de la sclerose en plaques, nous rapportons pour la premiere fois un cas dont la manifestation initiale de la maladie est une paralysie isolee du nerf moteur oculaire commun. Can. J. Neurol. Sci. 1986; 13:270-272 The onset of multiple sclerosis (MS) is monosymptomatic in gaze was possible. The right pupil was dilated and nonreactive to light approximately 45% of cases.1 When the disease presents as an and accomodation. Optic fundi were normal. A provisional diagnosis of posterior communicating aneurysm was made.
  • Pia, Ptosis, and Other Defects of Ocular Movement. Paradoxical

    Pia, Ptosis, and Other Defects of Ocular Movement. Paradoxical

    748 CLINICAL NEURO-OPHTHALMOLOGY gia, paralysis of vertical gaze, loss of convergence, exotro- EFFERENT ABNORMALITIES: ANISOCORIA pia, ptosis, and other defects of ocular movement. The presence of anisocoria usually indicates a structural defect of one or both irides or a neural defect of the efferent Paradoxical Reaction of the Pupils to Light and pupillomotor pathways innervating the iris muscles in one Darkness or both eyes. A careful slit-lamp examination to assess the health and integrity of the iris stroma and muscles is an Barricks et al. described three unrelated boys, 2, 6, and important step in the evaluation of anisocoria. If the irides 10 years of age, with congenital stationary night blindness, are intact, then an innervation problem is suspected. As most myopia, and abnormal electroretinograms, who showed a efferent disturbances causing anisocoria are unilateral, two ‘‘paradoxical’’ pupillary constriction in darkness (108). In simple maneuvers are helpful in determining whether it is a lighted room, all three patients had moderately dilated pu- the sympathetic or parasympathetic innervation to the eye pils; however, when the room lights were extinguished, the that is dysfunctional: (1) checking the pupillary light reflex patients’ pupils briskly constricted and then slowly redilated. and (2) measuring the anisocoria in darkness and in bright Subsequent investigators confirmed this observation and re- light. ported similar paradoxical pupillary responses in children When the larger pupil has an obviously impaired reaction and adults with congenital achromatopsia, blue-cone mono- to light stimulation, it is likely the cause of the anisocoria. chromatism, and Leber congenital amaurosis (109,110). In One can presume the problem lies somewhere along the addition, such responses occasionally occur in patients with parasympathetic pathway to the sphincter muscle.