1. Introduction.- 1.1. Anatomical Considerations.- 1.1.1. Course of the Facial Nerve in the Petrosal Bone.- 1.1.2. Composition and Fiber Spectrum of Facial Nerve.- 1.1.3. Intraneural Topography of Facial Nerve.- 1.2. Evaluation of Present Views on Etiology and Pathogenesis of Acute Facial Nerve Palsy.- 1.2.1. Idiopathic Facial Palsy (Bell's Palsy).- 1.2.2. Herpes Oticus with Concomitant Facial Palsy (Ramsey Hunt Syndrome).- 1.2.3. Bilateral Facial Palsies.- 2. Investigations, Part I: Intratemporal Stimulation of Facial Nerve for Localization of Conduction Block in Idiopathic Facial Palsy, Herpes Oticus, and Melkersson-Rosenthal Syndrome.- 2.1. Operative Access to the Internal Auditory Channel and Other Intrapetrosal Sections of the Facial Nerve.- 2.1.1. Intraoperative Stimulation and Recording Technique.- 2.1.2. Results of Intraoperative Stimulation of Facial Nerve in the Internal Acoustic Meatus and Facial Canal. Aspect of the Facial Nerve Under the Operative Microscope.- 2.2. Findings in Favor of a Revised Conception of the Relevant Pathogenetic Factors in Acute Facial Palsies.- 2.2.1. Histopathologic Findings in Idiopathic Facial Palsy.- 2.2.2. Histopathologic Findings in Herpes Oticus.- 2.2.3. Integration of Morphologic and Electrophysiologic Findings.- 3. Investigations, Part II: Electrophysiologic Investigations on the Natural History of Acute Facial Palsies.- 3.1. Electrodiagnosis of the Facial Nerve.- 1. General Considerations.- 2. Special Problems of Electrodiagnosis of the Facial Nerve.- 3. Electrodiagnostic Methods Hitherto Applied for Diagnosis in Facial Palsy.- 4. A New Method for the Determination of the Degree of Degeneration of Facial Nerve.- 3.2. Remarks on Some Clinical Features of Acute Facial Palsies.- 3.2.1. Implications of Topical Diagnosis.- 3.3. Case Reports.- 3.3.1. Discussion of the Graphical Presentation of Results.- 3.4. Results.- 3.4.1. Idiopathic Facial Palsy (Groups 1-9).- 3.4.2. General Principles that Emerge from the Histories of Idiopathic Facial Palsy.- 1. Nerve Fiber Degeneration.- 2. Conduction Block and the Beginning of its Recovery.- 3. Latency.- 4. Completion of Recovery from Conduction Block.- 5. Degree of Nerve Regeneration.- 6. Degree of Functional Recovery.- 7. Age.- 3.4.3. Herpes Oticus (Groups 1 and 2).- 3.4.4. Principles of Disease Evolution in Facial Palsy Associated with Herpes Oticus.- 3.4.5. Bilateral Facial Palsies: Case Reports.- 3.4.6. Bilateral Facial Palsies: Principles of Evolution.- 3.4.7. Acute Facial Palsies of Different Etiologies.- 3.4.8. Facial Palsies in Petrosal Bone Fractures.- 3.5. Prognosis of Acute Facial Palsies.- 3.6. Operation in Acute Facial Palsy: Transtemporal Decompression.- 3.6.1. Evolution of Operated Cases.- 3.7. Indications for Transtemporal Decompression of the Facial Nerve.- 3.8. On Drug Therapy of Idiopathic Facial Palsy.- Summary.- References.- Cases.- Author's Postscript.

Ocular myasthenia is a form of myasthenia gravis in which weakness is restricted to the ocular muscles and may produce significant visual disability. Patients present with fluctuating ptosis, diplopia, or a combination of both. Examination may show any type of ocular motility deficit ranging from isolated muscle palsy to complete ophthalmoplegia. Co-gan lid twitch, enhanced ptosis, peek sign, and saccadic fatigue are specific examination findings that support the clinical diagnosis of myasthenia gravis. Confirmation of the diagnosis is challenging with autoantibody serology, and repetitive nerve stimulation studies are often negative.

Research Articles| March 26 2010 Die okuläre Myasthenie Subject Area: Ophthalmology E. Esslen E. Esslen Neurologische Universitätsklinik, Kantonsspital (Dir.: Prof. G. Baumgartner), Zürich Search for other works by this author on: This Site PubMed Google Scholar Ophthalmologica (1973) 167 (4): 350–354. https://doi.org/10.1159/000306949 Article history Published Online: March 26 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation E. Esslen; Die okuläre Myasthenie. Ophthalmologica 1 April 1973; 167 (4): 350–354. https://doi.org/10.1159/000306949 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsOphthalmologica Search Advanced Search This content is only available via PDF. 1973Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. Article PDF first page preview Close Modal You do not currently have access to this content.

Forty patients with facial hyperkinesia (hemi-facial spasm and blepharospasm) were treated by selective extratemporal excision of facial nerve branches. Intraoperative bipolar faradic stimulation was used to detect the nerve branches which were particularly involved in the production of the spasm. Silver clips have been applied over the coagulated end of the proximal nerve stumps following section in order to avoid regeneration and to facilitate their radiologic identification if, in case of recurrence, subsequent chemical blocking of regenerated fibers should be necessary. The surgical follow-up results revealed that 80% of the patients with hemifacial spasm were still relieved from their disturbance at the end of the third postoperative year. A high rate of recurrence developed however in the group of patients with blepharospasm, leaving only 17% of the patients in a satisfactory condition three years following the operation.

In 11 of 12 patients submitted to total intratemporal surgical exposure of the seventh nerve because of idiopathic facial paralysis, morphological changes were observed proximally to the geniculate ganglion in the beginning of the fallopian canal and in the internal auditory meatus. The presence of pathology proximally to the geniculate ganglion in cases of Bell's palsy has been supported by the intra-operative electric stimulation of the exposed facial nerve in cases presenting at surgery with neuropraxia as well as by the preoperative iophendylate (Pantopaque) cisternography and the results of the lacrimal test. More material has to be collected in order to substantiate the preliminary findings. The accumulated evidence indicates, however, that the most critical part of the intratemporal course of the seventh nerve in Bell's palsy is situated proximally to the geniculate ganglion rather than towards the stylomastoid foramen.

Research Articles| March 30 2010 Internukleäre Ophthalmoplegie Subject Area: Ophthalmology A. Huber; A. Huber Universitäts-Augenklinik Zürich (Direktor: Prof. Dr. R. Witmer) und Neurologische Universitäts-Klinik (Direktor: Prof. Dr. G. Baumgartner) Search for other works by this author on: This Site PubMed Google Scholar E. Esslen E. Esslen Universitäts-Augenklinik Zürich (Direktor: Prof. Dr. R. Witmer) und Neurologische Universitäts-Klinik (Direktor: Prof. Dr. G. Baumgartner) Search for other works by this author on: This Site PubMed Google Scholar Ophthalmologica (1972) 165 (3-4): 320–326. https://doi.org/10.1159/000308515 Article history Published Online: March 30 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation A. Huber, E. Esslen; Internukleäre Ophthalmoplegie. Ophthalmologica 31 December 1972; 165 (3-4): 320–326. https://doi.org/10.1159/000308515 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsOphthalmologica Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1972Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.

Im Rahmen des Duane-Syndromes lassen sich als klinisch unterscheidbar 3 Typen herausdifferenzieren,Duane I mit vorwiegender Abduktionsbehinderung,Duane II mit vorwiegender Adduktionsbehinderung undDuane III mit Ab- und Adduktionsbehinderung, wobei allen Typen die mehr oder weniger ausgesprochene Lidspaltenverengerung und Retraktion des Bulbus beim Versuch zur Adduktion des befallenen Auges gemeinsam ist. Auf Grund elektromyographischer Untersuchungen steht heute fest, daß den Duane-Syndromen als pathogenetisches Prinzip eine paradoxe Innervation des Reclus externus des befallenen Auges zugrunde liegt. Für die Deutung dieser paradoxen Innervation wird die Möglichkeit einer abnormen Versorgung des Rectus externus mit Zweigen des Oculomotorius allein (Duane III) oder eine Doppelversorgung sowohl durch Zweige des Abducens und des Oculomotorius (Duane II, Duane I) diskutiert. Diesbezügliche anatomische Befunde sind beschrieben, jedoch bis heute noch nicht in Korrelation mit dem klinischen Befund eines Duane-Syndromes gebracht worden.