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Ein- und zweizeitige Sehnervenläsionen im Tiermodell und dessen klinischer Stellenwert

Single and temporally displaced second nerve lesions in an animal model and their clinical significance

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Zusammenfassung

Hintergrund

Die Indikation zur chirurgischen Optikusdekompression nach Trauma gilt als umstritten. Das chirurgische Trauma soll eine zusätzliche Nervenläsion erzeugen mit der Gefahr eines kompletten Visusverlusts. Alternativ wird eine konservative Hochdosis-Kortisontherapie empfohlen.

Methoden

In einem etablierten Tiermodell mit 29 Wistar-Ratten werden die funktionellen und morphologischen Läsionsfolgen einer kalibrierten ein- und zweizeitigen Optikuskompression untersucht.

Ergebnisse

In Abhängigkeit von der gewählten Läsionszeit und -stärke wurde eine lineare Abnahme der Neuronenzahl in der RGC- (Retinal-ganglion-cell-)Schicht sowie eine zunehmende Reaktivität für GFAP („glial fibrillary acidic protein“) als Zeichen einer zentralen Gliose der Astrozyten beobachtet, jedoch unabhängig davon, ob eine ein- oder zweizeitige Läsion vorlag.

Schlussfolgerungen

Die Indikation zur operativen Entlastung eines afferenzgeschädigten Auges sollte – insbesondere bei der geringen Morbidität des rhinochirurgischen Zugangswegs – großzügiger gestellt werden, um sekundäre Sehnervenschäden und Folgeschäden im zentralen visuellen System zu reduzieren, die mit dem Andauern der Läsion zunehmen können.

Abstract

Background

Surgical optic decompression after trauma has been discussed controversially. The surgical trauma is supposed to produce an additional nerve lesion with the danger of complete loss of vision. Alternatively, conservative high dose cortisone therapy has been recommended.

Methods

The functional and morphological consequences of a lesion after calibrated optic compression in one or two sessions were examined in an animal model using 29 Wistar rats.

Results

Depending on the duration and intensity of the lesion, we observed a linear decline in the number of neurons in the RGC (retinal ganglion cell) layer as well as an increasing reactivity to GFAP (glial fibrillary acidic protein) as an indication of central gliosis of astrocytes; however, this was independent on whether optic compression was performed in one or two sessions.

Conclusions

To reduce secondary damage to the visual nerve and the central visual system that might increase with a persisting lesion, the indication for surgical relief of an eye affected by afference should be considered liberally, especially in view of the low morbidity of rhinosurgical intervention.

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Literatur

  1. Anand VK, Sherwood C, Al-Mefty O (1991) Optic nerve decompression via transethmoid and supraorbital approaches. Operative techniques in otolaryngology. Head Neck Surg 2: 157–166

    Google Scholar 

  2. Berlis A, Putz R, Schumacher M (1992) Direct and CT measurements of canals and foramina of the skull base. Br J Radiology 65: 653–661

    Google Scholar 

  3. Brihaye J (1981) Transcranial decompression of optic nerve after trauma. In: Samii M, Janetta PJ (eds) The cranial nerves. Springer, New York, pp 116–124

  4. Busse H, Stoll W, Kroll P (1988) Dekompression des N. opticus. Klin Monatsbl Augenheilkd 193: 112

    Google Scholar 

  5. Gellrich NC, Gellrich MM, Bremerich A (1994) Influence of fetal brain grafts on axotomized retinal ganglion cells. Int J Oral Maxillofac Surg 23: 404–405

    Article  Google Scholar 

  6. Gellrich NC, Schimming R, Zerfowski M, Eysel UT (2002) Quantification of histological changes after calibrated crush of the intraorbital optic nerve in rats. Br J Ophthalmol 86: 233–237

    Article  PubMed  Google Scholar 

  7. Gossmann MD, Roberts DM, Barr CC (1992) Ophthalmic aspects of orbital injury – a comprehensive diagnostic and management approach. Clin Plastic Surg 19: 71–85

    Google Scholar 

  8. Hager G, Gerhardt HJ, Maruniak M (1975) Indikationen und Ergebnisse operativer Freilegung traumatisch geschädigter Sehnerven. Klin Monatsbl Augenheilkd 167: 515–526

    PubMed  Google Scholar 

  9. Holländer H, Bisti S, Maffei L, Hebel R (1984) Electroretinographic responses and retrograde changes after intracranial optic nerve section – a quantitative analysis in the cat. Exp Brain Res 55: 483–493

    PubMed  Google Scholar 

  10. Jiang RS, Hsu CY, Shen BH (2001) Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy. Rhinol 39 (2): 71–74

    Google Scholar 

  11. Jorissen M, Feenstra L (1992) Optic nerve decompression for indirect posterior optic nerve trauma. Acta Otolaryngol Belg 46: 311–324

    Google Scholar 

  12. Kennerdell JS, Amsbaugh GA, Meyers EN (1976) Transantral-ethmoidal decompression of optic canal fracture. Arch Ophthalmol 94: 1040–1043

    PubMed  Google Scholar 

  13. Kline LB, Morawetz RB, Swaid SN (1984) Indirect injury of the optic nerve. Neurosurgery 14: 756–764

    PubMed  Google Scholar 

  14. Klopfer J, Tielsch JM, Vitale S, See LC, Canner JK (1992) Ocular trauma in the United States. Arch Ophthalmol 110: 838–842

    PubMed  Google Scholar 

  15. Lang J (1981) Optic nerve, topographic anatomy. In: Samii M, Janetta PJ (eds) The cranial nerves. Springer, New York, pp 77–84

  16. Lang J (1988) Über die Cellulae ethmoidales posteriores und ihre Beziehungen zum Canalis opticus. HNO 36: 49–53

    PubMed  Google Scholar 

  17. Lentrodt J, Unsöld R, Bosche J (1991) Amaurose nach operativer Versorgung von Orbitabodenfrakturen — eine unvorhersehbare Komplikation? Fortschr Kiefer Gesichtschir 36: 150–151

    PubMed  Google Scholar 

  18. Lessel S (1991) Traumatic optic neuropathy and visual system injury. In: Shingleton, Hersch, Kenyon (eds) Eye trauma. Mosby Year Book, St. Louis, pp 371–379

  19. Lindenberg R, Walsh FB (1964) Vascular compressions involving intracranial pathways. Trans Am Acad Ophthalmol Otolaryngol 68: 679–694

    Google Scholar 

  20. Lipkin AF, Woodson GE, Miller RH (1987) Visual loss due to orbital fracture. Arch Otolaryngol Head Neck Surg 113: 81–83

    PubMed  Google Scholar 

  21. Lübben B, Stoll W, Grenzebach U (2001) Optic nerve decompression in the comatose and conscious patients after trauma. Laryngoscope 111 (2): 320–328

    PubMed  Google Scholar 

  22. Maniscalco JE, Habal MB (1971) Microanatomy of the optic canal. J Neurosurg 48: 402–406

    Google Scholar 

  23. Niho S, Murakami I, Sugita S, Sugita Y, Kawabe Y (1966) Decompression of the optic canal by the transethmoidal route. Acta Soc Ophthalmol Jpn 70: 343–351

    Google Scholar 

  24. Niho S, Niho M, Niho K (1970) Decompression of the optic canal by the transethmoidal route and decompression of the superior orbital fissure. Can J Ophthalmol 5: 22–40

    PubMed  Google Scholar 

  25. Niho M (1991) Rhinologic approach to optic nerve decompression. Otolaryngol Head Neck Surg 2: 167–172

    Google Scholar 

  26. Osguthorpe JD, Sofferman RA (1988) Optic nerve decompression. Otolaryngol Clin North Am 21: 155–169

    PubMed  Google Scholar 

  27. Panje WR, Gross CE, Anderson RL (1981) Sudden blindness following facial trauma. Otolaryngol Head Neck Surg 89: 941–948

    PubMed  Google Scholar 

  28. Perry VH (1981) Evidence for an amacrine cell system in the ganglion cell layer of the rat retina. Neurosci 6: 931–944

    Article  Google Scholar 

  29. Pringle JH (1922) Atrophy of the optic nerve following diffused violence of the skull. Br Med J 2: 1156–1157

    Google Scholar 

  30. Raveh J, Vuillemint H (1988) The surgical one-stage management of combined cranio-maxillo-facial and frontobasal fractures. J Craniomaxillofac Surg 16: 350–358

    PubMed  Google Scholar 

  31. Scheschy H, Benedikt O (1972) Optikusatrophie durch indirekte Traumen. Klin Monatsbl Augenheilkd 161: 309–315

    PubMed  Google Scholar 

  32. Sellebjerg F, Nielsen HS, Frederiksen JL, Olesen J (1999) A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology 22; 52 (7): 1479–1484

    Google Scholar 

  33. Sewall EC (1926) External operation on the ethnosphenoid-frontal group of sinuses under local anesthesia. Arch Otolaryngol 4: 401–411

    Google Scholar 

  34. Sewall EC (1928) Further development of the transsphenoid approach to the optic foramen. Ann Otol Rhinol Laryngol 37: 839–849

    Google Scholar 

  35. Sofferman RA (1991) Transnasal approach to optic nerve decompression. Operat Techn Otolaryngol Head Neck Surg 2: 150–156

    Google Scholar 

  36. Sofferman RA, Burlington VT (1981) Sphenoethmoid approach to the optic nerve. Laryngoscope 91: 184–196

    PubMed  Google Scholar 

  37. Spoor TC, Hartel WC, Lensink DB, Wilkinson MJ (1990) Treatment of traumatic optic neuropathy with corticosteroids. Am J Ophthalmol 110: 665–669

    PubMed  Google Scholar 

  38. Stanley JA, Baise GR (1968) The swinging flash light test to detect minimal optic neuropathy. Arch Ophthalmol 80: 769–771

    PubMed  Google Scholar 

  39. Thakar A, Mahapatra AK, Tandon DA (2003) Delayed optic nerve decompression for indirect optic nerve injury. Laryngoscope 113(1): 112–119

    Article  PubMed  Google Scholar 

  40. Wolin MJ, Lavin PJM (1990) Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am J Ophthalmol 109: 430–435

    PubMed  Google Scholar 

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Authors and Affiliations

  1. Klinik für Mund-, Kiefer- und Gesichtschirurgie, Medizinische Hochschule Hannover

    N.-C. Gellrich

  2. Chirurgische Klinik, Augusta-Kranken-Anstalt gGmbH Bochum

    J. Kankam

  3. Universitätsklinik für Hals-, Nasen- und Ohrenheilkunde und Poliklinik, Universitätsklinikum Freiburg

    W. Maier, A. Aschendorff & T. Klenzner

  4. Universitätsklinik für Hals-, Nasen- und Ohrenheilkunde und Poliklinik, Universitätsklinikum, Killianstraße 5, 79106, Freiburg

    J. Schipper

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  1. N.-C. Gellrich
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  2. J. Kankam
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  3. W. Maier
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  4. A. Aschendorff
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  5. T. Klenzner
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  6. J. Schipper
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Correspondence to J. Schipper.

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Gellrich, NC., Kankam, J., Maier, W. et al. Ein- und zweizeitige Sehnervenläsionen im Tiermodell und dessen klinischer Stellenwert. HNO 54, 761–767 (2006). https://doi.org/10.1007/s00106-006-1387-6

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  • DOI: https://doi.org/10.1007/s00106-006-1387-6

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