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Third Nerve Palsy: Analysis of 1400 Personally-examined Inpatients

Published online by Cambridge University Press:  02 December 2014

James R. Keane
James R. Keane*
Affiliation:
University of Southern California Medical School, Los Angeles, California, USA
*
6281 Vine Way, Los Angeles, California, 90068, USA.
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Abstract

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Background:

Most studies of third nerve palsy (TNP) antedate computerized imaging and focus primarily on chart review of referral outpatients.

Methods:

To compare a large contrasting population, I reviewed 1400 personally-examined municipal hospital inpatients with TNPs seen over 37 years.

Results:

TNPs were bilateral in 11%, complete in 33%, without other neurological signs (isolated) in 36%, and associated with recurrent cranial neuropathies in 7%. Third nerve damage occurred in the subarachnoid space in 32%, the cavernous sinus in 23%, the brainstem in 14%, as a nonlocalized peripheral neuropathy in 18% and at an uncertain location in 13%. Causes were trauma (26%), tumor (12%), diabetes (11%), aneurysm (10%), surgery (10%), stroke (8%), infection (5%), Guillain-Barre and Fisher syndromes (5%), idiopathic cavernous sinusitis (3%), benign self-limited (2%), miscellaneous (4%), and unknown (3%). Local causes, besides an abundance of trauma, included six cases involving cysticercosis, four with wound botulism, and one with coccidiomycotic meningitis. Of 234 patients with diabetes, microvascular ischemia was the cause of TNP in only two-thirds (five had aneurysms) and 53% of those with diabetic microvascular ischemia had pupillary involvement—often bilateral, suggesting concomitant autonomic neuropathy. Only 2% of aneurysms spared the pupil. Apainful onset occurred with 94% of aneurysm and 69% of diabetic cases.

Conclusions:

Bilateral TNPs, multiple cranial neuropathies, and accompanying neurological signs were common among our inpatients, as were causes rare in outpatient settings such as severe trauma, transtentorial herniation, midbrain strokes, and the Guillain-Barre syndrome. Few cases remained undiagnosed and nondiabetic ischemia was rare.

Résumé:

RÉSUMÉ:Contexte:

La plupart des etudes sur la paralysie du troisième nerf (PTN) sont antérieures à la tomodensitométrie et sont constituées principalement de revues de dossiers de patients externes.

Méthodes:

Afin d’examiner un volet différent de la PTN, j’ai révisé 1400 dossiers de patients atteints d’une PTN, hospitalisés dans un hospital municipal, que j’ai moi–même examinés au cours d’une période de 37 ans.

Résultats:

La PTN était bilatérale chez 11% des patients, complète chez 33%, sans autre signe neurologique (isolée) chez 36% et associée à des neuropathies crâniennes récurrentes chez 7%. La lésion du troisième nerf était située dans l’espace sous–arachnoïdien chez 32%, dans le sinus caverneux chez 23%, dans le tronc cérébral chez 14%, comme une neuropathie périphérique non localisée chez 18% et à un endroit indéterminé chez 13%. Les causes étaient un traumatisme chez 26%, une tumeur chez 12%, un diabète chez 11%, un anévrisme chez 10%, une chirurgie chez 10%, un accident vasculaire cérébral chez 8%, une infection chez 5%, un syndrome de Guillain–Barré ou de Fisher chez 5%, une sinusite caverneuse idiopathique chez 3%, une cause autolimitée bénigne chez 2%, des causes variées chez 4% et des causes inconnues chez 3%. Les causes locales, excluant les nombreux cas de traumatisme, comprenaient 6 cas de cysticercose, 4 de botulisme relié à une plaie et 1 cas de méningite à coccidiomycose. L’ischémie microvasculaire était la cause de la PTN chez seulement les deux tiers des 234 patients diabétiques dont 5 étaient porteurs d’anévrismes et 53% avaient une atteinte pupillaire, souvent bilatérale, ce qui est compatible avec la presence d’une neuropathie autonomique. La pupille n’était pas atteinte chez seulement 2% des patients porteurs d’anévrismes. Le début avait été douloureux chez 94% des patients porteurs d’anévrismes et 69% des diabétiques.

Conclusions:

La PTN bilatérale, les neuropathies crâniennes multiples et les signes neurologiques associés sont fréquents chez nos patients hospitalisés, de même que les étiologies qui sont rares chez les patients externes comme les traumatismes sévères, la hernie transtentorielle, les accidents vasculaires cérébraux et le syndrome de Guillain–Barré. Un diagnostic n’a pu être pose dans un très petit nombre de cas et l’ischémie non diabétique était rare.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 37 , Issue 5 , September 2010 , pp. 662 - 670
Copyright
Copyright © The Canadian Journal of Neurological 2010

References

1. Rucker, CW. Paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol. 1958;46:787–94.Google Scholar
2. Rucker, CW. The causes of paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol. 1966;61:1293–8.CrossRefGoogle ScholarPubMed
3. Rush, JA, Younge, BR. Paralysis of cranial nerves III, IV, and VI: cause and prognosis in 1000 cases. Arch Ophthalmol. 1981;99: 76–9.CrossRefGoogle Scholar
4. Richards, BW, Jones, FR Jr, Younge, BR. Causes and prognosis in 4278 cases of paralysis of the oculomotor, trochlear, and abducens cranial nerves. Am J Ophthalmol. 1992;113:489–96.CrossRefGoogle Scholar
5. Goldstein, JE, Cogan, DG. Diabetic ophthalmoplegia with special reference to the pupil. Arch Ophthalmol. 1960;64:592–600.CrossRefGoogle Scholar
6. Green, WR, Hackett, ER, Schlezinger, NS. Neuro-ophthalmologic evaluation of oculomotor nerve paralysis. Arch Ophthalmol. 1964;72:154–67.CrossRefGoogle ScholarPubMed
7. Cheek, CW, Simon, KA, Gay, AJ. Acquired cranial nerve lesions affecting the ocular system. Am J Ophthalmol. 1965;59:13–7.CrossRefGoogle ScholarPubMed
8. van Laere, E. La paralysie non traumatique du nerf oculomoteur commun. Apropos de 109 observations. Acta Neurol Belg. 1974; 74:182–92.Google Scholar
9. Teuscher, AU, Meienberg, O. Ischaemic oculomotor nerve palsy; clinical features and vascular risk factors in 23 patients. J Neurol. 1985;232:144–9.CrossRefGoogle ScholarPubMed
10. Kwan, ESK, Laucella, M, Hedges, TR jr, et al. A cliniconeuroradiologic approach to third cranial nerve palsies. AJNR Am J Neuroradiol. 1987;8: 459–68.Google ScholarPubMed
11. Berlit, P. Isolated and combined pareses of cranial nerves III, IV, and VI. A retrospective study of 412 patients. J Neurol Sci. 1991; 103:10–5.CrossRefGoogle Scholar
12. Wallace, SP, Mendez-Luck, C, Castafieda, X. Heading south: why Mexican immigrants in California seek health services in Mexico. Med Care. 2009:47:662–9.CrossRefGoogle ScholarPubMed
13. Keane, JR. Rhythmic pupillary oscillations accompanying a complete third nerve palsy. J Clin Neuro-ophthalmol. 1989;9: 169–70.Google ScholarPubMed
14. Keane, JR. Third nerve palsy due to penetrating trauma. Neurology. 1993:43:1523–7.Google Scholar
15. Keane, JR, Ahmadi, J. Most diabetic third nerve palsies are peripheral. Neurology. 1998;51;1510.Google Scholar
16. Keane, JR. Isolated brain stem third nerve palsy. Arch Neurol. 1988; 45:813–4.CrossRefGoogle ScholarPubMed
17. Keane, JR. Aneurysmal third nerve palsy presenting with pleocytosis. Neurology. 1996:46:1176.CrossRefGoogle ScholarPubMed
18. Rucker, CW. History of the numbering of the cranial nerves. Mayo Clin Proc. 1966;41:453–61.Google ScholarPubMed
19. Gowers, W. Diseases of the nervous system. Philadelphia: JB Lippincott Co; 1888. p. 612–16.Google Scholar
20. Duane, A. The extra-ocular muscles. In: Posey, WM, Spiller, WG, editors. The eye and the nervous system. Philadelphia: JB Lippincott Co; 1906. p. 222–41.Google Scholar
21. Keane, JR. Bilateral involvement of a single cranial nerve. Analysis of 578 cases. Neurology. 2005;65:950–2.Google ScholarPubMed
22. Keane, JR. Multiple cranial nerve palsies: analysis of 979 cases. Arch Neurol. 2005;62:1714–17.Google Scholar
23. Williams, HW. The diagnosis and treatment of diseases of the eye. Boston: Houghton, Mifflin & Co; 1881. p. 310.Google Scholar
24. Keane, JR. Ptosis and levator palsy caused by orbital roof fractures: three cases with subfrontal epidural hematomas. J Clin Neuroophthalmol. 1993;13:225–8.Google Scholar
25. Lam, BL, Thompson, HS, Corbett, JJ. The prevalence of simple anisocoria. Am J Ophthalmol. 187;104:69–73.CrossRefGoogle Scholar
26. Trobe, JD. Glaser JS, Post JD. Meningiomas and aneurysms of the cavernous sinus: neuro-ophthalmologic features. Arch Ophthalmol. 1978;96:457–67.Google Scholar
27. Keane, JR. Aneurysms and third nerve palsies. Ann Neurol. 1983; 14;696–7.CrossRefGoogle ScholarPubMed
28. Keane, JR. Intermittent third nerve palsy with cryptococcal meningitis. J Clin Neuroophthalmol. 1993;13:124–6.Google ScholarPubMed
29. Keane, JR. Functional diseases affecting the cranial nerves. In: Noseworthy, J, editor. Neurological therapeutics: principles and practice. 2nd ed. London: Martin Dunitz; 2006. p. 2202.Google Scholar
30. Keane, JR. Cavernous sinus syndrome: analysis of 151 cases. Arch Neurol. 1996;53:967–71.Google Scholar
31. Keane, JR. Third nerve palsies and angiography. Arch Neurol.1991; 48:470.CrossRefGoogle ScholarPubMed