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Year : 2006  |  Volume : 54  |  Issue : 3  |  Page : 173-175

Ocular motor nerve palsy: A clinical and etiological study

1 Kinshasa University Hospital, Kinshasa, Democratic Republic of Congo, USA
2 Saint Joseph Hospital, Kinshasa, Democratic Republic of Congo, USA

Correspondence Address:
Jean-Claude Mwanza
200 Glen Falls Lane, #205, Durham, NC 27713
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0301-4738.27068

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Purpose: To clinically describe cases of ocular motor nerve palsy and to determine the possible causes.
Materials and Methods:
Thirty-one consecutive patients with ocular motor nerve palsies were investigated. All underwent complete ophthalmological, as well as neurological, otorhinolaryngological and general examination. Computerised tomography (CT)-scan of the brain and complementary laboratory tests were obtained from each participant.
Paralysis of the sixth (38.4%) and the third (35.3%) cranial nerve were the most common. The Lees screen test was found to be very sensitive, confirming the diagnosis of ocular motor nerve palsy, even in cases with minimal manifestations. Complete ptosis and full mydriasis were mostly seen in isolated cases of the third cranial nerve palsy. The majority of eyes (63.2%) with third cranial nerve palsy had pupil sparing. Overall, an etiological diagnosis was made in 93.5% of cases. The common causes were vascular conditions (25.8%), otorhinolaryngologic diseases (19.7%) and trauma (12.9%). CT scan failed to reveal any abnormality in 54.8% of cases.
Patients with ocular motor nerve palsy should be carefully examined in close collaboration with other specialists, especially where sophisticated, complementary investigations are impossible.

Keywords: Etiology, ocular motor nerve palsy.

How to cite this article:
Mwanza JC, Ngweme GB, Kayembe DL. Ocular motor nerve palsy: A clinical and etiological study. Indian J Ophthalmol 2006;54:173-5

How to cite this URL:
Mwanza JC, Ngweme GB, Kayembe DL. Ocular motor nerve palsy: A clinical and etiological study. Indian J Ophthalmol [serial online] 2006 [cited 2023 Feb 8];54:173-5. Available from: https://www.ijo.in/text.asp?2006/54/3/173/27068

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Ocular motor nerve palsies (OMNPs) are commonly encountered in clinical practice and usually express an underlying local, regional or general disease. They may be unilateral or bilateral, may involve one or several nerves at the same time and may be obvious or sub clinical. In order to find out the etiology, it is important to carry out a detailed anamnesis, a careful clinical examination, as well as complementary investigations. No cause is found often, despite a battery of investigations.[1] To increase the chance of identifying the causes of OMNPs, a close collaboration between different specialists has been recommended.[1] This approach is widely used in industrialized countries, whereas in the developing world, particularly in sub-Saharan countries, such a policy is still difficult because of technical and financial problems. This short paper presents the results of the clinical and etiological aspects of OMNPs after using such a collaborative approach.

  Materials and Methods Top

Thirty-three consecutive patients with OMNP were enrolled and examined at the Department of Ophthalmology (DO), Kinshasa University Hospital (KUH), from January 1999 to January 2000. The inclusion criteria were: 1) presentation to the DO, KUH during the enrolment period with a recent OMNP (within 2 weeks of onset), 2) acceptance to undergo additional investigations whenever needed and 3) informed verbal consent. Because 2 patients missed examination by other specialists, only 31 were retained and evaluated. There were 17 men and 14 women, with a mean age of 41±14 years (range 10-57 years). Most of them (61.2%) were above 40 years of age.

An arrangement was made with the departments of otorhinolaryngology, internal medicine and neurology for their collaboration. They were especially asked to perform the investigations needed, free of charge. In case of difference of opinion, a meeting was held amongst the ophthalmologists and other investigators, in order to arrive at a consensus.

Each patient underwent a complete ophthalmologic evaluation, including a detailed anamnesis. The anamnesis also focused on risk factors in past and/or current ocular and general medical history and current or past medications. The visual acuity was measured using conventional methods. Pupils were checked for size, shape and light reflexes. The pupil was regarded as normal when its diameter was 4-5.5 mm. Miosis and mydriasis were considered when the diameter was less than 4 mm and greater than 7 mm, respectively. Mydriasis was further classified into mild (6-7 mm) and full (>7 mm). The upper lids were evaluated for ptosis by measuring the distance between the upper and lower margins using a transparent graduated rule, the Congolese reference values being 9±1.4 mm.[2] Ptosis was further classified into mild (4-8 mm), moderate (2-4 mm) and complete (<2 mm). Ocular motility was evaluated in all nine directions of gaze by means of a Lees-Lancaster screen, while ocular deviation and strabismus were assessed with the cover-uncover test. The red glass was used to investigate the diplopia.

In addition, all patients underwent neurological, cardio-vascular, endocrinologic and otorhinolaryngologic examinations and CT scanning. Whenever indicated, other clinical examinations such as odontological examinations were also done. Blood samples were taken from all patients for erythrocyte sedimentation rate, complete blood count, glycemia, VDRL and HIV antibodies. Other tests were done, if indicated on clinical grounds. The HIV-related palsy was considered in HIV-positive subjects, without any other pathology attributable to induce OMNPs. Cases of congenital OMNPs were not included in the study. Issues regarding the site of the lesion were not part of this study.

  Results Top

Symptoms as reported by the patients at presentation were as follows: visual impairment (4 patients =12.9%), ptosis (7 patients = 22.5%), diplopia (11 patients = 35.4%) and ocular deviation (29 patients = 93.5%).

The clinical examination did not reveal any case of visual impairment. Ptosis was observed in 13 patients (41.9%), among whom 6 had mild, 1 - moderate and 6 - complete ptosis. Complete ptosis was mostly seen in isolated cases of the third cranial nerve palsy [Table - 1]. Diplopia was objectively observed in all 11 patients who reported it at presentation and the Lees screen testing was abnormal in all patients.

The frequency distribution of different forms of OMNPs is displayed in the [Table - 1]. Isolated OMNPs were seen in 23 patients (74.1%), the sixth and the third cranial nerve being affected in 38.7% (12 patients) and 35.4% (11 patients), respectively.

Of 19 eyes with third cranial nerve palsy, among which 11 had isolated palsy, 7 (36.8%) had mydriasis, while the remainder had pupil sparing. In addition, full mydriasis was found to be more frequently associated with isolated third nerve palsy cases [Table - 1].

Overall, an etiological diagnosis could be made in 29 patients (93.5%) [Table - 1]. The common causes were vascular (25.8% = 8 patients), otorhinolaryngologic diseases (19.7% = 6 patients) and cranio-facial trauma (12.9% = 4 patients). Vascular diseases consisted of cerebro-vascular stroke as a complication of systemic arterial hypertension in all 8 patients. Otorhinolaryngologic conditions causing OMNPs were sinusitis (4 patients), sinus malignant tumor (1 patient) and complication of surgery in another single patient.

  Discussion Top

The etiology of OMNPs remains unknown in more than 25% of cases.[3],[4] It is however worth stressing that in the recent past, there has been a marked progress in investigative procedures, mainly in the field of imaging. This has helped increase the chances of arriving at an etiological diagnosis in cases of OMNP, in developed countries.[5] In the absence of advanced techniques such as magnetic resonance imaging, our protocol based on a tight multidisciplinary collaboration, has allowed us to determine the origin of the OMNP in most cases. Unlike many other studies, head trauma-related OMNPs were not excluded from this series of patients, which has substantially contributed to the proportion of causes found. We are aware of the small number of patents investigated in the present study; however, such a limitation may be counterbalanced by the advantage provided by the methodological approach.

In accordance with several previous reports,[6],[7] isolated cases of OMNP were more frequent. This study also showed that diplopia, which is an extremely disturbing phenomenon, remains the most common symptom.[8] Unlike some previous reports in which the frequency of diplopia was greater than 60%,[9],[10] this symptom was found in 35.4%, in the present study. This gap may be explained by the difference of the methodology applied. Indeed, instead of confirming it, other investigators have simply considered it as a subjective manifestation.

Paralysis of the sixth cranial nerve is recognized as the most common type, in most of the series throughout the literature,[4],[11] even though in some series, the third cranial nerve was the most affected.[6],[7] The low frequency of the fourth cranial nerve involvement may be due to the fact that congenital cases were excluded. Indeed, palsy of the fourth cranial nerve is mostly found to be congenital.[12],[13],[14]

Ptosis, in connection with third cranial nerve palsy may be of different degrees, as shown in the present study. All patients with mild ptosis were not aware of the abnormality. Moreover, this type of ptosis was not very obvious clinically, until objectively measured. Should any doubt arise on the presence or absence of ptosis in case of third cranial nerve palsy, we suggest that objective measurements be done.

In HIV-infected subjects, OMNPs may be due to a number of conditions, mainly opportunistic infections and intra-cranial tumors. Beside, HIV itself has been identified as an etiologic agent of OMNP, either by its direct effect on the nerves or by indirect immune mechanisms. The 3 HIV-positive patients did not show any obvious cause of OMNP.

The fact that CT-scan imaging failed to reveal any anomaly in 17 patients (54.8%), was not surprising. To date, it is well known that the resolution power and subsequently, the probability of disclosing lesions are lower with CT scan than with MRI. In addition, most cases were due to vascular and inflammatory causes, which are known to be hardly recognizable on CT-scan images.

In conclusion, we recommend that patients with OMNP be carefully clinically examined in close collaboration with other specialists, especially where sophisticated complementary investigations are impossible.

  Acknowledgments Top

The authors are very grateful to Drs. Kabasele P and Kilangalanga J (Department of Ophthalmology) for their constructive comments and advises throughout the execution of the study. We are deeply indebted to Drs. Lombe L (Department of Neurology), Lelo T (Department of Radiology) and Matanda M (Department of Otorhinolaryngology) for their close co-operation.

  References Top

Kerty E, Bakke SJ. Neurological imaging of the 3rd 4th and 6th cranial nerves. Tidssk Nor Laegeforen 2001;121:1366-8.  Back to cited text no. 1
Kaimbo KD. Mensurations palpιbrales chez les sujets congolais. J Fr Ophtalmol 1995;18:286-91.  Back to cited text no. 2
Richards BW, Jones FR, Younge BR. Causes and prognosis in 4278 cases of the oculomotor, trochlear and abducens cranial nerves. Am J Ophthalmol 1992;113:489-96.  Back to cited text no. 3
Rush JA, Younge BR. Paralysis of the cranial nerves III, IV and VI. Cause and prognosis in 1000 cases. Arch Ophthalmol 1981;99:76-9.  Back to cited text no. 4
Bianchi- Marzoli S, Bracanto R. Third, fourth and sixth cranial nerve palsies. Curr Opin Ophthalmol 1997;8:45-51.  Back to cited text no. 5
Berlit P. Isolated and combined pareses of cranial nerves III, IV and VI. A retrospective study of 421 patients. J Neurol Sci 1991;103:10-5.  Back to cited text no. 6
Batocchi AP, Evoli A, Majolini L, Lo Monaco M, Padua L, Ricci E, et al . Ocular palsies in the absence of other neurological or ocular symptoms: Analysis of 105 cases. J Neurol 1997;244:639-45.  Back to cited text no. 7
Mark AS. Oculomotor motion disorders: current imaging of cranial nerves 3, 4 and 6. Semin Ultrasound CT MR 1998;19:240-56.  Back to cited text no. 8
Mvogo CE, Bella-Hiag A, Ellong A, Ngosso A, Epesse M. Les paralysies oculo-motrices extrinsθques. Facteurs ιpidιmiologiques et cliniques. Mιd Afr Noire 1999;46:500-3.  Back to cited text no. 9
El Mansouri Y, Zaghoul K, Amroui A. Les paralysies oculo-motrices au cours du diabete. A propos de 12 cas. J Fr Ophtalmol 2000;23:14-8.  Back to cited text no. 10
Tiffin PA, MacEwen CJ, Craig EA, Clayton G. Acquired palsy of the oculomotor, trochlear and abducens nerves. Eye 1996;10:377-84.  Back to cited text no. 11
Flanders M, Draper J. Superior oblique palsy: Diagnosis and treatment. Can J Ophthalmol 1990;25:17-24.  Back to cited text no. 12
von Noorden GK, Murray E, Wong SY. Superior oblique paralysis: A review of 270 cases. Arch Ophthalmol 1986;104:1771-6.  Back to cited text no. 13
Mansour AM, Reinecke RD. Central trochlear palsy. Surv Ophthalmol 1986;30:279-97.  Back to cited text no. 14


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