|Year : 1984 | Volume
| Issue : 5 | Page : 447-453
Aetiological patterns of ocular motor nerve palsies
Vimala Menon, Jagmohan Singh, Prem Prakash
Dr. RP. Centre for Ophthalmic Sciences AIIMS, New Delhi, India
Dr. RP. Centre for Ophthalmic Sciences, AIIMS, New Delhi-110 029
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Menon V, Singh J, Prakash P. Aetiological patterns of ocular motor nerve palsies. Indian J Ophthalmol 1984;32:447-53
|How to cite this URL:|
Menon V, Singh J, Prakash P. Aetiological patterns of ocular motor nerve palsies. Indian J Ophthalmol [serial online] 1984 [cited 2021 Aug 1];32:447-53. Available from: https://www.ijo.in/text.asp?1984/32/5/447/27537
| Introduction|| |
Rucker in 1958 and 1966 reported on the distribution and causes of paralysis of third, fourth and sixth cranial nerves in two large series. In 1981 Rush and Younge, again analysed the 4etiological and distribution patterns in these nerve palsies in one thousand patients. The basic pattern was almost the same as far as frequency of these nerve palsies is concerned, with several differences from earlier reports in terms of various aetiological factors.
The present study was conducted at Dr. RP. Centre for Ophthalmic Sciences, AIIMS, New Delhi from 1981 to 1983 to analyse cases of acquired ocular motor palsies. 197 cases were selected from Strabismus and Neuroophthalmology clinics of the Centre.
| Material and methods|| |
197 acquired cases of ophthalmoplegia including those referred from Neurology and Neuro-surgery Departments were studies. These included both isolated nerve palsies and also those cases which had associated neurological deficit; to exclude speciality bias. Cases of myasthenia and other myopathies, congenital palsies, Graves'-ophthalmopathy and birth injuries were excluded from this study. Besides routine investigations, other procedures like C.S.F. analysis, radiological examination of skull, orbital fissures, optic foramina, paranasal sinuses, computerised tomography, and carotid angiography etc. were performed wherever indicated.
| Observations|| |
Age distribution analysis revealed that 75% of all cases were below 40 years of age. Maximum incidence of third nerve palsy (71%) was seen between 11-40 years; of fourth nerve between 30-5f years and of sixth cranial nerve in the 21-30 years age group. Multiple cranial nerve palsies were also observed to occur predominantly between 11-40 years of age.
There was only one case of bilateral third nerve palsy of undetermined aetiology while amongst 12 cases of fourth nerve involvement, not a single case had bilateral affection. 9 cases (10%) of sixth nerve paralysis had bilateral involvement: 4 of them had psuedotumor cerebri: 4 had intracranial neoplasm and the remaining patient had suffered head injury with fracture of skull. Bilaterality was observed in 5 cases (14.7%) of multiple nerve palsies; of which three had intracranial tumors; one patient was hypertensive and one case developed multiple ocular motor nerve palsies following encephalitis.
The sixth cranial nerve was affected most frequently in our series (88 cases). Third cranial nerve was the next most commonly injured nerve (63). There were 12 cases of fourth nerve palsy while 34 patients had multiple nerve involvement.
| Sixth cranial nerve|| |
Majority of the patients with sixth nerve palsy (32 cases) did not have any identifiable cause. Neoplasm accounted for 11 cases (12.5%): of these there were 5 cases off nasopharyngeal malignancies, 3 had pituitary tumors with parasellar extension; frontal lobe glioma, third ventricle tumor and metastasis from carcinoma of breast accounted for one case each [Table - 1].
Head injury was responsible for 9 cases (10.2%) of sixth nerve palsy with one patient having bilateral involvement. Associated optic nerve damage was seen in. one patient Except for one, all these patients showed either a partial or complete recovery in this category.
Vascular disease i.e. diabetes, hypertension and atherosclerosis resulted in 9 cases (10.2%) of sixth nerve palsy. Of these six patients had diabetes, 2 were hypertensive and in the remaining case there was evidence of atherosclerosis with calcification of intracavernous part of internal cartoid artery. Psuedotumor cerebri with no demonstrable intracranial space occupying lesion was present in 8 cases (9%); including 4 patients with bilateral affection. In our series, three patients had evidence of neurotuberculosis.
16 patients had sixth nerve palsy from a variety of causes: viral infection (3); Gradenigo's syndrome (2); meningitis (2); encephalitis (1); epidemic hamorrhagi.c conjunctivitis (1); electric shock(1); Herpes zoster (1); multiple sclerosis (2); psuedotumor of orbit (1); cysticecrosis of brain (1); aborted cavernous sinus thrombosis (1).
Associated visual loss in the form of optic atrophy was found in 6 cases (9%) and 12 patients (13.6%) had associated optic disc edema.
Neurological deficit accompanying sixth nerve palsy included: V nerve damage (6), VII nerve palsy (2), quadriparesis (1). convulsions (2), and VIII nerve involvement in one case. Partial or complete recovery occured in 24 cases (27.2%); amongst these, most of these cases were of either indeterminate (8) or vascular (7) aetiologies.
| Third cranial nerve|| |
The causes of paralysis involving the third cranial nerve (63 cases) are given in [Table - 2].
No identifiable cause could be attributed to most of the cases (30%). Head trauma caused third nerve palsy in 14 cases (22.2%): 5 of these had associated vision loss, with cortical blindness in one patient and homonymous hemianopia in. another. About half of these cases (6) had internal ophthalmoplegia and an equal number of patients did not show any recovery during the follow up period. Fractures of the skull could be demonstrated in only two patients. Associated neurological deficit in cases of post-traumatic third nerve paralysis consisted of V nerve involvement (2), VII nerve pasty (2) herniparesis and XII nerve paralysis in one case each.
Neoplasm related third nerve pasty was .observed in 6 patients (9.5%). There were three cases of meningiornas and remaining three cases had pituitary tumors with lateral extension. Amongst the vascular causes, diabetes was the causative factor in 2 and aneurysms of posterior communicating artery in another two cases.
An interesting observation in this category was the emergence of idiopathic inflammatory psuedorumors of orbit as an important cause of third nerve palsy (6 cases). The 14 miscellaneous cases were caused by a variety of the following agents: Weber's syndrome (3), multiple sclerosis(2), degenerative brain disease (1), drug induced (1), clivus ridge syndrome (1), post-operative complication of repair of perforating injury of globe (1), meningitis (2), neurofibromatosis (1) and migraine (1).
Irrespective of the aetiology, internal ophthalmopiegia was detected in about one third of cases (35%). Associated neurological deficit consisted of V nerve involvement (3) VII nerve palsy (5), herniparesis or quadriparesis (4) and XII nerve paralysis (1). Optic atrophy associated with third nerve palsy was seen in 8 cases (3 of them being post headtrauma plasies) and 3 patients had associated optic disc oedema, including one case of clivus ridge-syndrome. Third nerve paralysis showed partial or complete recovery in 15 cases (23%) including 6 cases of head injury.
| Multiple ocular motor cranial nerves|| |
Head injury was the most common cause (9 cases) of multiple nerve palsies [Table - 3]. Only one case had an obvious fracture of skull. Visual loss was observed in 5 cases; including one case of Berlin's oedema with optic atrophy. Except for one, all of them had associated internal ophthalmoplegia. Neurological deficit accompanying post traumatic multiple nerve palsies included VII nerve pasty (5 cases) and V nerve involvement in 2 cases.
Idiopathic inflammatory psuedotumor of orbit was the next common cause (8 cases); followed by neoplasm (7 cases). There were 2 cases of pituitary tumor and nasopharyngeal carcinoma each; one cerebellopontine angle tumor, one case of brainstem glioma and the remaining patient had a metastatic tumor from testicular malingancy.
5 patients had a variety of associated disorders: orbital cellulitis (2), Tolosa Hunt syndrome with positive syphilitic serology (1), Herpes zoster (1) and Tuberculoma of brain (1), The aetiology could not be determined in 5 patients [Table - 3].
Associated vision loss was found in more than half the cases (55%) in the form of optic atrophy. Similarly an almost equal number of cases (20) had associated involvement of intrinsic musculature of the eye. V and VII nerve involvement associated with multiple nerve palsies was seen in 7 cases each. 13 cases (38%) showed partial or complete recovery; majority (8 cases) being cases with idiopathic inflammatory psuedotumor of the orbit.
The distribution pattern analysis of multiple ocular motor nerve palsies revealed that the combined involvement of III, IV and VI nerves occured more frequently (50%) than any other combination.
| Fourth cranial nerve|| |
There were 12 cases of fourth nerve palsy [Table - 4] closed head injury was responsible for 5 cases of fourth nerve palsy including one cases with associated ataxic hemiparesis and another with superior altitudinal field defect. The aetiology remained obscure in 4 cases.
Other causes of fourth nerve palsy were diabetes (1), maxillary sinusitis (1), and post viral upper respiratory catarrh (1).
Partial recovery of function was observed in three cases (25%).
| Discussion|| |
In the present series of 197 cases of ocular motor cranial nerve palsies, majority of third nerve and multiple nerve palsies cases were in 11-40 years ago group, while the sixth nerve palsy was almost equally distributed amongst various age groups, the incidence being marginally higher in between 21-30 years of age. Fourth nerve plasy however was seen more often between 30 and 50 years of age. In earlier reports (Rama et al 1980); Rush and Younge (1981) all the cases were analysed together, irrespective of the nerve involved for determining the peak incidence; the drawback in this approach being that various nerve palsies have different aetiological patterns and the occurance of these causative factors has some relation to the various age groups.
[Table - 5] shows the comparison of fre. quency of nerve palsies between earlier reports and the present series. Like in earlie series sixth nerve was affected more frequen tly in our series (44.6%). 9 cases (10%) of case; of sixth nerve palsy had bilateral involvemen which is close to the figure of 8% reported by Rush and Younge (1981) and twice that of 5% reported by Shrader & Schlezinger (1960). In the present series bilateral sixth nerve palsy was observed more often (4 cases) with intracranial neoplasm as reported by Rush and Younge (1981). However, head injury was not the predominant cause of bilateral sixth nerve palsy in this series: Instead psuedotumor cerebri emerged as an alternate important cause (4 cases) for bilateral sixth nerve involvement.
The third cranial nerve was the next most commonly involvement nerve (32%) in the present series. This is comparable to an incidence of 27.4% to 33.5% reported before (Rucker, 1958; Rucker 1966; Krishna and Mehkari, 1973; Rama et al 1980; Rush and Younge, 1981. Only one patient with third nerve palsy of unknown aetiology had bilateral involvement (1.5%); which is comparable to the frequency quoted by Green and associates (1964).
Multiple cranial nerve palsies accounted for 17.3% of all cases. This figure is much lower than reported in the other two reports from India. Krishna and Mehkari (1973) found multiple cranial nerve involvement in 25% of their cases while Rama et al (1980) quoted an even higher incidence (35.5%) amongst their patients. The incidence of multiple nerve palsies in the present series goes well with that quoted in western literature (Rucker, 1958; Rush and Younge, 1981). We observed the same combination pattern of multiple nerve palsies as described by Rush and Younge (1981).
In patients with fourth nerve palsy which was observed in 6.1% of cases, none had a bilateral involvement, which is rather unusual. Rush and Younge (1981) reported bilateral involvement in 7.6% in their series. The actual incidence of fourth nerve palsy in the present series is much higher than that reported in other Indian series (0.5%)Krishna and Mehkari (1973); 1.1%-Rama etal. (1980).
A comparative analysis of causes of paralysis of cranial nerves amongst earlier reports and the present series [Table - 6] reveals that the present study is conspicuously different from others.
In our series of 197 cases of ophthalmoplegia, the largest group consisted of cases with undetermined aetiology (30.5%). This frequency is even higher than figures quoted in earlier reports. Despite the fact that sophisticated investigative procedures like ultrasonography and computed tomography of brain are available to us, we still have an embrassingly high proportion of cases with unknown aetiology.
Cases of head trauma (18.7%) were encountered more frequently in our series, than in reports by other Indian authors (Krishna and Mehkari 1973); Rama et al. 1980). Neoplasm caused 12.2% of all cases of paralysis involving third, fourth and sixth cranial nerves as compared to earlier reports of 26.3% in 1958. In our series, there was a decline in neoplasm caused sixth cranial nerve palsy (12.5%) compared to 30.9% of Rucker's (1966) series. A similar trend was noted by Rush and Younge in 1981.
Cases with palsies due to vascular disease and aneurysms were seen less often (7.1%) as compared to Western figures. On the contrary, Rama et al (1980) reported an incidence of 14% in a series of 90 Indian patients. Only 2 cases of aneurysms arising from posterior communicating artery were detected with third nerve involvement in the present series and both these patients had associated internal ophthalmoplegia.
Rama et al (1980) also could find only one case of aneurysmnal aetiology in their 90 patients and suggested that aneurysms are less common in South India. It is a matter of conjecture, whether this holds good for this part of the country as well.
Idiopathic inflammatory psuedotumors of orbit emerged as a significant cause of cranial nerve palsies especially cases with multiple nerve affection (23.5%) and third nerve palsies (9.5%). This could be due to the fact that ultrasonography is being employed quite frequently at this centre in these cases, rather than an actual spurt in the incidence of this particular condition. The prognosis for recovery is such cases was very good; out of 13 cases of multiple nerve palsies, in whom partial or complete recovery was observed, as many as 11 cases had idiopathic inflammatory psuedotumors of orbit.
Another interesting feature of this study was an almost complete eclipse of neurotuberculosis as an aetiological factor. Rama et al (1980) reported an incidence of as much as 21% with neurotuberculosis as the cause of various ocular rnotor cranial nerve palsies. In the present series, the incidence was only 2.I%; 3 cases with sixth nerve palsy and one case with combined third, fourth and sixth nerve involvement.
The pattern of recovery of sixth, third and fourth nerve palsies was almost similar; 27%, 23% and 25% respectively. In multiple ocular motor nerve palsies, the outlook for remission was comparatively better due to the emergence of I.I.P. as a significant aetiological factor. This is at variance with the observation made by Rush and Younge (1981) who found worse prognosis in these cases due to predominance of neoplasm related palsies in this group.
Syphilis was notably absent as a cause of ocular motor cranial nerve palsies except for one case of Tolosa Hunt syndrome with reactive VDRL test. Green et al (1964) reported an incidence of 9%-in cases with third nerve palsy due to syphilis. Shrader and Schlezinger (1960) also detected syphilitic aetiology in 10% of their cases with sixth nerve palsy. This trend can be attributed to the reduced prevalence and earlier and more effective treatment of syphilis these days.
| Summary|| |
There are to date only 3 reports available in the Indian literature with regard to aetiological pattern in acquired cranial nerve palsies. 197 cases of ophthalmoplegia have been analysed which included both isolated and mixed palsies. Isolated 6th nerve palsy was observed in 88 cases (44.6%) isolated 3rd nerve palsy in 63 cases (32.0%) while isolated 4th nerve palsy was seen in 12 cases (6.1%). The remaining 34 cases (17.3%) had involvement of 3rd, 4th & 6th nerves in various combinations. Isolated 4th nerve palsies were more common in this series as compared to other reports. The aetiological pattern of the cases has been discussed which also differs from previous reports.
| References|| |
Rucker C.W., 1958. Amer. J. Ophthalmol 46: 787.
Rucker C.W., 1966. Amer. J. Ophthalmol. 61: 1293-1298.
Rush J.A. and Younge B.R. 1981. Arch. Ophthalmol 99: 76.
Raina V., Vimala J.. Chander Shekhar M., Anjane_yulu C., and Dinakar 1..1980. Ind. J. Ophthalmoi. 28: 13-16.
Krishna A.G. and Mehkari M.B. Neurol. India (supple IV) Vol. 20: 584.
Green W.R, Hackett E.R, Schlezinger N.S., 1964. Arch. Ophthalmol. 72: 154-167.
Shrader E.C., Schlezinger N.S., 1960. Arch. Ophthalmol. 63: 84-91.
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6]