|Year : 1972 | Volume
| Issue : 4 | Page : 159-163
Aetiological study of the third, fourth and sixth cranial nerve paralysis
P Siva Reddy, R Chandrasekar Reddy, M Satapathy
Sarojini Devi Eye Hospital and Institute of Ophthalmology, Hyderabad, India
P Siva Reddy
Sarojini Devi Eye Hospital and Institute of Ophthalmology, Hyderabad
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Reddy P S, Reddy R C, Satapathy M. Aetiological study of the third, fourth and sixth cranial nerve paralysis. Indian J Ophthalmol 1972;20:159-63
|How to cite this URL:|
Reddy P S, Reddy R C, Satapathy M. Aetiological study of the third, fourth and sixth cranial nerve paralysis. Indian J Ophthalmol [serial online] 1972 [cited 2022 Jan 28];20:159-63. Available from: https://www.ijo.in/text.asp?1972/20/4/159/34644
A study of 100 cases of the Third, Fourth and Sixth cranial nerves was undertaken at the Institute of Ophthalmology and Sarojini Devi Eye Hospital, Hyderabad, to determine the relative frequency of the different nerves affected and the most probable aetiological factor operating in each case, with a hope that it will help in the management of those cases where the exact cause is difficult to find.
| Material and Methods|| |
This study is confined to only acquired paralysis of the Third. Fourth, and Sixth nerves excluding examples of supranuclear lesions, congenital anomalies and muscle disorders such as myasthenia gravis and other congenital anomalies.
The hundred cases were divided into six main groups depending upon nerve or combination of nerves paralysed.
As a rule every patient is required to submit to an exhaustive general and neuro-ophthalmologic examination and all the relevant laboratory investigations. Every patient is referred to the neurosurgeon and the ENT department for further examination and opinion.
Third Carnial Nerve:
In 8 of the 43 cases involving the III cranial nerve, the cause remained obscure at the first examination as well as throughout the period of observation and review at the hospital.
In 9 cases tuberculous meningitis was the aetiological factor. All these cases were strong Mantoux positive and the CSF analysis was highly suggestive of the disease with a low sugar and chloride content and pleocytosis mostly consisting of lymphocytes and polymorphs. Causes of paralysis of the Third Nerve:
Vascular disorders accounted for 9 cases of paralysis. All the cases showed evidences of varying degrees of arteriosclerosis. Diabetes was present in 8 cases and theremaining one case had hypertension.
Infective neuritis was presumably responsible for 6 cases of IIIrd. nerve paralysis. In all the cases antral wash was performed in the ENT Hospital and the washout was found to be purulent in almost all the cases. One case had suppurative otitis media in addition to infected sinuses.
In 3 cases the paralysis was attributable to intracranial vascular aneurysm. The site of the aneurysm was the Circle of Willis in all the cases as was proved by carotid angiography.
The remaining 8 cases in this category showed different causes. Trauma to the head sustained in road accidents were responsible for 2 cases. Syphilis accounted for 2 cases both of which showed complete iridoplegia. There were 2 cases of intracranial tumour of which one was metastatic. There was also one case each of orbital cellulitis and herpes zoster ophthalmicus. The case of herpes complicated by isolated III nerve palsy also had optic neuritis. In herpes zoster, paralysis of the ocular muscles presumably occurs from an extension of inflammation from the V cranial nerve to the other cranial nerves as they traverse the cavernous sinus (EDGARTON  TROUPP, KOSKINEN AND BOJORKISTEN  .
Pupillary reactions in III Nerve paralysis:
The condition of the pupils in case of isolated III nerve paralysis was significant and deserves mentioning. III nerve paralysis due to tumour or aneurysm usually exhibited either a fully dilated or a mid-dilated and sluggish pupil. In none of the cases in the above two categories were the pupils completely normal. In 7 out of 9 cases of paralysis due to tuberculous meningitis, the pupils were affected to varying degrees of inequality in size and shape and in the later stages they were invariably dilated and fixed. However, in marked contrast the pupillary reactions were completely normal in 7 cases out of 9 of vascular disorders. Only 2 cases with long standing diabetes showed abnormal pupillary reaction. Two cases of III nerve palsy with a syphilitic aetiology showed iridoplegia. In two out of the three cases of intracranial tumours there was iridoplegia. The condition of the the pupils in the other aetiological groups was not noteworthy.
Fourth Cranial Nerve:
There was only one case of isolated paralysis of the superior oblique muscle due to damage to the IV nerve in a road accident causing head injury to the patient. Haemorrhage into the nerve or direct pressure from outside was suspected. The cause however was only speculative and CSF analysis for xanthochromia was negative. The patient showed vertical muscle imbalance with associated diplopia.
Sixth Cranial Nerve:
In 6 out of the 30 cases of paralysis affecting the VI cranial nerve the cause remained unknown.
Tuberculous meningitis accounted for 8 cases, all of them occurring in patients under 15 years of age. Four patients at the first visit came with unmistakable signs of meningeal irritation and the diagnosis was easy in all the cases.
The paralysis in 3 patients was attributed to vascular disease based on objective evidence of arteriosclerosis. Diabetes was present in all the cases presumably contributing to the already diseased condition of the vessel walls.
As many as 7 cases came under the infective neuritis group. Four cases had dental sepsis and the remaining 3 cases had infected maxillary sinuses.
There was clinical evidence suggesting intracranial aneurysm in one case of VI nerve paralysis. Cerebral angiography subsequently revealed an aneurysm arising from the anterior portion of the Circle of Willis.
In the miscellaneous group there were 5 cases of abducens palsy. The cause was head injury in automobile accidents in 2 cases. Encephalitis accounted for 2 cases and the last case had an intracranial neoplasm.
The findings Of SHRADER AND SCHLEZINGER  may be compared here.
Multiple cranial nerve paralysis:
The incidence of multiple cranial nerve paralysis was relatively frequent, particularly the combination of III and VI cranial nerve paralysis.
The cause in four cases of paralysis of combined III and IV cranial nerves was difficult to determine in two cases. The other 2 cases were attributed to tuberculous meningitis.
Causes of paralysis of the Third & Sixth Nerves:
In four out of 12 cases of combined paralysis of the III and VI cranial nerves the cause was obscure. Three cases were directly the result of tuberculous meningitis. Pansinusitis of prolonged duration causing infective neuritis was responsible for 2 such cases. Amongst the miscellaneous group there was one case of head trauma, one due to intracranial metastasis from ethmoidal carcinoma, and one case due to carotid-cavernous fistula.
The cause of combined paralysis of the III, IV and VI cranial nerves remained unknown in 2 out of 10 such cases throughout the period of treatment and observation. Tuberculous meningitis with extensive damage at the base of the brain was responsible for 4 cases. Among the miscellaneous cases, there were two examples of carotid-cavernous fistula, one case of encephalitis and one case of orbital abscess in a child associated with axial proptosis.
| Comments|| |
The undetermined group is one of the largest groups and accounted for 22% of the cases as shown in [Table - 2] The cause remained unknown despite detailed investigation and prolonged observation.
The largest group by far comprised that of tuberculous meningitis accounting for 26% of the whole series. All the patients were below 15 years of age. This is in marked contrast to the report of RuCKER , whose series showed only a small percentage of cases of meningitis causing ocular muscle palsy. This could be due to the low incidence of tuberculosis in that country. In the majority of cases the pupils showed varying degrees of dilatation and anisocoria, particularly towards the later stages of the disease.
In tuberculous meningitis the base of the brain is covered with a gelatinous, greenish-yellow exudate extending from the chiasma in front to the cerebellum behind, filling up the spaces and surrounds and infiltrates the . optic chiasma, the vesseles of the Circle of Willis and the emerging cranial nerves and spreads out to the tips of the temporal lobes. The exudate gradually acquires a greyish colour and becomes tough in consistency resulting in strangulation of the emerging cranial nerves. This is the cause of the frequent pupillary changes in III nerve paralysis caused by tuberculous meningitis. According to KYRIELEIS pupillary involvement is present in 40% of all cases. He found the pupils fixed to light 15%, sluggish reaction to light in 15% and pronounced anisocoria in 10% of the cases.
Vascular disease accounted for 12% of the cases. All of them but one had diabetes. Arteriosclerotic changes were noted in all the cases. In all the 8 cases of isolated paralysis of the III nerve due to diabetes as the main cause, the pupils were normal and unaffected. The pathogenesis was demonstrated in a case at postmortem examination by DREYFUS, HAKIM AND ADAM  to be an ischaemic infarct within the centre of the nerve trunk due to occlusion of a nutrient artery. The nutrient artery being in the substance of the nerve, the pupillary fibres which lie along the surface are unaffected.
Infective neuritis accounted for 15% of the cases. Suppurative processes in associated structures is known to implicate the nerves. Infection in the accessory nasal sinuses particularly the ethmoids may often involve the III nerve (DUKE-ELDER  ). The close association of the III nerve with these air spaces explains the occurrence of the palsies. There was evidence of focal sepsis in most of the cases in the present series. Removal of these foci of sepsis was followed by considerable improvement.
Aneurysms accounted for 4% of the cases. They are said to occur intracranially more frequently than elsewhere in the body. The reason has not been adequately explained. A congenital defect of the tunica media is presumed to be the predisposing factor. This basic defect often aggravated by secondary factors such as arteriosclerosis, trauma and inflammation would explain the predilection for cerebal artery involvement. HYLAND AND BARNETT  . In the present series the site of the aneurysm was the anterior portion of the Circle of Willis in all the cases. In 3 out of the 4 cases the third nerve was affected.
The miscellaneous causes accounted for 21 % of the cases and have already been mentioned under the discussion of each nerve mentioned.
| Summary|| |
A study of 100 cases of paralysis of the III, IV and VI cranial nerves was made from the standpoint of aetiology. The undermined group accounted for 22% and tuberculous meningitis accounted for 26% of the cases. All the cases were below 15 years of age and the ocular palsies usually made their appearance during the second week of the developed disease. Vascular disease and aneurysm accounted for 12% and 4% respectivgly. Infective neuritis was presumed to be responsible for 15% of the cases. The cause of paralysis in the remaining 22% of the cases was associated with a variety of aetiological factors.
| References|| |
Dreyfus, P. M., Hakim, S., and Adam, R. D.: Diabetic Ophthalmoplegia, Arch. Neurol & Psychiat, 77: 337-349, 1957.
Duke-Elder, W. S.: Text book of ophthalmology, Mosby, London 1941.
Edgarton, A. E.: Herpes zoster ophthalmicus: Report of cases and review of literature, Arch. Oph., 34: 40-62, 114-153, 1945.
Hyland, H. H., and Barnett, H. J. M.: The pathogenesis of cranial nerve palsies associated with intracranial aneurysms, Proc. Roy. Soc. Med., 47: 141-146, 1954.
Klotz, H. A.: Paralysis of the Third cranial nerve., Survey of Ophth, Vol. 9, No. 2, April 1964.
Rucker, C. W.: Paralysis of the third, Fourth and Sixth cranial nerves, Am. J. Ophth, 46: 787-794, 1948.
Rucker, C. W., Dyer, J. A., Smith, D. C., and Taub, R. G.: The causes of acquired paralysis of the ocular muscles, Am. J. Ophth, 41: 951955, 1956.
Sharader E. C. and Schlezinger, N. S.: Neuro-ophthalmologic evaluation of abducens nerve paralysis, A. M. A. Arch. of Ophth, Vol. 63, 84-91, 1960.
Troupp, H., Koskinen, K., and Bojorkesten, G.: Ophthalmoplegia caused by Intracranial aneurysm, Acta. Ophth, 36: 79-86, 1958.
Walsh, F. B., Clinical Neuroophthalmology, Williams & Wilkins, Baltimore, 1947.
[Table - 1], [Table - 2]