|Year : 1973 | Volume
| Issue : 2 | Page : 90-91
Ophthalmoplegia of unknown etiology
HD Patel, S Nahar
Ramwadi Eye Hospital, Bombay, India
H D Patel
Ramwadi Eye Hospital, Bombay
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Patel H D, Nahar S. Ophthalmoplegia of unknown etiology. Indian J Ophthalmol 1973;21:90-1
In partial ophthalmoplegia, except for one or two, all extra-ocular muscles are paralysed. The etiology can be traumatic, vascular, inflammatory, etc. But there are 15 %,-20% of the cases of uncertain etiology - (DUKEELDER). 3 Idiopathic unilateral ophthalmolegia with paralytic proptosis which recovered spontaneously within 1 to 2 months has been variously attributed to transient myositis (DUNNINGTON AND BERKE; 4 BABEL 1 ) to serious tenonitis causing myositis (FERRALL; 5 DUKE ELDER; 3 ) to pariostitis of the superior orbital fissure (COLLIER 2 ; MORTADA 10 ); to neuritis of the peripheral ocular nerves (VON GRAEFE; 6 LANDESBERG. 7 UHTHOFF; 12 SUCKLING; 11 WILSON 13 ) and to blood cyst from an angiomatous malformation (MORTADA 8,9 ) pressing on the ocular nerves in the region of the superior orbital fissure. (DUKEELDER 3 ).
We are reporting a case of partial external ophthalmoplegia in which the etiology was not known and recovered in two years without any specific treatment.
| Case Report|| |
Patient J. C. S. a Hindu male, aged 34 years, salesman by profession attended the Ramwadi Eye Hospital, Bombay, on 24th April, 1969 with complaint of blurring of vision of and on.
There was no history of head trauma, exposure to cold, migraine, syphilis, or rheumatic pain, or any infective fever except four attacks of typhoid fever, the last one being in January 1969.
The patient was well nourished and his general health was normal. There was no glandular enlargement of any kind.
The temperature, blood pressure, pulse and heart were normal.
The motor and sensory systems, reflexes and sphincters were normal. There was no evidence of increased intra-cranial pressure.
All laboratory investigations were non-contributory.
The Mantaux test was negative. X-ray examination of the skull and the chest did not reveal any pathological lesion. Thymus shadow was absent.
Local examination on 24th April 1969, vision in both the eyes was 6/6 J 1 . Fundii and pupillary reactions were normal. Movements were normal except there was paresis of left lateral rectus muscle. After investigation he was treated with ten injections of Neurobion (a B 1 B 6 B 12 preparation) and Entodon. He was feeling better but was kept under observation.
On 8th July 1969 he reported with restricted upward movement in left eye. On examination in both the eyes vision, fundii and pupillary reactions were normal. Right eye was showing normal movements. There was paresis of superior and inferior recti, in addition to paralysis of lateral rectus of left eye. He was advised to consult a neurologist for recurrent attacks. On a provisional diagnosis of ocular myasthenia gravis, he was given prostigmin tablets for 30 days, but there was no relief.
Again lie consulted us, on 19th August 1969, with complaint of restricted movement also in the right eye and inability to open the right eye. On examination, the vision in both the eyes was 6/6 J 1 . Fundii and pupillary reactions were normal. There was paralysis of levator palpebrae superioris and medial rectos of right eye; and of the superior lateral and inferior recti of left eye. (Plate 1).
Again a course of ten injections of Neurobion and Entodon was repeated. But there was no relief. Then the patient was told that the disease would go by itself without any treatment in due course of time.
On 2nd December 1971 he came to hospital with complete recovery. (Plate 2).
A case external ophthalmoplegia of unknown etiology recovered in 2 years without any treatment. It was probably a case of virus etiology.
[Figure - 1]
[Table - 1]