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| CASE REPORT |
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| Year : 1998 | Volume
: 44
| Issue : 3 | Page : 76-7 |
Bilateral glaucomatocyclitic crisis in a patient with Holmes Adie syndrome.
P Puri, D Verma
Department of Ophthalmology, Hull Royal Infirmay, Hull, UK.
Correspondence Address:
P Puri
Department of Ophthalmology, Hull Royal Infirmay, Hull, UK.
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 0010703577 
A patient with pre-existing bilateral tonic pupils presented with simultaneous bilateral glaucomatocyclitic crisis. Deep tendon reflexes were absent although they were documented to be present 6 years ago. A possibility of a progressive autonomic dysfunction in both these conditions is discussed.
Keywords: Adie Syndrome, complications,diagnosis,Aged, Case Report, Female, Human, Iridocyclitis, complications,Ocular Hypertension, complications,
How to cite this article:
Puri P, Verma D. Bilateral glaucomatocyclitic crisis in a patient with Holmes Adie syndrome. J Postgrad Med 1998;44:76 |
Aetiology of glaucomaticocyclitic crisis (classically described as unilateral recurrent attacks of ocular hypertension with mild cyclitis) is unknown. A number of hypotheses relating it to a disturbance of autonomic nervous system has been postulated[1],[2],[3],[4]. Also Holmes-Adie syndrome More Details characterized by tonic pupillary reaction to light and loss of deep tendon reflexes[5] is known to be associated with a wide spread abnormality of autonomic nervous system in 40% of cases[6]. This communication presents a case of bilateral tonic pupils who presented with glaucomaticocyclitic crisis and absent deep tendon reflexes suggesting a progressive autonomic dysfunction as an underlying aetiopathogenic mechanism in both the conditions.
A 71-year-old Caucasian woman was referred by her optician for raised intraocular pressure and accompanying blurring of vision in both eyes. There was no history suggestive of pain, headache, haloes or photophobia. Ocular examination revealed a best corrected visual acuity of 6/9 in the right and 6/6 in the left eye. Slit lamp examination revealed mild ciliary congestion, mild corneal oedema, and two no-pigmented keratic precipitates on the posterior surface of the right cornea and a few cells in the aqueous without any flare. Left eye did not show any corneal edema with only one small non-pigmented keratic percipitate and occasional cells. Both pupils were dilated with sluggish reaction to light; accommodation was slow on changing gaze from distance to near. Both iridis were of similar colour with minimal pigmentation of anterior border layer and patchy atrophy of the stromal layer. Intra ocular pressures were 59 mm Hg in right and 36 mm Hg in the left eye. Gonioscopy revealed widely open angles. Fundus evaluation was normal with healthy discs. Central and peripheral fields were normal. There were bilateral absent knee jerks however, there was no postural hypotension. Full blood counts, random blood sugar and syphilis serology was normal. Patient had presented six years ago with bilateral dilated pupils when she was diagnosed to have bilateral Holmes Adie (tonic) pupils. Knee jerks were then demonstrated to be present. No further investigations into the cause were however performed. In view of her presentation and past history a diagnosis of glaucomaticocyclitic crisis and Holmes Adie syndrome was made. The patient was subsequently treated with Tab. Acetazolamide 500 mg. Orally (single dose) and G. timolol maleate 0.5% twice a day along with G prednisolone acetate 1% six times a day in both eyes. Follow up after six hour revealed pressure of 26 mm Hg in right and 16 mm Hg in left eye, which dropped further to 20 mm Hg in right and 16 mm Hg in left eye at 24 hours. Steroid eye drops were tapered over six weeks and anti glaucoma medication also stopped after six weeks. Intra ocular pressures after six weeks were maintained at 14 mm Hg in right and 16 mm Hg in left eye.
The aetiopathogenesis of glaucomaticocyclitic crisis is unknown. Its association with migraine, anisocoria and heterochromia suggested the possibility of an abnormality of auto immune system. Further demonstration of focal iris ischemia during an attack followed by dilatation and leakage on fluorescein angiography between the attacks also pointed towards the possibility of an abnormal reaction of autonomically innervated cilliary vessels[2] Masuda and Mishima following detection of a high level of prostaglandins in the anterior chamber during the interval between the crisis[3] also supported this theory of autoimmune imbalance.
On the other hand, aetiology of Holmes Adie Syndrome[4] characterized by loss of deep tendon reflexes and tonic pupillary reaction is also unknown although the characteristic pupillary abnormality is due to parasympathetic post ganglionic denervation[5]. In a study by Hope[6], wide spread abnormalities of the autonomic nervous system were seen in 40% of patients. It was further concluded that Holmes Adie Syndrome is commonly accompanied by progressive, mild but widespread autonomic involvement, which is rarely symptomatic. Association between the two conditions, which to the best of our knowledge has been reported for the first time, suggests that autonomic imbalance may be the missing link in the underlying pathogenic mechanism for glaucomaticocyclitic crisis and Holmes Adie pupils. Further more, absence of deep tendon reflexes, which were present at the time to diagnosis of Adie pupil, indicate the progressive nature of the disease, a fact reported by others as well.
| :: References | |  |
| 1. |
Poner A, Schlossman A. Syndrome of unilateral recurrent attacks of glaucoma with cycilitic symptoms. Arch Ophthalmol 1978; 39:517-35  |
| 2. | Raitta C, Vannas A. Galucomatocyclitic crisis Arch Opthalmol 1977; 95:608-12. |
| 3. | Masuda K, Mishima S. Prostaglandins and uveitis. Jap J Ophthalmol 1973; 17:166-70. |
| 4. | Holmes G. Paritial iridoplegia associated with symptoms of other disease if nervous system Trans Ophthalm Soc UK 1931; 51:209-18. |
| 5. | Bourgon R, Pilley SFJ. Cholinergic supersentivity of this sphincter in Adie tonic pupil. Am J Ophthalmol 1978; 85:373-7. |
| 6. | Hope Ross M, Bucharan TAS. Automatic function in Holmes-Adie Syndrome Eye 1990; 4:607-12.
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