Posner Schlossman Syndrome
(Glaucomatocyclitic Crisis)

By Stuart Macfarlane

Posner Schlossman Syndrome (PSS) is characterised by episodes of elevated IOP secondary to low-grade idiopathic iritis. It is otherwise known as Glaucomatocyclitic crisis. Its hallmark is a rise in IOP that is out of proportion to the degree of inflammation.

Mr PI, a 74 yo white male presented for review. He had a history of hazy vision in the left eye of 12 hours duration. BCVA was RE 6/5- and LE 6/9= and a left RAPD was present. Ophthalmoscopy revealed a normal right disc and advanced left disc pallor and cupping. Low-grade left corneal oedema was obvious with slitlamp examination. Only mild conjunctival injection was present. Investigation of the anterior chamber revealed minimal aqueous flare and small keratic precipitates primarily in the inferior half of the endothelium. Due to corneal oedema it was difficult to view the angles with gonioscopy however they appeared open and no posterior or anterior synechiae were present. Applanation tonometry was RE 18 and LE 55mmHg.

The diagnosis was made relatively easy by the existence of open angles, increased IOP, low-grade uveitis and the fact that he had a 20 year history of PSS. He was currently instilling timolol 0.5% twice daily to the left eye for secondary open angle glaucoma.

He was prescribed flarex drops hourly to the left eye with diamox tablets 500mg stat and advised to continue instilling timolol twice daily. At review 6 hours later IOP was RE 11 and LE 45mmHg. He took another 250mg diamox and was scheduled for review the next morning. At the subsequent review IOP was RE 9 and LE 22mmHg and the anti-inflammatory drops were tapered over the next few weeks. His IOP eventually stabilised at RE 14 and LE 13mmHg. Computerised perimetry, GDx, OCT and retinal photography were performed once his eye was quiet and comfortable.

He had a long history of PSS with the attacks initially occurring annually. As he aged the episodes have become less frequent, however due to the nerve head damage from each attack he sometimes has difficulty determining when he is having an attack. He can usually diagnose an episode by lighting a candle in a darkened room and looking for haloes secondary to corneal oedema. The attacks have caused secondary open angle glaucoma due to damage to his trabecular meshwork. His IOP is well controlled with timolol between episodes and he has been previously prescribed diamox for use during attacks.  Diamox was prescribed to lower his IOP as quickly as possible to minimise permanent damage to the nerve head and trabecular meshwork during each attack.

PSS patients have signs of anterior inflammation that are characteristically minimal with faint flare, rare cells, and only a few keratic precipitates that are small, flat, non-pigmented, and concentrated over the inferior half of the endothelium. The acute stage with rise in IOP can last up to a few weeks or as short as a day. The rise in IOP is more related to the duration of iritis rather than the degree and the condition is not associated with posterior synechiae. Depending on the IOP, corneal oedema may develop with subsequent haloes around lights.

Posner Schlossman Syndrome has two stages, iritis and increased IOP.

The aetiology of the iritis is unclear however has been proposed to be related to;

  • Abnormal vascular process
  • Autonomic defect
  • Allergic condition
  • Variation of developmental glaucoma
  • Cytomegalovirus (CMV) infection
  • HSV infection

There may be associations with allergic conditions and gastrointestinal diseases, most notably peptic ulcer disease. Prostaglandins, particularly prostaglandin E, have been found in higher concentration in the aqueous humour of patients during acute attacks. These levels return to normal between episodes.1

Currently the most accepted explanation is that HSV is linked to PSS. The trabecular meshwork is innervated by the trigeminal nerve and is a conduit for HSV. It has been proposed that HSV causes an inflammation of the trabecular meshwork, impeding aqueous outflow and increasing IOP. Both PSS and recurrent HSK may present with fine keratic precipitates, increased IOP and stress-induced unilateral attacks.

The rise in IOP is secondary to the iritis and the mechanism is thought to be from a reduction in outflow from inflammation of the trabecular meshwork. Gonioscopy reveals normal open angles without abnormal pigmentation. 2

PSS is uncommonly bilateral and typically presents between the second and fourth decade and is rarely encountered after the age of 60. 3 It is more common in males.

The following diagnoses need to be excluded.

Heterochromia may indicate Fuchs’ heterochromic uveitis. 1 Other uveitic glaucomas, which deserve consideration include phacolytic glaucoma (hypermature cataract and acute glaucoma), herpetic uveitis (HSV), acute angle closure glaucoma, iridocyclitis, chorioretinitis with anterior uveitis and secondary glaucoma with anterior uveitis from retinal detachment. 5

Gonioscopy needs to be performed to rule out angle-closure glaucoma or angle recession glaucoma. In a PSS glaucomatocyclitic crisis, the angles remain open.

Primary treatment is to resolve the inflammation, which will subsequently lead to an increase in aqueous outflow and consequently a reduction in IOP. In recalcitrant cases diamox 250mg qid may be required.

Some practitioners believe 1% apraclonidine can be prescribed during exacerbations of PSS. Four hours after instillation of 1% apraclonidine, IOP dropped 50.3% during acute PSS in one study.6

The disease usually runs its course with topical steroids not required between the acute stages. Prophylactic anti-inflammatory therapy is somewhat controversial and most practitioners do not feel that it prevents recurrences. 1

PSS may also be associated with POAG. In one study, twenty-six percent of PSS cases were diagnosed to have developed glaucoma as a result of repeated attacks4. Posner Schlossman patients may also more commonly be steroid responders, which is why flarex is generally initially prescribed, as it has less potential to cause a steroid response.

It can be concluded that surgery should be restricted to those cases with severe and disabling symptoms or to cases with progressive optic neuropathy with visual field loss, when the syndrome is associated with glaucoma. 7   


  1. Chandler, PA, Grant, WM. Glaucoma. Philadelphia: Lea and Febinger; 1986: p 363-375.
  2. Nagaraki S, Mishima, S. Aqueous humor dynamics in glaucomatocyclitic crisis.Investigative Ophthalmology 1976; 15: 365-370.
  3. Geurds EA, Gurwood AS.  Anterior uveitis, IOP, signal Posner Schlossman syndrome.Review of Optometry 1998; 135: 114 -119.
  4. Jap A, Sivakumar M, Chee SP.  Is Posner Schlossman Syndrome Benign? Ophthalmology 2001; 108 : 913-918.
  5. Kanski, J, McAllister J, Salmon J. Glaucoma, A Colour Manual of Diagnosis and Treatment. Boston: Butterworth Heinemann; 1989: p 88-89.
  6. Hong C, Song KY. Effect of apraclonidine hydrochloride on the attack of Posner-Schlossman syndrome. Korean J Ophthalmol 1993; 7: 28-33.
  7. Darchuk V, Sampaolesi J, Mato L, Nicoli C, Sampaolesi R. Optic nerve head behavior in Posner-Schlossman syndrome. Int Ophthalmol 2001; 23: 373-9.
  8. Yamamoto S, Pavan-Langston D, Tada R, Yamamoto R, Kinoshita S, Nishida K, Shimomura Y, Tano Y. Possible role of herpes simplex virus in the origin of Posner-Schlossman syndrome. Am J Ophthalmol 1995; 119: 796-8.
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