| disease | Glaucomatocyclitic Crisis Syndrome |
| alias | Glaucomatocyclitic Crisis, Posner-Schlossman Syndrome |
Glaucomatocyclitic crisis syndrome (hereinafter referred to as glaucomatocyclitic syndrome), also known as Posner-Schlossman syndrome, was comprehensively described by Posner and Schlossman in 1948 and 1953. This condition predominantly occurs in individuals aged 20 to 50, is rare in those over 50, and even more uncommon in those over 60. Lu Daoping reported that cases over 60 account for 5%.
bubble_chart Etiology
The exact cause of the disease is not yet fully understood. Some believe it may be related to allergic factors, focal infections, hypothalamic disorders, autonomic nervous system dysfunction, abnormal responses of the ciliary vascular nervous system, and abnormal development of the angle. In recent years, it has been discovered that during the attack stage of this disease, the concentration of prostaglandins (PG), particularly PGE, in the aqueous humor is significantly increased.
bubble_chart Clinical Manifestations
The main clinical manifestations of Posner-Schlossman syndrome are as follows:
1. The condition typically affects one eye and recurs in the same eye, with occasional bilateral involvement. Li Zhihui et al. (1982) reported that among 93 cases, 9 (10%) involved both eyes.
2. Episodic and recurrent elevation of intraocular pressure (IOP), with intervals ranging from months to 1–2 years. IOP can rise to 5.33–8.0 kPa (40–60 mmHg). Each episode of elevated IOP usually lasts 1–14 days and resolves spontaneously, though a minority may persist for up to a month, rarely extending to two months.
3. No subjective symptoms during attacks, only mild (grade I) discomfort. Even at the peak of an episode, there are no pronounced symptoms like headache or eye pain as seen in acute angle-closure glaucoma.
4. Vision is generally normal unless corneal edema occurs, leading to blurred vision.5. During an attack, the pupil is slightly dilated with preserved light reflex. Despite recurrent mild (grade I) cyclitis, posterior synechiae of the iris never develop.
6. Mild (grade I) cyclitis appears within 3 days of an IOP spike. Aqueous humor shows few floating cells, and aqueous flare is usually negative. Keratic precipitates (KP) typically appear within 3 days of the attack—grayish-white, fine or large and flat, resembling mutton fat, usually numbering fewer than 25 and clustered in the lower third of the cornea or hidden in the trabecular meshwork. KP disappear within days to a month after IOP normalizes. They may or may not reappear during IOP fluctuations, necessitating thorough examination.
7. No inflammatory cells are present in the vitreous.
8. The anterior chamber angle remains open during high IOP, with no peripheral anterior synechiae.
9. The fundus is generally normal unless coexisting with primary open-angle glaucoma, in which glaucomatous optic nerve and visual field damage may occur. However, during acute episodes, vascular shadow enlargement may be observed.
10. During high IOP, the "C" value is reduced but returns to normal during remission, along with IOP. Provocative tests are negative. This syndrome may coexist with primary open-angle glaucoma. Li Zhihui et al. (1982) reported a coexistence rate of 31%. For such cases, besides noting the clinical features of this syndrome, it is essential to assess for concurrent primary open-angle glaucoma to avoid delayed treatment of glaucomatous disease.
bubble_chart Treatment Measures
2. Surgical Treatment Surgery is not recommended for this syndrome, as it cannot prevent recurrence. However, close observation and long-term follow-up are necessary. If it coexists with primary or secondary open-angle glaucoma, posing a threat to visual function, surgical intervention should be considered.
