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This thesis investigates the accumulation of fluid in the yellow spot (macular edema) in ocular inflammation (uveitis). Macular edema may result in definitive loss of vision.Two methods of imaging of macular edema are fluorescein angiography (FA) and optical coherence tomography (OCT). The first method provides physiological information, the latter anatomical information. Comparison of FA and OCT images revealed that nearly half of the eyes had discrepant findings. In 30% of the eyes a mild fluorescein leakage was found but no retinal thickening or retinal cysts were seen on OCT. We speculate that in a thin retina a retinal thickening is not easily recognized. OCT revealed ME in 15% of the eyes with no leakage on FA. This discrepancy was common in inactive uveitis and also occurred more often in young patients with an intermediate uveitis. Possible explanations are that this type of edema is intracellularly located or that this edema represents the remains of accumulated fluid after the uveitis subsided and the active leakage had stopped. We emphasize the importance of performing both investigations. We investigated the significance of subretinal fluid in macular edema in uveitis. We conclude that SRD develops in the early stages of ME and uveitis but responds well to medical treatment. We propose a treatment algorithm where we suggest starting with periocular steroid injections (especially in those with unilateral ME) and if this is insufficient or in bilateral cases, immunomodulatory drugs are recommended. When inflammation is under control, but ME persists, the pump function of the retinal pigment epithelium can be stimulated by oral acetazolamide or somatostatin analogues. We investigated peripheral multifocal choroiditis (PMC), which is a chronic bilateral uveitis with vitritis and multiple punched out lesions in the retinal periphery in the absence of central chorioretinal lesions. A high association with sarcoidosis was found. A high cumulative incidence of ME of 81% was found and a prevalence of glaucoma of 35%, which is higher than in the general uveitis population. We report on a new characteristic of PMC, specifically papillitis, which was experienced by 95% of all PMC patients, resulting in 25% of the patients with optic atrophy. Despite many medical and surgical interventions, about 70% of the eyes had a visual acuity of at least 0.5 at ten years follow-up. The diagnosis of ocular sarcoidosis is difficult to prove and it frequently occurs that a uveitis is suspected to be related to sarcoidosis, but cannot be proven. Soluble interleukin-2 receptor (sIL-2R) and angiotensin-converting enzyme (ACE) are two markers that are used for the follow-up of systemic sarcoidosis patients but which have a low diagnostic sensitivity and specificity in the setting of uveitis. Although elevated intraocular levels of ACE or sIL-2R were found in sarcoidosis patients compared to non-inflammatory controls, a large overlap existed between the sarcoidosis-associated uveitis and the controls with infectious uveitis. We conclude that measurement of ACE and sIL-2R in aqueous humor in patients with uveitis did not represent a sensitive method for diagnosis of ocular sarcoidosis.