Central pulpy chorioretinopathy (“mesoplasia”) is one of the ten most common diseases of the posterior segment of the eye. Many patients have asked me many questions about this disease, so I would like to focus on some of the issues related to mesoplasia and discuss them with you. I. What kind of people are prone to “mesoplasia”? Type A personality is mainly characterized by impatience, strong personality, impulsiveness, strong sense of time and excessive pursuit of success, and a tendency to be aggressive. By the same token, the onset of the disease is also seen in white-collar workers who work under high pressure and spend long hours looking at computers, who are under stressful conditions such as chronic mental stress and overwork, which leads to increased levels of catecholamines and cortisol in the blood. Other risk factors include smoking, alcohol abuse, antibiotics and antihistamines, autoimmune diseases, hypertension, and adrenal tumors. Men are more likely to develop the disease than women, accounting for about 80% of all patients, and the age of onset is mostly between 30 and 50, with 20%-40% of patients having bilateral eye involvement. Secondly, what are the clinical manifestations of having mesoplasm? Patients have mild vision loss, distortion, small size and color vision change; central or paracentral dark spot; reduced contrast sensitivity; hyperopic refractive changes due to macular plasma detachment. Third, what tests are required for having middle pulp? Fluorescein fundus angiography (fluorescence angiography) is the most common test to confirm the diagnosis of mesophoria. The typical fluorescence angiography of mesoplasm is one or more fluorescein leaks in the area of the lesion, which expand as ink stains or smoke as the angiography progresses, and form a faint disc-like hyperfluorescence in the retinal detachment area in the late stage of the angiography. Patients with chronic mesoplasm may not show typical fluorescein leaks, but rather window-like translucent fluorescence or pigment-obscured fluorescence caused by diffuse retinal epithelial depigmentation or pigmentation in the posterior pole of the retina, on top of which some patients have a combination of fluorescein leaks. Fundus coherence optical tomography (OCT) allows dynamic monitoring of disease progression and quantitative assessment of treatment response. Choroidal angiography (ICGA) is now increasingly used in the diagnosis of mesoplasia. Choroidal angiography provides a diagnostic and differential diagnosis of the etiology and pinpoints abnormal choroidal vessels to guide PDT photodynamic therapy. Fourth, can I recover from mesoplasm by myself? Most patients with mesoplasia recover on their own in 4~6 months after acute onset, and their vision can mostly return to normal, so it is considered a self-limiting disease. However, in some patients, visual function changes such as visual distortion, decreased contrast sensitivity and abnormal color vision can persist. In a small number of patients, the course of the disease is prolonged for more than 6 months. Those with diffuse RPE loss in the lesion area are defined as chronic mesoplasia. This group of patients has more severe lesions, often with permanent vision loss. Long-term persistence may lead to choroidal neovascularization (CNV) and even permanent vision loss. About 30% to 50% of patients with CNV have recurrence after the first attack, and 10% of patients have more than 3 recurrences. Repeated or untreated cases can damage visual function, leading to abnormalities in central vision, contrast sensitivity, color vision, etc. About 5% of patients have severely impaired visual function. V. Does mesophoria require treatment? Based on the understanding that mesophoria is a self-limiting disease, many ophthalmologists follow a conservative treatment strategy for mesophoria. In one case, no treatment is given and the disease is left alone; in the other case, patients are given vitamin C, vitamin B1, lutin, dibazol, creatinine, and other “placebo” treatments. Due to the self-limiting nature of mesoplasm, these treatments also seem to provide satisfactory “results”. For conservative treatment, most patients improve on their own after 4-6 months of disease, but it is important to emphasize that patients with mesoplasia who have had the disease for more than 3 months are at risk of irreversible visual impairment, with 5% of these patients even having severely impaired vision. Previously, the more common treatment for mesoplasia was laser photocoagulation. The clinical study of indocyanine green choroidal angiography (ICGA) for mesoplasia revealed that the choroidal vascular hyperpermeability corresponding to the lesion in mesoplasia patients triggered localized plasma retinal detachment, which further deepened the understanding of the nature of the pathological basis of mesoplasia. Therefore, the current view is that the pathogenesis of mesoplasia is due to choroidal capillary dilation and leakage, and laser photocoagulation cannot resolve the choroidal capillary dilation and leakage, so many patients still relapse after treatment. In addition, the use of laser for lesions in the positive central region of the macula (under the central recess or within the macular avascular zone) will result in severe loss of vision. For patients treated with laser, it may also cause paracentral dark spot or even damage Bruch’s membrane leading to CNV formation. In recent years, successful treatment of mesoplasia with photodynamic therapy (PDT) has been reported in the domestic and international literature. The mechanism is that PDT leads to embolization of the choroidal capillary network, thus preventing leakage due to increased permeability of the choroidal capillaries. Although the clinical course of some mesoplasms is somewhat self-limiting, a longer course will still produce irreversible visual impairment, and active treatment is still recommended if safe and effective treatments are available; compared with previous drug and laser photocoagulation treatments, PDT with reduced photosensitizer doses is safe and effective in the treatment of mesoplasms and deserves further exploration and promotion. This is our basic view on the treatment of mesoplasm at present. Other treatments for mesoplasm include reducing patient stressors, discontinuing glucocorticoids, lowering blood pressure, reducing blood catecholamine and glucocorticoid concentrations, and other etiology-specific treatments. Treatment with micropulse lasers, transpupillary thermotherapy, and intraocular injections of anti-vascular endothelial growth factor drugs have also been attempted. However, these approaches have not gained widespread acceptance to date.