Retinal pigmentary changes

Retinal pigmentary changes, visual field defects, color vision loss Retinal pigmentary changes, disturbances of dark adaptation, color vision loss, visual field defects Impairment of dark adaptation, visual field defects, vascular attenuation Color vision disturbances, entoptic phenomena Color vision disturbances... 

Chlorpromazine (Thorazine) and thioridazine (Mellaril), both phenothiazine derivatives, are used for their antipsychotic effects in the control of severely disturbed or agitated behavior and in schizophrenia. Thioridazine has a higher incidence of antimuscarinic effects but a lower incidence of extrapyramidal symptoms. Pigmentary changes of the retina have been reported occasionally in association with chlorpromazine therapy, although it is recognized that only thioridazine produces retinal toxicity. 

Pigmentary changes (discrete RPE pigment scattering perifoveally with depigmented surround can be in retinal periphery) accompanying CV loss, visual acuity,VF defects, decreased dark adaptation. 

Side effects of these drugs include CNS effects (e.g., headache, nervousness, insomnia, and others), rashes, dermatitis, pigmentary changes of the skin and hair, gastrointestinal disturbance (e.g., nausea), and reversible ocular toxicities such as cycloplegia and corneal deposits. Potentially serions retinal toxicity is uncommon when the currently recommended doses are used and is least common with hydroxychloroquine. However, because of the possibility of permanent damage associated with the retinopathy, an ophthalmologic evaluation should be done at baseline and every 3 months when chloroquine is used and every 6 to 12 months when hydroxychloroquine is used. If retinal abnormalities are noted, antimalarial therapy should be discontinued or the dose reduced. ... 

Erom this point of view the retinal changes are of particular interest. While phytanic acid could well play an (unfavorable) role in the rhodopsine cycle (Wald 1960, Baum et al. 1965), in the majority of patients with pigmentary retinitis this change develops in the absence of phytanic acid storage, either as a disease of its own or during the course of other disorders such as a-beta-lipoproteinemia (see page 382). 

Thioridazine can cause significant retinal toxicity, leading to reduced visual acuity, changes in color vision, and disturbances of dark adaptation.These symptoms typically occur 30 to 90 days after initiation of treatment. The fundus often appears normal during the early stages of symptoms, but within several weeks or months a pigmentary... 

In TD, pathogenetic discussions center around the abnormality of plasma HDL and the deposition of cholesterol esters in reticuloendothelial tissues. Other changes, such as a low plasma level of carotenes in adult cases, apparently result from the decreased concentration of LDL and are, in contrast to those of a-j8-lipoproteinemia, without clinical consequences in TD. Of interest is the existence in the Kentucky kindred of cases with pigmentary retinitis (see fig.[5) such subjects had low or normal plasma HDL, and a relation between the retinopathy and TD is improbable. On the other hand, splenic bone marrow inhibition in one subject is most probably a result of the underlying disease. This has not been established for the occurrence of coronary thrombosis in one patient, in whom an autopsy was not performed and the condition of the vasculature is not known. A predisposition in TD toward the development of atherosclerotic lesions cannot be excluded. 

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