Introduction

Anosognosia, a neurological condition, involves a lack of awareness of one's neurological or psychiatric deficits. Anton Syndrome (AS), an unusual form of anosognosia, manifests as bilateral vision loss coupled with denial of blindness. This systematic review delves into 64 studies encompassing 72 AS cases to explore demographics, clinical presentations, treatments, and outcomes.

Materials and Methods

The study rigorously followed PRISMA guidelines, screening PubMed, Google Scholar, and Scopus databases without timeframe limitations. Only English human studies providing full text were included. Data underwent thorough assessment, examining patient demographics, etiological variables, and treatment modalities.

Results

Sixty-four studies met the stringent inclusion criteria. Examining 72 AS cases showed a median age of 55 (6 to 96 years) with no gender preference. Hypertension (34.7 %) and visual anosognosia (90.3 %) were prevalent. Stroke (40.3 %) topped causes. Management included supportive (30.6 %) and causal approaches (30.6 %). Improvement was seen in 45.8 %, unchanged in 22.2 %, and deterioration in 11.1 %. Anticoagulation correlated with higher mortality (p < 0.05).

Discussion

AS, an unusual manifestation of blindness, stems mainly from occipital lobe damage, often due to cerebrovascular incidents. The syndrome shares features with Dide-Botcazo syndrome and dates back to Roman times. Its causes range from strokes to rare conditions like multiple sclerosis exacerbation. Accurate diagnosis involves considering clinical presentations and imaging studies, distinguishing AS from similar conditions.

Conclusion

This comprehensive review sheds light on AS's complex landscape, emphasizing diverse etiologies, clinical features, and treatment options. Tailored treatments aligned with individual causes are crucial. The study's findings caution against blanket anticoagulation therapy, suggesting a nuanced approach. Further research is pivotal to refine diagnostics and optimize care for AS individuals.