The present study provides a comprehensive clinical characterization of neurological, cognitive, and systemic manifestations in post-COVID syndrome within a Caucasian cohort. The findings demonstrate a high prevalence of persistent symptoms, particularly sensory disturbances, cognitive complaints, and fatigue. Importantly, symptom distribution was heterogeneous, supporting the concept that post-COVID syndrome is a multidimensional clinical entity rather than a uniform condition.

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One of the most consistent observations in this study was the high prevalence of sensory symptoms, particularly anosmia and ageusia, affecting more than half of the cohort. These findings are in line with previous reports indicating that olfactory and gustatory dysfunction are among the most common and persistent features of post-COVID syndrome, even in patients with initially mild disease.12 Boscolo-Rizzo et al. reported similar patterns of persistence in smell and taste dysfunction, highlighting their clinical relevance as long-term sequelae of SARS-CoV-2 infection.13,14 This consistency across studies supports the reliability of sensory dysfunction as a hallmark feature of post-COVID neurological involvement.

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In addition to sensory disturbances, cognitive symptoms were highly prevalent, with nearly half of the participants reporting memory impairment and a substantial proportion demonstrating executive dysfunction and attention deficits.15 These findings are consistent with emerging evidence suggesting that cognitive impairment is a central component of post-COVID syndrome. A recent meta-analysis by Premraj et al. described a high frequency of cognitive and neuropsychiatric manifestations in post-COVID populations, reinforcing the concept that cognitive dysfunction is not an isolated phenomenon but part of a broader neuropsychological spectrum.10,16

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A key finding of the present study is the association between disease severity and symptom burden. Patients with severe acute COVID-19 demonstrated a significantly higher prevalence of cognitive complaints, fatigue, and neuropathic symptoms compared to those with mild disease. This pattern suggests a dose–response relationship, in which greater systemic involvement during the acute phase is associated with a higher risk of long-term neurological sequelae. These findings are consistent with previous observations that severe infection is associated with increased risk of persistent neurological complications, potentially reflecting greater systemic stress, inflammatory burden, and organ involvement during the acute phase.

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In contrast, sensory symptoms such as anosmia and ageusia were distributed relatively evenly across severity groups, suggesting that these manifestations may be less dependent on systemic disease severity and more related to localized mechanisms, such as viral effects on olfactory pathways. This distinction between severity-dependent and severity-independent symptoms highlights the heterogeneity of post-COVID neurological involvement and suggests that different pathophysiological mechanisms may underlie specific symptom domains.

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From a clinical perspective, the high prevalence of fatigue and cognitive complaints is particularly relevant, as these symptoms are closely associated with reduced functional capacity and quality of life. Although the present study did not focus on mechanistic pathways, the observed co-occurrence of cognitive and systemic symptoms suggests that these manifestations may cluster within specific clinical phenotypes. The identification of such patterns may facilitate improved patient stratification and targeted management strategies in clinical practice.

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The findings of this study also underscore the importance of comprehensive clinical assessment in patients with post-COVID syndrome. The wide distribution of symptoms across neurological, cognitive, and systemic domains suggests that a multidisciplinary approach is required, integrating neurological evaluation, cognitive screening, and psychological assessment. Early identification of high-risk patients, particularly those with severe acute disease or multiple persistent symptoms, may improve long-term outcomes through timely intervention and rehabilitation strategies.

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This study has several limitations that should be acknowledged. First, the cross-sectional design limits the ability to assess temporal dynamics or causal relationships between variables. Second, symptom assessment relied in part on patient-reported outcomes, which may be subject to reporting bias. Third, although the cohort was relatively large and well-characterized, it represents a specific regional population, which may limit generalizability to other populations. Nevertheless, the study provides valuable insights into the clinical phenotype of post-COVID syndrome in an underrepresented Caucasian cohort.

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In summary, the present study demonstrates that a broad and heterogeneous spectrum of neurological, cognitive, and systemic manifestations characterizes post-COVID syndrome. Sensory dysfunction, cognitive impairment, and fatigue represent the most prominent features, while disease severity appears to influence the burden of cognitive and systemic symptoms. These findings contribute to a better understanding of the clinical phenotype of post-COVID syndrome and provide a foundation for future longitudinal and mechanistic studies.

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The relatively long median interval since infection reflects the prolonged recruitment period and should be considered when interpreting patterns of symptom persistence.

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The present findings should be interpreted primarily as a descriptive characterization of symptom distribution among individuals with persistent post-COVID manifestations, rather than as a formal phenotypic classification of post-COVID syndrome.

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Several limitations should be considered. First, because participants were recruited from outpatient and follow-up settings and all had persistent symptoms, the cohort is not representative of all individuals recovering from COVID-19. Therefore, the reported frequencies should not be interpreted as general population prevalence. Second, the long median interval since infection may introduce recall bias and may reflect differences related to viral variants, reinfections, and vaccination status. Third, unadjusted comparisons may be influenced by age, sex, BMI, comorbidities, and hospitalization status