Abstract

Background: Cerebral venous thrombosis (CVT) is commonly associated with intracranial hypertension (IH), though its neuroimaging markers remain less well-defined. This study aims to systematically review and compare neuroimaging markers of IH in CVT and idiopathic IH (IIH) to better understand their diagnostic implications.

Methods: A systematic review and meta-analysis were conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. From inception to 2024, we searched PubMed, Web of Science, and Scopus for observational studies and randomized controlled trials focusing on neuroimaging findings in primary IH (i.e., IIH) and IH secondary to CVT. Data were extracted on neuroimaging outcomes, including peri-optic cerebrospinal fluid (CSF) pressure, optic nerve head protrusion, and others.

Results: Six studies met the eligibility criteria, comprising three cohort studies and three case-control studies, with a combined total of 301 patients. The results indicated that peri-optic CSF pressure (Odds ratio [OR]: 5.85, P = 0.0002), optic nerve head protrusion (OR: 4.1, P = 0.02), sclera flattening (OR: 2.2, P = 0.04), and empty sella (OR: 3.25, P = 0.03) were observed more frequently in patients with IIH than in those with CVT and IH. However, when comparing CVT with IH to controls, optic nerve tortuosity did not show a significant difference (OR: 2.20, P = 0.18). Increased ventricular volume (Mean difference: 1.76, P P = 0.002) were more common in CVT with IH patients compared to the control group.

Conclusion: Typical neuroimaging characteristics of IH (e.g., empty sella) are more frequently observed in idiopathic cases (i.e., IIH) than in secondary causes, such as IH resulting from CVT. These differences have the potential to enhance diagnostic precision and facilitate the development of improved imaging protocols.

Keywords: Cerebral venous thrombosis, Intracranial hypertension, Magnetic resonance imaging, Neuroimaging, Systematic review

INTRODUCTION

Intracranial hypertension (IH) can result from secondary causes such as tumors, infections, or obstructions in cerebrospinal fluid (CSF) or blood flow, including cerebral venous thrombosis (CVT).[ 21 ] IH frequently accompanies CVT, presenting in the early stages in approximately 40% of cases[ 46 , 47 ] and persisting as a chronic issue in around 10% of patients.[ 23 ] It is associated with visual impairment[ 16 ] and poses an increased risk of long-term morbidity and mortality.[ 20 ] Delayed onset of IH may occur in patients with regressive thrombosis.[ 16 , 36 ] In individuals without brain lesions, common risk factors for IH include clot formation in the dominant and bilateral transverse sinuses,[ 19 ] thrombosis in the superficial veins,[ 32 ] and the development of collateral vessels linking the dural sinuses to deep cerebral veins.[ 5 ] Diagnosing IH related to CVT typically requires invasive CSF pressure measurement.[ 28 ] Papilledema serves as a highly specific indicator of IH, with specificity rates between 95% and 100%.[ 17 , 34 ] The current standard for diagnosing IH relies on invasive intracranial pressure (ICP) assessment through lumbar puncture (LP), which carries potential risks, including bleeding, infection, and soft-tissue scarring.[ 42 ] Consequently, recent studies have focused on developing non-invasive methods for ICP evaluation.

Over the past decade, magnetic resonance imaging (MRI) has revealed certain features associated with increased ICP.[ 1 , 3 ] These include an empty sella, narrowing of the transverse sinus, dilation of the optic nerve sheath (ONS), protrusion of the optic nerve, flattening of the posterior sclera, and vertical curvature of the optic nerve.[ 30 , 52 ] Most MRI findings linked to elevated ICP reported in the literature have been observed in individuals with idiopathic IH (IIH). However, it remains unclear whether these MRI markers also occur during acute ICP elevation, such as IH caused by CVT. Previous studies have demonstrated that many MRI findings associated with IIH are not specific to this condition. Regardless of whether IH is idiopathic (e.g., IIH) or secondary to space-occupying lesions like tumors, the MRI indicators and findings often remain consistent.[ 29 , 41 ] To address this, we conducted a systematic review and meta-analysis to investigate neuroimaging markers associated with IIH and IH secondary to CVT and to compare these findings. These distinctions hold potential for improving diagnostic accuracy, advancing imaging protocols, and enabling less invasive approaches to monitor disease progression.

METHODS

Adhering to the Cochrane handbook of systematic reviews of interventions at each step,[ 29 ] and following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement’s guidelines, we conducted this systematic review and meta-analysis.[ 38 ]

Database searching

We conducted a database search using the following strategy: “Cerebral venous thrombosis” AND “intracranial hypertension” AND “Neuroimaging” OR “Magnetic resonance imaging” OR “MRI” OR “Computed tomography” OR “CT.” The search was performed across PubMed, Web of Science, and Scopus from inception to 2024 to identify articles eligible for inclusion in our study.

Screening

Following the database search, duplicates were removed using EndNote version 7.[ 18 ] The remaining articles were then uploaded to Rayyan software[ 40 ] for screening. The screening process was conducted in two stages. Initially, two independent authors screened the articles by title and abstract to assess eligibility. Articles passing this stage underwent full-text screening. Discrepancies were resolved either through consensus or by consulting a senior author for a final decision.

Eligibility criteria

The screening process employed predefined inclusion and exclusion criteria. Eligible studies included observational studies (cohort, cross-sectional, or case–control) and randomized controlled trials (RCT) focusing on neuroimaging findings in IH secondary to CVT or IIH. Case reports and reviews were excluded from the study. Gray literature and preprints were excluded from this review. These sources were omitted to ensure the inclusion of peer-reviewed studies only.

Quality assessment

The quality of the included observational cohort and case– control studies was evaluated using the Newcastle–Ottawa scale (NOS) tool recommended by Cochrane. This tool comprises eight questions, each earning a maximum of one star, except for the comparability question, which can receive up to two stars. Consequently, the total possible score ranges from zero to nine. Studies scoring between 0 and 3 were classified as low quality, those scoring 4–6 as moderate quality, and those scoring 7–9 as high quality.[ 50 ]

Data extraction

Two independent authors performed data extraction using Microsoft Excel sheets. Extracted baseline data included study design, sample size, age, population, and gender, alongside outcomes such as the event and total occurrence of neuroimaging findings. These findings encompassed peri-optic CSF pressure, optic nerve head protrusion, sclera flattening, optic nerve tortuosity, empty sella, and ventricular volume.

Statistical analysis

The meta-analysis of the included studies was performed using review manager version 5.4 software. Events and totals of dichotomous variables were pooled to calculate the odds ratio (OR), while mean differences (MD) were determined for continuous variables, with a 95% confidence interval (CI) and a significance threshold of P = 0.05. Heterogeneity was assessed using the I² statistic and its corresponding P-value. A fixed-effect model was applied due to the absence of heterogeneity among the included studies.

RESULTS

Database searching and screening

The database search initially identified 127 articles, of which 51 were duplicates, leaving 76 articles eligible for title and abstract screening. From these, 66 articles were excluded, and 10 proceeded to full-text screening. Ultimately, six articles were selected for inclusion in the meta-analysis[ 18 , 30 , 39 , 41 , 48 , 53 ] [ Figure 1 ].

Figure 1:

PRISMA flow diagram of the study selection process. The diagram illustrates the systematic screening and selection of studies included in the meta-analysis. A total of 127 records were initially identified through database searching. After removing 51 duplicates, 76 records remained for title and abstract screening. Of these, 66 articles were excluded based on irrelevance or insufficient data. Ten full-text articles were assessed for eligibility, resulting in the final inclusion of six studies in the meta-analysis. The flow follows the PRISMA guidelines, detailing the number of records at each stage: Identification, screening, eligibility, and inclusion. IH: Intracranial hypertension, CVT: Cerebral venous thrombosis, IIH: Idiopathic intracranial hypertension, PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-Analyses.

Baseline characteristics

This meta-analysis comprised six studies, including three cohort studies comparing patients with CVT and IH to those with IIH, and three case–control studies comparing CVT and IH patients to a control group without IH. Collectively, the studies involved 301 patients. Specifically, the control group consisted of 87 patients, compared to 84 patients with IH secondary to CVT. In addition, 73 patients with IIH were compared to 57 patients with CVT-related IH. The baseline characteristics of these studies are outlined in Table 1 .

Table 1:

Baseline characteristics of the included studies.

Quality assessment

Based on the NOS criteria, four of the included studies were classified as high quality, while the remaining two were deemed to be of moderate quality [ Table 2 ].

Table 2:

Quality assessment of the included studies using Newcastle-Ottawa scale.

Meta-analysis

The meta-analysis demonstrated that certain neuroimaging findings were notably more frequent in patients with IIH compared to those with CVT and IH. These included peri-optic CSF pressure (OR: 5.85, 95% CI: 2.29–14.95, P = 0.0002; [ Figure 2 ]), optic nerve head protrusion (OR: 4.1, 95% CI: 1.19–14.08, P = 0.02; [ Figure 3 ]), sclera flattening (OR: 2.2, 95% CI: 1.05–4.6, P = 0.04; [ Figure 4 ]), and empty sella (OR: 3.25, 95% CI: 1.09–9.67, P =0.03; [ Figure 5 ]). In contrast, there were no significant differences between the two groups regarding optic nerve tortuosity [ Figure 6 ]. When compared to the control group, patients with CVT and IH had a higher likelihood of optic nerve tortuosity, but this difference was not statistically significant (OR: 2.20, 95% CI: 0.69– 7.04, P = 0.18; Figure 7 ]). However, sclera flattening (OR: 6.68, 95% CI: 2.05–21.78, P = 0.002; [ Figure 8 ]) and increased ventricular volume (MD: 1.76, 95% CI: 1–2.53, P < 0.00001; [ Figure 9 ]) were significantly more prevalent in CVT with IH patients. No substantial heterogeneity was observed across all evaluated outcomes.

Figure 2:

Comparison of peri-optic CSF pressure between idiopathic IIH and CVT-IH. Forest plot demonstrates significantly higher odds of increased peri-optic CSF pressure in IIH patients compared to CVT-IH (OR: 5.85; 95% CI: 2.29–14.95; P = 0.0002). No heterogeneity was detected. CSF: Cerebrospinal fluid, OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, IIH: Idiopathic intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 3:

Optic nerve head protrusion is compared between IIH and CVT-IH patients. The forest plot indicates that optic nerve head protrusion is significantly more prevalent in IIH than in CVT-IH patients (OR: 4.1; 95% CI: 1.19–14.08; P = 0.02). Statistical heterogeneity was minimal across included studies. OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, IIH: Idiopathic intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 4:

Sclera flattening comparison between IIH and CVT-IH groups. The forest plot reveals a significantly higher occurrence of sclera flattening in IIH patients (OR: 2.2; 95% CI: 1.05–4.6; P = 0.04). These findings support the greater prominence of posterior globe deformities in IIH. OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, IIH: Idiopathic intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 5:

Empty sella prevalence between IIH and CVT-IH patients. Forest plot analysis shows that IIH patients have a significantly higher frequency of empty sella (OR: 3.25; 95% CI: 1.09–9.67; P = 0.03). This finding reinforces the role of sellar morphology as a neuroimaging marker of IIH. OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, IIH: Idiopathic intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 6:

Optic nerve tortuosity in IIH versus CVT-IH patients. The forest plot demonstrates no significant difference in the frequency of optic nerve tortuosity between groups, suggesting this feature may not distinguish between IIH- and CVT-related IH. OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, IIH: Idiopathic intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 7:

Optic nerve tortuosity in CVT-IH patients versus control subjects without intracranial hypertension. Although tortuosity was more common in CVT-IH, the difference did not reach statistical significance (OR: 2.20; 95% CI: 0.69–7.04; P = 0.18). OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 8:

Sclera flattening in CVT-IH patients compared to controls. The forest plot indicates a significantly higher occurrence of sclera flattening in CVT-IH patients (OR: 6.68; 95% CI: 2.05–21.78; P = 0.002), suggesting this feature is associated with elevated intracranial pressure. OR: Odds ratio, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, M-H: Mantel–Haenszel method.

Figure 9:

Ventricular volume comparison between CVT-IH patients and controls. Forest plot shows significantly increased ventricular volume in CVT-IH patients (MD: 1.76; 95% CI: 1.00– 2.53; P < 0.00001), indicating a measurable structural change related to intracranial hypertension. MD: Mean difference, CI: Confidence interval, CVT: Cerebral venous thrombosis, IH: Intracranial hypertension, M-H: Mantel–Haenszel method.

DISCUSSION

Main findings

The present study demonstrated that neuroimaging findings such as peri-optic CSF pressure, optic nerve head protrusion, sclera flattening, and empty sella were more pronounced in IIH patients compared to those with IH secondary to CVT. Conversely, findings including sclera flattening and increased ventricular volume were more prominent in IH patients secondary to CVT when compared to the control group. Thus, while neuroimaging abnormalities are evident in both conditions, they appear to be more prevalent among IIH patients.

Discrimination between IIH and CVT-related IH

When comparing neuroimaging in IIH and IH secondary to CVT, it is well-established that both conditions share several clinical and radiologic features. Although IIH patients tend to have a higher incidence of females and individuals who are overweight compared to those with CVT, the clinical overlap between the two conditions is notable. It has been previously highlighted that at least, one-third of CVT patients present with a syndrome featuring isolated elevated ICP (headaches and papilledema), which is clinically indistinguishable from IIH.[ 7 ] As a result, the diagnosis of CVT in many cases relies solely on brain imaging. Despite significant advancements in MRI technology over the past decade, misinterpretation of brain MRI scans still leads to delayed identification of CVT, especially in patients with isolated elevated ICP. Many clinicians who assess patients with isolated elevated ICP do not routinely use magnetic resonance venography (MRV) to visualize the intracranial venous system. Instead, they often request that radiologists exclude CVT based solely on standard brain MRI. Establishing and disseminating clear evidence-based guidelines emphasizing MRV as a crucial diagnostic tool for detecting CVT in patients with isolated ICP elevation is lacking. Integrating MRV into standard diagnostic algorithms could encourage its routine use. Ridha et al.,[ 41 ] suggested that, in such cases, identifying imaging features of elevated ICP, such as abnormalities in the sella turcica, dilatation of the ONS, and globe flattening, may be helpful. Indeed, while both IIH and CVT patients exhibited MRI signs of elevated ICP, these findings were more common in IIH patients than in those with CVT.

Pathophysiology

CVT is often associated with IH. The formation of blood clots or narrowing of the cerebral venous sinuses results in increased pressure in the brain’s veins, a condition known as intracranial venous hypertension. This elevated pressure contributes to increase ICP by obstructing the normal absorption of CSF at the arachnoid villi. Venous hypertension is commonly observed in CVT patients and is responsible for typical symptoms of raised ICP, such as headaches, papilledema, and changes in mental status, which are frequently seen in these individuals.[ 7 ] The precise cause of IIH remains unclear and is an ongoing topic of debate.[ 9 ] However, the role of venous hypertension in IIH is well recognized, particularly in patients with transverse sinus stenosis (TSS), which is detectable through brain MRV. Several researchers have emphasized the importance of venous hypertension as a common mechanism underlying conditions such as IIH and CVT, both of which are characterized by isolated elevated ICP.[ 14 , 33 ] While prior studies have investigated the clinical and radiologic features of IIH and CVT, the work by Ridha et al.[ 41 ] is notable for focusing solely on IIH patients with cerebral venous stenosis detected through high-quality contrast-enhanced MRV. All the IIH patients in this study had bilateral TSS, likely causing impaired venous drainage and increased pressure in the brain’s veins, similar to what occurs in CVT patients with obstructed venous sinuses. This strengthens the comparison between IIH and CVT patients in terms of venous hemodynamics.

Use of MRI as a discriminative tool in previous reports

Patients suspected of having IIH, along with those experiencing headaches from other causes, frequently undergo cranial MRI.[ 10 ] While MRI plays a crucial role in distinguishing between individuals with IIH and those without, LP is considered a simple and effective diagnostic method, widely recognized as the gold standard for diagnosing IIH. The diagnosis of IIH has been associated with several brain MRI abnormalities.[ 1 , 8 , 35 ] These include optic nerve head protrusion, posterior scleral flattening, increased peri-optic CSF, optic nerve tortuosity, partial empty sella, tonsillar herniation, enlargement of Meckel’s cave, and meningocele, which are well-established MRI findings in IH.[ 1 , 8 , 35 ] However, further investigation is required to clarify the diagnostic value and practical application of these signs in clinical practice.

The role of neuroimaging findings in distinguishing between IIH and secondary causes of IH has been studied only in a few studies.[ 15 , 30 , 41 , 43 ] Hingwala et al.[ 30 ] reported that patients with IIH exhibited a higher incidence of globe flattening and optic nerve head protrusion compared to those with malignancies. Subgroup analyses comparing IIH patients with venous hypertension – mainly those with CVT – showed that nerve sheath buckling was more frequent in patients with venous hypertension, while globe flattening was more common in those with IIH.[ 30 ] In another study by Ridha et al.,[ 41 ] it was found that none of the abnormal neuroimaging signs indicative of increased ICP were specific to IIH or able to differentiate it from other causes of IH, such as CVT.

The effect of body mass index (BMI) on diagnosis and risk factor of IH

Onder and Kisbet[ 39 ] reported that the BMI values were notably higher in the IIH group compared to the CVT group (31.0 vs. 25.9; P = 0.022). However, no correlation was found between BMI and MRI findings. The association between IIH and obesity is well-established in the scientific literature,[ 4 , 25 , 44 , 51 ] although the exact pathophysiological mechanisms linking obesity to IIH remain unclear.[ 51 ] Obesity is typically regarded as a contributing factor to IIH, rather than the sole cause,[ 44 ] though debates on this topic continue. A previous study[ 25 ] investigating pressure changes outside the skull in IIH patients concluded that weight does not directly contribute to the development of the condition. Instead, the authors suggested that IIH might either be a primary cause of weight gain in these patients or exacerbate pre-existing weight issues. The study by Onder and Kisbet[ 39 ] further supports the link between elevated BMI and IIH. However, the lack of any correlation between BMI and LP opening pressure or MRI findings does not provide sufficient evidence to suggest that obesity plays a critical role in the condition’s development. Future large-scale studies are needed to clarify these issues.

Causes of IH in CVT patients

Several interconnected mechanisms contribute to the elevated risk of IH in CVT. First, the size and specific location of the blood clot play a significant role in the likelihood of developing intracranial hemorrhage.[ 2 , 19 , 24 , 47 ] In addition, the rise in endogenous pressure may be influenced by local thrombosis, which is contingent on the extent of collateral circulation. Moreover, reduced trans-vessel pressure, such as when thrombosis impacts Pacchioni granulations, can lead to diminished pressure-dependent CSF absorption through glymphatic pathways.[ 37 ] It is also important to recognize that although rare, dural arteriovenous fistula can contribute to or exacerbate CVT, resulting in increased intravenous pressure and ICP.[ 12 , 49 ] Finally, the impaired blood flow within the veins can cause fluid accumulation, tissue necrosis, and bleeding, ultimately leading to elevated pressure within the skull.[ 14 ]

MRI in CVT-related IH

The study by Schuchardt et al.[ 48 ] demonstrated that an enlargement in the diameter of the ONS serves as a valuable diagnostic marker for IH in acute CVT cases.[ 6 , 22 ] This aligns with the findings of Dong et al.,[ 17 ] which involved patients with IH and controls classified according to the severity of pituitary gland dysfunction. Other neuroimaging markers were found to be less informative. Although optic nerve tortuosity is more commonly observed in IH patients, its sensitivity in accurately detecting IH in acute CVT cases is limited.[ 45 ] Dong et al.[ 17 ] found no significant differences in ocular bulb size, pituitary grade, or the size of the lateral and fourth ventricles between CVT patients with and without IH at baseline.

Reversibility of neuroimaging findings in CVT

There is currently no data regarding the effectiveness of neuroimaging in monitoring the progression of CVT over time, particularly in determining the appropriate duration for anticoagulation treatment when incomplete recanalization occurs. The reversibility of neuroimaging markers varied, with ocular findings showing the highest frequency of reversibility.[ 48 ] Notably, there was a significant reduction in the frequency of ONS diameter enlargement, bulbar fattening, and pituitary grading, and the reversibility of these changes was associated with the categorization of IH. However, despite a noticeable decrease, the enlargement of ONS diameter did not return to baseline levels in all eight out of eight IH patients when compared to both the control group and patients without IH. Pituitary grade remained elevated in patients with IH. Given that symptoms of IH improved in most patients, it is unlikely that IH will persist throughout the follow-up period. The resolution of IH neuroimaging findings may depend on factors such as the duration of IH, tissue elasticity, and the time needed for normalization. In patients with IIH who have papilledema, neuroimaging markers of IH remain evident even after symptoms and papilledema have subsided.[ 11 ] The average time for the reversal of papilledema in CVT patients was 6 months.[ 36 ] Studies involving the infusion of substances into the spinal canal[ 26 ] and postmortem analysis have shown a correlation between the widening of the ONS diameter and a temporary increase in CSF pressure.[ 27 ] However, full reversibility of ONS diameter was not achieved following prolonged high pressure exposure.[ 27 ] While treatment for IH can reverse empty sella, pituitary compression may persist due to anatomical changes in the sellar region, similar to observations in IIH.[ 11 ]

LIMITATIONS

Study design

Most of the included studies were observational in nature (cohort or case–control), which may introduce inherent biases such as selection bias and confounding. In addition, no RCT were identified that specifically addressed neuroimaging findings in IH secondary to CVT versus IIH.

Sample size and study number

The number of included studies was small (n = 6), with a total sample size of 301 patients. This limits the statistical power and generalizability of the findings. Subgroup analyses were constrained due to insufficient data.

Heterogeneity in imaging protocols

There was considerable variability in MRI protocols and imaging criteria used across studies. This heterogeneity may influence the reliability and consistency of reported imaging markers of IH.

Language and publication bias

Only studies published in English were included, which may introduce language bias and exclude relevant data from non-English sources. Furthermore, potential publication bias cannot be excluded, as studies with negative or inconclusive findings may be underreported.

We focused on incorporating published studies from indexed databases, which may have resulted in the omission of relevant unpublished or gray literature, potentially introducing a bias toward studies with positive outcomes. To minimize this risk, we conducted a systematic search across multiple databases and reviewed the references of included studies.

Lack of longitudinal data

Most studies were cross-sectional, lacking longitudinal follow-up to assess the evolution or resolution of imaging markers over time. Future studies should evaluate these markers in relation to clinical outcomes and treatment response.

Future directions

Future research should include larger, multicenter studies with standardized MRI protocols and prospective designs. The integration of advanced imaging techniques and automated quantification tools could improve diagnostic precision. In addition, exploring imaging correlations with clinical outcomes may enhance risk stratification and inform management strategies in patients with IH due to CVT and IIH.

CONCLUSION

This systematic review and meta-analysis demonstrate that neuroimaging findings associated with IH in CVT show distinct patterns when compared to IIH. While some neuroimaging markers, such as optic nerve head protrusion and sclera flattening, are more common in IIH, increased ventricular volume and sclera flattening were more prevalent in CVT-related IH. These differences have the potential to enhance diagnostic precision and facilitate the development of improved imaging protocols.

Ethical approval:

The Institutional Review Board approval is not required.

Declaration of patient consent:

Patient’s consent was not required as there are no patients in this study.

Financial support and sponsorship:

This work was supported by the deanship of scientific research, vice presidency for graduate studies and scientific research, King Faisal University, Saudi Arabia (Grant No. KFU241582).

Conflicts of interest:

There are no conflicts of interest

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Disclaimer

The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.

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