Elshaarawy O, Lan S, Mueller J, Mueller S. Critical flicker frequency improves after alcohol detoxification and is associated with liver stiffness. World J Gastroenterol 2025; 31(36): 107703 [DOI: 10.3748/wjg.v31.i36.107703]
Corresponding Author of This Article
Sebastian Mueller, PhD, Professor, Center for Alcohol Research, University of Heidelberg, In Neuenheimer Feld 350, Heidelberg 69120, Baden-Württemberg, Germany. sebastian.mueller@urz.uni-heidelberg.de
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Observational Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Omar Elshaarawy, Shuai Lan, Johannes Mueller, Sebastian Mueller, Center for Alcohol Research, University of Heidelberg, Heidelberg 69120, Baden-Württemberg, Germany
Omar Elshaarawy, Department of Hepatology and Gastroenterology, National Liver Institute, Menoufia University, Menoufia 32511, Egypt
Omar Elshaarawy, Department of Gastroenterology, Liverpool University, Liverpool L78XP, United Kingdom
Author contributions: Elshaarawy O and Mueller J contributed to conceptualization; Lan S conducted the experiments; Mueller J performed the data analysis; Mueller S acquired funding and designed the study; Elshaarawy O and Lan S contributed equally as co-first authors. All authors contributed to writing-draft, writing-revision, and approved to submit the final version.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of University of Heidelberg, No. S150-2015.
Informed consent statement: All study participants, or their legal guardians, provided written consent prior to study enrollment.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Data sharing statement: There is no additional data available.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Sebastian Mueller, PhD, Professor, Center for Alcohol Research, University of Heidelberg, In Neuenheimer Feld 350, Heidelberg 69120, Baden-Württemberg, Germany. sebastian.mueller@urz.uni-heidelberg.de
Received: April 7, 2025 Revised: May 18, 2025 Accepted: August 22, 2025 Published online: September 28, 2025 Processing time: 165 Days and 16.8 Hours
Abstract
BACKGROUND
Critical flicker frequency (CFF) is a quantitative tool for assessing hepatic encephalopathy (HE), particularly minimal HE, which is associated with poor prognosis in liver cirrhosis. Alcohol-related liver disease (ALD) is a leading global cause of cirrhosis; however, the effects of alcohol on CFF and its relationship with liver stiffness (LS) remain underexplored.
AIM
To study the impact of alcohol withdrawal on CFF and its correlation with LS in ALD patients.
METHODS
A total of 108 patients were included: 93 heavy drinkers hospitalized for detoxification, 15 with non-ALD etiologies, and 20 healthy controls. CFF was measured using the Hepatonorm analyzer, and LS via transient elastography (FibroScan). Baseline and post-detoxification assessments were conducted in 57 ALD patients.
RESULTS
The cohort had a mean age of 53.7 ± 13.8 years, with 74% male participants. CFF measurements were reliable, with 97.2% of patients showing an interquartile range < 20%. ALD patients exhibited significantly lower CFF compared to controls. Receiver operating characteristic analysis for overt HE (n = 12) yielded an area under the curve of 0.66 (95% confidence interval: 0.49-0.84, P = 0.0142), with an optimal cutoff of 36.5 Hz. CFF significantly improved post-detoxification. Patients with LS > 17 kPa had lower CFF, while those with intermediate LS showed no significant difference.
CONCLUSION
CFF is influenced by HE severity and acute alcohol exposure, showing improvement after detoxification. Its weak correlation with fibrosis stage suggests that CFF serves as a sensitive neurocognitive marker in ALD.
Core Tip: This study demonstrates that critical flicker frequency (CFF), a non-invasive marker of neurocognitive function, significantly improves following alcohol detoxification in patients with alcohol-related liver disease (ALD). CFF was reduced in ALD patients and correlated with liver stiffness, particularly post-detoxification, highlighting its utility in detecting minimal hepatic encephalopathy. These findings underscore CFF’s value in assessing alcohol-related neurotoxicity and monitoring therapeutic response, supporting its integration into routine evaluation of patients with ALD and cirrhosis.
Citation: Elshaarawy O, Lan S, Mueller J, Mueller S. Critical flicker frequency improves after alcohol detoxification and is associated with liver stiffness. World J Gastroenterol 2025; 31(36): 107703
Alcohol remains a major global health concern, contributing to approximately three million deaths annually and playing a key role in the development of chronic liver disease[1-4]. As a systemic toxin, alcohol exerts deleterious effects on multiple organ systems, with over 200 distinct pathological conditions linked to its consumption[1]. Among the most severely affected organs are the liver and brain, where hepatic encephalopathy (HE) represents a critical complication in advanced liver disease[2]. HE commonly manifests in the setting of decompensated cirrhosis[5,6], further worsening an already poor prognosis[7]. Its onset often signals life-threatening complications, such as infections or gastrointestinal hemorrhage, necessitating prompt recognition and intervention[8,9].
The diagnosis of HE traditionally relies on clinical assessment, including the detection of asterixis and psychomotor impairment. While quantitative diagnostic tools have refined severity assessment[10-12], simpler bedside tests such as the number connection test remain widely used despite their limitations due to confounding factors[7,13]. Minimal HE (MHE), a subclinical form of HE characterized by subtle neurocognitive dysfunction, has gained increasing recognition due to its prognostic significance. Accurate detection of MHE is crucial, as it can predict the progression to overt HE and impact patient outcomes[13]. Critical flicker frequency (CFF) testing has emerged as a robust, non-invasive psychophysical tool for assessing MHE, offering valuable insights into neurocognitive integrity by evaluating visual cortical function[13-17]. Its diagnostic accuracy and predictive value in identifying complications, including post-transjugular intrahepatic portosystemic shunt outcomes, underscore its clinical relevance[18-22].
Despite growing evidence on CFF as a marker of neurocognitive dysfunction in cirrhosis, the direct impact of alcohol on CFF remains poorly understood[16,23,24]. Given alcohol’s neurotoxic effects and its interplay with hepatic fibrosis severity[25,26], this study investigates dynamic changes in CFF among heavy drinkers before and after detoxification. By integrating liver stiffness (LS) measurements and laboratory parameters, we here aim to investigate the impact of alcohol withdrawal on CFF and its correlation with LS in alcohol-related liver disease (ALD) patients.
MATERIALS AND METHODS
Study design and ethical approval
This study was conducted at the Salem Medical Center, Heidelberg, Germany, to assess the utility of CFF and LS measurements in heavy alcohol users and patients with ALD. The study design is shown in Figure 1. Ethical approval was obtained from the Ethics Committee of the University of Heidelberg, and all participants provided written informed consent in accordance with the Declaration of Helsinki.
Figure 1 Flowchart illustrating the study design and patient selection process.
ALD: Alcohol-related liver disease; LS: Liver stiffness; US: Ultrasound; CFF: Critical flicker frequency.
Participant recruitment
A total of 117 Caucasian patients aged 18-75 years were enrolled, meeting the inclusion criteria of chronic excessive alcohol consumption (≥ 1 year, exceeding three units/day for men and two units/day for women). Baseline assessments for patients admitted for detoxification were conducted within 24 hours of admission, prior to the initiation of specific detoxification pharmacotherapy, to capture the acute effects of alcohol and early withdrawal. The timing relative to the last alcohol intake varied but was typically within the preceding 12-48 hours for this group. Withdrawal severity was not systematically quantified using standardized scales (e.g., Clinical Institute Withdrawal Assessment of Alcohol) as part of this specific research protocol, which should be considered a limitation; however, all patients received standard institutional detoxification protocols managed by the clinical team. Exclusion criteria included the presence of other chronic liver diseases, malignancies and conditions interfering with CFF or LS measurements. Additionally, 20 healthy volunteers served as controls. A subset of ALD patients underwent repeat assessments after a mean detoxification period of 5.3 days.
CFF measurement
CFF was measured using the Hepatonorm analyzer (R&R Medi-Business, Germany) following established protocols[14]. Testing was conducted in a semi-darkened environment, and CFF was recorded as the median frequency at which flickering light was perceived. Patients were instructed to fixate on the light-emitting diode and indicate verbally the point at which the flickering light appeared continuous (ascending frequency) and the point at which continuous light started to flicker (descending frequency). The mean of these two readings was taken for each measurement, and the median of five such valid measurements constituted the final CFF value. Patient cooperation and understanding were assessed prior to and during the test. A CFF threshold of < 39 Hz was used to define MHE, in accordance with American Association for the Study of Liver Diseases and European Association for the Study of the Liver guidelines[20,27] and served as the primary method for MHE diagnosis in this study, as specific additional neuropsychological tests were not systematically performed across all participants for this research purpose. Overt HE was clinically diagnosed by the attending physicians based on the West Haven criteria, considering clinical signs such as asterixis, altered consciousness, and psychomotor abnormalities.
LS assessment
LS was measured via transient elastography (FibroScan, Echosens, France), adhering to standardized protocols[4,28]. Reliable LS measurements were defined as an interquartile range (IQR)/median ratio < 30%. Additionally, ultrasound imaging was performed to exclude confounding conditions such as biliary obstruction or vascular congestion.
Statistical analysis
Data were analyzed using SPSS Statistics version 25. Continuous variables are presented as means ± SD, while categorical variables are expressed as frequencies. Group comparisons were conducted using the independent Student’s t-test, and follow-up data were analyzed with the paired t-test. Correlations were assessed using the Spearman correlation coefficient. The diagnostic performance of CFF was evaluated via receiver operating characteristic curve analysis. A P value < 0.05 was considered statistically significant.
RESULTS
Patient characteristics and CFF performance
Of the 117 patients initially enrolled, 9 were excluded due to invalid CFF assessments, primarily due to difficulties in understanding or performing the test. This included three patients who consistently reported flickering, one who perceived multiple visual targets, and five who were unable to follow instructions. The final analysis included 108 patients, yielding a mean CFF of 40.5 ± 6.1 Hz and an IQR of 2.6 ± 2.0 Hz. Measurement reliability was high, with 97.2% of patients exhibiting an IQR < 20% and 83.3% with an IQR < 10%. Patient characteristics are shown in Table 1. Among the 93 patients diagnosed with ALD, cirrhosis was confirmed in 30% of cases based on established clinical criteria. In comparison, cirrhosis was observed in 33% of patients with non-ALD etiologies. HE was diagnosed in 9.7% of ALD patients and 20% of non-ALD patients. Using a diagnostic threshold of < 39 Hz for CFF, 42% of ALD patients and 73% of non-ALD patients were classified as having MHE.
Table 1 Patient characteristics of the total cohort (n = 108).
Figure 2A illustrates the distribution of CFF values across healthy controls (n = 20), ALD patients (n = 93), and non-ALD patients (n = 15). A significant reduction in CFF was noted in both patient groups compared to controls (P < 0.05 for ALD; P < 0.001 for non-ALD). Notably, a subset of ALD patients exhibited CFF values exceeding those of healthy volunteers. Receiver operating characteristic analysis for the entire cohort (n = 108) with overt HE (n = 12) demonstrated moderate diagnostic utility for CFF, with an area under the curve of 0.66 (95% confidence interval: 0.49-0.84, P = 0.0142; see Figure 2B). The optimal CFF cutoff for detecting overt HE was identified as 36.5 Hz.
Figure 2 Critical flicker frequency in patients with and without alcohol-related liver disease and diagnostic accuracy to detect hepatic encephalopathy.
A: Critical flicker frequency (CFF) in patients with alcohol-related liver disease, non-alcohol-related liver disease etiologies, and healthy volunteers (controls). The mean CFF is significantly lower in disease groups compared to controls. However, a wider spread of CFF values is observed among patients, with some individuals showing higher CFF values than controls; B: Receiver operating characteristic curve for the detection of overt hepatic encephalopathy (n = 12). The area under the curve was 0.66 (95% confidence interval: 0.49-0.84, P = 0.0142), with an optimal cutoff for hepatic encephalopathy at 36.5 Hz. P values were determined using Tukey’s test. ALD: Alcohol-related liver disease; CFF: Critical flicker frequency. aP < 0.05, cP < 0.001.
Correlations between CFF, laboratory parameters, and imaging
Spearman correlation coefficients revealed significant associations between CFF and various clinical parameters (Table 2). A negative correlation was observed with age (r = -0.20, P = 0.036) and LS (r = -0.26, P = 0.042), while positive correlations were found with pack-years of alcohol consumption (r = 0.249, P = 0.03), serum potassium levels (r = 0.259, P = 0.01), and platelet counts (r = 0.32, P = 0.001). Although trends were noted for HE grade, bilirubin, and creatinine, these did not reach statistical significance.
Table 2 Spearman correlation coefficient with all patients (alcohol-related liver disease and non-alcohol-related liver disease, n = 108).
CFF and cirrhosis in patients undergoing alcohol detoxification
To examine the effect of alcohol detoxification on CFF, data from 57 ALD patients who underwent structured detoxification were analyzed. From the initial cohort of 93 ALD patients, 23 were excluded as CFF measurements were not performed within 24 hours of admission, and 13 were excluded due to incomplete evaluations for cirrhosis. Among the remaining 57, 44 patients underwent a second CFF measurement approximately after one week of detoxification, with an average interval of 5.4 ± 1.5 days. Table 3 summarizes the clinical characteristics of this subset, which consisted of 71% male patients with a mean age of 50.6 ± 12.9 years, a mean body mass index (BMI) of 26.7 ± 5.1 kg/m², and a mean daily alcohol consumption of 137 ± 120 g/day over an average period of 16.7 ± 9.7 years. Cirrhosis was confirmed in 17.5% of patients (n = 10).
Table 3 Patient characteristics of the detoxification cohort (n = 57) for patients with critical flicker frequency measurements before and after detoxification (n = 44).
Figure 3 Effect of cirrhosis status on critical flicker frequency and alcohol detoxification stratified by cirrhosis status.
A: Critical flicker frequency (CFF) in patients with cirrhosis (n = 10) and without cirrhosis (n = 47) compared to controls (n = 20). Cirrhotic patients exhibit significantly lower CFF values than controls. P values were determined using Tukey’s test; B: Changes in CFF following alcohol detoxification in patients with pre- and post-detoxification measurements (n = 44). CFF was analyzed in subgroups of patients with cirrhosis (n = 6) and without cirrhosis (n = 38). CFF significantly increases in the no-cirrhosis group after alcohol detoxification. P values were determined using paired samples t-test. CFF: Critical flicker frequency. aP < 0.05, cP < 0.001.
Among the 44 patients assessed pre- and post-detoxification, 40.1% (n = 18) initially recorded CFF values below the MHE diagnostic threshold of 39 Hz. Following detoxification, only 13.6% (n = 6) remained below this threshold, reflecting a substantial improvement in neurocognitive function. Spearman correlations in this subset, shown in Table 4, revealed significant associations between pre-detoxification CFF and BMI (r = -0.55, P = 0.015) and platelet count (r = 0.48, P = 0.001). After detoxification, CFF correlated significantly with serum sodium (r = -0.53, P = 0.027) and LS (r = 0.64, P = 0.03), suggesting that alcohol abstinence may better elucidate the link between hepatic dysfunction and neurocognitive impairment.
Table 4 Spearman correlations for critical flicker frequency before and after alcohol detoxification (n = 44).
Comparison of CFF in cirrhosis stratified by LS and imaging
Baseline CFF values were compared among patients stratified by LS and ultrasound findings. Among 108 patients with valid CFF data, 85 underwent ultrasound evaluation, and 60 had LS measurements. Patients were grouped into LS categories of < 6 kPa, 6-17 kPa, and > 17 kPa, with the latter threshold indicative of cirrhosis. The results are shown in Figure 4. CFF values were significantly lower in patients with LS > 17 kPa compared to those with LS < 6 kPa (P < 0.05; Figure 4A). However, no significant difference was observed between the 6-17 kPa and < 6 kPa groups. Similarly, patients with ultrasonographic evidence of cirrhosis exhibited lower CFF values, although this trend did not reach statistical significance (Figure 4B).
Figure 4 Comparison of critical flicker frequency.
A: Liver stiffness intervals; B: Ultrasonographic signs of cirrhosis. Patients with liver stiffness > 17 kPa exhibited significantly lower critical flicker frequency values than those with LS < 6 kPa (P < 0.05). The difference between patients with and without sonographic signs of cirrhosis did not reach statistical significance. P values were determined using an unpaired independent samples t-test. CFF: Critical flicker frequency. aP < 0.05.
DISCUSSION
This study highlights three key findings: (1) CFF improves significantly following alcohol withdrawal, indicating that alcohol exerts direct neurotoxic effects; (2) CFF is an effective tool for detecting subclinical encephalopathy in ALD, capturing a spectrum of neurocognitive deficits that may not be apparent on clinical examination; and (3) Although the correlation between CFF and LS was modest, particularly in patients with advanced fibrosis, the association suggests that CFF may partially reflect hepatic structural changes alongside functional deficits.
Our data demonstrate that alcohol abstinence leads to a marked improvement in CFF, particularly in patients without cirrhosis. This improvement likely reflects the reversal of acute, direct neurotoxic effects of alcohol on the central nervous system, such as temporary cortical suppression and altered neurotransmitter function, which can impair visual temporal processing. The observation that CFF can normalize in a substantial portion of patients soon after detoxification supports this notion of a reversible component. This supports the hypothesis that CFF reflects cortical processing of visual stimuli[29] and is influenced by both acute and chronic alcohol consumption[25,26]. It is important to distinguish these acute, reversible effects from the more chronic, potentially structural neuro-adaptive changes or damage (e.g., neuronal loss, gliosis, white matter alterations) that can occur with long-term heavy alcohol use, especially in the context of cirrhosis. These chronic changes may contribute to the persistent CFF deficits observed in some patients, particularly those with more advanced liver disease, even after a period of abstinence. The normalization of CFF in approximately half of the patients initially classified as having MHE highlights its sensitivity as a marker for subtle cognitive impairment[30]. This reversibility positions CFF as a promising biomarker not only for detection but also for monitoring therapeutic response during early abstinence. Early detection is clinically relevant, as even mild cognitive dysfunction increases the risk of accidents, particularly those involving motor vehicles[31,32].
Patients with advanced fibrosis or cirrhosis exhibited less robust recovery in CFF following detoxification, suggesting that structural and functional changes in the brain may contribute to persistent neurocognitive deficits. The interplay of elevated neurotoxins, such as ammonia, and irreversible structural alterations likely perpetuates encephalopathy despite alcohol cessation[14,19,33]. These findings underscore the need for tailored management strategies in cirrhotic patients to address persistent cognitive impairment[34,35], potentially including neuroprotective agents or cognitive rehabilitation, although further research is needed in these areas. For instance, studies utilizing magnetic resonance spectroscopy have shown altered brain metabolite profiles (e.g., decreased myo-inositol, increased glutamine/glutamate) in cirrhotic patients, indicative of osmotic stress and impaired glial function, which can persist even with abstinence and contribute to cognitive deficits[36]. Furthermore, advanced neuroimaging techniques like diffusion tensor imaging have revealed white matter microstructural abnormalities in patients with ALD and cirrhosis, suggesting axonal damage and demyelination that may not fully recover and could underpin lasting CFF impairments[36].
Our results corroborate previous studies demonstrating the association between CFF and LS, particularly after detoxification. LS, as assessed via transient elastography, is a well-established indicator of fibrosis severity and long-term prognosis in chronic liver disease[4,37,38]. As alcohol cessation reduces the confounding effects of hepatocyte swelling and necrosis on LS measurements, CFF emerges as a complementary marker for identifying patients at high risk for progressive encephalopathy and adverse outcomes[39].
While CFF demonstrates significant potential as a diagnostic and prognostic tool, its clinical application is not without challenges. Successful CFF measurement depends on patient cooperation, visual acuity, and a controlled testing environment. Patients with advanced HE, particularly those classified as West Haven grades III-IV, often struggle to complete the test reliably due to impaired cognitive function. This is supported by our findings, where some ALD patients exhibited higher measurements than controls, possibly due to delayed button pressing caused by slower response times. Additionally, external factors such as optical aids, ambient light conditions, and operator variability can introduce inconsistencies in measurement.
This study has several limitations. The sample size, particularly for subgroup analyses such as cirrhotic patients and non-ALD etiologies, was relatively small, which may limit the generalizability of these specific findings. However, recruitment of participants, particularly those with ALD requiring detoxification is difficult due to the inherent challenges in engaging this patient population. The heterogeneity of the cohorts, including ALD, non-ALD, and healthy controls, while providing comparative insights, also introduces variability. Potential confounders such as specific comorbidities (e.g., diabetes, hypertension, though major interfering conditions were exclusion criteria), concurrent medications, and detailed nutritional status beyond BMI were not exhaustively controlled for in this analysis. The follow-up period of approximately 5.3 days post-detoxification is short and primarily captures acute changes; longer-term follow-up would be needed to assess the persistence of CFF improvements and their correlation with sustained abstinence and liver function recovery.
Despite these limitations, the relative independence of CFF from variables such as age, sex, and educational background strengthens its applicability across diverse clinical populations. Furthermore, while detoxification protocols were standardized, variations in individual responses, medication use during detoxification (though aimed at managing withdrawal), and baseline nutritional status were not exhaustively controlled for and could represent confounding factors. However, further standardization of testing protocols and validation across different patient cohorts are necessary to enhance its utility in routine practice.
The findings of this study underscore the need for longitudinal investigations to establish CFF as a validated marker for disease progression and therapeutic response in ALD. Integration of CFF into multi-parametric diagnostic models, alongside LS and biochemical markers, could refine risk stratification algorithms for HE. Additionally, interventional studies evaluating the impact of specific therapies, such as ammonia-lowering agents and nutritional interventions, on CFF could provide valuable insights into the mechanisms underlying neurocognitive dysfunction in chronic liver disease.
This study highlights the utility of CFF as non-invasive tool for detecting and monitoring subclinical HE in patients with ALD despite of its moderate accuracy in this study. CFF provides valuable insights into disease severity and neurocognitive function, reflecting both the direct neurotoxic effects of alcohol and underlying hepatic dysfunction. Importantly, CFF responds dynamically to alcohol cessation, offering a sensitive measure of therapeutic impact.
CONCLUSION
In summary, incorporating CFF testing into standard clinical practice has the potential to enhance the early identification and management of patients at risk for HE. Future efforts should focus on optimizing testing protocols, validating its use in broader patient populations, and exploring its integration with other diagnostic modalities to improve outcomes in chronic liver disease.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Gastroenterology and hepatology
Country of origin: Germany
Peer-review report’s classification
Scientific Quality: Grade A, Grade B, Grade B
Novelty: Grade A, Grade B, Grade B
Creativity or Innovation: Grade A, Grade B, Grade B
Scientific Significance: Grade A, Grade B, Grade B
P-Reviewer: Ghannam WM, MD, Professor, Egypt; Shomura M, PhD, Professor, Japan; Twohig P, MD, Assistant Professor, FRCPC, United States S-Editor: Wu S L-Editor: A P-Editor: Zhang L
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