Purpose of the studyHepatitis C virus (HCV) is associated with neuropsychiatric complaints. Previous studies have associated cognitive alterations with HCV infection but have often included confounding factors in their samples. This study compares the cognitive performance between patients with HCV infection (HCV patients) and a control group while excluding other factors that may cause cognitive impairment.Study designThis cross-sectional study was conducted from March 2010 through June 2011. HCV infected patients and healthy individuals between the ages of 18 and 80 years were considered eligible. The exclusion criteria included well established causes of cognitive impairment such as depression and cirrhosis. Study participants underwent neuropsychological testing involving measures of attention, memory, abstraction, visuoconstructive abilities, and executive function.ResultsOf 138 initial patients, 47 were excluded because of their medical records, three refused to participate, 23 did not attend the consultation, and 32 were excluded because of having Beck Depression Inventory (BDI) scores >11. In all, 33 patients underwent neuropsychological testing; however, three were excluded because of having hypothyroidism, and one was excluded because of having a cobalamin deficiency. For the control group, of the 33 healthy individuals that were selected, four were excluded because of having BDI scores >11. Thus, the final analysis included 29 HCV patients and 29 control participants. The groups did not differ in education, age, or gender. No statistically significant differences were found between the groups regarding cognitive performance.ConclusionsIn this study using strict selection criteria, there was no evidence of an association between HCV infection and cognitive impairment.
Since the discovery of HCV in 1989, several diseases have been related to chronic infection by this virus. Often, patients with hepatitis C virus (HCV) complain of cognitive impairment even before the development of hepatic cirrhosis, which they described as "brain fog." Several studies have proposed a link between chronic HCV infection and the development of cognitive alterations, but the inclusion of confounding factors in their samples significantly limits the analysis of the results. In this article, we will give an overview about cognitive dysfunction in patients with HCV.
Minimal hepatic encephalopathy is a syndrome caused by liver cirrhosis and accompanied by a broad spectrum of cognitive symptoms. The objective of the present study was to describe the prevalence of minimal hepatic encephalopathy in cirrhotic patients and to compare their cognitive performance with controls using standardized tests. Patients receiving medication or experiencing comorbidities associated with cognitive disorders were excluded. The final cohort was compared with a control-matched group using the Mini-Mental State Examination (MMSE), as well as Simple Drawing, Clock Drawing, Rey Auditory-Verbal Learning Test (RAVLT), Random Letter, Stroop, Trail-Making Test (TMT) A and B, Boston Naming, Category Verbal Fluency, Digit Span, Constructional Praxis, Processing Speed, and Similarities Tests. The results indicated no differences in the prevalence of cognitive complaints spontaneously reported by 29 patients with cirrhosis versus 22 healthy controls. The most affected tests included: MMSE (26.3 ± 2 vs. 28.1 ± 1.8 points; p = 0.004), learning (35.4 ± 9 vs. 41 ± 9.1 points; p = 0.041), retroactive interference (0.67 ± 0.22 vs. 0.84 ± 0.16 points; p = 0.004), and recognition (8.7 ± 2.6 vs. 11.2 ± 4.1 points; p = 0.024) in RAVLT, TMT-A (63.2 ± 29.3 vs. 47.6 ± 16.5 s; p = 0.029) and TMT-B (197.9 ± 88.1 vs. 146.8 ± 76.5 s; p = 0.03). No differences were observed with respect to age, gender, and education. In conclusion, MMSE proved to be a useful tool for detecting global cognitive impairment experienced by cirrhosis patients. Moreover, the most impaired cognitive functions were verbal episodic memory and information processing speed. These findings suggest that minimal hepatic encephalopathy represents a disorder that affects the medial temporal system and, possibly, the prefrontal cortex, and this requires further study.
Minimal hepatic encephalopathy is a syndrome caused by cirrhosis, with a broad spectrum of clinical manifestations. Its diagnosis is based on abnormal results of cognitive and neurophysiological tests, but there are no universally available criteria, especially in Brazil, where local testing standards are required. The objective of the present study was to compare the performance of the mini-mental state examination (MMSE), Rey’s auditory-verbal learning test (RAVLT), psychometric score of hepatic encephalopathy (PHES), topographic mapping of brain electrical activity (TMBEA) and long-latency auditory evoked potential (P300) in the detection of minimal hepatic encephalopathy in Brazil. From 224 patients with cirrhosis included in the global sample, 82.5% were excluded due to secondary causes responsible for cognitive or neurophysiological dysfunction. The final sample consisted of 29 cirrhotics, with predominance of A5 Child-Pugh classification, and 29 controls paired in critical variables such as age, educational level, gender, professional category, scores suggestive of mild depression, association with compensated type 2 diabetes mellitus and sociodemographic characteristics. Overall, performance on cognitive tests and TMBEA did not show a statistically significant difference. There was a marked difference in P300 latency adjusted for age, with patients with cirrhosis showing a mean of 385 ± 78 ms (median of 366.6 ms) and healthy volunteers exhibiting a mean of 346.2 ± 42.8 ms (median of 348.2 ms) (p < 0.01). These findings suggest that, in the earliest stages of cirrhosis, age-adjusted P300 latency was superior to cognitive assessment and TMBEA for detection of minimal hepatic encephalopathy.
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