Visual attention in cirrhotic patients: A study on covert visual attention orienting

Amodio, Piero; Marchetti, P.; Piccolo, F. Del; Campo, Giovanni; Rizzo, Cristiano; Iemmolo, R.M.; Gerunda, G.E.; Caregaro, L.; Merkel, Carlo; Gatta, Angelo

doi:10.1002/hep.510270608

Cited by 53 publications

(20 citation statements)

References 25 publications

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“…However, the inclusion of even a small number of patients with cirrhosis and hepatic encephalopathy might well be responsible for the correlations observed. In addition, sustained attention, which was found to be abnormal in almost half of the study group, is known to be impaired in patients with hepatic encephalopathy [17,18] . When the same authors administered a similar test battery to an independent group of HCV-infected patients, 33% of whom had cirrhosis, there was no correlation between perceived cognitive impairment, fatigue or depression and neuropsychological performance, which suggests that the latter might not be clinically relevant [19] .…”

Section: Cognitive Alterations In Patients With Hcv Liver Diseasementioning

confidence: 90%

Neuropsychological alterations in hepatitis C infection: The role of inflammation

Senzolo¹

2011

WJG

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About 50% of patients with hepatitis C virus (HCV) infection complain of neuropsychiatric symptoms, "brain fog", weakness, fatigue, and exhibit some degree of quality of life impairment, irrespective of the severity of liver disease. Since the first observation of HCV-related cognitive deficits, 10 studies have been published that have evaluated neuropsychiatric performance in patients with HCV infection and different degrees of hepatic impairment�� Unfortunately, these have often included patients with cirrhosis, patients who had acquired the infection through previous intravenous drug misuse, who had a history of relatively recent treatment with interferon, or were on psychoactive medication�� In addition, different neuropsychological batteries and tests that explored different cognitive domains were used, which makes the results of the studies difficult to compare�� Finally, limited information is available on the pathogenesis of HCV-related cognitive impairment�� Cerebral and/or systemic inflammation may be important players but their potential role has not been substantiated by experimental data�� The present review outlines the available evidence of the presence of cognitive impairment in patients with HCV infection, with a focus on the potential relationship with cerebral and/or systemic inflammation.

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Section: Cognitive Alterations In Patients With Hcv Liver Diseasementioning

confidence: 90%

Neuropsychological alterations in hepatitis C infection: The role of inflammation

Senzolo¹

2011

WJG

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“…30 There is considerable evidence that patients with cirrhosis, particularly those with evidence of hepatic encephalopathy, exhibit attentional dysfunction, more specifically, deficits of complex attentional skills. [31][32][33][34][35] Their inability to disengage previously focused attention 35 may play a role in their inability to track small moving objects.…”

Section: Discussionmentioning

confidence: 99%

Disruption of smooth pursuit eye movements in cirrhosis: Relationship to hepatic encephalopathy and its treatment

et al. 2005

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Smooth pursuit eye movements (SPEM) are the conjugate movements used to track the smooth trajectory of small dots. Jerky or 'saccadic' ocular pursuit has been reported in patients with cirrhosis, but no formal assessment of SPEM has ever been undertaken. The aim of this study was to evaluate SPEM in patients with cirrhosis and varying degrees of hepatic encephalopathy. The patient population comprised 56 individuals (31 men, 25 women) of mean age 51.1 (range, 25-70) years, with biopsy-proven cirrhosis, classified, using clinical, electroencephalographic, and psychometric variables, as either neuropsychiatrically unimpaired or as having minimal or overt hepatic encephalopathy; patients were further categorized in relation to their treatment status. The reference population comprised 28 healthy volunteers (12 men, 16 women) of mean age 47.3 (range, 26-65) years. SPEM was assessed using an electro-oculographic technique. Visual inspection of the SPEM recordings showed clear disruption of smooth pursuit in the patients with minimal hepatic encephalopathy, and more pronounced disruption, if not complete loss, of smooth pursuit in patients with overt hepatic encephalopathy. The differences observed in quantifiable SPEM indices between the healthy volunteers/unimpaired patients and those with overt hepatic encephalopathy were significant (P < .05). In conclusion, SPEM performance is impaired in patients with hepatic encephalopathy in parallel with the degree of neuropsychiatric disturbance: the pathophysiology of these changes is unknown, but retinal, extrapyramidal, and attentional abnormalities are likely to play a role. Treatment status confounds the classification of neuropsychiatric status and should be taken into account when categorizing these patients. (HEPATOLOGY 2005;42:772-781.)

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“…The mechanism of this inability to learn is unclear but may reflect that hyperammonemia induces an attention deficit that is crucial for learning and has been suggested as being central to the development of minimal HE. 37,38 Patients who have minimal HE are likely to have marked abnormalities of attention that include all of the domains such as working memory, alertness, selective attention, attention shift, and visual and acoustic vigilance. 37,38 Those with cirrhosis but without evidence of minimal HE had normal attention test results.…”

Section: Discussionmentioning

confidence: 99%

“…37,38 Patients who have minimal HE are likely to have marked abnormalities of attention that include all of the domains such as working memory, alertness, selective attention, attention shift, and visual and acoustic vigilance. 37,38 Those with cirrhosis but without evidence of minimal HE had normal attention test results. Although the battery of tests used in this study requires intact "attention," these tests do not specifically test "attention" and suitable studies will need to be performed to address this question.…”

Section: Discussionmentioning

confidence: 99%

Induced hyperammonemia alters neuropsychology, brain MR spectroscopy and magnetization transfer in cirrhosis

et al. 2003

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Hyperammonemia is a universal finding after gastrointestinal hemorrhage in cirrhosis. We administered an oral amino acid solution mimicking the hemoglobin molecule to examine neuropsychological changes, brain glutamine levels, and brain magnetization transfer ratio (MTR). Forty-eight metabolically stable patients with cirrhosis and no evidence of "overt" hepatic encephalopathy (HE) were randomized to receive 75 g of amino acid solution or placebo; measurements were performed before and 4 hours after administration. Neuropsychological tests included the Trails B Test, Digit Symbol Substitution Test, memory subtest of the Randt battery, and reaction time. Plasma was collected for ammonia and amino acid measurements, and brain metabolism was studied using proton magnetic resonance (MR) spectroscopy in the first 16 randomized patients. In 7 other patients, MTR was measured. A significant increase in ammonia levels was observed in the amino acid group (amino acid group, 76 ؎ 7.3 to 121 ؎ 6.4 mol/L; placebo, 83 ؎ 3.3 to 78 ؎ 2.9 mol/L; P < .001). Neuropsychological function improved significantly in the placebo group, but no significant change in neuropsychological function was observed in the amino acid group. Brain glutamate/glutamine (Glx)/creatine (Cr) ratio increased significantly in the amino acid group. MTR decreased significantly from 30 ؎2.9 to 23 ؎ 4 (P < .01) after administration of the amino acid solution. In conclusion, an improvement in neuropsychological test results followed placebo, which was not observed in patients administered the amino acid solution. Induced hyperammonemia resulted in an increase in brain Glx/Cr ratio and a decrease in MTR, which may indicate an increase in brain water as the operative mechanism. A mmonia is believed to be central in the pathogenesis of hepatic encephalopathy (HE). [1][2][3][4] It is well known that upper gastrointestinal bleeding in cirrhotic patients produces hyperammonemia and precipitates HE. [1][2][3][4][5][6] Simulating the metabolic effects of upper gastrointestinal bleeding by oral administration of erythrocytes has been shown to induce hyperammonemia and behavioral disturbance in portacaval-shunted rats. 7 In an uncontrolled study, we showed that oral administration of an amino acid solution that is identical to the amino acid profile of hemoglobin results in deterioration in memory test results, suggesting that this may be a clinically valid model to study the pathogenesis of HE. 8 Although the data relating arterial ammonia concentration to the severity of HE are controversial, there is growing evidence that greater arterial ammonia concentrations are observed in more severe states of HE. 3,4,9 In a recent study in patients with acute liver failure, an arterial concentration of ammonia greater

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Visual attention in cirrhotic patients: A study on covert visual attention orienting

Cited by 53 publications

References 25 publications

Neuropsychological alterations in hepatitis C infection: The role of inflammation

Neuropsychological alterations in hepatitis C infection: The role of inflammation

Disruption of smooth pursuit eye movements in cirrhosis: Relationship to hepatic encephalopathy and its treatment

Induced hyperammonemia alters neuropsychology, brain MR spectroscopy and magnetization transfer in cirrhosis

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