The impact of liver disease on cognitive functioning and mood.

The following review discusses some of the cognitive and functional problems in liver disease. Some medical literature is included which is consistent with difficulties reported by patients. Prevalence, possible causes, and types of liver disease are reviewed, including an outline of various complications associated with the disease. Hepatic encephalopathy (HE) is one such complication and a general background to this is given. It has been suggested that subgroups of patients with liver disease have mild cognitive deficits and demonstrate poorer performances on neuropsychological tests compared with matched controls. This has been termed minimal hepatic encephalopathy (MHE), a syndrome that occurs in patients with liver disease without overt symptoms of hepatic encephalopathy. The full spectrum of cognitive impairment in MHE is unknown (Collie, 2005). Research has attempted to understand the profile of cognitive deficits in patients with liver disease. Studies have investigated various areas of functioning (e.g. psychomotor skills, attention and memory) by neuropsychological testing. The main studies are presented in the review. Some of the limitations of the minimal hepatic encephalopathy hypothesis are discussed. There is some debate about possible causes of observed cognitive deficits and various psychological models including health (coping and quality of life) and clinical (mood issues) are proposed. Further research and clinical implications are also discussed

Minimal hepatic encephalopathy: consensus statement of a working party of the Indian National Association for study of the liver

Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30-45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party

The burden of minimal hepatic encephalopathy: from diagnosis to therapeutic strategies

Minimal hepatic encephalopathy (MHE) is the mildest form of hepatic encephalopathy (HE). It affects the performance of psychometric tests focused on attention, working memory, psychomotor speed, and visuospatial ability, as well as electrophysiological and other functional brain measures. MHE is a frequent complication of liver disease, affecting up to 80% of tested patients. By being related to falls, an impairment in fitness to drive and the development of overt HE, MHE severely affects the lives of patients and caregivers by altering their quality of life and their socioeconomic status. MHE is detected in clinically asymptomatic patients using appropriate psychometric tests and neurophysiological methods that highlight neuropsychological alterations, such as video-spatial orientation deficits, attention disorders, memory, reaction times, electroencephalogram slowing, prolongation of latency-evoked cognitive potentials, and reduction in the critical flicker frequency. Several treatments have been proposed for MHE treatment, including non-absorbable disaccharides, poorly absorbable antibiotics such as rifaximin, probiotics and branched-chain amino acids. However, because of the multiple diagnosis methods, the various endpoints of treatment trials and the variety of agents used in trials, the treatment of MHE is not currently recommended as routine, but only on a case-by-case basis

Minimal Hepatic Encephalopathy: Silent Tragedy

Hepatic encephalopathy (HE) is brain dysfunction caused by both acute and chronic liver diseases that produces a spectrum of neuropsychiatric symptoms in the absence of other known brain diseases. Minimal hepatic encephalopathy (MHE) is the mildest form of this spectrum. MHE is defined as HE without symptoms on clinical or neurological examination, but with deficits in the performance of psychometric tests, working memory, psychomotor speed, and visuospatial ability. Minimal hepatic encephalopathy is associated with impaired driving skills and increased risk of motor vehicle accidents and has been associated with increased hospitalizations and death. Despite its clinical importance, a large number of clinicians had never investigated whether their cirrhotic patients might have MHE. Although, there is no single gold standard test for diagnosis of MHE, a combination of two neuropsychological tests or psychometric hepatic encephalopathy score battery test and/or neurophysiological test is standard for diagnosis of MHE. It was found that, treatment for MHE improves neuropsychiatric performance and quality of life and decreases the risk of developing overt HE (OHE). The agents used to treat OHE have been tested in patients with MHE. In particular, lactulose, rifaximin, probiotics and l-ornithine and l-aspartate (LOLA) have all been shown to be beneficial, with documented improvement in psychometric performance after treatment

Hepatic encephalopathy

Hepatic encephalopathy (HE) is a prognostically relevant neuropsychiatric syndrome that occurs in the course of acute or chronic liver disease. Besides ascites and variceal bleeding, it is the most serious complication of decompensated liver cirrhosis. Ammonia and inflammation are major triggers for the appearance of HE, which in patients with liver cirrhosis involves pathophysiologically low-grade cerebral oedema with oxidative/nitrosative stress, inflammation and disturbances of oscillatory networks in the brain. Severity classification and diagnostic approaches regarding mild forms of HE are still a matter of debate. Current medical treatment predominantly involves lactulose and rifaximin following rigorous treatment of so-called known HE precipitating factors. New treatments based on an improved pathophysiological understanding are emerging

A Study on Minimal Hepatic Encephalopathy.

INTRODUCTION : Minimal Hepatic Encephalopathy (MHE) is the earliest stage of hepatic encephalopathy and is associated with changes in cognitive functions, in electrophysiological parameters and in cerebral neurochemical/ neurotransmitter homeostasis. MHE can be observed in patients with cirrhosis who have no clinical evidence of hepatic encephalopathy. Prevalence is estimated to be about 30% - 60% in cirrhotics without overt clinical signs of hepatic encephalopathy 1-7 . Probability of clinical hepatic encephalopathy after follow up of 3years was estimated to be 50% in patients with MHE compared to 8% in cirrhotics without MHE, whether this course of events is affected by early treatment needs to be studied. MHE often manifested with sleep disturbances or subtle behavioral changes that are more apparent to the patient’s family than to the clinician. The behavioral changes are due predominantly to subtle impairment of cognitive function resulting from bilateral dysfunction of forebrain and parieto-occipital regions, because verbal abilities are usually preserved in this stage of hepatic encephalopathy. Cerebral dysfunction is not detectable by the routine clinical examination but only by neuropsychological or neurophysiological measures. Patients with MHE perform worse than healthy controls especially in tests of psychomotor speed, visual perception and attention. Some of these patients also show a pathologic slowing of the electroencephalogram (EEG) and Prolonged Latencies of Exogenous (Visual Evoked Potentials (VEP), Somatosensory Evoked Potentials (SSEP) and Brainstem Auditory Evoked Potentials (BAEP) and endogenous evoked potentials (P300). A consensus has emerged that patients with MHE should be treated. Only limited numbers of studies are available to analyze the importance of encephalopathy. Hence psychometric and neurophysiological tests to diagnose minimal hepatic encephalopathy. AIM OF THE STUDY : To find out the prevalence of Minimal Hepatic Encephalopathy in cirrhotic patients with the help of Number connection test (NCT), Electroencephalogram (EEG) and Brainstem auditory evoked potential (BAEP). CONCLUSION : Minimal Hepatic Encephalopathy is proved undoubtedly impairs quality of life observed in patients with cirrhosis who have no overt encephalopathy, medical intervention can improve both cognitive function and health related quality of life. Hence screening for Minimal Hepatic Encephalopathy is important in cirrhotics to provide them a good quality of life, driving skills which is impaired in Minimal Hepatic Encephalopathy by interfering at the early stage of the disease to prevent progression to overt encephalopathy which has got a high mortality. Diagnosis of MHE requires high index of suspicion, useful three diagnostic tools are NCT, EEG and BAEP. This study showed 48% had abnormal NCT, 30% had abnormal EEG, 24% had abnormal BAEP with combined prevalence of MHE 64%. This study suggested that Number connection test (NCT), Electroencephalogram (EEG) and Brainstem auditory evoked potentials (BAEP) are valid tools for the screening of minimal hepatic encephalopathy in cirrhotic patients of various etiology as there is a greater likelihood of overt encephalopathy development in the immediate follow up period in patients with an abnormality detected by these tests than in patients with no such abnormality. Seven patients developed overt encephalopathy within a period of 2months in the one year follow up period. Large scale study may be needed to enlighten these aspects. These tools can be used for screening for MHE in patients with cirrhosis

Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a complex neurological syndrome, characteristic of patients with liver disease, that causes a wide and complex spectrum of nonspecific neurological and psychiatric manifestations, ranging from a subclinical entity such as minimal or covert hepatic encephalopathy to a deep form in which a complete alteration of consciousness can be observed: overt hepatic encephalopathy. Both minimal and overt hepatic encephalopathy have a high impact on patients, caregivers, and national health services, driving substantial consumption of economic resources. In this Special Issue, we discussed the current state-of-the-art research, address ongoing knowledge gaps, and ongoing controversies related to the pathogenesis, diagnosis, and therapeutic management of hepatic encephalopathy

A Study on Minimal Hepatic Encephalopathy in Cirrhotics.

INTRODUCTION : Hepatic encephalopathy includes a spectrum of transient and reversible neurological and psychiatric manifestations usually found in patients with chronic liver disease and portal hypertension. Its occurrence indicates a poor prognostic factor with a projected one year survival rate of 43%. It occurs in 50% to 70% of cirrhotic patients. The least severe form of hepatic encephalopathy, which is not recognized on clinical examination is Minimal hepatic encephalopathy (MHE). It impairs health related quality of life (HRQOL). It can be detected by using sensitive tests like number connection tests, line tracing tests and figure connection tests, EEG, visual, auditory and somatosensory evoked potentials. Ammonia levels are found to be elevated in patients with minimal hepatic encephalopathy and therefore can play a role in the causation of minimal hepatic encephalopathy. Minimal hepatic encephalopathy has a subtle but negative impact on a patient’s spatial and motor skills, the ability to perform complex tasks such as driving, and even quality of life. Some studies have reported that patients with MHE can progress and later on develop overt hepatic encephalopathy. Due to its negative impact on daily living, it has been suggested that the failure to diagnose this condition could be classified as a medical error. Helicobacter pylori, a gram negative microaerophilic bacteria produces ammonia from urea, which is absorbed in the gastric lumen into circulation.Infection with these bacteria can result in hyperammonemia and hepatic encephalopathy and eradication of these bacteria results in decreased ammonia levels. AIM AND OBJECTIVES : 1. To study the incidence of minimal hepatic encephalopathy in asymptomatic cirrhotics. 2. To study the prevalence of helicobacter pylori in asymptomatic cirrhotics with minimal hepatic encephalopathy. CONCLUSION : This study shows the high incidence of minimal hepatic encephalopathy in asymptomatic cirrhotic patients. This study proves that the prevalence of H.pylori is markedly high in patients with minimal hepatic encephalopathy