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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic encephalopathy is considered to be a reversible metabolic encephalopathy, which occurs as a complication of hepatocellular failure and is associated with increased portal-systemic shunting of gut-derived nitrogenous compounds. Its manifestations are most consistent with a global depression of CNS function, which could arise as a consequence of a net increase in inhibitory neurotransmission, due to an imbalance between the functional status of inhibitory (e.g., GABA) and excitatory (e.g., glutamate) neurotransmitter systems. In liver failure, factors that contribute to increased GABAergic tone include increased synaptic levels of GABA and increased brain levels of natural central benzodiazepine (BZ) receptor agonists. Ammonia, present in modestly elevated levels, may also augment GABAergic tone by direct interaction with the GABAA receptor, synergistic interactions with natural central BZ receptor agonists, and stimulation of astrocytic synthesis and release of neurosteroid agonists of the GABAA receptor. Thus, there is a rationale for therapies of HE that lower ammonia levels and incrementally reduce increased GABAergic tone towards the physiologic norm.
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PMID:Pathogenesis of hepatic encephalopathy. 1123 1

Minimal hepatic encephalopathy (HE) is a major cause of premature retirement in cirrhotics. The decision on the earning capability of a patient is usually based on clinical judgement, considering the patient's complaints and clinical findings such as nervousness and depression. In a comprehensive psychometric study we were able to show that cirrhotic patients, who are considered to be unable to earn their living, differ significantly from those who are working, in tests evaluating psychomotor function and in personality and subjective well-being scores representing nervousness, aggressiveness, depression. The latter scores are considered to represent the individual discrepancies between professional demands and cerebral performance. Since minimal HE affects psychomotor function but not verbal abilities this discrepancy exists predominantly in "blue collar workers." In accordance with this 60% of "blue collar" (in contrast to 20% of "white collar") workers of our patient group were considered unfit for work. Working ability is an essential element of quality of life in Western societies. Thus, an impairment of working capability is of major impact on quality of life in cirrhotics.
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PMID:Quality of life in cirrhotics with minimal hepatic encephalopathy. 1172 87

Cerebrocortical minislices derived from control rats ("control slices") and from rats with thioacetamide (TAA)-induced hepatic failure showing moderate hyperammonemia and symptoms of hepatic encephalopathy (HE) ("HE slices"), were incubated with physiological saline in the absence or presence of 5 mM ammonium acetate ("ammonia"), at potassium ion (K+) concentrations ranging from 5 to 15 mM. The efflux of endogenous aspartate (Asp), glutamate (Glu) and taurine (Tau) to the incubation medium was assayed by HPLC. At 5 mM K+, perfusion of control slices with ammonia did not affect Glu and slightly depressed Asp efflux. Raising K+ concentrations in the incubation medium to 7.5 led to inhibition of Glu and Asp efflux by ammonia and the inhibitory effect was further potentiated at 10 mM K+. The inhibition was also significant at 15 mM K+. This suggests that, depression of excitatory neurotransmission associated with acute hyperammonemia is more pronounced under conditions of intense neuronal activity than in the resting state. HE moderately increased the efflux of Glu and Asp, and the stimulatory effect of HE on Glu and Asp efflux showed virtually no variation upon changing K+ concentration up to 15 mM. Ammonia strongly, and HE moderately, increased Tau efflux at 5 mM K+. However, both the ammonia- and HE-dependent Tau efflux decreased with increasing K+ concentration in the medium and was no longer significant at 10 mM concentration, indicating that intense neuronal activity obliterates the neuroprotective functions of this amino acid triggered by hyperammonemia.
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PMID:Effects of ammonia and hepatic failure on the net efflux of endogenous glutamate, aspartate and taurine from rat cerebrocortical slices: modulation by elevated K+ concentrations. 1202 Jun 8

A number of studies have reported an association between chronic hepatitis C (HCV) infection and significant impairments in health-related quality of life (QOL), which are independent of the severity of liver disease. There are numerous reports documenting the prevalence of symptoms such as fatigue and depression in chronic HCV infection, which may in part account for the reductions in quality of life. Although there are a large number of potential explanations for these symptoms, including depression and anxiety associated with the diagnosis of HCV infection or substance abuse, there has been recent interest in the possibility of a biological effect of HCV infection on cerebral function. There is emerging evidence of mild, but significant neurocognitive impairment in HCV infection, which cannot be attributed to substance abuse, coexistent depression or hepatic encephalopathy. In vivo magnetic resonance spectroscopy and neurophysiological studies have suggested that a biological mechanism may underlie these cognitive findings. The recent detection of HCV genetic sequences in post mortem brain tissue raises the intriguing possibility that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment.
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PMID:Cerebral dysfunction in chronic hepatitis C infection. 1261 63

Hepatic encephalopathy is a frequent complication of cirrhosis. Portal-systemic shunts and depression of hepatic function are the primary underlying abnormalities. Arterial blood ammonia levels are frequently elevated during hepatic encephalopathy and are lower when a clinical improvement is established. Glutamine synthesis is part of the metabolic pathway for ammonia cerebral detoxification that induces ATP and glutamate (excitatory neurotransmitter) depletion. Plasma levels of branched chain amino acids are reduced in patients with cirrhosis, this event allows aromatic amino acids to cross the hemato-liquoral barrier through exchange with glutamine. Cerebral excess of aromatic amino acids promotes the synthesis of octopamine and feniletiletanolamine, weak neurotransmitters. Benzodiazepine-like substances may affect GABA-ergic transmission by interacting with their receptors on the GABA-benzodiazepine complex. Therapy is aimed at controlling the events that may precipitate the acute encephalopathy, at reducing the ammonia levels, and correcting the neurotransmission abnormalities.
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PMID:[Hepatic encephalopathy. Pathogenesis and therapy]. 1284 6

Hepatitis C virus (HCV) infection is a major public-health-care problem, with over 170 million infected worldwide. Patients with chronic HCV infection often complain of various cognitive problems as well as symptoms of depression, anxiety, and fatigue. Relatively little is known, however, about the specific cognitive deficits that are common among HCV patients, and the influence of psychiatric symptomatology on cognitive functioning. In the current study of 21 chronically infected HCV patients, we assessed subjective cognitive dysfunction, depression, anxiety, and fatigue and compared these symptom areas to cognitive tests assessing visuoconstruction, learning, memory, visual attention, psychomotor speed, and mental flexibility. Results revealed that cognitive impairment ranged from 9% of patients on a visuoconstruction task to 38% of patients on a measure of complex attention, visual scanning and tracking, and psychomotor speed, and greater HCV disease severity as indicated by liver fibrosis was associated with greater cognitive dysfunction. Objective cognitive impairment was not related to subjective cognitive complaints or psychiatric symptomatology. These findings suggest that a significant portion of patients with chronic HCV experience cognitive difficulties that may interfere with activities of daily living and quality of life. Future research using cognitive measures with HCV-infected patients may assist researchers in identifying if there is a direct effect of HCV infection on the brain and which patients may be more likely to progress to cirrhosis and hepatic encephalopathy.
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PMID:Cognitive functioning and psychiatric symptomatology in patients with chronic hepatitis C. 1463 43

Hepatic encephalopathy is the most obvious neurological consequence of chronic hepatitis C virus (HCV) infection. There are also case reports of HCV-associated cerebral vasculitis. This review is concerned with the possibility of an effect of HCV on cerebral dysfunction, occurring at an early stage of chronic infection, prior to the development of cirrhosis and unrelated to vasculitis. There is emerging evidence of mild, but significant neurocognitive impairment in HCV infection, which cannot be attributed to substance abuse, coexistent depression, or hepatic encephalopathy. In vivo magnetic resonance spectroscopy and neurophysiological studies have suggested that a biological mechanism may underlie these cognitive findings. The recent detection of HCV genetic sequences in postmortem brain tissue raises the intriguing possibility that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment.
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PMID:Central nervous system involvement in hepatitis C virus infection. 1555 29

Protein-energy malnutrition (PEM) is a prevalent observation in cirrhotic patients. In advanced cirrhotic patients with hepatic encephalopathy, dietary protein should be restricted to the low level of 0.5 g/kg/day. In such a strictly protein restricted diet, branched amino acid-enriched nutritious products should be prescribed to improve PEM. Avoidance of day-time or nocturnal fasting by frequent meals and late evening snacks is another recommendation for prevention of PEM. The n-3 polyunsaturated fatty acids (PUFA) modulate lymphocyte proliferation and eicosapetaenoic acid (EPA) up-regulates the metabolic action of insulin. The dietary n-6/n-3 PUFA ratio should be maintained between 2.8 and 3.2 in chronic liver disease. Oxidative stress is suggested as a trigger in the progression of chronic liver disease. Antioxidant vitamins; Vitamins A, E and C and carotenes may be useful to prevent the progression of chronic liver disease. Zinc depression occurs in advanced liver disease and it reduces taste and immune function. A goal of dietary management in chronic liver disease should be preventing PEM and blocking progression to hepatic cancer, and improving quality of life.
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PMID:Chronic hepatic disease and dietary instruction. 1560 46

Hepatic encephalopathy is characterized by disturbances of motor and cognitive functions involving the basal ganglia. So far no standards for assessment of neuropsychiatric abnormalities (disorders of sleep, mood, anxiety and personality) in subclinical hepatic encephalopathy have been defined. Using an animal model of mild (subclinical) hepatic encephalopathy we investigated now striatum-related behaviors and cortico-striatal synaptic plasticity in rats 2 months after introduction of a portacaval shunt and sham-operated matched controls. In a novel open field portacaval shunt rats displayed less locomotor activity; unlike controls they also showed no habituation to the field and no recall of the field environment after 24 h, indicative of cognitive deficit. The elevated-plus maze test indicated no differences in fear/anxiety in the portacaval shunt animals. Tetanic stimulation of cortical afferents in magnesium-free solution evoked an N-methyl-D-aspartate-dependent long-term potentiation in sham-operated animals. In portacaval shunt animals long-term potentiation was significantly impaired. Histamine, a potent modulator of cortico-striatal transmission, induced a larger long-term depression of field potentials in control compared with portacaval shunt rats. In conclusion, a combination of electrophysiological and behavioral approaches has revealed functional changes in cortico-striatal transmission. These data are relevant for understanding the mechanisms of motor and cognitive dysfunctions in hepatic encephalopathy patients and for the development of precise psychometric tests, evaluating cognitive deficits in subclinical hepatic encephalopathy.
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PMID:Deficits in cortico-striatal synaptic plasticity and behavioral habituation in rats with portacaval anastomosis. 1603 90

It has been reported that hepatitis C virus (HCV) infection is associated with cognitive dysfunction, fatigue and depression, which do not correlate with the severity of liver disease and cannot be accounted for by hepatic encephalopathy or drug abuse. There is also emerging evidence that HCV infection can have negative neurocognitive effects in HIV-infected cohorts. Magnetic resonance spectroscopy has suggested the likely existence of a biological basis for these effects. HCV replicative forms have recently been detected in autopsy brain tissue and the infected cells have been identified as CD68-positive (macrophages/microglia). These findings raise the possibility that HCV infection of the brain could be directly related to the reported neuropsychological and cognitive changes. HCV is not strictly hepatotropic, as it can also replicate in leukocytes, including monocytes/macrophages. The latter cells could provide access of HCV into the central nervous system ('Trojan horse' mechanism) in a process similar to that postulated for HIV-1. In support of this hypothetical mechanism come reports showing a close relationship between HCV sequences present in the brain and cerebrospinal fluid and sequences found in lymph nodes and peripheral blood mononuclear cells. However, despite some similarities there is a fundamental difference between HIV-1 and HCV infection as the latter does not progress into AIDS-type dementia.
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PMID:Emerging evidence of hepatitis C virus neuroinvasion. 1625 11


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