Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy

Kale, Ravindra A.; Gupta, Rakesh K.; Saraswat, Vivek A.; Hasan, Khader M.; Trivedi, Richa; Mishra, Asht M.; Ranjan, Piyush; Pandey, Chandra M.; Narayana, Ponnada A.

doi:10.1002/hep.21114

Cited by 184 publications

(197 citation statements)

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“…23 Most of the studies of these treatment modalities have found improvement in psychometry, [19][20][21][22][23] ammonia level, 20,23,24 and cerebral edema. 46 We did not measure ammonia level in our patients; however, we believe that improvement in the MHE in our patients most likely was related to the same mechanism. Lactulose was chosen as a modality of intervention in this study because the drug is cost effective, easily available, and effective in reducing blood ammonia.…”

Section: Discussionmentioning

confidence: 72%

“…Several lines of evidence suggest that the pathogenesis of MHE is similar to that of overt HE. [15][16][17] Several treatment modalities that reduce ammonia level have been tried in order to treat this condition, for example, dietary protein manipulation, 18 branched-chain amino acids, 19 L-ornithine L-aspartate, 20 lactulose, 21,22,46 and probiotics. 23 Most of the studies of these treatment modalities have found improvement in psychometry, [19][20][21][22][23] ammonia level, 20,23,24 and cerebral edema.…”

Section: Discussionmentioning

confidence: 99%

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Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy

et al. 2007

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Minimal hepatic encephalopathy (MHE) has a negative effect on patients' daily functioning. Thus far, no study has investigated the effect of treatment-related improvement in cognitive functions on health-related quality of life (HRQOL). We measured psychometric performance by number and figure connection tests parts A and B, picture completion, and block design tests and HRQOL by the Sickness Impact Profile (SIP) of 90 patients with cirrhosis on inclusion into the study and 3 months later. A Z score less than ؊2 on the neuropsychological (NP) tests was considered abnormal. Sixty-one (67.7%) patients had MHE. They were randomly assigned in a 1:1 ratio to receive treatment (lactulose) for 3 months (n ‫؍‬ 31) or no treatment (n ‫؍‬ 30) in a nonblinded design. H epatic encephalopathy (HE) is a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction diagnosed after exclusion of other known brain diseases. The Working Party at the 11th World Congress of Gastroenterology, Vienna, under the Organization Mondiale de Gastroentrologie proposed a multiaxial definition of HE that defined both the type of hepatic abnormality (type A, B, or C) and the duration and characteristics of neurological manifestations (episodic, persistent, or minimal HE) in chronic liver disease. 1 HE has been considered a continuous dimension that could be measured with 1 index to summarize several neurological domains, such as cognition, emotion, behavior, and biologic rhythms. Minimal hepatic encephalopathy (MHE) represents a portion of this dimension and is the mildest form of HE. Whereas patients with HE have impaired intellectual functioning, personality changes, altered level of consciousness, and neuromuscular dysfunction, patients with MHE have no recognizable clinical symptoms of HE but do have mild cognitive and psychomotor deficits. In the absence of a "gold standard" for determining MHE, neuropsychological (NP) and neurophysiological methods have been the most trusted and widely used tests to diagnose this condition. 1,2 MHE is considered clinically relevant for at least 3 reasons. First, it impairs patients' daily functioning and

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy

et al. 2007

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“…36 Recent MRI studies of patients with ALF demonstrate evidence of interstitial brain edema as well as cytotoxic edema, implying there may be a vasogenic component to the cerebral edema in ALF. 37,38 In an animal model of ALF, astrocyte swelling, extravascular and interstitial edema has been described. However, brain capillary endothelial cells and their tight junctions appeared intact.…”

Section: Ammonia and The Brain: The Sick Astrocytementioning

confidence: 99%

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

222

169

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The syndrome we refer to as Hepatic Encephalopathy (HE) was first characterized by a team of Nobel Prize winning physiologists led by Pavlov and Nencki at the Imperial Institute of Experimental Medicine in Russia in the 1890's. This focused upon the key observation that performing a portocaval shunt, which bypassed nitrogen-rich blood away from the liver, induced elevated blood and brain ammonia concentrations in association with profound neurobehavioral changes. There exists however a spectrum of metabolic encephalopathies attributable to a variety (or even absence) of liver hepatocellular dysfunctions and it is this spectrum rather than a single disease entity that has come to be defined as HE. Differences in the underlying pathophysiology, treatment responses and outcomes can therefore be highly variable between acute and chronic HE. The term also fails to articulate quite how systemic the syndrome of HE can be and how it can be influenced by the gastrointestinal, renal, nervous, or immune systems without any change in background liver function. The pathogenesis of HE therefore encapsulates a complex network of interdependent organ systems which as yet remain poorly characterized. There is nonetheless a growing recognition that there is a complex but influential synergistic relationship between ammonia, inflammation (sterile and non-sterile) and oxidative stress in the pathogenesis HE which develops in an environment of functional immunoparesis in patients with liver dysfunction. Therapeutic strategies are thus moving further away from the traditional specialty of hepatology and more towards novel immune and inflammatory targets which will be discussed in this review. ( J CLIN EXP HEPATOL 2015;5:S7-S20) H epatic encephalopathy (HE) is the term used to encapsulate the broad spectrum of neuropsychiatric disturbances associated with both acute and chronic liver failure (ALF and CLF, respectively), as well as porto-systemic bypass in the absence of hepatocellular disease. The clinical manifestations of HE can be extremely heterogeneous in nature, with symptoms presenting anywhere on a continuum spanning from seemingly normal cognitive performance, right the way through to states of confusion, stupor and coma. In between these extremes, patients with HE may exhibit signs such as inattentiveness, blunted affect, impairment of memory or reversal of the sleep-wake cycle, as well as physical manifestations such as tremor, myoclonus, asterixis and deep tendon hyperreflexia.ALF is defined by the onset of coagulopathy alongside any degree of encephalopathy in patients with no evidence of pre-existing liver disease. 1 The presence of HE in those with ALF is prognostic, with up to a quarter of cases developing raised intracranial pressure. 2 Patients presenting with ALF are at risk of developing its cardinal, lifethreatening feature, cerebral edema. Left untreated, cerebral edema can rapidly progress to cause herniation of the uncus through the falx cerebri, leading to compression of the brainstem and, ultimately, death. H...

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“…MHE being a preclinical stage of HE has similar pathogenesis. [20][21][22] Ammonia is metabolized only by astrocytes in brain and increased ammonia levels causes rise in intracellular glutamine levels leading onto low-grade cerebral edema and HE. 23 Ammonia also modulates glutamate neurotransmission and induces neurosteroid production in neurons, leading to a positive modulatory effect on the gamma-aminobutyric acid-A receptor.…”

Section: Pathogenesis Of Minimal Hepatic Encephalopathymentioning

confidence: 99%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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Minimal hepatic encephalopathy (MHE) is the mildest form of the spectrum of neurocognitive impairment in cirrhosis. It is a frequent occurrence in patients of cirrhosis and is detectable only by specialized neurocognitive testing. MHE is a clinically significant disorder which impairs daily functioning, driving performance, work capability and learning ability. It also predisposes to the development of overt hepatic encephalopathy, increased falls and increased mortality. This results in impaired quality of life for the patient as well as significant social and economic burden for health providers and care givers. Early detection and treatment of MHE with ammonia lowering therapy can reverse MHE and improve quality of life. ( J CLIN EXP HEPATOL 2015;5:S42-S48) H epatic encephalopathy (HE) is a neurocognitive disorder in which brain function is impaired and is associated with both acute and chronic liver dysfunction. 1 It is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Minimal HE (MHE) is the mildest form of spectrum of HE which is characterized by subtle cognitive and psychomotor deficits in the absence of recognizable clinical symptoms of HE. 2 It occurs in patients with liver dysfunction and/or portosystemic shunts. In MHE, neurocognitive abnormalities primarily affect attention, speed of information processing, executive control, motor ability and coordination in an individual. 3 In 1970, Zeegen et al 4 first described this condition when they discovered that 38% of patients who had undergone portal decompression surgery scored abnormal in Reitan trail making test (number connection test). Eight years later, the term subclinical HE 5 was introduced to describe these patients. Since then, this condition was described under various names like early HE, latent HE, subclinical HE and finally minimal HE. The latest classification combines MHE and grade 1 HE into covert HE while higher grades are classified as overt HE, thus simplifying the clinical schema so that HE can be uniformly diagnosed. 6 Covert HE means that the mental defect is not detectable by the clinician using conventional testing and is not noticeable to the patient. However, it is significant because these patients usually have neuropsychiatric and neurophysiological abnormalities on advanced testing which are not enough to cause disorientation or asterixis. MHE is regarded as a preclinical stage of HE and ammonia and systemic inflammation plays an important role in its pathogenesis similar to HE. Ammonia lowering therapies were used in the treatment of MHE and found to be effective.MHE is clinically significant as it impairs daily functioning, health related quality of life (HRQOL) and driving skills, predicts the development of overt HE and is associated with poor survival. 7-11 Overt HE develops in >50% of MHE patients within three years. 10 These patients pose a significant burden to their care givers depending on the severity of cognitive dysfunction. 2,12 Considering all ...

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Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy

Cited by 184 publications

References 38 publications

Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy

Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Minimal Hepatic Encephalopathy Impairs Quality of Life

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