Incomplete improvement of visuo-motor deficits in patients with minimal hepatic encephalopathy after liver transplantation

Mechtcheriakov, Sergei; Graziadei, Ivo; Mattedi, Michael; Bodner, Thomas; Kugener, André; Hinterhuber, Hartmann; Marksteiner, Josef; Vogel, Wolfgang

doi:10.1002/lt.20009

Cited by 88 publications

(79 citation statements)

References 35 publications

(39 reference statements)

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“…The type cognitive assessment throughout the studies includes several components that are affected in MHE, such as attention, concentration, psychomotor speed and verbal and visuospatial short-term memory. Therefore, most of the studies consider also the persistence or worsening of preexisting cognitive deficits as POCD [27][28][29]22,[37][38][39][40][41][42], in accordance with the statement that successful LT should remove HE [27,31,32]. MHE predicts OHE [43], but it is often clinically missed [44].…”

Section: Pocd In Lt Recipientsmentioning

confidence: 73%

Postoperative cognitive dysfunction after liver transplantation

Aceto

Perilli

Lai

et al. 2015

General Hospital Psychiatry

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Section: Pocd In Lt Recipientsmentioning

confidence: 73%

Postoperative cognitive dysfunction after liver transplantation

Aceto

Perilli

Lai

et al. 2015

General Hospital Psychiatry

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“…This potentially helps explain the persisting neurological complications in patients following liver transplantation [6,[22][23][24]. Furthermore, even though liver transplantation dramatically improves the clinical neurological status, there is evidence in the literature to suggest that minimal HE may persist due to unknown irreversible changes in the brain [25,26]. Therefore full recovery and reversibility of HE following liver transplantation is currently under scrutiny [23].…”

Section: Discussionmentioning

confidence: 99%

Neuropathological changes in the brain of pigs with acute liver failure

Kristiansen

Lindal

Myreng

et al. 2010

Scandinavian Journal of Gastroenterology

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Kristiansen, R.G. et al., 2010. Neuropathological changes in the brain of pigs with acute liver failure. Scandinavian journal of gastroenterology, 45(7-8) ABSTRACTObjective. Cerebral edema is a serious complication of acute liver failure (ALF), which may lead to intracranial hypertension and death. An accepted tenet has been that the blood-brain barrier is intact and that brain edema is primarily caused by a cytotoxic etiology due to hyperammonemia. However, the neuropathological changes in ALF have been poorly studied. Using a well characterized porcine model we aimed to investigate ultrastructural changes in the brain from pigs suffering from ALF. Materials and methods. Sixteen female Norwegian Landrace pigs weighing 27-35 kg were randomised into two groups: ALF (n = 8) and sham operated controls (n = 8). ALF was induced with an end-to-side portacaval shunt followed by ligation of the hepatic arteries. Biopsies were harvested from three different areas of the brain (frontal lobe, cerebellum, and brain stem) following eight hours of ALF and analyzed using electron microscopy. Results. Profound perivascular and interstitial edema were found in all three areas. Disruption of pericytic and astrocytic processes were seen, reflecting breakdown/lesion of the blood-brain barrier in animals suffering from ALF. Furthermore, neurons and axons were edematous and surrounded by vesicles. Severe damage to Purkinje neuron (necrosis) and damaged myelin were seen in the cerebellum and brain stem, respectively. Biopsies from sham operated animals were normal. Conclusions. Our data support the concept that vasogenic brain edema plays an important role in the development of intracranial hypertension in pigs with ALF.

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“…In patients undergoing liver transplantation for cirrhosis, the deficits related to MHE may improve (33); however, a significant number of patients demonstrate only marginal or even no improvement in their visuomotor or visuoconstructive functioning (34). This led to the hypothesis that there may be two types of MHE: delirium-like MHE, which is reversible with transplant; and 'dementia-like MHE', which is not reversible with transplant (35).…”

Section: Treatmentmentioning

confidence: 99%