Cerebral metabolite alterations in patients with posttransplant encephalopathy after liver transplantation

Pflugrad, Henning; Tryc, Anita Blanka; Goldbecker, Annemarie; Barg‐Hock, Hannelore; Strassburg, Christian P.; Klempnauer, Jürgen; Lanfermann, Heinrich; Weißenborn, Karin; Raab, Peter

doi:10.1371/journal.pone.0221626

Cited by 14 publications

(12 citation statements)

References 39 publications

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“…For instance, brain MRI analysis identified alterations in cerebral metabolites in patients with post-transplant encephalopathy vs patients without posttransplant encephalopathy. Moreover, both groups had similar alterations in cerebral metabolites pre-LT, suggesting that intra-operative factors associated with LT (surgery duration, complications, time under anesthesia, and others) may influence cerebral osmolytes and neurological performance after LT [24]. Nevertheless, further studies are needed to precisely understand to what extent intra-operative factors/insults impact brain function and contribute to neurological complications post-LT.…”

Section: Intra-operative Factors and Neurological Complicationsmentioning

confidence: 96%

“…Clinical neurological complications following LT include seizures, cerebrovascular complications, ischemic stroke, CNS infection, brain hemorrhage (hemorrhagic stroke), osmotic demyelination syndrome, cerebral embolism, central pontine myelinolysis and posterior reversible encephalopathy syndrome [17,21,22]. Moreover, some neurological complications after LT such as post-transplant encephalopathy, alteration consciousness, disorientation, confusion, memory impairment, headaches, difficulty concentrating, focal motor deficits, fatigue, sleep impairment, and mood disorders could last for years [16,[23][24][25][26] with neuropathological abnormalities found in up to 72% of patients at autopsy [27]. In some cases, global cognitive impairments were reported to be present 9-12 months following LT [28].…”

Section: Neurological Complications Following Liver Transplantationmentioning

confidence: 99%

“…In acute liver failure (ALF), intracranial hypertension impairs cerebral blood flow [52] increasing the risk of brain injury during LT [53]. Independent of HE, alterations in cerebral osmolytes have been shown to be associated with post-transplant encephalopathy [24]. Different detrimental factors in end-stage liver disease including inflammation, malnutrition/sarcopenia, altered glucose metabolism, and systemic hemodynamics alterations (hyperdynamic state, hypovolemia) are associated in some degree with increased risk of post-transplant neurological complications [40,[54][55][56].…”

Section: He: the Vulnerable Brainmentioning

confidence: 99%

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Hepatic Encephalopathy: From Metabolic to Neurodegenerative

2021

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Hepatic encephalopathy (HE) is a neuropsychiatric syndrome of both acute and chronic liver disease. As a metabolic disorder, HE is considered to be reversible and therefore is expected to resolve following the replacement of the diseased liver with a healthy liver. However, persisting neurological complications are observed in up to 47% of transplanted patients. Several retrospective studies have shown that patients with a history of HE, particularly overt-HE, had persistent neurological complications even after liver transplantation (LT). These enduring neurological conditions significantly affect patient's quality of life and continue to add to the economic burden of chronic liver disease on health care systems. This review discusses the journey of the brain through the progression of liver disease, entering the invasive surgical procedure of LT and the conditions associated with the post-transplant period. In particular, it will discuss the vulnerability of the HE brain to peri-operative factors and post-LT conditions which may explain non-resolved neurological impairment following LT. In addition, the review will provide evidence; (i) supporting overt-HE impacts on neurological complications post-LT; (ii) that overt-HE leads to permanent neuronal injury and (iii) the pathophysiological role of ammonia toxicity on astrocyte and neuronal injury/damage. Together, these findings will provide new insights on the underlying mechanisms leading to neurological complications post-LT.

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Section: Intra-operative Factors and Neurological Complicationsmentioning

confidence: 96%

Section: Neurological Complications Following Liver Transplantationmentioning

confidence: 99%

Section: He: the Vulnerable Brainmentioning

confidence: 99%

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Hepatic Encephalopathy: From Metabolic to Neurodegenerative

2021

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“…Furthermore, dysfunction in superior frontal gyrus, lingual gyrus, inferior occipital gyrus, thalamus, putamen, and caudate structures was manifested in cirrhotic patients with previous OHE after LT (Zhang et al, 2017 ). Moreover, around 30% of cirrhotic patients develop post-transplant encephalopathy, and brain metabolites alterations (glutamine/glutamate increased, myo-Inositol, and choline decreased) have been found in these patients (Pflugrad et al, 2019 ). Then, recuperation is a slow process, and requires a long-term monitoring in order to detect post-operatory alterations or residual dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Cognitive Impairment After Resolution of Hepatic Encephalopathy: A Systematic Review and Meta-Analysis

et al. 2021

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Hepatic encephalopathy (HE) is one of the most disabling metabolic diseases. It consists of a complication of liver disease through the action of neurotoxins, such as excessive production of ammonia from liver, resulting in impaired brain function. Its prevalence and incidence are not well known, although it has been established that up to 40% of cirrhotic patients may develop HE. Patients with HE episodes display a wide range of neurological disturbances, from subclinical alterations to coma. Recent evidence suggests that the resolution of hepatic encephalopathy does not fully restore cognitive functioning in cirrhotic patients. Therefore, the aim of this review was to evaluate the evidence supporting the presence of lingering cognitive deficits in patients with a history of HE compared to patients without HE history and how liver transplant affects such outcome in these patients. We performed two distinct meta-analysis of continuous outcomes. In both cases the results were pooled using random-effects models. Our results indicate that cirrhotic patients with a history of HE show clear cognitive deficits compared control cirrhotic patients (Std. Mean Difference (in SDs) = −0.72 [CI 95%: −0.94, −0.50]) and that these differences are not fully restored after liver transplant (Std. Mean Difference (in SDs) = −0.72 [CI 95%: −0.94, −0.50]).

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“…Among the known organic substances regulating the osmotic pressure of neuroglial cells, significantly increased concentration of inositol and myoinositol in the plasma and brain tissue of patients with liver cirrhosis developing ODS have been reported. 20 Abnormalities in myoinositol concentrations have been found in dogs suffering from HE, supporting the theory of a reduced capacity to respond to osmotic changes in these dogs. 21 …”

Section: Discussionmentioning

confidence: 69%

Diagnosis of post-attenuation neurological signs syndrome in a cat with refractory status epilepticus and clinical response to therapeutic plasma exchange

Niemann

Beckmann

Iannucci

et al. 2022

Journal of Feline Medicine and Surgery Open Reports

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Case summary An 8-year-old female spayed British Shorthair cat that underwent surgical portosystemic shunt (PSS) attenuation developed progressive neurological signs 7 days postoperatively. Neurological signs progressed, despite medical management, and seizure activity became rapidly refractory to anticonvulsants. The diagnosis of post-attenuation neurological signs (PANS) was made based on the timing of the occurrence of clinical signs following surgery, absence of hyperammonaemia and suggestive MRI findings of the brain. The cat developed status epilepticus that required treatment with general anaesthesia and mechanical ventilation, from which the cat could not be effectively weaned without the recurrence of seizures. Therapeutic plasma exchange (TPE) was performed as a rescue therapy for PANS and associated refractory status epilepticus. A total of two plasma volumes were processed during one single TPE session. The seizure activity resolved immediately after the TPE session, the cat showed progressive improvement of neurological signs and remained stable thereafter. No significant complications associated with the TPE were observed. The cat was discharged 11 days after admission and was fully recovered. Relevance and novel information This is an unusual report of PANS diagnosed in a cat based on clinical and MRI findings. The cat developed refractory status epilepticus and had a positive outcome following TPE as rescue therapy. The MRI findings in this report could be useful for the diagnosis of PANS in cats. We speculate that TPE could be taken into consideration as a possible therapeutic intervention in PANS syndrome.

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Cerebral metabolite alterations in patients with posttransplant encephalopathy after liver transplantation

Cited by 14 publications

References 39 publications

Hepatic Encephalopathy: From Metabolic to Neurodegenerative

Hepatic Encephalopathy: From Metabolic to Neurodegenerative

Cognitive Impairment After Resolution of Hepatic Encephalopathy: A Systematic Review and Meta-Analysis

Diagnosis of post-attenuation neurological signs syndrome in a cat with refractory status epilepticus and clinical response to therapeutic plasma exchange

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