The neurology of liver failure

Lewis, M. B.; Howdle, P D

doi:10.1093/qjmed/hcg110

Cited by 80 publications

(57 citation statements)

References 89 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, a disturbance of sleep is recognized as one of the early signs of hepatic encephalopathy [5,6,7]. Reversal of sleep rhythm, drowsiness and lethargy are classic signs of this disease, and their presence and entity are used to define the clinical stages of hepatic encephalopathy [8,9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

et al. 2008

View full text Add to dashboard Cite

Abstract:Objective: Sleep disturbance and excessive daytime sleepiness have been reported in patients with hepatic cirrhosis. The objective of this study was to evaluate daytime somnolence and sleep complaints in a group of 178 patients with cirrhosis compared to a control group.Method: Sleep features and excessive daytime sleepiness were evaluated by the Basic Nordic Sleep Questionnaire (BNSQ) and the Epworth Sleepiness Scale (ESS). We collected clinical and laboratory data, neurological assessment and EEG recording in cirrhotic patients. Results:Patients with cirrhosis complained of more daytime sleepiness (p<0.005), sleeping badly at least three times a week (p<0.005), difficulties falling asleep (p<0.01) and frequent nocturnal awakening (p<0.005) than controls. We found a poor correlation between sleep disorders and clinical or laboratory parameters. Conclusion: Our results confirm previous literature reports suggesting a high prevalence of sleep disturbance in patients with cirrhosis.Insomnia and daytime sleepiness are the main complaints. Sleep disorders are probably a multifactorial phenomenon.

show abstract

Section: Introductionmentioning

confidence: 99%

Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

et al. 2008

View full text Add to dashboard Cite

show abstract

“…(HEPATOLOGY 2008;48:1184-1192 H yperammonemia (HA) is a well-known complication of acute and chronic liver diseases and plays a central role in the pathogenesis of hepatic encephalopathy (HE). [1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. 6-9 Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency.…”

mentioning

confidence: 99%

“…[1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. [6][7][8][9] Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency.…”

mentioning

confidence: 99%

“…13 Classical treatments of HE, except through liver transplantation and liver replacement therapies, consist in decreasing the ammonia production of urease-positive bacteria by antibiotics or decreasing the ammonia absorption into the gut by acidifying the colon content with nonabsorbable sugars such as lactulose. 4,[13][14][15] However, these treatments are insufficient due to their side effects, toxicities, poor compliance by patients, and the lack of clear effect on survival. [16][17][18] Increasing evidence indicates that probiotics, such as Lactobacillus, promote the growth of non-urease producing species, lower the intestinal pH and reduce the absorption of ammonia in the colonic lumen, 19 and could be efficient to treat HA and HE.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

et al. 2008

View full text Add to dashboard Cite

Hyperammonemia is a common complication of acute and chronic liver diseases. Often accompanied with side effects, therapeutic interventions such as antibiotics or lactulose are generally targeted to decrease the intestinal production and absorption of ammonia. In this study, we aimed to modulate hyperammonemia in three rodent models by administration of wild-type Lactobacillus plantarum, a genetically engineered ammonia hyperconsuming strain, and a strain deficient for the ammonia transporter. Wild-type and metabolically engineered L. plantarum strains were administered in ornithine transcarbamoylase-deficient Sparse-fur mice, a model of constitutive hyperammonemia, in a carbon tetrachloride rat model of chronic liver insufficiency and in a thioacetamide-induced acute liver failure mice model. Constitutive hyperammonemia in Sparse-fur mice and hyperammonemia in a rat model of chronic hepatic insufficiency were efficiently decreased by Lactobacillus administration. In a murine thioacetamide-induced model of acute liver failure, administration of probiotics significantly increased survival and decreased blood and fecal ammonia. The ammonia hyperconsuming strain exhibited a beneficial effect at a lower dose than its wild-type counterpart. Improved survival in the acute liver failure mice model was associated with lower blood ammonia levels but also with a decrease of astrocyte swelling in the brain cortex. Modulation of ammonia was abolished after administration of the strain deficient in the ammonium transporter. Intestinal pH was clearly lowered for all strains and no changes in gut flora were observed. Conclusion: Hyperammonemia in constitutive model or after acute or chronic induced liver failure can be controlled by the administration of L. plantarum with a significant effect on survival. The mechanism involved in this ammonia decrease implicates direct ammonia consumption in the gut. (HEPATOLOGY 2008;48:1184-1192 H yperammonemia (HA) is a well-known complication of acute and chronic liver diseases and plays a central role in the pathogenesis of hepatic encephalopathy (HE). [1][2][3][4][5] This neurological dysfunction results, at least in part, from an increase in plasma ammonia level and the severity of the symptoms correlates with blood ammonia level. 6-9 Animal models used in studying hyperammonemic disorders are multiple: fulminant hepatic failure, 10 chronic liver failure, 11 or urea cycle deficiency. 12 Ammonia is produced by many tissues but its major external source results from deaminase and urease activities of the gut flora. Although its absorption occurs through the intestinal epithelium, ammonia is carried by the portal vein into the liver where it is metabolized into urea. 13 Classical treatments of HE, except through liver transplantation and liver replacement therapies, consist in decreasing the ammonia production of urease-positive bacteria by antibiotics or decreasing the ammonia absorption into the gut by acidifying the colon content with nonabsorbable sugars such as lactulose. 4,[13][14][1...

show abstract

“…12,13 In the early stages, demyelination seems to predominate, but as the disease progresses axonal loss occurs, and this is likely to be irreversible. 2,14 Occasionally, demyelination has also been found in the ventral pyramidal tracts, in the posterior columns and spinocerebellar tracts. A recent study also documented in an HM patient a delayed onset posterior column dysfunction (proprioception and vibratory sensory loss) and a small fiber length-dependent axonal polyneuropathy, 15 both progressing concomitantly with the motor deficits.…”

Section: Discussionmentioning

confidence: 99%

Central motor and sensory conduction in patients with hepatic myelopathy

Nardone

Orioli²,

Höller

et al. 2014

Spinal Cord

View full text Add to dashboard Cite

Study design: Experimental neurophysiological study. Objectives: The hepatic myelopathy (HM) is characterized by progressive weakness and spasticity of the lower extremities, while there are only a few reports of sensory impairment. However, sensory function has been poorly explored in HM. We believe that an electrophysiological assessment of dorsal columns by somatosensory evoked potentials (SEPs) and of cortico-spinal lateral tracts by motor evoked potentials (MEPs) should be of considerable value in the functional evaluation of the spinal cord involvement in patients with HM. Setting: Salzburg (Austria) and Merano (Italy). Methods: Eight patients diagnosed with HM were studied with MEPs and SEPs. Neurological examination revealed different degrees of cortico-spinal tract involvement in all patients and sensory abnormalities in three patients. Results: Central motor conduction to lower limb muscles was abnormal in all patients, while central sensory conduction was abnormal in seven out of the eight patients. Both central motor and sensory conduction to upper limbs are normal in all patients. Conclusion:The main finding is that electrophysiological evidence of central sensory involvement is present in a very high percentage of patients with HM, and that the threshold for electrophysiological abnormalities is below that for clinical manifestations. Therefore, central sensory and motor conduction studies are sensitive methods for detecting, localizing and monitoring spinal cord damage in HM.

show abstract

The neurology of liver failure

Cited by 80 publications

References 89 publications

Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents

Central motor and sensory conduction in patients with hepatic myelopathy

Contact Info

Product

Resources

About