Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study.

Videen, John S.; Michaelis, Thomas; Pinto, Priscila Rech; Ross, Brian D.

doi:10.1172/jci117728

Cited by 179 publications

(112 citation statements)

References 38 publications

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“…The Cho resonance contains contributions from phosphocholine and glycerophosphorylcholine; available evidence suggests that glycerophosphorylcholine, which comprises at least half of the MR-visible peak (Miller et al, 1996), is a cerebral osmolyte (Lien et al, 1990;Videen et al, 1995). Chronic renal failure, for example, associated with a prolonged hyerposmotic state, demonstrates a positive correlation between MRS-derived Cho and serum osmotic pressure (Sasaki et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

Zahr

Mayer

Rohlfing

et al. 2013

Neuropsychopharmacol

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Ventricular enlargement, a common in vivo marker of aging, disease, and insult, is presumed to reflect atrophy of surrounding brain regions. Pathological mechanisms underlying ventricular enlargement, however, are likely specific to the condition under investigation. Here, multimodal imaging, incorporating structural magnetic resonance imaging (MRI), MR spectroscopy (MRS), and diffusion weighted imaging (DWI), was used in rats exposed to binge ethanol (EtOH) to provide insight into a mechanism of reversible ventricular enlargement. During intoxication, MRI revealed expansion of ventricles, but volume changes in dorsal or ventral hippocampi, caudateputamen, or thalamus were not detectible. MRS of whole-brain parenchyma showed decreases in N-acetylasparate (NAA) and tissue water T2, and increases in choline-containing compounds (Cho). DWI showed decreased diffusivity selective to the thalamus. All MR parameters returned to baseline with 7 days of recovery. Rapid recovery of ventricular volume and the absence of detectable tissue volume reductions in brain regions adjacent to ventricles argue against atrophy as a mechanism of ventricular expansion. Decreased tissue water T2 and decreased thalamic diffusivity suggest lower tissue water content and a role for both NAA and Cho, as osmolytes is proposed. Together, these data support a model of fluid redistribution during acute EtOH intoxication and recovery to account for rapid ventricular volume changes.

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Section: Discussionmentioning

confidence: 99%

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

Zahr

Mayer

Rohlfing

et al. 2013

Neuropsychopharmacol

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show abstract

“…The coordinate losses of both electrolytes and organic osmolytes from the brain cells enable a very effective regulation of brain volume during hyponatremia. 16,17 The effectiveness of this mechanism in preventing lethal edema depends, among other factors, on the severity of hyponatremia and rate of reduction of the serum sodium concentration, adaptation being more efficient in chronic hyponatremia than in acute hyponatremia. There is evidence that such cerebral adaptation to hyponatremia also occurs in cirrhosis.…”

Section: Brain Adaptation To Hyponatremiamentioning

confidence: 99%

Hyponatremia in cirrhosis: Pathogenesis, clinical significance, and management

Ginès¹,

Guevara²

2008

Hepatology

280

269

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Hyponatremia is a frequent complication of advanced cirrhosis related to an impairment in the renal capacity to eliminate solute-free water that causes a retention of water that is disproportionate to the retention of sodium, thus causing a reduction in serum sodium concentration and hypo-osmolality. The main pathogenic factor responsible for hyponatremia is a nonosmotic hypersecretion of arginine vasopressin (or antidiuretic hormone) from the neurohypophysis related to circulatory dysfunction. Hyponatremia in cirrhosis is associated with increased morbidity and mortality. There is evidence suggesting that hyponatremia may affect brain function and predispose to hepatic encephalopathy. Hyponatremia also represents a risk factor for liver transplantation as it is associated with increased frequency of complications and impaired short-term survival after transplantation. The current standard of care based on fluid restriction is unsatisfactory. Currently, a new family of drugs, known as vaptans, which act by antagonizing specifically the effects of arginine vasopressin on the V2 receptors located in the kidney tubules, is being evaluated for their role in the management of hyponatremia. The short-term treatment with vaptans is associated with a marked increase in renal solute-free water excretion and improvement of hyponatremia. Long-term administration of vaptans seems to be effective in maintaining the improvement of serum sodium concentration, but the available information is still limited. Treatment with vaptans represents a novel approach to improving serum sodium concentration in cirrhosis.

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“…59,91,94 Consequently, alterations in mI levels have the potential to reflect abnormalities in both membrane metabolism and intracellular signaling mechanisms. 59 Decreased levels of mI have been observed in cases of chronic hepatic encephalopathy, hypoxic encephalopathy, stroke, tumor, and hyponatremia, 91,95 while increased concentrations have been observed in conditions such as Alzheimer's disease, diabetes mellitus, recovered hypoxia, hyperosmolar states, and the neonatal brain. 91 Concerning membrane metabolism in particular, abnormally high levels of mI have also been associated with cases of MS plaque, HIV infection, and metachromatic leukodystrophy, and these findings have led some researchers to label mI as a breakdown product of myelin.…”

Section: Impaired Phospholipid Metabolism In Bipolar Disordermentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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Magnetic resonance spectroscopy (MRS) affords a noninvasive window on in vivo brain chemistry and, as such, provides a unique opportunity to gain insight into the biochemical pathology of bipolar disorder. Studies utilizing proton ( 1 H) MRS have identified changes in cerebral concentrations of N-acetyl aspartate, glutamate/glutamine, choline-containing compounds, myo-inositol, and lactate in bipolar subjects compared to normal controls, while studies using phosphorus ( 31 P) MRS have examined additional alterations in levels of phosphocreatine, phosphomonoesters, and intracellular pH. We hypothesize that the majority of MRS findings in bipolar subjects can be fit into a more cohesive bioenergetic and neurochemical model of bipolar illness that is both novel and yet in concordance with findings from complementary methodological approaches. In this review, we propose a hypothesis of mitochondrial dysfunction in bipolar disorder that involves impaired oxidative phosphorylation, a resultant shift toward glycolytic energy production, a decrease in total energy production and/or substrate availability, and altered phospholipid metabolism. Molecular Psychiatry (2005) 10, 900-919.

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Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study.

Cited by 179 publications

References 38 publications

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

Hyponatremia in cirrhosis: Pathogenesis, clinical significance, and management

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

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