Dialysis encephalopathy: Neuropathologic aspects

Winkelman, Marc D.; Ricanati, Edmond S.

doi:10.1016/s0046-8177(86)80203-9

Cited by 24 publications

(8 citation statements)

References 41 publications

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“…In case of Al encephalopathy, significant Al content was observed in hippocampus, occipito-parietal cortex, cerebellum and striatum. This topographic distribution correlates with the clinical defects in higher cortical functions, including aphasia [43,44]. It is interesting to note in the above studies that Al tends to accumulate more in the cortex and hippocampus, both in normal and AD brains [45].…”

Section: Introductionmentioning

confidence: 79%

“…Quantitative investigations using SIMS have indicated that these intracellular concentrations can exceed 500 ppm of Al, and it is thus relevant to consider whether pathological changes are associated with intraneuronal accumulation. Studies in patients with dialysis encephalopathy have shown the presence of NFTs [62,129,137] and of spongiform changes in the neuropil [43]. Nuclear immunostaining with an antibody to the N-terminal region of the APP has been shown in patients with chronic renal failure.…”

Section: Can the Sole Involvement Of Al In Ad Be Accepted?mentioning

confidence: 99%

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Aluminium in Alzheimer?s disease: are we still at a crossroad?

Gupta

Anitha

Hegde

et al. 2005

CMLS, Cell. Mol. Life Sci.

280

147

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Aluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimer's disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.

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Section: Introductionmentioning

confidence: 79%

Section: Can the Sole Involvement Of Al In Ad Be Accepted?mentioning

confidence: 99%

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Gupta

Anitha

Hegde

et al. 2005

CMLS, Cell. Mol. Life Sci.

280

147

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“…A number of factors are probably involved in causing disturbed cognitive function, such as the increased daily aluminum intake due to aluminum containing phosphate-binding gels (Altmann et aI., 1989), the persistent exposure to the so called dial ysis disequilibrium, where ionic disturbances and sometimes water intoxication are induced, hypoten sive and hypoxic episodes during and after dialysis, and, despite the treatment, some degree of uremia. Neuropathologically, a diffuse affection, i.e., a spongy change consisting of vacuoles located in the neuropil of neurons and astrocytes throughout the cerebral cortex was described in patients with dial ysis encephalopathy (Winkelman and Ricanati, 1986). The neuropathologic correlate to the more subtle mental changes seen in patients nowadays have not yet been described.…”

Section: Resultsmentioning

confidence: 99%

Increased Cerebral Blood Flow in Anemic Patients on Long-Term Hemodialytic Treatment

Vorstrup

Lass

Waldemar

et al. 1992

J Cereb Blood Flow Metab

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Summary: CBP was measured in 15 patients on chronic hemodialytic treatment. CBP was measured with xenon-133 inhalation using single photon emission tomography. In addition, computerized tomography (CT) and a neuro logical examination were done prior to hemodialysis. Mean CBP was 66.2 ± 17.3 (SD) ml 100 g-I min-I, which was significantly higher (t-test, p < 0.05) than for an age-matched control group (54.7 ± 10.2 ml 100 g-I min -I). However, the hematocrit for the patients was considerably lower, 0.30 ± 0.07, as compared to 0.43 ± 0.03 in the controls. A significant negative correlation was observed between CBP and the hematocrit (y = -1.79x + 120.7, r = -0.71, p < 0.01). Calculating CBP from this equation in the dialyzed patients using a hematAs focal or diffuse brain tissue damage is invari ably followed by a reduction in CBF, there are rea sons to expect a CBF decrease in patients on long term hemodialytic treatment. First, the renal dis ease itself may cause uremic encephalopathy (Olsen, 1961;Tyler, 1968), although today most pa tients will receive hemodialysis early in the course of their disease to prevent long-standing severe ure mia. Second, a severe progressive neurological syn drome called dialysis dementia evolves in a number of patients regularly treated with hemodialysis. The etiology of this syndrome was originally found to relate to a high aluminum content in the dialysate (Alfrey et aI., 1976;Alfrey, 1987). Lately, it has Received November 22, 1991; final revision received March 18, 1992; accepted March 18, 1992. Address correspondence and reprint requests to Dr. Sissel Vorstrup, Department of Neurology, Rigshospitalet, 9, Blegdamsvej, 2100 Copenhagen, Denmark.Abbreviations used: CT, computed tomography; CM, can thomeatal (plane); Hct, hematocrit; PET, positron emission to mography. 745ocrit of 0.43 yielded a mean CBP value of 43.7 mlloo g-I min -I, i.e., 20% below the expected. Two patients showed a focal CBP decrease. CT showed central or cor tical atrophy in five patients, and two had small hypo dense lesions. The neurological examination revealed slight to moderate dementia in seven cases. Although mean CBP was found to be increased by 21% as com pared to the control group, an even higher CBP level would have been expected to outweigh the decreased ox ygen carrying capacity of the blood. The findings suggest a lowered metabolic demand of the brain tissue, probably due to subtle brain damage. Key Words: Anemia-CBP Hemodialysis.been suggested that even the moderately increased aluminum levels in the blood, often seen in these patients because of a high daily intake of aluminum containing phosphate-binding gels, may cause de mentia (Altmann et aI., 1989). Third, hypotensive episodes, arterial hypoxemia, and fluctuations in electrolytes and cerebral water content may occur during hemodialysis and cause subtle subclinical brain tissue damage (Savazzi et aI., 1985). Finally, the underlying process for the renal disease could cause brain damage and thereby decrease CBF. We therefore studied the in...

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“…Spongiform change of the superficial cortical layers has also been described in dialysis encephalopathy, or Alfrey's syndrome, a condition marked by stuttering, aphasia, dementia, myoclonus, and seizures in patients on chronic renal hemodialysis [221. The spongiform alteration predominates in the upper three cortical layers of the frontal, temporal, and parietal cortex of both hemispheres, left greater than right [22]. Spongiform change of the upper cortical layers has also been reported in familial Alzheimer's disease [ 5 ] in association with neurofibrillary tangles and senile plaques, and in parkinsonian dementia complex of Guam (191.…”

Section: Discussionmentioning

confidence: 99%

Progressive aphasia without dementia: Two cases with focal spongiform degeneration

Kirshner

Tanrıdağ

Thurman

et al. 1987

Annals of Neurology

150

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Two patients with the syndrome of progressive aphasia without evidence of generalized dementia underwent postmortem neuropathological examinations. In both patients, characteristic changes of Alzheimer's disease, Pick's disease, or Creutzfeldt-Jakob disease were absent. Both patients showed a focal spongiform change involving primarily layer 2 of the left inferior frontal gyrus (and temporal cortex in Patient 1) and a mild astrocytosis in layer 2 and deeper cortical layers. This focal, spongiform cortical degeneration in patients with progressive aphasia does not appear to duplicate any known central nervous system degenerative disease.

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Dialysis encephalopathy: Neuropathologic aspects

Cited by 24 publications

References 41 publications

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Increased Cerebral Blood Flow in Anemic Patients on Long-Term Hemodialytic Treatment

Progressive aphasia without dementia: Two cases with focal spongiform degeneration

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