CT and angiographic correlation of severe neurological disease in toxemia of pregnancy

Lewis, L. K.; Hinshaw, David B.; Will, Albrecht; Hasso, Anton N.; Thompson, Joseph R.

doi:10.1007/bf00341945

Cited by 109 publications

(38 citation statements)

References 14 publications

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“…35 Cerebral vasospasm and increased vascular resistance parallel the process in other organs. 40,[46][47][48][49][50] The placenta is fetal tissue (fetal human leukocyte antigens typing) and requires unique immune modulation to remain isolated from the maternal circulation. 36,51 Placental-maternal immune reaction has been postulated.…”

Section: Clinical/biologic Features Common To Pres-associated Conditionsmentioning

confidence: 99%

“…CA and MRA demonstrate focal vasoconstriction, focal vasodilation, string-of-beads appearance, and vessel pruning, undoubtedly reflecting endothelial dysfunction (increased and decreased vessel tone) or reduced flow. 21,24,37,40,46,47,[94][95][96] Diffuse vasoconstriction is also present. 24 These features have been noted in hypertensive as well as nonhypertensive patients and have been shown to reverse.…”

Section: Evidence Of Hypoperfusion In Presmentioning

confidence: 99%

See 1 more Smart Citation

Posterior Reversible Encephalopathy Syndrome, Part 2: Controversies Surrounding Pathophysiology of Vasogenic Edema

Bartynski¹

2008

AJNR Am J Neuroradiol

948

790

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SUMMARY:Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic state accompanied by a unique brain imaging pattern typically associated with a number of complex clinical conditions including: preeclampsia/eclampsia, allogeneic bone marrow transplantation, solid organ transplantation, autoimmune diseases and high dose cancer chemotherapy. The mechanism behind the developing vasogenic edema and CT or MR imaging appearance of PRES is not known. Two theories have historically been proposed: 1) Severe hypertension leads to failed auto-regulation, subsequent hyperperfusion, with endothelial injury/vasogenic edema and; 2) vasoconstriction and hypoperfusion leads to brain ischemia and subsequent vasogenic edema. The strengths/weaknesses of these hypotheses are reviewed in a translational fashion including supporting evidence and current available imaging/clinical data related to the conditions that develop PRES. While the hypertension/hyperperfusion theory has been most popular, the conditions associated with PRES have a similar immune challenge present and develop a similar state of T-cell/endothelial cell activation that may be the basis of leukocyte trafficking and systemic/cerebral vasoconstriction. These systemic features along with current vascular and perfusion imaging features in PRES appear to render strong support for the older theory of vasoconstriction coupled with hypoperfusion as the mechanism.T he mechanism of posterior reversible encephalopathy syndrome (PRES) is not known. Two opposing hypotheses are commonly cited, but the issue is controversial: 1) The current more popular theory suggests that severe hypertension exceeds the limits of autoregulation, leading to breakthrough brain edema; 2) the earlier original theory suggests that hypertension leads to cerebral autoregulatory vasoconstriction, ischemia, and subsequent brain edema. The issues surrounding these theories are reviewed to summarize the potential values of each mechanism. Current Popular Theory: Hypertension, Failed Autoregulation, HyperperfusionSevere hypertension with failed autoregulation, injury to the capillary bed, and hyperperfusion remains the most popular theory for the brain edema that develops in PRES. [1][2][3][4] This concept is naturally intuitive, due to the frequent presence of hypertension at toxicity, and was originally embraced as the cause of eclampsia, historically labeled as a "hypertensive disorder of pregnancy." The hypertension/hyperperfusion theory is primarily based on blood pressure exceeding the autoregulation limits of the brain. AutoregulationAutoregulation is an intrinsic function of the vasculature of the brain, designed to maintain a stable blood flow in the face of fluctuating blood pressure. 5,6 Under normal circumstances, brain vessels possess intrinsic vascular tone.7 With autoregulation, vasodilation occurs as blood pressure drops and vasoconstriction occurs as blood pressure increases. [5][6][7] This function is regulated by the endothelium with release of relaxing factors (endothelium-de...

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Section: Clinical/biologic Features Common To Pres-associated Conditionsmentioning

confidence: 99%

Section: Evidence Of Hypoperfusion In Presmentioning

confidence: 99%

Posterior Reversible Encephalopathy Syndrome, Part 2: Controversies Surrounding Pathophysiology of Vasogenic Edema

Bartynski¹

2008

AJNR Am J Neuroradiol

948

790

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] On CT or MR imaging studies, the edema is often widespread but predominates in the parietal and occipital regions, likely leading Hinchey et al 15 to suggest the "posterior" description. A substantial experience with PRES has evolved; and though more widely recognized, controversy still exists as to the mechanism responsible for the brain edema.…”

mentioning

confidence: 99%

Posterior Reversible Encephalopathy Syndrome, Part 1: Fundamental Imaging and Clinical Features

Bartynski¹

2008

AJNR Am J Neuroradiol

969

890

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SUMMARY:Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic state coupled with a unique CT or MR imaging appearance. Recognized in the setting of a number of complex conditions (preeclampsia/eclampsia, allogeneic bone marrow transplantation, organ transplantation, autoimmune disease and high dose chemotherapy) the imaging, clinical and laboratory features of this toxic state are becoming better elucidated. This review summarizes the basic and advanced imaging features of PRES, along with pertinent features of the clinical and laboratory presentation and available histopathology. Many common imaging/clinical/laboratory observations are present among these patients, despite the perception of widely different associated clinical conditions.

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“…[1][2][3][4][5][6][7][8] The imaging appearance was originally noted in patients with preeclampsia/eclampsia, after transplantation (solid-organ transplantation or allogeneic bone marrow transplantation [allo-BMT]), or in the setting of severe hypertension. [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] The wider spectrum of patients who develop this toxicity was highlighted by Hinchey et al in 1996, 24 and the term "PRES" was used to characterize the typical and unique imaging appearance. The mechanism of PRES is not yet determined; however, it is thought to be related to endothelial cell dysfunction/injury leading to blood-brain barrier leakage, with resultant cortical and subcortical vasogenic edema.…”

mentioning

confidence: 99%

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

Hefzy¹,

Bartynski²,

Boardman³

et al. 2009

AJNR Am J Neuroradiol

291

227

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CT and angiographic correlation of severe neurological disease in toxemia of pregnancy

Cited by 109 publications

References 14 publications

Posterior Reversible Encephalopathy Syndrome, Part 2: Controversies Surrounding Pathophysiology of Vasogenic Edema

Posterior Reversible Encephalopathy Syndrome, Part 2: Controversies Surrounding Pathophysiology of Vasogenic Edema

Posterior Reversible Encephalopathy Syndrome, Part 1: Fundamental Imaging and Clinical Features

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

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