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(Stroke. 1997;28:1082-1085.)
© 1997 American Heart Association, Inc.
Articles |
Diffusion-Weighted Imaging Discriminates Between Cytotoxic and Vasogenic Edema in a Patient With Eclampsia
From the Departments of Radiology (P.W.S., R.G.G.) and Neurology (F.S.B., L.H.S.), Massachusetts General Hospital, Boston.
Correspondence to Pamela W. Schaefer, MD, Gray 285, Massachusetts General Hospital, Fruit St, Boston, MA 02114.
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Abstract |
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 Top Abstract IntroductionCase ReportDiscussionReferences |
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Background The pathophysiology of eclampsia remains unclear. While the majority of patients develop reversible T2 hyperintense signal abnormalities on MR scans and reversible neurological deficits, some patients do develop infarctions (permanent T2 hyperintense abnormalities) and permanent neurological impairment. Routine MRI cannot prospectively differentiate between these two patient groups. Echo-planar diffusion-weighted imaging, however, is a new technique that clearly differentiates between cytotoxic and vasogenic edema.
Case Description A 30-year-old woman developed symptoms consistent with eclampsia 24 hours after delivering premature twins. An MRI demonstrated extensive, diffuse T2 hyperintense signal abnormalities involving subcortical white matter and adjacent gray matter with a posterior predominance, consistent with either infarction or hypertensive ischemic encephalopathy. Diffusion-weighted images demonstrated increased diffusion, consistent with vasogenic edema and hypertensive ischemic encephalopathy.
Conclusions Unlike routine MRI, diffusion-weighted imaging reliably differentiates between vasogenic edema and cytotoxic edema. Consequently, in eclamptic patients diffusion-weighted imaging can afford clear differentiation between hypertensive ischemic encephalopathy and infarction, two very different entities with very different treatment protocols. Diffusion-weighted imaging should be performed in all eclamptic patients and should greatly affect their management.
Key Words: brain edema • eclampsia • hypertension • magnetic resonance imaging
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Introduction |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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Eclampsia is characterized clinically by hypertension, edema, proteinuria, and seizures in women during the second half of pregnancy or in the immediate postpartum period. The pathophysiology remains unclear.1 2 3 4 One proposed mechanism is that cerebral vasospasm induced by severe hypertension results in ischemia and consequent cytotoxic edema. This is supported by angiographic findings of diffuse or focal vasospasm and by infarctions in some patients.1 2 5 Pathological findings of widespread arteriolar vasospasm and thrombosis and gross and microscopic infarctions also support this theory.6 7 An alternative theory is that acute hypertension in eclampsia induces loss of autoregulation with passive dilatation of cerebral arterioles; hydrostatic pressure results in the extravasation of proteins and fluid into the interstitium.8 9 10 Multiple reports of reversible T2 hyperintense white matter lesions with a predominance in the posterior circulation (where there is less vasomotor sympathetic innervation) as well as increased perfusion with SPECT scanning in patients with both eclampsia and hypertensive ischemic encephalopathy support this latter theory.8 11 12 13 14 15 16 17
Echo-planar diffusion-weighted imaging is a new technique by which images sensitive chiefly to the molecular diffusion of water molecules can be generated. It has been well documented that acute infarction with the development of cytotoxic edema is characterized by markedly decreased diffusion.18 19 20 21 22 It has also been demonstrated that increased interstitial water, which is found in vasogenic edema, demonstrates increased diffusion.4 23 24 We describe a patient with eclampsia with multiple large abnormal T2 hyperintense regions in whom we used diffusion-weighted imaging to differentiate between vasogenic and cytotoxic edema.
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Case Report |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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A 30-year-old right-handed woman was transferred to our hospital at 29 weeks of gestation complaining of dyspnea and tachycardia. She presented in preterm labor complicated by gestational diabetes and borderline preeclampsia, with elevated transaminases (SGOT, 114 U/L; SGPT, 122 U/L; alkaline phosphatase, 138 U/L; lactate dehydrogenase, 416 U/L), hyperuricemia (uric acid, 11.9 mg/dL), pulmonary edema, proteinuria (24-hour urinary total protein, 297 mg/L; creatinine, 858 mg), and mild hypertension (blood pressure, 158/108 mm Hg). Her pulmonary edema was treated with furosemide. Tocolytic therapy with terbutaline and magnesium did not arrest labor, and she delivered premature twins by cesarean section within 48 hours. That night she experienced severe neck and occipital pain, and the following day she had a generalized, tonic-clonic seizure. Intravenous magnesium therapy was initiated, and a noncontrast enhanced head CT demonstrated multiple 3- to 15-mm hypodensities in the parietal lobes involving gray and white matter and in the left frontal subcortical white matter. She was evaluated by the Massachusetts General Hospital Stroke Service 36 hours after her seizure and was found to be alert and oriented with fluent speech and no cognitive deficits. Her fundi were benign. She had a few beats of gaze-evoked horizontal nystagmus with gaze to either side and a slightly flattened left nasolabial fold. Strength, sensation, and cerebellar function were normal. Deep tendon reflexes were increased in the right upper limb, and a Hoffmann's reflex was elicited in the right hand. An MRI was obtained on a 1.5-T GE Signa system with echo-planar capabilities provided by Advanced NMR Systems. Fast spin-echo, T2-weighted images (TR, 4200 ms; TE, 104 ms; ETL, 8; FOV, 20x20 cm; matrix, 256x192; slice thickness, 5 mm with 1 mm gap; 1 NEX) (Figure
, panel A)
demonstrated extensive T2 hyperintensity involving the gray and
subcortical white matter in all lobes with predominance in the temporal
and occipital lobes as well as in the frontal and parietal convexities;
small T2 hyperintense foci were also seen in the cerebellar hemispheres
bilaterally. Isotropic diffusion-weighted images (single-shot EPI;
diffusion gradients applied in six orthogonal directions with effective
gradient amplitude of 14 mT/m; TR, 6000 ms; TE, 108 ms; FOV, 40x20 cm;
matrix, 256x128; slice thickness 6 mm with 1 mm gap; 1 NEX;
b value of 1221 s/mm2) (Figure, panel B)
demonstrated increased diffusion in most of these regions with four
sampled ADCs ranging from 1.2 to
1.8x10-3 mm2/s. Four sampled
ADCs in normal subcortical white matter ranged from 0.68 to
0.88x10-3 mm2/s; no areas of
decreased diffusion were identified. Repeated physical examination 3
days later revealed new onset of bilateral cerebellar dysmetria,
overshoot with leftward saccades, mild truncal ataxia, and pronounced
horizontal nystagmus on left lateral gaze. A repeated MRI demonstrated
partial decrease in the extent of some of the T2 hyperintense regions
with corresponding partial resolution of the abnormally increased
diffusion. MR angiography of the neck showed no evidence of vertebral
artery dissection. Transthoracic
echocardiography was normal. The patient improved
rapidly, and within 3 weeks all previously noted neurological
abnormalities had resolved. Follow-up MRI at that time demonstrated
complete resolution of the T2 signal abnormalities (Figure, panel C)
and of the corresponding regions of increased diffusion (Figure, panel
D); four ADCs sampled in locations similar to those of the initial
elevated ADCs returned to normal values and ranged from 0.53 to
0.88x10-3 mm2/s.
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Discussion |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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The clinical hallmarks of eclampsia are hypertension, peripheral edema, proteinuria, and seizures. Other neurological findings include headaches, loss of vision, mental status changes, and coma. Previously reported neuroimaging findings include reversible CT hypodense and MRI T2 hyperintense abnormalities seen predominantly in the subcortical white matter and basal ganglia,8 11 12 13 14 15 increased perfusion on SPECT imaging,11 occasional infarctions,5 11 13 diffuse vasoconstriction on angiography,1 5 13 and intracerebral hemorrhage.25 While the pathophysiology of eclampsia remains unclear, the clinical, pathological, and neuroimaging findings have led to two major hypotheses. Based on angiographic findings of vasoconstriction, permanent infarctions in the more severely affected patients, and pathological findings of arteriolar vasoconstriction, vessel thrombosis, and infarctions,6 7 one proposed mechanism is hypertension-induced vasoconstriction causing ischemia with the development of cytotoxic edema.1 3 An alternative view suggests that eclampsia is a form of hypertensive encephalopathy; hypertension induces a loss of autoregulation,8 9 10 11 which leads to passive arteriolar dilatation, opening of tight junctions, extravasation of macromolecules, and vasogenic edema. This theory is supported by multiple reports of reversible T2 hyperintense abnormalities, increased perfusion with SPECT imaging, and animal models demonstrating focal areas of arteriolar dilatation separated by segments of normal vessel.
One would predict that the appropriate management of acute hypertension in eclampsia would be different under the two competing hypotheses. If cerebral vasospasm were the underlying pathophysiological mechanism, then the vasospasm would have to be severe enough to cause distal ischemia and cytotoxic edema. Cerebral perfusion to these regions should be further reduced by the acute lowering of mean arterial pressure, and additional ischemic injury should ensue. Treatment then ought to resemble that which is initiated for vasospasm from other etiologies, such as for the vasospasm associated with subarachnoid hemorrhage. In this setting, mean arterial pressure is increased and intracranial pressure is reduced to ensure adequate cerebral perfusion pressure. Several observations do not support this hypothesis in the majority of patients with eclampsia. First, most patients respond well to reductions in mean arterial pressure, and ischemic infarction or permanent neurological injury is rarely seen. Second, some angiographic studies of eclamptic patients with neurological impairment have been unrevealing,26 indicating that vasospasm of large or medium-sized vessels as seen on angiography is not necessary to cause the clinical syndrome. Third, the degree of ischemia necessary to cause cytotoxic edema (failure of the ATP-dependent ion pumps) results in depression of neuronal cellular function. However, patients with eclampsia often have relatively minor neurological impairment compared with the rather extensive territory of T2 signal abnormality, making it unlikely that these regions are in fact ischemic. For these reasons, it is likely that hypertension-induced vasogenic edema is the underlying pathophysiological mechanism in most eclampsia cases. However, a small percentage of patients do develop infarctions and permanent neurological deficits; in some of these patients, vasospasm has been demonstrated on angiograms.
To date, there has not been a reliable method of distinguishing between vasogenic and cytotoxic edema in the living patient at the onset of eclampsia at a time when this knowledge could greatly affect management. On conventional MRI, vasogenic edema is usually marked by T2 hyperintensity predominantly involving white matter, and cytotoxic edema is marked by T2 hyperintensity involving gray matter, white matter, or both. Conventional MRI cannot clearly distinguish between these different types of edema. Echo-planar diffusion-weighted imaging, however, is a new technique that clearly distinguishes between the two. With very strong gradient pulses, images sensitive chiefly to molecular diffusion of water molecules can be generated. Regions with cytotoxic edema demonstrate diffusion coefficients that are decreased compared with those of white matter.18 19 20 21 22 In the setting of acute stroke, this is thought to result from decreased Na+,K+-ATPase activity in glial cell membranes and consequent decrease in water molecule transport. Conversely, regions with vasogenic edema demonstrate diffusion coefficients that are markedly increased compared with those of normal white matter.4 23 24
In our patient, routine fast spin-echo, T2-weighted MR images demonstrated multiple regions of extensive T2 signal abnormality involving both white and gray matter. These were interpreted as representing either infarctions or multiple areas of vasogenic edema; we could not readily differentiate between the two. On diffusion-weighted imaging, all T2 hyperintense regions demonstrated markedly increased diffusion, consistent with vasogenic edema; no regions of decreased diffusion to suggest cytotoxic edema were identified. These findings were consistent with the fact that our patient had relatively minor neurological impairment. These initial findings strongly support the pathophysiological mechanism of hypertension-induced vasogenic edema. We were able to confidently lower blood pressure, avoid further invasive evaluation, and defer anticoagulation therapy because we were confident that the patient had not developed thromboembolic infarctions. Follow-up imaging demonstrated complete resolution of the diffusion and T2 abnormalities and confirmed our hypothesis.
Our data confirm only that we could accurately identify that the MRI T2 signal abnormality in our patient represents vasogenic edema. Occasionally patients, for unclear reasons, develop infarctions and permanent neurological deficits. Diffusion-weighted imaging is noninvasive, requires 126 seconds to perform, and in the near future will be readily available on most MR scanners. Since this technique accurately distinguishes between vasogenic and cytotoxic edema, we believe that this technique will be an invaluable tool in helping physicians to optimize the treatment of eclamptic patients from the onset; the majority who develop vasogenic edema will undergo blood pressure reduction and supportive measures, while the rare patient who develops infarction will undergo more aggressive therapy. Further prospective evaluation of these patients is needed to test our hypothesis.
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Selected Abbreviations and Acronyms |
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Received December 26, 1996; revision received February 27, 1997; accepted February 27, 1997.
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R. B. Schwartz, S. K. Feske, J. F. Polak, U. DeGirolami, A. Iaia, K. M. Beckner, S. M. Bravo, R. A. Klufas, R. Y. C. Chai, and J. T. Repke Preeclampsia-Eclampsia: Clinical and Neuroradiographic Correlates and Insights into the Pathogenesis of Hypertensive Encephalopathy Radiology, November 1, 2000; 217(2): 371 - 376. [Abstract] [Full Text]
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C Oppenheim, D Galanaud, Y Samson, M Sahel, D Dormont, B Wechsler, and C Marsault Can diffusion weighted magnetic resonance imaging help differentiate stroke from stroke-like events in MELAS? J. Neurol. Neurosurg. Psychiatry, August 1, 2000; 69(2): 248 - 250. [Abstract] [Full Text] [PDF]
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G. W. Albers, M. G. Lansberg, A. M. Norbash, D. C. Tong, M. W. O'Brien, A. R. Woolfenden, M. P. Marks, and M. E. Moseley Yield of diffusion-weighted MRI for detection of potentially relevant findings in stroke patients Neurology, April 25, 2000; 54(8): 1562 - 1567. [Abstract] [Full Text] [PDF]
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J. R. Carhuapoma, P. Y. Wang, N. J. Beauchamp, P. M. Keyl, D. F. Hanley, and P. B. Barker Diffusion-Weighted MRI and Proton MR Spectroscopic Imaging in the Study of Secondary Neuronal Injury After Intracerebral Hemorrhage Stroke, March 1, 2000; 31(3): 726 - 732. [Abstract] [Full Text] [PDF]
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M. J. Cooney, W. G. Bradley, S. C. Symko, S. T. Patel, and P. K. Groncy Hypertensive Encephalopathy: Complication in Children Treated for Myeloproliferative Disorders-Report of Three Cases Radiology, March 1, 2000; 214(3): 711 - 716. [Abstract] [Full Text]
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K.-O. Lovblad and C. Basssetti Diffusion-Weighted Magnetic Resonance Imaging in Brain Death Stroke, February 1, 2000; 31(2): 539 - 542. [Abstract] [Full Text] [PDF]
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J. M. Provenzale CT and MR Imaging of Nontraumatic Neurologic Emergencies Am. J. Roentgenol., February 1, 2000; 174(2): 289 - 299. [Full Text] [PDF]
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M. Yoneda, M. Maeda, H. Kimura, A. Fujii, K. Katayama, and M. Kuriyama Vasogenic edema on MELAS: A serial study with diffusion-weighted MR imaging Neurology, December 1, 1999; 53(9): 2182 - 2182. [Abstract] [Full Text] [PDF]
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R. L. Robertson, L. Ben-Sira, P. D. Barnes, R. V. Mulkern, C. D. Robson, S. E. Maier, M. J. Rivkin, and A. J. d. Plessis MR Line-Scan Diffusion-Weighted Imaging of Term Neonates with Perinatal Brain Ischemia AJNR Am. J. Neuroradiol., October 1, 1999; 20(9): 1658 - 1670. [Abstract] [Full Text]
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S. G. Pavlakis, Y. Frank, and R. Chusid Topical Review: Hypertensive Encephalopathy, Reversible Occipitoparietal Encephalopathy, or Reversible Posterior Leukoencephalopathy: Three Names for an Old Syndrome J Child Neurol, May 1, 1999; 14(5): 277 - 281. [Abstract] [PDF]
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E. Keller, S. Flacke, H. Urbach, and H. H. Schild Diffusion- and Perfusion-Weighted Magnetic Resonance Imaging in Deep Cerebral Venous Thrombosis Stroke, May 1, 1999; 30(5): 1144 - 1146. [Abstract] [Full Text] [PDF]
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R. L. Robertson, S. E. Maier, C. D. Robson, R. V. Mulkern, P. M. Karas, and P. D. Barnes MR Line Scan Diffusion Imaging of the Brain in Children AJNR Am. J. Neuroradiol., March 1, 1999; 20(3): 419 - 425. [Abstract] [Full Text]
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A. R. Woolfenden, M. W. O'Brien, R. E. Schwartzberg, A. M. Norbash, and D. C. Tong Diffusion-Weighted MRI in Transient Global Amnesia Precipitated by Cerebral Angiography Stroke, November 1, 1997; 28(11): 2311 - 2314. [Abstract] [Full Text]
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