- Email: [email protected]
Eclampsia and postpartum cerebral angiopathy: a response
Journal of the Neurological Sciences 178 (2000) 77–78 www.elsevier.com / locate / jns
Reply to Letter to the Editor
Eclampsia and postpartum cerebral angiopathy: a response A.K. Shah M.D.* Department of Neurology, Wayne State University, Detroit Medical Center, Detroit, MI 48201, USA Received 4 April 2000; accepted 6 April 2000
We appreciate the interest of Dr. Zunker and colleague in the case reports we published [1]. They suggest the diagnosis of postpartum angiopathy (PCA) in patient 2. We disagree for the following reasons. First, the patient developed hypertension in association with headache, which was followed by seizures: a common clinical scenario in patients with eclampsia. Second, urinalysis showed proteinuria. Third, she did not suffer from permanent brain injury, as shown by the neurological exam and imaging studies. Fourth, she had a subarachnoid hemorrhage without an associated intracerebral hemorrhage: indeed there was no petechial hemorrhage on MR imaging. The subarachnoid hemorrhage (with a small amount of blood in the sulci over a frontal lobe) was similar to a common autopsy finding of ‘‘pia-arachnoid hemorrhage’’ in the series of eclampsia cases described by Sheehan and Lynch [2]. Fifth, the cerebral angiogram performed after the subarachnoid hemorrhage showed narrowing of only a small segment of the internal carotid arteries without multifocal segmental narrowing. These findings do not establish diagnosis of PCA in this patient. Cerebral vasospasm is known to occur following subarachnoid hemorrhage and also in eclampsia. These facts support diagnosis of eclampsia in this patient. It is not clear whether postpartum cerebral angiopathy differs from eclampsia. Many cases of so-called PCA described in the literature assume the diagnosis just on the basis of the occurrence of the syndrome during the postpartum period and on the presence of multifocal narrowing of cerebral vessels on angiogram [3–6]. In many instances, the clinical and radiological features were similar to what is seen in eclampsia, such as transient neurological deficits and hyperintense lesions on T2 *Tel.: 11-313-745-4280; fax: 11-313-993-0643. E-mail address: [email protected] (A.K. Shah).
weighted MR images. The angiographic changes were also reversible in some patients. In some cases, the neurological syndrome apparently followed administration of vasoactive medication, such as ergot preparation, sumatriptan, sympathomimetic drugs or bromocriptine. However, ergot alkaloids and bromocriptine are frequently used during the postpartum period for control of uterine hemorrhage or suppression of lactation. There is insufficient evidence to suggest any relationship with these drugs to this neurological syndrome. On the other hand, 4-vessel cerebral angiography or MR angiography in eclampsia have shown narrowing of the cerebral vessels [7,8]. Similarly, increased blood flow velocity in cerebral arteries examined by transcranial doppler (TCD) in women with eclampsia suggests narrowing of the cerebral vessels [9]. Transient neurological deficits are characteristic of eclampsia. Traditionally, eclampsia is believed to occur during third trimester of pregnancy or within 48 hours of delivery. However, late postpartum eclampsia is a well-known entity [10]. In a prospectively collected case series by us, the first seizure was more likely to occur in postpartum period, compared to the intrapartum and prepartum periods [11]. These facts raise several important questions. Are eclampsia and PCA just different manifestations of the same underlying pathophysiologic process or are they fundamentally different? Are transient neurological deficits and MR imaging changes characteristic of eclampsia? Do angiographic changes suggest the etiology and distinguish between two conditions? Which patients are at risk for stroke or intracranial hemorrhage? Magnesium sulfate is a proven therapy for eclampsia. Should we use this for PCA? The other comment by Zunker and colleagues is about the discrepancy between our findings of normal diffusion weighted images and the findings of Schwartz et al. showing increased diffusion in areas with abnormal signal on T2 weighted images [12]. It is difficult to speculate
0022-510X / 00 / $ – see front matter 2000 Elsevier Science B.V. All rights reserved. PII: S0022-510X( 00 )00375-0
78
A.K. Shah / Journal of the Neurological Sciences 178 (2000) 77 – 78
about the reasons behind this apparent difference. Most likely it represents technical dissimilarities between the studies. However, both findings are in sharp contrast of decreased diffusion found in stroke. Clinically, this is very useful as acute or subacute stroke stands out as area of markedly increased signal on DWI. I strongly agree with Zunker and colleagues’ comments about the usefulness of other MR techniques such as MR angiography, MR venography, and perfusion measurements in patients with eclampsia. Transcranial Doppler (TCD) is certainly a useful tool in the management of eclampsia. It is a non-invasive bedside method that can be used in monitoring cerebral blood flow serially. To what extent it aids in management of eclampsia beyond diagnosis is still unknown.
References [1] Shah AK, Whitty JE. Usefullness of combined T2 and diffusion weighted MR imaging in women with eclampsia. J Neurol S 1999. [2] Sheehan HL, Lynch JR. Cerebral lesions in Pathology of Toxemia of Pregnancy. Churchill Livingstone, London, 1973, pp. 524–84. [3] Barinagarrementeria F, Cantu C, Balderrama J. Postpartum cerebral angiopathy with cerebral infarction due to ergonovine use. Stroke 1992;23:1364–6.
[4] Raroque HG, Tesfa G, Purdy P. Postpartum cerebral angiopathy. Is there a role for sympathomimetic drugs? Stroke 1993;24:2108–10. [5] Comabella M, Alvarez-sabin J, Rovira A, Codina A. Bromocriptine and Postpartum cerebral angiopathy: A causal relationship? Neurology 1996;46:1754–6. [6] Granier I, Garcia E, Geissler A, Boespflug MD, Durand-Gasselin J. Postpartum cerebral angiopathy associated with the administration of sumatriptan and dihydroergotamine- a case report. Intensive Care Medicine 1999;25(5):532–4. [7] Will AD, Lewis KL, Hinshaw DB, Jordan K, Cousins LM, Hasso AN, Thompson JR. Cerebral vasoconstriction in toxemia. Neurology 1987;37:1555–7. [8] Sengar AR, Gupta Rk, Dhanuka AK, Roy R, Das K. MR imaging; MR angiography, and MR spectroscopy of the brain in eclampsia. AJNR 1997;18:1485–90. [9] Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and transcranial Doppler sonographic findings in eclampsia. Br J Obstet Gynecol 1997;104(10):1165–72. [10] Lubarsky Sl, Barton JR, Friedman SA, Nasreddine S, Ramadan MK, Sibai BM. Late postpartumeclampsia revisited. Obstet Gynecol 1994;83:502–5. [11] Shah AK, Nikhar NK, Watson CR, Shah JR, Whitty JE, Cotton DB. New Onset Peri-partum Seizures – Insight into a common disorder. Presented at the 50th Annual Meeting of the American Academy of Neurology, Minneapolis, Minnesota. Neurology 1998;50(suppl. 4):A253. [12] Schwartz RB, Mulkern RV, Gudjartsson H, Jolez F. Diffusion weighted MR imaging in hypertensive encephalopathy: Clues to pathogenesis. Am J Neuroradiol 1998;19:859–62.
Reply to Letter to the Editor
Eclampsia and postpartum cerebral angiopathy: a response A.K. Shah M.D.* Department of Neurology, Wayne State University, Detroit Medical Center, Detroit, MI 48201, USA Received 4 April 2000; accepted 6 April 2000
We appreciate the interest of Dr. Zunker and colleague in the case reports we published [1]. They suggest the diagnosis of postpartum angiopathy (PCA) in patient 2. We disagree for the following reasons. First, the patient developed hypertension in association with headache, which was followed by seizures: a common clinical scenario in patients with eclampsia. Second, urinalysis showed proteinuria. Third, she did not suffer from permanent brain injury, as shown by the neurological exam and imaging studies. Fourth, she had a subarachnoid hemorrhage without an associated intracerebral hemorrhage: indeed there was no petechial hemorrhage on MR imaging. The subarachnoid hemorrhage (with a small amount of blood in the sulci over a frontal lobe) was similar to a common autopsy finding of ‘‘pia-arachnoid hemorrhage’’ in the series of eclampsia cases described by Sheehan and Lynch [2]. Fifth, the cerebral angiogram performed after the subarachnoid hemorrhage showed narrowing of only a small segment of the internal carotid arteries without multifocal segmental narrowing. These findings do not establish diagnosis of PCA in this patient. Cerebral vasospasm is known to occur following subarachnoid hemorrhage and also in eclampsia. These facts support diagnosis of eclampsia in this patient. It is not clear whether postpartum cerebral angiopathy differs from eclampsia. Many cases of so-called PCA described in the literature assume the diagnosis just on the basis of the occurrence of the syndrome during the postpartum period and on the presence of multifocal narrowing of cerebral vessels on angiogram [3–6]. In many instances, the clinical and radiological features were similar to what is seen in eclampsia, such as transient neurological deficits and hyperintense lesions on T2 *Tel.: 11-313-745-4280; fax: 11-313-993-0643. E-mail address: [email protected] (A.K. Shah).
weighted MR images. The angiographic changes were also reversible in some patients. In some cases, the neurological syndrome apparently followed administration of vasoactive medication, such as ergot preparation, sumatriptan, sympathomimetic drugs or bromocriptine. However, ergot alkaloids and bromocriptine are frequently used during the postpartum period for control of uterine hemorrhage or suppression of lactation. There is insufficient evidence to suggest any relationship with these drugs to this neurological syndrome. On the other hand, 4-vessel cerebral angiography or MR angiography in eclampsia have shown narrowing of the cerebral vessels [7,8]. Similarly, increased blood flow velocity in cerebral arteries examined by transcranial doppler (TCD) in women with eclampsia suggests narrowing of the cerebral vessels [9]. Transient neurological deficits are characteristic of eclampsia. Traditionally, eclampsia is believed to occur during third trimester of pregnancy or within 48 hours of delivery. However, late postpartum eclampsia is a well-known entity [10]. In a prospectively collected case series by us, the first seizure was more likely to occur in postpartum period, compared to the intrapartum and prepartum periods [11]. These facts raise several important questions. Are eclampsia and PCA just different manifestations of the same underlying pathophysiologic process or are they fundamentally different? Are transient neurological deficits and MR imaging changes characteristic of eclampsia? Do angiographic changes suggest the etiology and distinguish between two conditions? Which patients are at risk for stroke or intracranial hemorrhage? Magnesium sulfate is a proven therapy for eclampsia. Should we use this for PCA? The other comment by Zunker and colleagues is about the discrepancy between our findings of normal diffusion weighted images and the findings of Schwartz et al. showing increased diffusion in areas with abnormal signal on T2 weighted images [12]. It is difficult to speculate
0022-510X / 00 / $ – see front matter 2000 Elsevier Science B.V. All rights reserved. PII: S0022-510X( 00 )00375-0
78
A.K. Shah / Journal of the Neurological Sciences 178 (2000) 77 – 78
about the reasons behind this apparent difference. Most likely it represents technical dissimilarities between the studies. However, both findings are in sharp contrast of decreased diffusion found in stroke. Clinically, this is very useful as acute or subacute stroke stands out as area of markedly increased signal on DWI. I strongly agree with Zunker and colleagues’ comments about the usefulness of other MR techniques such as MR angiography, MR venography, and perfusion measurements in patients with eclampsia. Transcranial Doppler (TCD) is certainly a useful tool in the management of eclampsia. It is a non-invasive bedside method that can be used in monitoring cerebral blood flow serially. To what extent it aids in management of eclampsia beyond diagnosis is still unknown.
References [1] Shah AK, Whitty JE. Usefullness of combined T2 and diffusion weighted MR imaging in women with eclampsia. J Neurol S 1999. [2] Sheehan HL, Lynch JR. Cerebral lesions in Pathology of Toxemia of Pregnancy. Churchill Livingstone, London, 1973, pp. 524–84. [3] Barinagarrementeria F, Cantu C, Balderrama J. Postpartum cerebral angiopathy with cerebral infarction due to ergonovine use. Stroke 1992;23:1364–6.
[4] Raroque HG, Tesfa G, Purdy P. Postpartum cerebral angiopathy. Is there a role for sympathomimetic drugs? Stroke 1993;24:2108–10. [5] Comabella M, Alvarez-sabin J, Rovira A, Codina A. Bromocriptine and Postpartum cerebral angiopathy: A causal relationship? Neurology 1996;46:1754–6. [6] Granier I, Garcia E, Geissler A, Boespflug MD, Durand-Gasselin J. Postpartum cerebral angiopathy associated with the administration of sumatriptan and dihydroergotamine- a case report. Intensive Care Medicine 1999;25(5):532–4. [7] Will AD, Lewis KL, Hinshaw DB, Jordan K, Cousins LM, Hasso AN, Thompson JR. Cerebral vasoconstriction in toxemia. Neurology 1987;37:1555–7. [8] Sengar AR, Gupta Rk, Dhanuka AK, Roy R, Das K. MR imaging; MR angiography, and MR spectroscopy of the brain in eclampsia. AJNR 1997;18:1485–90. [9] Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and transcranial Doppler sonographic findings in eclampsia. Br J Obstet Gynecol 1997;104(10):1165–72. [10] Lubarsky Sl, Barton JR, Friedman SA, Nasreddine S, Ramadan MK, Sibai BM. Late postpartumeclampsia revisited. Obstet Gynecol 1994;83:502–5. [11] Shah AK, Nikhar NK, Watson CR, Shah JR, Whitty JE, Cotton DB. New Onset Peri-partum Seizures – Insight into a common disorder. Presented at the 50th Annual Meeting of the American Academy of Neurology, Minneapolis, Minnesota. Neurology 1998;50(suppl. 4):A253. [12] Schwartz RB, Mulkern RV, Gudjartsson H, Jolez F. Diffusion weighted MR imaging in hypertensive encephalopathy: Clues to pathogenesis. Am J Neuroradiol 1998;19:859–62.