Cerebral vasospasm in eclampsia.

Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1,000 words (typed double-spaced) in length and may be subject to editing or abridgment. To the Editor: I read with interest the article by Trommer et al 1 and the letter by Dr. Goodlin. 2 1 failed to see a reply from either Dr. Trommer or the editor, but instead saw a letter from Dr. Brick 3 in the next issue of Stroke. I feel both letters need further clarification and offer my comments. First, I agree in principle with Dr. Goodlin's points regarding a subspecialty journal and the proper diagnosis of reported patients. However, a strict definition reflects our lack of understanding of eclampsia. Also, defining eclampsia solely in terms of seizures may give a false sense of security and deny early intervention to preeclamptic women with subtle neurologic symptoms (i.e., headache, blurring of vision, etc.). We know through neuroradiologic studies that cerebral lesions may be present even in these patients 4-5 and that treatment is thereby warranted. In fact, patients with seizures may show no lesions on computed tomograms, with minimal reversible lesions on magnetic resonance images, whereas patients without seizures and only "blurring of vision" may have diffuse permanent lesions. 6 ' 7 Nobody can predict who will deteriorate or how fast, so even patients with "minor" neurologic symptoms deserve equal attention. Perhaps this is why many physicians still use the older, but all-inclusive, term toxemia and accept the unpopular concept of eclampsia without seizures. Second, Dr. Goodlin's comment that "this type of cerebral vasospasm has been recognized for the last 45 years" needs clarification. Though such patients have indeed been known for years, I had no knowledge of direct in vivo evidence to support cerebral vasospasm until a few years ago. Review of the literature shows that angiography was first reported in "toxemia" by Beck and Menezes in 1981.' However, this patient had concom-itant intracranial hemorrhage. A subsequent report by Will et al' also showed hemorrhage in two of three patients. It is possible therefore that the hemorrhage caused the vasospasm. The report of Trommer et al provides some of the first clear angiographic evidence for vasospasm. Third, although Trommer et al 10 and Brick" agree on the possible role of the female reproductive hormones, the authors fail to highlight differences in their cases. One was clearly toxemic with diffuse …