have involved the whole LST. Three patients showed superficial sensory disturbance of the arm and leg, sparing the face. This is caused by partial involvement of the LST. DL can manifest as contralateral superficial sensory disturbance in various patterns, which are 1) hemisensory change; 2) segmental sensory changes of the face and trunk and arm; 3) arm, trunk, and leg, sparing the face; and 4) arm or leg, sparing the face. Decreased vibratory sense in the contralateral leg was attributable to involvement of the lateral part of the ML, which predominantly conveys deep sensations of the leg. These sensory changes in patients with rLPI can display various segmental patterns. Favorable outcome could be related to the localization of rLPI, allowing sufficient collateral circulation by the arterial network with anteromedial arteries, vertical anastomosis of the lateral arteries, and extensive distribution of CST fibers of the leg in the rostral lateral pontine base. References 1. Bassetti C, Bogousslavsky J, Barth A, Regli F. Isolated infarcts of the pons. Neurology 1996;46:165–175. 2. Duvernoy HM. The human brainstem and cerebellum. Surface, structure, vascularization, and three-dimensional sectional anatomy with MRI. Vienna: Springer-Verlag, 1995. 3. Nieuwenhuys R, Voogd J, van Huijzen C. The human central nervous system. A synopsis and atlas. Berlin: Springer-Verlag, 1988. 4. Haerer AF. DeJong’s the neurologic examination. 5th ed. Philadelphia: JB Lippincott, 1992. 5. van Swieten JC, Koudstaal PJ, Visser MC, Schouten HJA, van Gijn J. Interobserver agreement for the assessment of handicap in stroke patients. Stroke 1988;19:604 – 607. 6. Brodal A. Neurological anatomy in relation to clinical medicine. Oxford: Oxford University Press, 1981. 7. Schneider R, Gautier J-C. Leg weakness due to stroke. Site of lesions, weakness patterns and causes. Brain 1994;117:347–354. 8. Englander RN, Netsky MG, Adelman LS. Location of human pyramidal tract in the internal capsule. Anatomic evidence. Neurology 1975;25:823–826. 9. Urban PP, Wicht S, Vucorevic G, et al. The course of corticofacial projections in the human brainstem. Brain 2001;124:1866 –1876. 10. Matsumoto S, Okuda B, Imai T, Kameyama M. A sensory level on the trunk in lower lateral brainstem lesions. Neurology 1988;38: 1515–1519. Non-aneurysmal primary subarachnoid hemorrhage in pregnancy-induced hypertension and eclampsia A.K. Shah, MD Abstract—Clinical as well as neuroimaging studies of women with eclampsia or pregnancy-induced hypertension (PIH) have described a variety of neurologic manifestations, including intraparenchymal brain hemorrhage. Autopsy studies have described pia-arachnoid hemorrhage in women who died of eclampsia, but radiographic studies have found only intraparenchymal hemorrhage. The author describes clinical and radiographic features in three women with subarachnoid hemorrhage associated with PIH. NEUROLOGY 2003;61:117–120 Pregnancy-induced hypertension (PIH) is a multisystem disorder, occasionally associated with neurologic manifestations. Eclampsia is defined as seizures or coma occurring in the setting of PIH. Clinically, stroke, intraparenchymal hemorrhage, or transient neurologic deficits are described.1 Neuroimaging studies have described transient hypodensities affecting white matter or deep nuclei as well as occasional intraparenchymal hemorrhage on CT scan. More recently, MRI was found to be more sensitive than CT scanning, and usually shows transient hyperintense lesions on T2-weighted MR images.2 Materials and methods. Patients were recruited from a women’s hospital in a metropolitan area with approximately 6000 deliveries per year. Data were collected in a prospective study of women with new onset of seizures in the peripartum period. A neurologist performed history and physical examination, usually within 24 hours, and all patients had neuroimaging study performed. Patients were selected for the current study if they met the following criteria: absolute blood pressure (BP) greater than 140/90 mm Hg, or rise of systolic BP by 30 mm Hg or diastolic BP by 15 mm Hg from baseline, during late pregnancy or early postpartum period with proteinuria or edema; documented subarachnoid hemorrhage (SAH) by either CT scan of head or CSF analysis; and normal conventional four-vessel angiogram, including venous phase. All clinical, laboratory, and radiologic data of the selected patients were reviewed. Case 1. A 21-year-old primipara developed sudden rise in blood pressure within a few hours of the delivery and had unwitnessed transient loss of consciousness the following day. Two hours later, she had two witnessed generalized tonic-clonic seizures. She denied headache initially, but reported mild headache a few days later. Her neurologic examination was unremarkable. CT scan of the head performed on the day of seizures is shown in figure 1. MRI of the brain showed multiple hyperintense lesions From Wayne State University/Detroit Medical Center, Detroit, MI. Received December 11, 2002. Accepted in final form March 13, 2003. Address correspondence and reprint requests to Dr. A.K. Shah, Dept. of Neurology, 8D-8, UHC, 4201, St Antoine, Detroit, MI 48201; e-mail: ashah@med.wayne.edu Copyright © 2003 by AAN Enterprises, Inc. 117 Figure 1. (A) Higher cuts of head CT scan without contrast show small subarachnoid blood filling sulci over the left hemisphere (arrow). (B) Slightly lower cuts at the level of lateral ventricles show hyperdensity in the left sylvian fissure (arrowhead) compared to the right side. on T2-weighted images predominantly involving the white matter. Cerebral angiogram 2 days later had normal results. During another unrelated admission to the hospital 18 months later, she did not have any neurologic complaints or deficits. Case 2. A 17-year-old, 38 weeks pregnant primigravida was admitted for sickle cell crisis with severe pain and evidence of hemolysis on the laboratory examination. She responded well to hydration and analgesics. Three days later, she went into spontaneous labor and delivered vaginally. Two days postpartum, she developed rapidly worsening hypertension (maximum BP 160/102 mm Hg) and proteinuria. She had complex partial seizures and had a secondarily generalized tonic-clonic seizure later that day. Her neurologic examination was remarkable for mild recent memory deficit and left-sided hyperreflexia that resolved quickly. Initial CT scan of the brain had normal results, and MRI showed a small occipital hyperintense lesion on T2-weighted images. She was treated with MgSO4 and recovered well. Four days later, she developed new sudden, sharp, severe unilateral temporal pain. There was no clinical or laboratory evidence of sickle cell crisis. A repeat CT scan of the head revealed focal SAH over the frontal convexity (figure 2). Cerebral angiogram 2 days later had normal results. Six months follow-up showed normal results on neurologic examination and brain MRI. Case 3. A 27-year-old multipara developed sudden, sharp occipital headache immediately after a vaginal delivery. She developed mild hypertension, but was discharged the next day. Five days later, she returned to the emergency department because of worsening headache, nausea, and vomiting. Her examination was remarkable for BP 176/92 mm Hg, mild neck stiffness, and mild generalized edema. Her laboratory evaluation showed 4⫹ proteinuria. A head CT scan from the emergency department showed SAH over the right frontoparietal convexity and interhemispheric fissure. Her cerebral angiogram had normal results. On most recent follow-up examination 3 years after SAH, results of neurologic examination were normal. Results. As described above, three women were included in the study. All three women were African American. Two women were selected from a prospective study (from a total of 40 women in the study) of patients who had new onset seizures in the peripartum period. An additional patient with SAH in setting of PIH without seizures or coma was also identified. All three women had onset of symptoms during the postpartum period. Two women developed sudden headache, but headache was not severe in one (Case 3) and she was initially discharged without neuroimaging. The third patient developed mild headache several days after the occurrence of SAH. None were taking medications except analgesics, vitamins, or MgSO4 before SAH. Head CT scan revealed SAH in all women. The subarachnoid blood was localized over frontal lobe convexity in Figure 2. Head CT scan without contrast shows a small area of subarachnoid blood filling the cortical sulci over the right frontal lobe (small black arrows) (Case 2). 118 NEUROLOGY 61 July (1 of 2) 2003 one patient; another patient had blood over the convexity extending into the sylvian fissure. The third patient showed SAH in similar distribution with extension into the sylvian and interhemispheric fissures. A conventional fourvessel angiogram was performed within 2 to 4 days of the occurrence of SAH in all women, and failed to reveal any intracranial aneurysm, vasospasm, focal narrowing, or abnormality during the venous phase. The laboratory evaluation showed normal platelet count, blood urea nitrogen, creatinine, prothrombin time (PT), partial thromboplastin time (PTT), aspartate aminotransferase, and alanine aminotransferase in all women and negative urine drug screen in two who were tested. All patients recovered well without any permanent neurologic deficits. Discussion. The aim of this study is to report SAH as an unusual neurologic complication of PIH and describe its clinical and radiographic characteristics. The underlying etiology of SAH in the women reported here is unlikely to be intracranial aneurysm, cortical venous sinus thrombosis, or ruptured arterial-venous malformation (AVM). The clinical presentation, course of illness, and location of SAH on imaging studies were not typical of aneurysmal rupture. These women did not have any medical condition to suspect mycotic aneurysm, and all were afebrile. In addition, conventional angiogram failed to detect aneurysm. Similarly, cortical venous sinus thrombosis or AVM is also unlikely considering the clinical and radiographic data. SAH is five times more common in pregnant women compared to nonpregnant women of the same age.3 However, higher incidence is due to SAH from intracranial aneurysms or vascular malformations. There are little, if any, clinico-radiologic data on nonaneurysmal SAH related to eclampsia or PIH. The CT findings reported in patients with eclampsia include hypodensities affecting white matter or deep nuclei and intraparenchymal hemorrhages.2,4,5 The exact incidence of intracranial hemorrhage (ICH) in PIH is difficult to judge. Nonetheless, it is probably rare, as head CT scan did not show ICH in any of the 20 patients (out of a total of 65) who had the test.5 In our series of 40 patients with eclampsia who underwent neuroimaging, two women (5%) developed SAH, but none had intraparenchymal hemorrhage.6 Headache is a common but not a universal symptom in eclampsia, but is usually very severe in SAH. In this series, two out of three women had headache, but one had only mild pain that failed to trigger neuroimaging initially (Case 3). This clinical scenario is strikingly different from the classic presentation of SAH with explosive thunderclap headache. This may be due to the presence of a small amount of blood over the cerebral convexity in these women. The location of SAH in these women also differs from the typical finding in SAH from cerebral aneurysm rupture. The blood in aneurysmal SAH is usually located in the basal brain cisterns, with more serious hemorrhages extending into the sylvian fis- sure, interhemispheric fissure, and ventricular system and rarely over the convexities.7 In contrast, our patients had blood over the convexity of the frontal/ parietal lobes extending into the sylvian fissure or interhemispheric fissure. Another interesting fact is that SAH occurred in all women during the postpartum period. The underlying cause of primary SAH in women with PIH remains obscure. Because the amount of blood as detected by CT scan was small, and primarily located over cerebral convexity, the source is unlikely to be a large or medium-sized artery. One possibility is that the SAH is a result of rupture of cortical petechiae over the surface of the brain. However, in two patients who had brain MRI, the images did not reveal any evidence of petechial hemorrhages. In an autopsy series of women with eclampsia, petechial hemorrhage and pia-arachnoid hemorrhage were among the gross pathologic findings. However, the brain under the pia-arachnoid hemorrhage rarely shows petechial hemorrhage.8 The location of pia-arachnoid hemorrhage is similar to that of blood seen in patients reported here, as defined by the CT scan. Thus, cortical petechiae leaking blood into the subarachnoid space is less likely to be an explanation for SAH in these women. One of the proposed underlying pathophysiologic mechanisms of eclampsia is that of forced vasodilatation. The vasodilatation results from sudden accelerated hypertension that exceeds cerebral vessels’ ability to autoregulate cerebral blood flow by vasoconstriction. This may result in leakage of fluid in the interstitial space. This theory can explain transient hyperintense lesions on T2-weighted brain MR images in women with eclampsia.9 One can hypothesize that SAH in these women is due to the rupture of small pial blood vessel (possibly a small vein as it has thinner walls) due to sudden unchecked rise in blood pressure, combined with failed autoregulation, allowing the high arterial pressure to be transmitted to small pial blood vessels. These vessels also lack support by surrounding interstitial or neuronal tissue, making them vulnerable to rupture. This may explain the small amount of subarachnoid blood over the cerebral convexity seen in these patients, because venous bleeding is under significantly lower pressure compared to the arterial bleed, and venous bleed can be self-restricting by the tamponade effect of hematoma itself. The mortality rate in eclampsia is low, but it is high in aneurysmal SAH. The presence of SAH in eclampsia appears to carry benign short- and longterm prognosis. None of our patients developed permanent neurologic deficits on follow-up examination, 6 months to 3 years later. The lower morbidity may be due to location and amount of blood in the subarachnoid space. There are a few limitations of the study, which are inherent in a retrospective analysis of clinical data. There was no follow-up vascular imaging study to evaluate for possible occult AVM or aneurysm. There July (1 of 2) 2003 NEUROLOGY 61 119 was no detailed evaluation for coagulation function, except routine complete blood count and PT/PTT, which had normal results. Patients with sickle cell anemia are at higher risk of hemorrhagic stroke and the potential role of sickle cell disease in Case 2 cannot be evaluated in this study. Although larger studies are needed to confirm these findings, a few comments can be offered from the findings of this series. SAH should be included into the spectrum of neurologic manifestations of severe PIH. Headache may not be severe in these patients, and occurrence of SAH in patients with PIH appears to carry relatively a benign prognosis. Acknowledgment The author thanks Drs. S. Chaturvedi and J. Whitty for their help. References 1. Donaldson JO. Eclampsia. In: Devinsky O, Feldman E, Hainline B, eds. Neurological complications of pregnancy. New York: Raven Press, 1994; 25–33. 2. Dahmus MA, Barton JR, Sibai BM. Cerebral imaging in eclampsia. Magnetic resonance imaging versus computed tomography. Am J Obstet Gynecol 1992;167:935–941. 3. Fox MW, Harms RW, Davis DH. Selected neurologic complications of pregnancy. Mayo Clin Proc 1990;65:1595–1618. 4. Brown CEL, Purdy P, Cunningham FG. Head computed tomographic scans in women with eclampsia. Am J Obstet Gynecol 1988;159:915–920. 5. Sibai BM, Spinnato JA, Watson DL, Lewis JA, Anderson. Eclampsia IV. Neurological findings and future outcome. Am J Obstet Gynecol 1985; 152:184 –192. 6. Shah AK, Whitty J. Characteristics of headache in women with eclampsia. Neurology 1999;52(suppl 2):A285–A86. 7. Mayer SA, Bernardini GL, Brust JCM, Solomon RA. Subarachnoid hemorrhage. In: Rowland LP, ed. Merritt’s neurology. Philadelphia: Lippincott Williams & Wilkins, 2000;260 –267. 8. Sheehan HL, Lynch JB. Cerebral lesions. In: Pathology of toxemia of pregnancy. Edinburgh: Churchill Livingstone, 1973;524 –553. 9. Shah AK, Whitty JE. Brain MRI in peripartum seizures: usefulness of combined T2 and diffusion weighted MR imaging. J Neurol Sci 1999;166: 122–125. Ipsilateral neglect versus hemianopic compensation Anna M. Barrett, MD; B. Lee Peterlin, DO; and Kenneth M. Heilman, MD Abstract—Hemianopic patients may make line bisection errors in the direction of contralesional space, which could represent functional compensation or might be due to ipsilateral neglect. The authors report a patient with stroke with left homonymous hemianopsia and contralesional (leftward) bias on the line bisection task while upright, lying on his left side, and sitting with head bent 90 degrees leftward. Because hemianopic compensation should map retinotopically and the patient consistently erred body-leftward, the authors conclude that his contralesional errors are consistent with ipsilateral neglect. NEUROLOGY 2003;61:120 –123 Hemianopic patients may make contralesional line bisection (LB) errors.1,2 A compensatory contralesional bias may require awareness; active contralesional eye or head turning, or both; and preferential contralesional hemispatial attention. However, nonhemianopic patients may also err contralesionally3 (ipsilateral neglect [IpN]). Hemianopia could result from posterior cerebral artery (PCA) infarction, affecting geniculocalcarine pathways, calcarine cortex, and potentially the thalamus. Because IpN may follow thalamic infarction,4 contralesional LB bias after PCA stroke could represent either a compensatory bias or IpN. We examined a 50-year-old patient with right temporal-occipital and ventrolateral thalamic infarction and right caudate hemorrhage (figure 1). He had left-sided homonymous hemianopia; face, arm, and leg (4⫹/5) hemiparesis and mild incoordination; and hemihypesthesia. Echocardiogram showed a small patent foramen ovale. The patient received clopidogrel 75 mg daily. The patient demonstrated left spatial neglect (day 3 poststroke, left-sided line cancellation omissions, left auditory extinction to bilateral stimulation, drawing copy omitted left-sided details). He erred 15 mm leftward, however, bisecting a 21-cm line. Whereas hemianopic visual defects map retinotopically, IpN might respect environment, head, or body-centered coordinates.5 By dissociating these reference frames, we wished to learn whether compensatory bias or IpN better explained the patient’s errors. From the Division of Neurology (Drs. Barrett and Peterlin), Pennsylvania State College of Medicine, Hershey; the Department of Neurology (Dr. Heilman), University of Florida College of Medicine, Gainesville; and the Neurology Service (Dr. Heilman), Veterans Affairs Medical Center, Gainesville, FL. Supported by the Department of Medicine, PA State College of Medicine, the National Institute of Neurological Disorders and Stroke, National Institutes of Health (A.M.B.), the Penn State General Clinical Research Center (A.M.B.), and the Department of Veteran Affairs (K.M.H.). Received July 24, 2002. Accepted in final form February 21, 2003. Address correspondence and reprint requests to Dr. Anna M. Barrett, 500 University Avenue, Division of Neurology (H037), Penn State College of Medicine, Hershey, PA 17033; e-mail: amb33@psu.edu 120 Copyright © 2003 by AAN Enterprises, Inc. Non-aneurysmal primary subarachnoid hemorrhage in pregnancy-induced hypertension and eclampsia A.K. Shah Neurology 2003;61;117-120 DOI 10.1212/01.WNL.0000069609.36517.A3 This information is current as of July 8, 2003 Updated Information & Services including high resolution figures, can be found at: http://www.neurology.org/content/61/1/117.full.html References This article cites 6 articles, 0 of which you can access for free at: http://www.neurology.org/content/61/1/117.full.html##ref-list-1 Citations This article has been cited by 7 HighWire-hosted articles: http://www.neurology.org/content/61/1/117.full.html##otherarticles Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): All Medical/Systemic disease http://www.neurology.org//cgi/collection/all_medical_systemic_disease Subarachnoid hemorrhage http://www.neurology.org//cgi/collection/subarachnoid_hemorrhage Permissions & Licensing Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions Reprints Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus Neurology ® is the official journal of the American Academy of Neurology. 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