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Reversal of acute ischemic hypodense lesions on computed tomography
] Stroke Cerebrovasc Dis 1993;3:240-243 © 1993 National Stroke Association
Reversal of Acute Ischemic Hypodense Lesions on Computed Tomography D. K. Kim, M.D., Ph.D., Marc R. Mayberg, M.D., '[oseph M. Eskridge, M.D., David W. Newell, M.D., and H. Richard Winn, M.D.
Hypodense ischemic lesions on computed tomography (CT) are usually associated with cerebral infarction and permanent tissue injury. We describe three cases of acute ischemic lesions detected by CT that rapidly resolved following therapy. In two cases, the appearance of hypodense lesions was associated with the onset of vasospasm after subarachnoid hemorrhage, and resolution correlated with successful treatment. In the third case, multiple acute hypodense lesions in a patient with eclampsia improved following treatment with diuretic agents. Key Words: Computed tomography-Cerebral ischemia-Hypodense lesions-VasospasmEclampsia.
Computed tomography (CT) has become an indispensable tool in the diagnosis of cerebral infarction (1,2). Low-density lesions in characteristic vascular distributions as detected by CT are the hallmark of evolving or established cerebral infarction from 3 to 5 days after onset of ischemia (3,4). However, the significance of early CT changes associated with cerebral ischemia remains uncertain. We present three cases with acute hypodense CT lesions that resolved over several days. The etiology of these lesions remains uncertain, but vasospasm may be the mechanism with two of the cases. With the third case, the hypodense lesions that improved in concert with the resolution of clinical deficits appear to be an unusual complication of eclampsia.
From the Departments of Neurological Surgery and lRadiology, University of Washington Medical School, Seattle, WA, U.S.A. Address correspondence and reprint requests to Dr. M. R Mayberg at Department of Neurological Surgery, RI-10, University of Washington Medical School, Seattle, WA98195, U.S.A. 240
] STROKE CEREBROVASC DIS, VOL. 3, NO .4, 1993
Case Reports Case 1 A 40-year-old man was transferred to the University of Washington Medical Center 9 days after suffering a subarachnoid hemorrhage (SAH). On physical examination, moderate meningismus was present, but no focal findings were notable. CT showed subarachnoid blood in the basal cisterns on the right and occipital horn of the right lateral ventricle. Cerebral angiography on admission revealed a right posterior cerebral artery (PCA) aneurysm (P2 segment) as well as moderately severe diffuse vasospasm, including that of the right PCA and basilar artery. After clipping of the aneurysm on the day of admission, the neurologic examination remained normal except for a right superior quadrantmopsia. CT on the second postoperative day demonstrated hypodensity in the distribution of the right PCA (Fig. I, left), which correlated with decreased perfusion in the same distribution by single-photon emission computed tomography (SPECT) using 99Tc (5-7) . Transcranial Doppler (TeD) examination demonstrated increased velocity
REVERSIBLE ISCHEMIC CT LESIONS
Fi~e 1. Cl'scans for Case 1. Left: Postoperativeday2. A rig!lt oc.clpl~al hJ!podellse lesionilltJ!e right posterior cerebral artery dis-
tribution IS dem?"strated. Right: Postoperative day 16. Near complete resolutionof theacute hypodellse lesion ill the right occipitallobe is shoum.
in the left middle cerebral artery (MCA) consistent with vasospasm (8,9). Cerebral angiography showed severe basilar artery and bilateral PCA vasospasm, more prominent on the right. The patient underwent successful angioplasty of the basilar artery and both PCAs (10) and was treated with hypertensive, hypervolemic therapy. Subsequent TCD evaluations on postoperative days three and six (posthemorrhage days 12 and 15) showed mild residual left MCA vasospasm with resolving right PCA vasospasm (Fig. 2). On day of discharge (postoperative day 9), the quadrantnopsia had resolved. Follow-up CT 2 weeks later showed complete resolution of the hypodense lesion in the right occipital region (Fig. 1, right).
Case 2 A 47-year-old woman was admitted with SAH following three episodes of severe headache over the preceding week. On physical examination, the pa-
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tient was mildly lethargic without focal neurologic deficits. CT revealed subarachnoid blood in the basal cisterns and a hematoma in the right sylvian fissure . Cerebral angiography demonstrated multiple aneurysms, including right MCA, anterior communicating artery (ACoA), right ophthalmic artery, left pericallosal artery, and left posterior communicating artery. The right MCA, ACoA, and ophthalmic aneurysms were clipped through a right pterional approach; at surgery, it was apparent that the MCA aneurysm was the source of the hemorrhage. Postoperatively, the patient was confused and somnolent. CT at this time showed a diffuse hypodense region in the right MCA distribution extending into the occipital lobe (Fig. 3, left). Cerebral angiography on postoperative day 1 demonstrated vasospasm of the right MCA branches distal to the trifurcation. SPECT revealed hypoperfusion in the right MCA distribution. The patient was treated with hypertensive, hypervolemic therapy and gradually improved. By postoperative day 8, the patient was fully oriented, and neurologic examination was normal except for dysphasia. Follow-up CT on postoperative day 15 demonstrated nearly complete resolution of the hypodense lesions (Fig. 3, right).
Case 3
80
..._-_ .
Figure 3. CTscansforCase 2. Left: Postoperative day 3. Diffuse parenchspna! hypodellselesions ill the right middle cerebral artery alldright posterior cerebral artery distributions are demonstrated. Right: P?stoperativeday20. Nearcomplete resolution of thehypodellse lesions are demonstrated. Thegray-white differelltiation is clearly evidellt.
4
5
6
Pos t-Ope ra tiv e D ay
Figure 2. Sequelltial TCD velocities ill Case 1. BA, basilar artery; PCA, posterior cerebral artery.
A 23-year-old woman with a history of cocaine abuse presented in labor and pre-eclampsia. Urine toxicology screen detected opiate metabolites. Following vaginal delivery of a normal neonate, the patient developed acute neurologic deterioration manifested initially with headache and blurry vision, then progressive coma necessitating intubation. CT demonstrated diffuse, severe edema and hypodense J STROKE CEREBROVASC DIS, VOL. 3, NO.4, 1993
241
D.KKIMETAL
Figure 4. CTscans forCase 3. Left: Postpartum day 1. Diffuse Ilypodense parenchymal lesions of bilateral watershed zones, left greater than right, are depicted. Theleft posterior cerebral artery distributionhqpodense lesion is particularly notable. Right: Postpartum day 6. Resolution of the diffuse Irypodense lesions are shown. A small residual leftoccipiial hvpodense lesion is evident.
lesions of bilateral watershed zones, more prominent on the left (Fig. 4, left). Mannitol and lasix were administered, and an intracranial pressure (ICP) monitor was inserted, with initial readings of 18 mm Hg. The patient remained unresponsive for 12 h, during which time the ICP returned to normal levels following several infusions of mannitol. When the patient awoke, she manifested a right hemiparesis and rightsided neglect, which resolved over several days. TCD examination revealed increased velocities in the MCA bilaterally. Repeat CT on postpartum day 2 revealed remarkable resolution of the previous hypodense lesions, with only a minimal residual left occipital hypodense region (Fig.4, right). On discharge, the patient demonstrated only mild memory deficits.
Discussion CT remains the initial study of choice in the diagnosis of acute stroke (5,11,12). Although hemorrhagic strokes will be immediately evident on CT, ischemic strokes usually become evident within hour to days and are usually manifest on serial scans (3,4). Nonetheless, a small category of acute hypodense lesions detected by CT may not be indicative of cerebral infarction but rather may represent acute ischemic lesions that are potentially reversible with proper clinical management. This report presents three cases of reversible acute hypodense CT lesions associated with clinical improvement and hemodynamic evidence of improved local blood flow. Unlike the "fogging effect," the appearance of hypodense lesions in these cases was not associated with local edema (13,14).
242
J STROKE CEREBROVASC DIS, VOL. 3, NO.4, 1993
A common factor in the three cases presented in this report was presumptive cerebral ischemia. In Case 1, the resolution of the clinical neurologic deficit due to vasospasm correlated with normalization of basilar artery and right PCA velocities by TCD and resolution of the hypodense lesions on CT. In Case 2, angiography demonstrated distal MCA vasospasm, which correlated with SPECT evidence ofhypoperfusion for that vascular distribution. TCD is less sensitive in detecting distal vasospasm in this setting (9). The rapid resolution of clinical deficits and CT hypodense lesions in Case 1 following angioplasty contrasts with the more gradual improvement noted in Case 2, suggesting a direct relationship between ongoing cerebral ischemia and the presence of CT abnormalities. Case 3 is distinguishable from the other two cases in several ways, including the treatment, which comprised management of ICP with diuresis. Generalized elevated cerebral arterial blood velocities by TCD in this case were interpretable as either diffuse vasospasm or hyperdynamic flow. Although cocaineinduced ischemia has been described (15,16), the clinical course in this case appears to be more typical for the neurologic complications of eclampsia (17,18). In the absence of confirmatory angiographic data, vasospasm cannot be dismissed as the etiology. Nonetheless, cortical blindness associated with occipital lobe hypodense lesions on CT or magnetic resonance imaging (MRI) has been previously noted with eclampsia (19,20). Moreover, several reports have observed that hypodense lesions associated with eclampsia may be reversible (21-23) . The basis of the CT findings with eclampsia has been postulated to be venous congestion, as suggested by angiography in one case (24). This explanation is consistent with the resolution of clinical deficits in association with the resolution of the CT findings after medical management of the ICP with diuresis. The management of systematic ischemic hypodense lesions as detected by CT is facilitated by data derived from angiography, TCD, assessment of cerebral blood flow, and ICP monitoring; these diagnostic measures enable institution of specific therapies based on the nature of the lesion. Consistent with the findings in this report, a recent communication suggested that initial CT scans in the setting of vasospasm after SAH may not necessarily correlate with final clinical outcome (25). Rapid advances in MRI angiography and MRI techniques that provide information on blood and cerebrospinal fluid flow characteristics may provide greater information in the evaluation of acute stroke (26,27).
REVERSIBLE ISCHEMIC CT LESIONS
References 1. Davis KR, Tavares JM, New PF, et aI. Cerebral infarction diagnosis by computerized tomography. Analysis and evaluation of finding. Compui Tomogr 1975 ;124: 643-60. 2. Kinkel WR, Jacobs L Computerized axial transverse tomography in cerebrovascular disease. Neurology 1976;26:924-30. 3. Ionue Y, Takemota K, Miyamoto T, et aI. Sequential computed tomography scans in acute cerebral infarction. Radiology 1980;135:655-62. 4. Wall SO, Brandt-Zwadzki M, Jeffrey RB,et aI. High frequency CT findings within 24 hours after cerebral in farction. AJNR 1981;2:553-7. 5. Campbell JK, Houser 0 , Stevens JC, et aI. Computed tomography and radionuclide imaging in th e evaluation of ischemic stroke. Radiology 1978;126:695-702. 6. Hill TC. Single-photon emission computed tomography to study cerebral function in man. JNucl Med 1980; 21:1197-9. 7. Holmes RA, Chaplin SB, Royston KG, et aI. Cerebral uptake and retention of Tc-99m-hexamethyleneamine oxime (Tc-99m-HMPAO). Nucl Med Commun 1985;6: 443-7. 8. Aaslid R, Huber P, Nomes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 1984;60:37-41. 9. Newell OW, Winn HR. Evaluation of vasospasm using transcranial Doppler. COl/temp Neurosurg 1989;11: 1-6. 10. Newell OW, Eskridge JM, Mayberg MR, et aI. Angloplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 1989; 71:654-60. 11. Heiss WD, Herholz K,Beecher-Schwarz HG, et aI. PET, CT, and MR imaging in cerebrovascular disease. JComput Tomogr 1986;10 :903-11 . 12. Liliequist B, Lindquist M, Valdimarsson E. Computed tomography and subarachnoid hemorrhage. Neuroradiology 1977;14:21-6. 13. Becker H, Desch H, Hacker H, et aI. CT fogging effect with ischemic cerebral infarcts. Neuroradiology 1979; 18:85-192.
14. Skriver EB,Olsen TS. Transient di sappearance of cerebral infarcts on the CT scans, the so-called fogging effect. Neuroradiology 1981;22:61-5. 15. Golbe U, Merkin MD . Cerebral infarction in a user of free-base cocaine ("crack"). Neurology 1986 ;36:16024. 16. Mody CK, Miller BL, McIntyre HB, et aI. Neurologic complications of cocaine abuse. Neurology 1988;38: 1189-93. 17. Colosimo CJr, Fileni A, Moschini M, etaI. CT findings in eclampsia. Neuroradiology 1985;27:313-7. 18. Wiebers DO. Ischemic cerebrovascular complications of pregnancy. Arch NeuroI1985;42:1106-13. 19. Beeson JH, Duda EE. Computed axial tomography scan demonstration of cerebral edema in eclampsia preceded by blindness. Obstet GYI/ecol 1982;60:52932. 20. Duncan R, Hadley 0, Bone I, et aI. Blindness in eclampsia: CT and MR imaging. J Neurol Neurosurg Psychiatry 1989;52:899-902. 21. Naheedy MH, Biller J, Schiffer M, et aI. Toxemia of pregnancy: cerebral CT find ings. J Comput Assist Tomogr 1985;9:497-501. 22. Vandenplas 0, Dive A, Dooms G, Mahieu P. Magnetic resonance evaluation of severe neurological disorders in eclampsia. Neuroradiology 1990 ;32:47-9. 23. Vandermarcq P, Desbordes JM, Bataille B, et aI. Reversible cerebral lesions in eclampsia: clinical and x-ray computed tomographic study. J Radiol 1989;70:5036. 24. Nakakita K, Tanaka S, Fujii C, Kohama A. Circulatory disturbance of deep cerebral veins in eclampsia. No T Shinkei 1990;42:239-43. 25. Gomez CR, Burger SK, Puricelli M, et aI. Early computed tomography demonstration of cerebral infarction does not correlate with clinical outcome. J Stroke Cerebrovasc Dis 1992;2:146-50. 26. Tsuruda JS, Saloner 0, Anderson C. Noninvasive evaluation of cerebral ischemia. Circulation 1991;83(Suppl 1):177-89. 27. Warach S, Li W, Ronthal M, et aI. Acute cerebral ischem ia: evaluation with dynamic contrast enhanced MR imaging and MR angiography. Radiology 1992; 182:417.
J STROKE CEREBROVASC DIS, VOL. 3, NO.4,
1993
243
Reversal of Acute Ischemic Hypodense Lesions on Computed Tomography D. K. Kim, M.D., Ph.D., Marc R. Mayberg, M.D., '[oseph M. Eskridge, M.D., David W. Newell, M.D., and H. Richard Winn, M.D.
Hypodense ischemic lesions on computed tomography (CT) are usually associated with cerebral infarction and permanent tissue injury. We describe three cases of acute ischemic lesions detected by CT that rapidly resolved following therapy. In two cases, the appearance of hypodense lesions was associated with the onset of vasospasm after subarachnoid hemorrhage, and resolution correlated with successful treatment. In the third case, multiple acute hypodense lesions in a patient with eclampsia improved following treatment with diuretic agents. Key Words: Computed tomography-Cerebral ischemia-Hypodense lesions-VasospasmEclampsia.
Computed tomography (CT) has become an indispensable tool in the diagnosis of cerebral infarction (1,2). Low-density lesions in characteristic vascular distributions as detected by CT are the hallmark of evolving or established cerebral infarction from 3 to 5 days after onset of ischemia (3,4). However, the significance of early CT changes associated with cerebral ischemia remains uncertain. We present three cases with acute hypodense CT lesions that resolved over several days. The etiology of these lesions remains uncertain, but vasospasm may be the mechanism with two of the cases. With the third case, the hypodense lesions that improved in concert with the resolution of clinical deficits appear to be an unusual complication of eclampsia.
From the Departments of Neurological Surgery and lRadiology, University of Washington Medical School, Seattle, WA, U.S.A. Address correspondence and reprint requests to Dr. M. R Mayberg at Department of Neurological Surgery, RI-10, University of Washington Medical School, Seattle, WA98195, U.S.A. 240
] STROKE CEREBROVASC DIS, VOL. 3, NO .4, 1993
Case Reports Case 1 A 40-year-old man was transferred to the University of Washington Medical Center 9 days after suffering a subarachnoid hemorrhage (SAH). On physical examination, moderate meningismus was present, but no focal findings were notable. CT showed subarachnoid blood in the basal cisterns on the right and occipital horn of the right lateral ventricle. Cerebral angiography on admission revealed a right posterior cerebral artery (PCA) aneurysm (P2 segment) as well as moderately severe diffuse vasospasm, including that of the right PCA and basilar artery. After clipping of the aneurysm on the day of admission, the neurologic examination remained normal except for a right superior quadrantmopsia. CT on the second postoperative day demonstrated hypodensity in the distribution of the right PCA (Fig. I, left), which correlated with decreased perfusion in the same distribution by single-photon emission computed tomography (SPECT) using 99Tc (5-7) . Transcranial Doppler (TeD) examination demonstrated increased velocity
REVERSIBLE ISCHEMIC CT LESIONS
Fi~e 1. Cl'scans for Case 1. Left: Postoperativeday2. A rig!lt oc.clpl~al hJ!podellse lesionilltJ!e right posterior cerebral artery dis-
tribution IS dem?"strated. Right: Postoperative day 16. Near complete resolutionof theacute hypodellse lesion ill the right occipitallobe is shoum.
in the left middle cerebral artery (MCA) consistent with vasospasm (8,9). Cerebral angiography showed severe basilar artery and bilateral PCA vasospasm, more prominent on the right. The patient underwent successful angioplasty of the basilar artery and both PCAs (10) and was treated with hypertensive, hypervolemic therapy. Subsequent TCD evaluations on postoperative days three and six (posthemorrhage days 12 and 15) showed mild residual left MCA vasospasm with resolving right PCA vasospasm (Fig. 2). On day of discharge (postoperative day 9), the quadrantnopsia had resolved. Follow-up CT 2 weeks later showed complete resolution of the hypodense lesion in the right occipital region (Fig. 1, right).
Case 2 A 47-year-old woman was admitted with SAH following three episodes of severe headache over the preceding week. On physical examination, the pa-
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tient was mildly lethargic without focal neurologic deficits. CT revealed subarachnoid blood in the basal cisterns and a hematoma in the right sylvian fissure . Cerebral angiography demonstrated multiple aneurysms, including right MCA, anterior communicating artery (ACoA), right ophthalmic artery, left pericallosal artery, and left posterior communicating artery. The right MCA, ACoA, and ophthalmic aneurysms were clipped through a right pterional approach; at surgery, it was apparent that the MCA aneurysm was the source of the hemorrhage. Postoperatively, the patient was confused and somnolent. CT at this time showed a diffuse hypodense region in the right MCA distribution extending into the occipital lobe (Fig. 3, left). Cerebral angiography on postoperative day 1 demonstrated vasospasm of the right MCA branches distal to the trifurcation. SPECT revealed hypoperfusion in the right MCA distribution. The patient was treated with hypertensive, hypervolemic therapy and gradually improved. By postoperative day 8, the patient was fully oriented, and neurologic examination was normal except for dysphasia. Follow-up CT on postoperative day 15 demonstrated nearly complete resolution of the hypodense lesions (Fig. 3, right).
Case 3
80
..._-_ .
Figure 3. CTscansforCase 2. Left: Postoperative day 3. Diffuse parenchspna! hypodellselesions ill the right middle cerebral artery alldright posterior cerebral artery distributions are demonstrated. Right: P?stoperativeday20. Nearcomplete resolution of thehypodellse lesions are demonstrated. Thegray-white differelltiation is clearly evidellt.
4
5
6
Pos t-Ope ra tiv e D ay
Figure 2. Sequelltial TCD velocities ill Case 1. BA, basilar artery; PCA, posterior cerebral artery.
A 23-year-old woman with a history of cocaine abuse presented in labor and pre-eclampsia. Urine toxicology screen detected opiate metabolites. Following vaginal delivery of a normal neonate, the patient developed acute neurologic deterioration manifested initially with headache and blurry vision, then progressive coma necessitating intubation. CT demonstrated diffuse, severe edema and hypodense J STROKE CEREBROVASC DIS, VOL. 3, NO.4, 1993
241
D.KKIMETAL
Figure 4. CTscans forCase 3. Left: Postpartum day 1. Diffuse Ilypodense parenchymal lesions of bilateral watershed zones, left greater than right, are depicted. Theleft posterior cerebral artery distributionhqpodense lesion is particularly notable. Right: Postpartum day 6. Resolution of the diffuse Irypodense lesions are shown. A small residual leftoccipiial hvpodense lesion is evident.
lesions of bilateral watershed zones, more prominent on the left (Fig. 4, left). Mannitol and lasix were administered, and an intracranial pressure (ICP) monitor was inserted, with initial readings of 18 mm Hg. The patient remained unresponsive for 12 h, during which time the ICP returned to normal levels following several infusions of mannitol. When the patient awoke, she manifested a right hemiparesis and rightsided neglect, which resolved over several days. TCD examination revealed increased velocities in the MCA bilaterally. Repeat CT on postpartum day 2 revealed remarkable resolution of the previous hypodense lesions, with only a minimal residual left occipital hypodense region (Fig.4, right). On discharge, the patient demonstrated only mild memory deficits.
Discussion CT remains the initial study of choice in the diagnosis of acute stroke (5,11,12). Although hemorrhagic strokes will be immediately evident on CT, ischemic strokes usually become evident within hour to days and are usually manifest on serial scans (3,4). Nonetheless, a small category of acute hypodense lesions detected by CT may not be indicative of cerebral infarction but rather may represent acute ischemic lesions that are potentially reversible with proper clinical management. This report presents three cases of reversible acute hypodense CT lesions associated with clinical improvement and hemodynamic evidence of improved local blood flow. Unlike the "fogging effect," the appearance of hypodense lesions in these cases was not associated with local edema (13,14).
242
J STROKE CEREBROVASC DIS, VOL. 3, NO.4, 1993
A common factor in the three cases presented in this report was presumptive cerebral ischemia. In Case 1, the resolution of the clinical neurologic deficit due to vasospasm correlated with normalization of basilar artery and right PCA velocities by TCD and resolution of the hypodense lesions on CT. In Case 2, angiography demonstrated distal MCA vasospasm, which correlated with SPECT evidence ofhypoperfusion for that vascular distribution. TCD is less sensitive in detecting distal vasospasm in this setting (9). The rapid resolution of clinical deficits and CT hypodense lesions in Case 1 following angioplasty contrasts with the more gradual improvement noted in Case 2, suggesting a direct relationship between ongoing cerebral ischemia and the presence of CT abnormalities. Case 3 is distinguishable from the other two cases in several ways, including the treatment, which comprised management of ICP with diuresis. Generalized elevated cerebral arterial blood velocities by TCD in this case were interpretable as either diffuse vasospasm or hyperdynamic flow. Although cocaineinduced ischemia has been described (15,16), the clinical course in this case appears to be more typical for the neurologic complications of eclampsia (17,18). In the absence of confirmatory angiographic data, vasospasm cannot be dismissed as the etiology. Nonetheless, cortical blindness associated with occipital lobe hypodense lesions on CT or magnetic resonance imaging (MRI) has been previously noted with eclampsia (19,20). Moreover, several reports have observed that hypodense lesions associated with eclampsia may be reversible (21-23) . The basis of the CT findings with eclampsia has been postulated to be venous congestion, as suggested by angiography in one case (24). This explanation is consistent with the resolution of clinical deficits in association with the resolution of the CT findings after medical management of the ICP with diuresis. The management of systematic ischemic hypodense lesions as detected by CT is facilitated by data derived from angiography, TCD, assessment of cerebral blood flow, and ICP monitoring; these diagnostic measures enable institution of specific therapies based on the nature of the lesion. Consistent with the findings in this report, a recent communication suggested that initial CT scans in the setting of vasospasm after SAH may not necessarily correlate with final clinical outcome (25). Rapid advances in MRI angiography and MRI techniques that provide information on blood and cerebrospinal fluid flow characteristics may provide greater information in the evaluation of acute stroke (26,27).
REVERSIBLE ISCHEMIC CT LESIONS
References 1. Davis KR, Tavares JM, New PF, et aI. Cerebral infarction diagnosis by computerized tomography. Analysis and evaluation of finding. Compui Tomogr 1975 ;124: 643-60. 2. Kinkel WR, Jacobs L Computerized axial transverse tomography in cerebrovascular disease. Neurology 1976;26:924-30. 3. Ionue Y, Takemota K, Miyamoto T, et aI. Sequential computed tomography scans in acute cerebral infarction. Radiology 1980;135:655-62. 4. Wall SO, Brandt-Zwadzki M, Jeffrey RB,et aI. High frequency CT findings within 24 hours after cerebral in farction. AJNR 1981;2:553-7. 5. Campbell JK, Houser 0 , Stevens JC, et aI. Computed tomography and radionuclide imaging in th e evaluation of ischemic stroke. Radiology 1978;126:695-702. 6. Hill TC. Single-photon emission computed tomography to study cerebral function in man. JNucl Med 1980; 21:1197-9. 7. Holmes RA, Chaplin SB, Royston KG, et aI. Cerebral uptake and retention of Tc-99m-hexamethyleneamine oxime (Tc-99m-HMPAO). Nucl Med Commun 1985;6: 443-7. 8. Aaslid R, Huber P, Nomes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 1984;60:37-41. 9. Newell OW, Winn HR. Evaluation of vasospasm using transcranial Doppler. COl/temp Neurosurg 1989;11: 1-6. 10. Newell OW, Eskridge JM, Mayberg MR, et aI. Angloplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 1989; 71:654-60. 11. Heiss WD, Herholz K,Beecher-Schwarz HG, et aI. PET, CT, and MR imaging in cerebrovascular disease. JComput Tomogr 1986;10 :903-11 . 12. Liliequist B, Lindquist M, Valdimarsson E. Computed tomography and subarachnoid hemorrhage. Neuroradiology 1977;14:21-6. 13. Becker H, Desch H, Hacker H, et aI. CT fogging effect with ischemic cerebral infarcts. Neuroradiology 1979; 18:85-192.
14. Skriver EB,Olsen TS. Transient di sappearance of cerebral infarcts on the CT scans, the so-called fogging effect. Neuroradiology 1981;22:61-5. 15. Golbe U, Merkin MD . Cerebral infarction in a user of free-base cocaine ("crack"). Neurology 1986 ;36:16024. 16. Mody CK, Miller BL, McIntyre HB, et aI. Neurologic complications of cocaine abuse. Neurology 1988;38: 1189-93. 17. Colosimo CJr, Fileni A, Moschini M, etaI. CT findings in eclampsia. Neuroradiology 1985;27:313-7. 18. Wiebers DO. Ischemic cerebrovascular complications of pregnancy. Arch NeuroI1985;42:1106-13. 19. Beeson JH, Duda EE. Computed axial tomography scan demonstration of cerebral edema in eclampsia preceded by blindness. Obstet GYI/ecol 1982;60:52932. 20. Duncan R, Hadley 0, Bone I, et aI. Blindness in eclampsia: CT and MR imaging. J Neurol Neurosurg Psychiatry 1989;52:899-902. 21. Naheedy MH, Biller J, Schiffer M, et aI. Toxemia of pregnancy: cerebral CT find ings. J Comput Assist Tomogr 1985;9:497-501. 22. Vandenplas 0, Dive A, Dooms G, Mahieu P. Magnetic resonance evaluation of severe neurological disorders in eclampsia. Neuroradiology 1990 ;32:47-9. 23. Vandermarcq P, Desbordes JM, Bataille B, et aI. Reversible cerebral lesions in eclampsia: clinical and x-ray computed tomographic study. J Radiol 1989;70:5036. 24. Nakakita K, Tanaka S, Fujii C, Kohama A. Circulatory disturbance of deep cerebral veins in eclampsia. No T Shinkei 1990;42:239-43. 25. Gomez CR, Burger SK, Puricelli M, et aI. Early computed tomography demonstration of cerebral infarction does not correlate with clinical outcome. J Stroke Cerebrovasc Dis 1992;2:146-50. 26. Tsuruda JS, Saloner 0, Anderson C. Noninvasive evaluation of cerebral ischemia. Circulation 1991;83(Suppl 1):177-89. 27. Warach S, Li W, Ronthal M, et aI. Acute cerebral ischem ia: evaluation with dynamic contrast enhanced MR imaging and MR angiography. Radiology 1992; 182:417.
J STROKE CEREBROVASC DIS, VOL. 3, NO.4,
1993
243