AUTHOR(S): Medlock, Michael D., M.D.; Olivero, William C., M.D.; Hanigan, William C., M.D., Ph.D.; Wright, Robert M., M.D.; Winek, Sally Jo, M.D. Department of Neuroscience (MDM, WCO, WCH, SJW) and Department of Radiology (RMW), University of Illinois College of Medicine at Peoria, Peoria, Illinois Neurosurgery 31; 870-876, 1992 ABSTRACT: FROM 1985 TO 1991, 13 children were diagnosed at the University of Illinois College of Medicine at Peoria, Saint Francis Medical Center, with cerebral venous thrombosis (CVT) by magnetic resonance imaging scan. Ages ranged from newborn to 5 years. Six children were premature neonates, five were term neonates and two were 5 years old. In the premature neonates, thrombosis was usually associated with other problems. All the term neonates had seizures. In all neonates, thrombosis resolved without any specific treatment. In the two older children, one presented with pseudotumor cerebri and one with coma. These children required neurosurgical intervention. Follow-up magnetic resonance imaging scans were obtained in 9 of 13 children and showed thrombus resolution in each case. Three children were studied in the acute and convalescent stages by magnetic resonance angiography using time-of-flight techniques. Each follow-up magnetic resonance angiogram showed improvement in venous flow consistent with their clinical course and other imaging studies. We conclude that 1) CVT in children encompasses a range of clinical conditions which may or may not require neurosurgical intervention; 2) magnetic resonance imaging is superior to other modalities for the diagnosis of CVT; and 3) magnetic resonance angiography is an alternative means to monitor the evolution of CVT and efficacy of therapeutic intervention. KEY WORDS: Cerebral venous thrombosis; Magnetic resonance angiography; Magnetic resonance imaging; Neonates Early descriptions from autopsy studies suggested that cerebral venous thrombosis (CVT) was a grave, often pre-terminal condition associated with many diseases (5,9). Angiography, and then computed tomography, provided progressively less invasive means for diagnosis and established the association of CVT with many other diseases. With magnetic resonance imaging (MRI) and now MR angiography, the diagnosis can be made even more accurately and noninvasively. This report describes the risk factors, clinical presentations, radiological findings, and Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 treatment in 13 children with CVT. PATIENTS AND METHODS From 1985 to 1991, 13 children were diagnosed with CVT at the University of Illinois College of Medicine at Peoria, Saint Francis Medical Center. The hospital records and cerebral imaging studies of these children were reviewed. All of the children had MR imaging, two had arterial digital subtraction (DS) angiography and three had MR angiography. MRI scans were done with a 0.5- or 1.5-T Siemens Magnetom scanner (Erlangen, Germany). MR angiography was performed on the 1.5-T scanner using limited flip angle gradient recalled echo (timeof-flight) techniques. Fast low angle shot (FLASH) sequences were used to study one child and fast imaging with steady precession (FISP) sequences were used to study two children. Each child's most recent developmental outcome was obtained from office charts and by phone calls to parents or caretakers. None was lost to follow-up. Three of these children were included in a previous report by Hanigan et al. (16). RESULTS For comparison purposes, these 13 children were divided into 3 age groups: 6 premature neonates, 5 full-term neonates, and 2 older children, both 5 years of age. Table 1 summarizes the findings in the premature neonates. In three of these children, MRI scanning was done because of a questionably abnormal cerebral sonogram performed routinely to rule out periventricular hemorrhage (PVH). One child with a Grade 4 PVH had seizures that were difficult to control, which prompted MRI scan. One child had MRI scan because of a questionably abnormal computed tomographic (CT) scan of the head, and one child had Escherichia coli meningitis and seizures. None of the children required any specific treatment for their CVT. Follow-up MRI was performed in five of the six children at 8 days, 26 days, 27 days, 47 days, and 8 months after the initial study. In each case there was complete or near complete recanalization of the major venous channels. In the two children in whom follow-up more than 2 years was available, one child is developmentally normal and one has mild psychomotor retardation. Table 2 summarizes the findings in the term neonates. All five term infants had seizures or probable seizures; three had no known risk factors, one had asphyxia related to abruptio placentae, and one had hydrocephalus with PVH. Of the three without any other central nervous system insult, two have had no further seizures after hospital discharge, and one has persistent daily seizures. Two of these children are developmentally normal and three are developmentally delayed. Again, as in the premature newborns, none of these children required any specific treatment for their thrombosis. Follow-up MRI scan was done in three of these children 43 days, 65 days, and 4 months after the initial study. All studies showed recanalization of the major sinuses. Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Neurosurgery 1992-98 November 1992, Volume 31, Number 5 870 Children with Cerebral Venous Thrombosis Diagnosed with Magnetic Resonance Imaging and Magnetic Resonance Angiography Clinical Study CASE REPORTS Patient 1 A 6-day-old female infant (Patient 6 in Table 1) was admitted for hypotonia and lethargy. She was born at 36 weeks estimated gestational age and weighed 2470 g. Her parents were mentally deficient. At the time of presentation, she was in respiratory distress, hypotonic, and hyporeflexic. Cerebrospinal fluid contained 4450 red blood cells/mm3, 17 white blood cells/mm3, glucose 2.0 mmol/L (normal, 2.224.44), and protein 1.01 g/L (normal, 0.15-0.45). There was neither PVH nor seizures. CT scan at 11 days of age showed superior sagittal sinus hyperdensity consistent with thrombosis. MRI scan at 14 days of age showed superior sagittal sinus and right transverse sinus thrombosis with two small left frontal lobe hemorrhages. MR angiogram obtained immediately after the spin-echo images at 14 days of age showed no flow in multiple intracranial sinuses and, at 21 days of age, an MR angiogram showed improved venous flow (Fig. 1). MRI scan at 21 days of age showed recanalization of both sinuses. Acquisition time for these images was 6 minutes. Karyotyping showed a deletion of the short arm of chromosome 18. She has had no further seizures and is not taking anticonvulsant medication. At 7 months' chronological age, her developmental age is estimated at 4 months. Patient 2 A 5-year-old boy fell backwards, struck his head on a coffee table, and suffered a depressed skull fracture of the left occipital bone. He was followed without surgery. MRI scan confirmed the presence of a depressed skull fracture but showed little underlying parenchymal abnormality and no extraaxial hemorrhage. MR angiography showed occlusion of the dominant left transverse sinus (Fig. 2, top). Acquisition time for these images was 9.5 minutes. Over the next several weeks he had three admissions for worsening headaches. Lumbar puncture showed an opening pressure of 400 mm H2O. Cerebrospinal fluid protein, glucose, and cell count were normal. Each lumbar puncture provided him with only temporary relief of headache and intracranial hypertension. Forty-one days after injury, DS angiography confirmed the continued occlusion of the left transverse sinus. He underwent elevation of the fracture. Postoperative MRI scanning and angiography showed recanalization of the sinus (Fig. 2, bottom). One year later, he had no further headache and was neurologically normal. Patient 3 A 5-year-old boy presented with increasing lethargy. He sustained a mild head injury with no loss of consciousness 1 week before admission. He had several days' history of headache and malaise. He had Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 a generalized tonic-clonic seizure during evaluation in the emergency room. His family and other members of the community had atypical pneumonialike infections. A CT scan was interpreted as normal on images transmitted by phone at night. Review of the actual films later in the morning revealed a hyperdense transverse sinus. Lumbar puncture showed 2250 red blood cells/mm3 and 23 white blood cells/mm3. The opening pressure was not measured. He rapidly became comatose and required intubation. MRI scan showed a right parietal lobe venous infarct and a left frontal lobe hematoma. MR angiogram showed extensive thrombosis of the internal and external venous systems (Fig. 3, top). Acquisition time for these images was 5.5 minutes. Acyclovir and antibiotics were begun. An intracranial pressure (ICP) monitor showed normal or near normal pressure. Over the next several days, he was treated with heparin and diuretics; however, his ICP climbed to 70 torr. Pentobarbital-induced electroencephalogram burst suppression was unsuccessful in controlling his ICP. Systemic urokinase was begun at 60,000 U/hr (Abbokinase, Abbott Laboratories, North Chicago, IL) and continued for 4 days. After this, DS angiography showed sluggish venous flow and persistent thrombus in the anterior superior sagittal sinus. Cerebrospinal fluid cultures were negative for bacteria. His ICP gradually normalized over the next several days, and he was extubated. Repeat DS angiography showed normal venous flow and resolution of all thrombus. Two days after the DS angiogram, a repeat MR angiogram showed improved flow in all venous channels (Fig. 3, bottom). At 15 months after illness, he was normal intellectually with a mild pronator drift. DISCUSSION The natural history of cerebral venous thrombosis is variable. Reports before the use of conventional angiography were based only on postmortem examination. In the Byers and Hass (9) autopsy series of 50 children with CVT, 26 cases were associated with bacterial infection and 24 cases were not (9). Even after the advent of angiography, the prognosis was felt to be poor. Askenasy et al. (2) described three patients with angiographically confirmed sagittal sinus thrombosis, all of whom died. Averback (4) reported seven patients with aseptic CVT, five of which were fatal. In Bailey and Hass' report (5) of 33 children with pathologically confirmed aseptic CVT, the majority of children had severe nutritional disturbances from vomiting and diarrhea and 31 died. Recent reports suggest a more variable outcome. In a series by Scotti et al. (32), of eight children with CVT diagnosed by angiography, six of which were aseptic, they noted only one child who died. In a series by Bousser et al. (7), of 38 adult patients, only 4 died. Since the introduction of high resolution CT and MRI scans, the diagnosis has been made more frequently, many times with good outcome, even in comatose patients (7,17,34). There have been numerous case reports, but a limited series of children with CVT not related to contiguous infection. Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Both older children, Patients 2 and 3, required neurosurgical intervention. Their case histories, along with the neonate in whom we obtained acute and convalescent MR angiograms, are presented in detail. Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 spin-echo images. Paradoxical enhancement caused by slow flowing blood can produce high signal on T1weighted images which can be confused with thrombosis. By changing the imaging plane, the high signal will become low signal excluding thrombosis (23,37) . The diagnosis can be made even without clinical suspicion (3). In a review of 234 children with neurological disorders who underwent 261 MRI scans of the head, 2 showed dural sinus thrombosis (27) . Rivkin et al. (28) reported six neonates with MRI scan-diagnosed CVT who presented with lethargy and hypotonia and had a benign clinical course without specific treatment. MR angiography has been used in the diagnosis of CVT. The two most useful MR angiographic techniques are generally classed as limited flip angle gradient recalled echo (time-of-flight) and phase contrast images. Phase contrast images require longer acquisition times, which are more likely to compromise pediatric imaging. Both techniques require improvements before small vessel disease can be adequately imaged. We used two different time-offlight techniques, FISP and FLASH. Our MR angiograms produced by both of these methods were consistent with the clinical course of the patients, CT scans, DS angiography, and T1- and T2-weighted spin-echo MRI scans. MR angiography has also been used successfully to study cerebrovascular disease in neonates and infants with arterial occlusive disease and stroke from various causes (22,30). To our knowledge there have been no reports of MR angiograms performed in children with CVT. Even with the recent advances in neuroimaging and earlier diagnosis of sinus occlusion, treatment remains controversial. The dilemma is whether to use anticoagulation, usually heparin, to prevent further thrombosis, to use fibrinolytic therapy such as urokinase to lyse the clot, and/or to symptomatically treat the elevated ICP with steroids, mannitol, acetazolamide, etc. The dilemma persists because the natural history is not known. DiRocco et al. (12) treated five patients with a combination of heparin and systemic urokinase with good results. Several of the patients had focal neurological deficits and one was in a coma. In a large series of 38 cases described by Bousser et al. (7), most patients were treated with anticoagulation and steroids. Gettelfinger and Kokmen (15), in treating seven patients with superior sagittal sinus thrombosis, recommended that anticoagulation should not be used but recommended antiedema agents. Higashida et al. (18) treated a neonate with infusion of urokinase directly into the superior sagittal sinus with a good outcome. Thromboplastin has been used in the intracranial sinuses, subarachnoid space, and brain parenchyma with good clot lysis and few complications in animal models (1,21). Although there have been rare case reports of surgical treatment of aseptic sinus occlusion, treatment now appears to be primarily medical (26,32,36). An ICP monitor may be helpful in the management, although it precludes MRI scanning. Transfemoral instillation of fibrinolytic agents by an interventional neuroradiologist may play a role in selected patients. Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. The presenting clinical picture can vary from asymptomatic to coma with focal neurological deficits. Confusion, headache, hemiplegia, and seizures are common symptoms. Papilledema and focal deficits are also common (7,33). A common presentation in the newborn period is seizures and full fontanels. Dural sinus occlusion can also cause the clinical syndrome of pseudotumor cerebri. Before the advent of antibiotics, the association of dural CVT with chronic mastoiditis or chronic otitis was a common presentation in children. Today, this is rarely seen. Other associated conditions include dehydration, asphyxia, polycythemia, systemic malignancy, trauma, meningitis, pregnancy, oral contraceptives, sickle cell trait, and coagulation abnormalities (6,8,14, 20,24,31,32,35,38) . Little has been written on whether or not there are any maternal risk factors which predispose a newborn to CVT. In the mothers of the premature infants in our series, three had preeclampsia and two had premature rupture of the membranes. In the full-term newborn pregnancies, one mother had preeclampsia, one had oligohydramnios, one had abruptio placentae, and one had a history of illicit drug abuse. Of the 11 newborns, 6 mothers were smokers; all of the term neonates' mothers and one of the premature neonates' mothers. More data is needed to determine whether any of these conditions are causally related to CVT. The diagnosis is confirmed with neuroimaging. Until recently the modality of choice was intraarterial iodinated contrast angiography. Findings include nonvisualization of the venous sinuses either partial or complete, increase in the arteriovenous circulation time, collateral venous pathways, reversal of flow in the obstructed sinus, and mass affect from venous infarct (33,39). We have found angiography useful only when MRI scanning was not available or when an ICP monitor precluded the use of MRI scanning. With the availability of high resolution CT scanning, a noninvasive diagnosis was made with increased accuracy. Findings included dural and tentorial enhancement, dilatation of transcerebral intermedullary veins, the cord sign, i.e., visualization of thrombosed veins, and the empty delta sign (13,27). Brain involvement may show hemorrhagic infarcts, edema, compression, or enlargement of the ventricles (15,25,27,29) . In our series, several CT scans were interpreted as normal when MRI scans showed unequivocal CVT. MRI scanning is superior to CT scanning in the diagnosis of venous thrombosis. By 1989, MRI was described as the imaging modality of choice (5,10,11,13, 19,20,24,29,37) . In high field magnetic resonance, acute sinus thrombosis is isointense on T1-weighted images and markedly hypointense on T2-weighted images. Sinus thrombosis in an intermediate stage has a high signal intensity on T1- and T2-weighted spinecho images (10,23). Daniels et al. (10) have described a gradient recall echo MR sequence in which the normal sinus and veins are hyperintense but lose signal with complete occlusion. They think this may be the best method for diagnosis of acute sinus thrombosis, which can be missed on T2-weighted ACKNOWLEDGMENT The authors thank Mrs. JoAnna Gass for assistance in the preparation of the manuscript. Received, April 7, 1992. Accepted, June 12, 1992. Reprint requests: William C. Olivero, M.D., Department of Neuroscience, University of Illinois College of Medicine at Peoria, P.O. Box 1649, Peoria, IL 61656. REFERENCES: (1-39) 1. 2. 3. 4. Alexander LF, Yamamota Y, Ayoubi S, AlMefty O, Smith RR: Efficacy of tissue plasminogen activator in the lysis of thrombosis of the cerebral venous sinus. Neurosurgery 26:559-564, 1990. Askenasy HM, Kosary IZ, Braham J: Thrombosis of the longitudinal sinus. Diagnosis by carotid angiography. Neurology 12:288-292, 1962. Atkinson EA, Fairburn B, Heathfield KWG: Intracranial venous thrombosis as a complication of oral contraception. Lancet 1:914- 918, 1970. Averback P: Primary cerebral venous thrombosis in young adults: The diverse manifestations of an underrecognized disease. Ann Neurol 3:81-86, 1978. Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. Bailey O, Hass GM: Dural sinus thrombosis in early life: I. The clinical manifestations and extent of brain injury in acute sinus thrombosis. J Pediatr 11:755-771, 1937. 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Arch Neurol 38:431-435, 1981. Eick JJ, Miller KD, Bell KA, Tutton RH: Computed tomography of deep cerebral venous thrombosis in children. Radiology 140:399- 402, 1981. Fairburn B: Intracranial venous thrombosis complicating oral contraception: Treatment by anticoagulant drugs. Br Med J [Clin Res] 2:647, 1973. Gettelfinger DM, Kokmen E: Superior sagittal sinus thrombosis. Arch Neurol 34:2-6, 1977. Hanigan WC, Tracy PT, Tadros WS, Wright RM: Neonatal cerebral venous thrombosis. Pediatr Neurosci 14:177-183, 1988. Hanley DF, Feldman E, Borel CO, Rosenbaum AE, Goldberg AL: Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension. Stroke 19:903-909, 1988. Higashida RT, Helmer E, Halbach VV, Hieshima GB: Direct thrombolytic therapy for superior sagittal sinus thrombosis. AJNR 10:S4-S6, 1989. Hulcelle PJ, Dooms GC, Mathurin P, Cornelis G: MRI assessment of unsuspected dural sinus thrombosis. Neuroradiology 31:217- 221, 1989. Kaufman HH, Schochet S, Koss W, Herschberger J, Bernstein D: Efficacy and safety of tissue plasminogen activator. Neurosurgery 20:403-407, 1987. Lewin JS, Masaryk TJ, Modic MT, Ross JS, Stork EK, Wiznitzer M: Extracorporeal membrane oxygenation in infants: Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Most of the children in our series received no treatment specific for CVT. Many of the neonates have developmental delays; because of their multiple medical problems, it is impossible to determine the precise role that CVT played in this delay. Three of the four children presenting with seizures without other known central nervous system risk factors have not had persistent seizures. In the two children receiving treatment, one presented with signs and symptoms consistent with pseudotumor cerebri secondary to traumatic occlusion of the dominant transverse sinus. His symptoms resolved after removal of the depressed bone fragment and subsequent sinus recanalization. In those cases in which an anatomical obstruction causes symptomatic sinus thrombosis, surgery appears warranted, but the surgeon should anticipate significant blood loss. In the other child who presented with seizures and coma, systemic urokinase was instituted as a last resort, and he made an excellent recovery. The temporal relationship between the institution of fibrinolytic therapy, the onset of clinical recovery, the DS angiogram results, and the MR angiogram results in our case suggested, but by no means proved, a causal relationship. In summary, we have reported our experience with 13 children with CVT. In the newborn period, CVT is frequently a self-limited disease requiring no treatment. 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This article by Medlock et al. shows us how well this entity is diagnosed by magnetic resonance imaging (MRI) angiography in a wide variety of pediatric patients, and it is clear that some perplexing clinical problems might be clarified by the use of this technique. In particular, their Patient 2, who had a pseudo-tumor syndrome in association with a depressed fracture obliterating the left transverse sinus, was particularly instructive. The authors used excellent clinical judgment in withholding immediate elevation of this potentially serious fracture, which was associated with no intracranial pathology. They confirmed the continued presence of increased intracranial pressure, demonstrated the occluded transverse sinus by MRI angiography, and the reappearance of flow in the sinus after elevation of the fracture accompanied by resolution of the clinical problem. This short acquisition time of the MRI studies suggest that this technique could become more widely used in the appropriate clinical setting. R. Michael Scott Boston, Massachusetts This article addresses a complex issue of the occurrence of cerebral venous thrombosis in a myriad of diseases in childhood. In a retrospective analysis spanning 6 years, the authors review 13 children with deep cerebral venous thrombosis as a part of their clinical syndromes. The diagnosis in each child was made with MRI scan, and follow-up MRI scans were obtained in 9 of 13 children. The authors categorize their children into three groups: premature neonates, term neonates, and two older children. This varied clinical spectrum was looked at with MRI to define the presence of venous thrombosis as a part of their clinical spectrum. The radiological findings were consistent in these patients with various degrees of venous thrombosis. What association this finding had with any of the clinical syndromes is difficult to discern. In one case, the individual with depressed skull fracture, his clinical syndrome was more than likely the result of venous occlusion secondary to the bony fragment rather than thrombosis. This paper presents an excellent discussion of Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. 22. Angiographic and parenchymal evaluation of brain with magnetic resonance imaging. Radiology 173:361-365, 1989. Macchi PJ, Grossman RI, Gomori JM, Goldberg HI, Zimmerman RA, Bilaniuk LT: High field MR imaging of cerebral venous thrombosis. J Comput Assist Tomogr 10:1015, 1986. Murphy MF, Clarke CRA, Brearley RL: Superior sagittal sinus thrombosis and essential thrombocythaemia. Br Med J [Clin Res] 287:1344, 1983. Nüssel F, Huber P: High resolution computed tomography of superior sagittal sinus thrombosis and abnormalities. Neuroradiology 31:307-311, 1989. 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Scotti LN, Goldman RL, Hardman DR, Heinz ER: Venous thrombosis in infants and children. Radiology 112:393-399, 1974. Shaenboen MJ, Matzura TM, Disbro MA: Magnetic resonance imaging of dural sinus thrombosis with resolution. JAOA 89:794804, 1989. Sigsbee B, Deck MDF, Posner JB: Nonmetastatic superior sagittal sinus thrombosis complicating systemic cancer. Neurology 29:139- 146, 1979. Sindou M, Mercier P, Bokor J, Brunon J: Bilateral thrombosis of the transverse sinuses: Microsurgical revascularization with venous bypass. Surg Neurol 13:215-220, 1980. Steinherz PG, Miller LP, Ghavimi F, Allen JC, Miller DR: Dural sinus thrombosis in children with acute lymphoblastic leukemia. JAMA 246:2837-2839, 1981. Tarras S, Gadia C, Meister L, Roldan E, cerebral venous thrombosis and reviews the literature as to the use of MRI in its diagnosis. I think it is very important, and the authors appropriately point out the fact that the temporal relationship of the diagnostic tests for cerebral venous thrombosis by no means proves a causal relationship. This is an interesting and well written paper and one which brings to our attention the very common association of cerebral venous thrombosis and various other primary diseases. For instance, it is not uncommon in the neonate with vein of Galen malformation to find associated cerebral venous thrombosis as a part of the picture. In fact, deep cerebral venous anomalies and occlusions we now realize form a part of the pathological process in the vein of Galen malformations. Again, it is important to realize this process (cerebral venous thrombosis) represents a paraphenomenon of the primary pathological process although it may contribute to presentation and outcome. Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. J. Parker Mickle Gainesville, Florida Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Figure 1. MR angiogram at 14 days old (top, FLASH, TR/TE/flip angle = 31/10/50, unenhanced) showed diminished flow in the superior sagittal sinus (arrows) and internal cerebral venous system (arrowheads) flow. MR angiogram at 21 days old (bottom, FLASH, TR/TE/flip angle = 31/10/50, unenhanced) showed recanalization of the superior sagittal sinus and improved flow in the internal venous system. Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Figure 2. Preoperative MR angiogram 3 days after the injury (top, TR/TE/flip angle = 40/7/20, unenhanced) showed thrombosis of the left transverse sinus from the torcula to the vein of Labbe. Postoperative MR angiogram (bottom, TR/TE/flip angle = 40/7/20, unenhanced) shows restoration of flow through the sinus. Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Figure 3. MR angiogram on the day of admission (top, FISP, TR/TE/flip angle = 23/13/20, gadolinium diethylene-triamine-pentaactic acid-enhanced) showed extensive thrombosis of the superior sagittal sinus (arrows) and internal venous system (arrowheads). Follow-up MR angiogram (bottom, FISP, TR/TE/flip angle = 23/13/20, unenhanced) showed improved flow in the internal and external venous systems even with contrast enhancement on convalescent study. Table 2. Term Neonatesa Downloaded from https://academic.oup.com/neurosurgery/article-abstract/31/5/870/2549004 by guest on 31 March 2018 Redistribution of this article permitted only in accordance with the publisher’s copyright provisions. Table 1. Premature Neonatesa