1990;85;737Pediatrics Elke H. Roland, Olof Flodmark and Alan Hill Thalamic Hemorrhage With Intraventricular Hemorrhage in the Full-Term Newborn http://pediatrics.aappublications.org/content/85/5/737 the World Wide Web at: The online version of this article, along with updated information and services, is located on ISSN: 0031-4005. Online ISSN: 1098-4275. PrintIllinois, 60007. Copyright © 1990 by the American Academy of Pediatrics. All rights reserved. by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from PEDIATRICS Vol. 85 No. 5 May 1990 737 Thalamic Hemorrhage With Intraventricular Hemorrhage in the Full-Term Newborn Elke H. Roland, MD; Olof Flodmark, MD, PhD; and Alan Hill, MD, PhD From the Division of Neurology, Department of Pediatrics, and Department of Radiology, University of British Columbia, British Columbia’s Children’s Hospital, Vancouver, British Columbia, Canada ABSTRACT. Intraventricular hemorrhage is an uncom- mon problem in the full-term newborn. In a review of 19 full-term infants with intraventricular hemorrhage diag- nosed on computed tomography prior to 1 month of age, thalamic hemorrhage associated with the intraventricular hemorrhage was documented in 12 infants. Thus, tha- lamic hemorrhage appears to be the most common source of intraventricular hemorrhage in this age group, partic- ularly in infants who had uneventful birth histories and in whom clinical abnormalities (signs of increased intra- cranial pressure, seizures, altered level of consciousness) developed after the first week of life. The majority of these infants had predisposing factors for cerebral venous infarction such as sepsis, cyanotic congenital heart dis- ease, and coagulopathy. The clinical appearance and out- come for infants with thalamic hemorrhage/intraventric- ular hemorrhage were similar to those in infants with intraventricular hemorrhage originating from other sites, except for an increased incidence of cerebral palsy in infants with thalamic hemorrhage/intraventricular hemorrhage. Definitive diagnosis was made on the basis of characteristic radiologic abnormalities. Pediatrics 1990;85:737-742; thakimic hemorrhage, intraventricular hemorrhage, newborn, cerebral infarction. Intraventricular hemorrhage occurs commonly in the premature infant as a result of rupture of fragile vessels in the subependymal germinal matrix. In contrast, intraventricular hemorrhage occurs much less frequently in the full-term newborn. Docu- mented sources of hemorrhage in this age group are more diverse and include residual germinal matrix, choroid plexus, vascular malformation or tumor, as well as extension of hemorrhagic cerebral infarc- tion. Occasionally, intraventricular hemorrhage may result from coagulopathy.”2 In a review of 19 full-term newborns with intra- ventricular hemorrhage, we identified an unusually high incidence of thalamic hemorrhage in associa- tion with the intraventricular hemorrhage. In this study, we describe the clinical appearance, associ- ations, and radiologic features and sequelae at 18 months of age in this group of infants. In addition, we provide a review of the literature on the uncom- mon entity of thalamic hemorrhage/intraventricu- lar hemorrhage in the full-term newborn. METHODS Study Population The study population comprised all full-term newborns (1 1 boys, 8 girls) admitted to British Columbia’s Children’s Hospital between January 1980 and May 1987 in whom intraventricular hem- orrhage was diagnosed by computed tomography (CT) prior to 1 month of age. This hospital, the only pediatric tertiary referral center for the prov- ince of British Columbia, has approximately 39 900 full-term deliveries per year. Infants who had intra- cerebral, subdural, subarachnoid, or posterior fossa hemorrhage without accompanying intraventricu- lar hemorrhage were excluded. We reviewed the clinical and radiologic features as well as the out- come of infants who had thalamic hemorrhage in association with intraventricular hemorrhage. Radiologic Investigations Received for publication May 2, 1988; accepted Jun 2, 1989. Reprint requests to (A.H.) Division ofNeurology, British Colum- bia’s Children’s Hospital, 4480 Oak St, Vancouver, British Co- lumbia, Canada V6H 3V4. PEDIATRICS (ISSN 0031 4005). Copyright © 1990 by the American Academy of Pediatrics. CT scans of the head without contrast enhance- ment were performed on all infants, often at the referring hospital at the time of onset of clinical abnormalities. Later, follow-up CT scans were per- formed both with and without contrast enhance- at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from 738 THALAMIC HEMORRHAGE AND NEWBORN ment on all infants at least 3 weeks following the original diagnosis of intraventricular hemorrhage in an attempt to identify underlying cerebrovascu- lar abnormalities. Scans were performed with a General Electric 8800 CT/T scanner. Axial and coronal sections of 5-mm thickness were viewed using a window width of 60 Hounsfield units and a window level of 30 Hounsfield units. Cerebral ultrasonography was not performed rou- tinely at the onset of clinical abnormalities, either because of lack of easy availability of the technique at the referring hospitals during the initial years of the study or because it was considered redundant following diagnosis by CT. Serial cranial ultrasound scans were performed to document posthemor- rhagic ventricular dilation. Cerebral angiography was performed in three of the infants with thalamic hemorrhage/intraventricular hemorrhage. Rapid sequence, including late venous phase images, was obtained using a magnification technique. Neurologic Outcome Neurologic examination was performed by a pe- diatric neurologist on all infants at 18 months of age. Developmental outcome was assessed accord- ing to the Gesell Developmental Scale and was classified as follows: (1) normal; (2) mild/moderate delay-mild abnormalities of muscle tone that did not interfere with ambulation; (3) severe delay- developmental level of less than a 12-month age level, ie, impaired ambulation often associated with spastic quadriplegia, microcephaly, and seizures. The incidence of neurologic sequelae in infants with thalamic hemorrhage/intraventricular hemorrhage was compared with that of infants with intraven- tricular hemorrhage from other sources. Statistical Analysis The incidence of neurologic sequelae in infants with thalamic hemorrhage/intraventricular hem- orrhage as compared with those with intraventric- ular hemorrhage from other sources was analyzed statistically by means of the two-tailed version of the Fisher exact test. RESULTS Radiologic Features Review of the CT scans of the 19 full-term infants with intraventricular hemorrhage demonstrated in- creased tissue attenuation in the region of the thal- amus, consistent with unilateral thalamic hemor- rhage as the most probable source of intraventric- ular hemorrhage in 12 infants (63%, Fig 1). The presence of localized subependymal hemorrhage in association with intraventricular hemorrhage sug- gested residual germinal matrix as the source of hemorrhage in three infants (16%). In 4 infants (21%), no definite source of hemorrhage could be identified and intraventricular hemorrhage was presumed to originate most probably from choroid plexus. Decreased tissue attenuation suggestive of tha- lamic infarction adjacent to the hemorrhage in the thalamus was shown in the CT scans of three of the infants with thalamic hemorrhage/intraventric- ular hemorrhage performed during the acute phase of illness (Fig 2). Furthermore, increased attenua- tion in the region of the straight sinus (Fig 1) was observed on noncontrast CT scans of two other Fig 1. Noncontrast CT scan of brain of full-term new- born with thalamic hemorrhage/intraventricular hemor- rhage. Note increased attenuation in location of straight sinus (arrow). Fig 2. Noncontrast CT scan of brain of full-term new- born with thalamic hemorrhage/intraventricular hemor- rhage. Note decreased tissue attenuation (arrow) in thai- amus adjacent to hemorrhage in thaiamus. at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from ARTICLES 739 patients with thalamic hemorrhage/intraventricu- lar hemorrhage. In one patient, failure of opacifi- cation of the ipsilateral internal cerebral vein suggestive of venous occlusion was shown in cere- bral angiography (Fig 3). In this patient, the vein of Galen, inferior sagittal sinus, and straight sinus appeared normal angiographically. No abnormal attenuation in the straight sinus was shown in CT scan. Angiographic results were normal in the two other infants. In all patients, follow-up contrast-enhanced CT scans obtained at least 3 weeks after the initial diagnosis of intraventricular hemorrhage did not demonstrate unusual areas of enhancement sugges- tive of vascular malformations. In addition, there was normal filling of major cerebral venous sinuses with contrast material. Clinical Features All infants with intraventricular hemorrhage had sudden onset of dramatic neurologic abnormalities. Prior to this presentation, 16 infants appeared nor- mal. Of the 7 infants in whom intraventricular hemorrhage developed before 2 days of age, 3 had moderate hypoxic-ischemic encephalopathy. Clini- cal features were nonspecific for the site of origin of the intraventricular hemorrhage and included one or more of the following: vomiting, seizures, apnea, lethargy, irritability, bulging fontanel, and Fig 3. Cerebral angiogram, venous phase, demonstrates nonopacification of internal cerebral vein at time of visualization of inferior sagittal sinus (arrow). These two vascular structures are normally visualized simultane- ously. TABLE 1. Time of Onset of Clinical Abnormalities in Full-Term Infants With Intraventricular Hemorrhage Origin of No. of Infants Intraventricular Hemorrhage “Early Onset” “Late Onset” <48 H 3-28 D ofAge of Age (n=7) (n=12) Thalamus 2 10 Residual germinal matrix 3 0 Unknown (possibly choroid 2 2 plexus) abnormal movements, eg, opisthotonic posturing or jitteriness. The ages at onset of clinical abnormalities of patients in our series are listed in Table 1. The . clinical and radiologic features of the 12 infants in this series who had thalamic hemorrhage/intraven- tricular hemorrhage as well as 8 additional infants described previously in the literature are summa- rized in Table 2. In the 7 infants in whom abnor- malities occurred early, ie, prior to 48 hours of age, hemorrhage originated from residual germinal ma- trix in 3 infants, and most probably originated from choroid plexus in 2 infants. Only 2 infants with thalamic hemorrhage/intraventricular hemorrhage (patients 7 and 9 in Table 2) had clinical abnor- malities during the first 2 days of life. In 3 infants in whom symptoms developed early, including 1 infant with thalamic hemorrhage/intraventricular hemorrhage (patient 9), there was evidence sugges- tive of acute birth asphyxia, eg, Apgar scores of less than 5 at 5 minutes or need of positive pressure ventilation for longer than 2 minutes following delivery. In 12 infants, the birth histories were uncompli- cated and clinical abnormalities did not become evident until later, between 3 and 28 days of age (mean 10 days). Of the 12 infants with thalamic hemorrhage/intraventricular hemorrhage, 10 were in this group. Predisposing factors for cerebral ye- nous thrombosis in this group (sepsis, congenital heart disease, coagulopathy, and electrolyte dis- turbance) were identified in 5 of the 10 infants with thalamic hemorrhage/intraventricular hemorrhage (patients 1, 2, 6, 10, 11). Neurologic Outcome The neurologic sequelae at 18 months of age are summarized in Table 3. One infant with intraven- tricular hemorrhage which probably originated from choroid plexus also sustained severe birth asphyxia and died during the neonatal period. The incidence of developmental delay, hydrocephalus, and seizures that persisted beyond 6 months of age was similar in infants with thalamic hemor- at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from TABLE 2. Clinical Features of Full-Term Infants With Thalamic Hemorrhage/Intraventricular Hemorrhage Source and Sex and Age Major Clinical Radiologic Perinatal/ Patient No. Birth Wt (g) (d) Features Findings Postnatal Complications Present study 1 M, 3000 12 Vomiting, lethargy, sei- LTH/IVH, nonopaci- Urinary tract in- zures fication of internal fection cerebral vein (by angiogram) 2 M, 2970 14 Irritability, focal sei- RTH/IVH, decreased Urinary tract in- zures attenuation in thal- fection amus 3 F, 2970 6 Opisthotonus, seizures RTH/IVH, normal None angiogram 4 M, 3320 26 Seizures, irritability, LTH/IVH Pregnancy-induced tense fontanelle hypertension 5 M, 2890 25 Apnea, vomiting, coma LTH/IVH None 6 M, 2890 27 Lethargy, vomiting, RTH/IVH, normal Hyponatremia, vi- gastrointestinal hem- angiogram tamin K defi- orrhage ciency 7 F, 3140 0.5 Apnea, focal seizures LTH/IVH, decreased None attenuation in thal- amus 8 M, 3750 6 R focal seizures LTH/IVH, increased Heavy meconium- attenuation vein of stained liquor, Galen normal Apgar scores 9 M, 3870 2 Seizures, respiratory Bilateral TH/IVH Asphyxia, cyanotic arrest congenital heart disease 10 F, 3280 5 Seizures, apnea RTH/IVH Polycythemia 11 F, 3170 8 Vomiting, coma RTH/IVH, increased Sepsis attenuation in straight sinus 12 M, 2970 5 Seizures, apnea LTH/IVH, decreased None attenuation in thal- amus Palma et al#{176} 13 M, 3250 7 R focal seizures LTH/IVH Prolonged labor, normal Apgar scores 14 M, 3500 26 Opisthotonus, tense LTH/IVH Prolonged rupture fontanelle of membranes Mitchell and O’Tuama3 15 F, 3850 12 Vomiting, dehydration, LTH/IVH None tense fontanelle Trounce et a14 16 F, 3110 11 Vomiting, dehydration, LTH/IVH None tense fontanelle 17 M, 3000 14 Focal seizures, irritabil- RTH/IVH None ity 18 F, 3260 12 Vomiting, opistho- RTH/IVH None tonus, sunsetting eyes 19 M, 2950 13 Generalized seizures, RTH/IVH None opisthotonus, abnor- mal eye movements Primhak and Smith#{176} 20 M, 3340 1.5 Focal seizures, apnea, LTH/IVH Prolonged labor feeding problems * Abbreviations: R, right; L, left; TH, thalamic hemorrhage; IVH, intraventricular hemorrhage. rhage/intraventricular hemorrhage compared with with thalamic hemorrhage/intraventricular hem- infants with intraventricular hemorrhage from orrhage compared with infants with intraventricu- other sources. The incidence of cerebral palsy, usu- lar hemorrhage from other sources (P < .05), how- ally hemiparesis, was significantly higher in infants ever. Only a small minority of infants with thalamic 740 THALAMIC HEMORRHAGE AND NEWBORN at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from TABLE 3. Neurologic Outcome at 18 Months of Age* ARTICLES 741 Neurologic Infants With Infants With P Outcome Germinal Matrix! Intraventricular Hemorrhage and Choroid Plexus! Intraventricular Hemorrhage (n = 7) Thalamic Hemorrhage! Intraventricular Hemorrhage (n = 12) Values Normal 0 2 .51 Developmental delay Mild/moderate 5 9 .99 Severe 1 1 .99 Hydrocephalus 2 7 .35 Seizures (after 1 mo of age) 4 8 .99 Cerebral palsyt 2 10 .05t Death 1 0 .37 * Germinal matrix/intraventricular hemorrhage + choroid plexus/intraventricular hemorrhage and thalamic hemor- rhage/intraventricular hemorrhage were compared using the two-tailed version of Fisher’s exact test. 1 P < .05 denotes statistically significant difference between groups. hemorrhage/intraventricular hemorrhage (2 pa- tients) appeared normal neurologically at follow- up. In the majority (10 patients), there was at least mild or moderate developmental delay. DISCUSSION Intraventricular hemorrhage is an uncommon problem in the full-term newborn. In contrast to the premature newborn, in whom intraventricular hemorrhage originates almost exclusively from sub- ependymal germinal matrix, the origin of intraven- tricular hemorrhage in the full-term infant is more diverse.13 According to our data, extension of tha- lamic hemorrhage may be the most common cause of intraventricular hemorrhage in the full-term newborn, an observation that has not been reported previously in this age group. The pathogenesis of thalamic hemorrhage/intra- ventricular hemorrhage in the full-term newborn is not clear. Hemorrhage into thalamus and basal ganglia has been described previously in the full- term newborn in association with coagulation disorders1 and hypoxic-ischemic cerebral injury.47 In such instances, the thalamic and striatal hem- orrhage was bilateral and was not associated with intraventricular hemorrhage. Several isolated cases have been reported of unilateral thalamic hemor- rhage associated with intraventricular hemorrhage in full-term newborns who appeared otherwise healthy.2’3’8’9 In these instances, because of the close proximity of large venous channels to the ventric- ular wall, the intraventricular hemorrhage was con- sidered to represent a secondary phenomenon re- sulting from extension of the thalamic hemorrhage. Thalamic hemorrhage has been described in adults and older children in the context of chronic hypertension.10” Similarly, in studies in both ex- perimental animals12 and human infants a role was suggested for intermittent episodes of hypertension in the genesis of intraventricular hemorrhage in the newborn.13”4 Hypertension was not observed in our patients, however. Furthermore, although thalamic hemorrhage has been documented in the context of hypoxic-ischemic cerebral injury,47 a role for birth asphyxia was not supported by the high Apgar scores, lack of other evidence of perinatal asphyxia, and late appearance of hemorrhage ie, often after 1 week of age. The possibility of hemorrhage from a vascular malformation cannot be excluded entirely in our patients (cerebral angiography was not per- formed in all infants because of its potential mor- bidity in this age group). The absence of vascular abnormalities or recurrent hemorrhage on follow- up CT scans argues against this possibility, how- ever. The clinical appearance of thalamic hemorrhage! intraventricular hemorrhage was characterized by sudden onset of marked neurologic abnormalities in all patients. The clinical features, with the ex- ception of timing of onset of problems, were gen- erally nonspecific and did not permit diagnosis of the location of hemorrhage. Thus, the clinical pres- entation was similar to that observed in full-term infants with intraventricular hemorrhage of other origin and consisted principally of signs of in- creased intracranial pressure, seizures, and dimin- ished level of consciousness. In a recent report8 of 4 full-term newborns with thalamic hemorrhage! intraventricular hemorrhage, persistent downward deviation of the eyes was observed in two infants. The authors speculated that this clinical feature may be pathognomonic of hemorrhage in this lo- cation. We did not observe this sign in any of our patients with thalamic hemorrhage/intraventricu- lar hemorrhage, however. Late onset of clinical abnormalities, ie, often after 4 days of age, in as- sociation with an uneventful birth history occurred at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from 742 THALAMIC HEMORRHAGE AND NEWBORN in the majority of cases of thalamic hemorrhage! intraventricular hemorrhage (17 of 20 patients). The clinical abnormalities of late onset appear to be characteristic of this condition. This suggests that thalamic hemorrhage/intraventricular hemor- rhage may be a result of postnatal causes. Predis- posing factors for venous thrombosis (sepsis, con- genital heart disease, and hematologic disturb- ances) were documented in 6 of the 12 infants with thalamic hemorrhage/intraventricular hemorrhage in our study. Although the diagnosis of thalamic hemorrhage! intraventricular hemorrhage in our patients was made radiologically on the basis of CT findings, it may also be established by cranial ultrasonog- raphy.6’7 In three infants in whom thalamic hem- orrhage was less extensive, there was decreased tissue attenuation in the thalamus adjacent to the hemorrhage in the CT scans, which is consistent with hemorrhagic infarction in that region (Fig 2). Furthermore, the observation of increased atten- uation in the region of the straight sinus on CT scans of two infants with thalamic hemorrhage/ intraventricular hemorrhage performed without contrast enhancement (Fig 1), as well as the ab- sence of opacification of the ipsilateral internal cerebral vein during cerebral angiography in one patient (Fig 3), raises the possibility that venous occlusion may play a role in the pathogenesis of hemorrhagic thalamic infarction.15’16 An associa- tion between thrombosis of the internal cerebral vein and hemorrhagic thalamic infarction has been demonstrated previously by neuropathologic stud- ies in young infants. Intraventricular hemorrhage was not uncommon, presumably because of the proximity of the larger venous channels to the ventricular walls.17 Except for a significantly greater incidence of cerebral palsy in infants with thalamic hemor- rhage/intraventricular hemorrhage, the outcome of these patients did not differ significantly from that of infants with intraventricular hemorrhage from other sources. A variable neurologic outcome was suggested in previous reports3’8’9 of infants with unilateral thalamic hemorrhage/intraventricular hemorrhage. In contrast, infants with bilateral tha- lamic hemorrhage following birth asphyxia have uniformly poor prognosis and have either died or developed severe neurologic sequelae.47 According to our data, neurologic sequelae, eg, hydrocephalus, seizures, and cerebral palsy (especially hemiplegia), are common following thalamic hemorrhage/intra- ventricular hemorrhage and occur in the majority of cases. Only a minority of infants appeared neu- rologically and developmentally normal at 18 months of age. In summary, a high incidence of thalamic hem- orrhage is suggested by our data as a cause of intraventricular hemorrhage in the full-term new- born. This is seen especially in infants with Un- eventful birth histories and infants in whom clinical abnormalities develop after 1 week of age. Both the clinical appearance during the newborn period and neurologic outcome appear similar to that of full- term infants with intraventricular hemorrhage originating from other sites. Thus, although tha- lamic hemorrhage/intraventricular hemorrhage may be suspected on the basis of clinical features, definitive diagnosis is based on radiologic abnor- malities observed either on CT scans, cranial ultra- sonography, or cerebral angiography. REFERENCES 1. Volpe JJ. Neurology of the Newborn. Philadelphia, PA: WB Saunders Co; 1987 2. Palma PA, Miner ME, Morriss FH, et al. Intraventricular hemorrhage in the neonate born at term. Am J Dis Child. 1979;133:941-944 3. Mitchell W, O’Tuama L. Cerebral intraventricular hemor- rhages in infants: a widening age spectrum. Pediatrics. 1980;65:35-39 4. Kotagal 5, Toces 5, Kotagal P, Archer C. Symmetric hi- thalamic and striatal hemorrhage following perinatal hy- poxia in a term infant. J Comput Assist Tomogr. 1983;17:353-355 5. Voit T, Lemburg P. Damage of thalamus and basal ganglia in asphyxiated full-term neonates. Neuropediatrics. 1987; 18:176-181 6. Kreusser KL, Schmidt RE, Shackelford GD, Volpe JJ. Value of ultrasound for identification of acute hemorrhagic necro- sis of thalamus and basal ganglia in an asphyxiated term infant. Ann Neurol. 1984;16:361-363 7. Donn SM, Bowerman RA, DiPietro MA, Gebarski S. Son- ographic appearance of neonatal thalamic-striatal hemor- rhage. J Ultrasound Med. 1984;3:231-233 8. Trounce JQ, Dodd KL, Fawer C-L, Fielder AR, Punt J, Levene MI. Primary thalamic haemorrhage in the newborn: a new clinical entity. Lancet. 1985;1:190-192 9. Primhak RA, Smith MF. Primary thalamic hemorrhage in first week of life. Lancet. 1985;1:635 10. Waishe TM, David KR, Fisher CM. Thalamic hemorrhage: a computed tomographic-clinical correlation. Neurology. 1977;27:217-’222 11. Livingston JH, Brown JK. Intracerebral haemorrhage after the neonatal period. Arch Dis Child. 1986;61:538-544 12. Goddard J, Lewis RM, Armstrong DL, Zeller RS. Moderate, rapidly induced hypertension as a cause of intraventricular hemorrhage in the newborn beagle model. ,J Pediatr. 1980;96:1057-1060 13. Wimberley PD, Lou HC, Pedersen H, et al. Hypertensive peaks in the pathogenesis of intraventricular hemorrhage in the newborn: abolition by phenobarbitone sedation. Acta Pediatr Scand. 1982;71:537-542 14. Young RSK, Liberthson RR, Zalneraitis EL. Cerebral hem- orrhage in neonates with coarctation of the aorta. Stroke. 1982;13:491-494 15. Wendling LR. Intracranial venous sinus thrombosis: diag- nosis suggested by computed tomography. Am J Roentgenol. 1978;130:978-980 16. Rao KC, Knipp HC, Wagner EJ. Computed tomographic findings in cerebral sinus and venous thrombosis. Radiology. 1981;140:391-398 17. Ehlers H, Courville CB. Thrombosis of internal cerebral veins in infancy and childhood: Review of literature and report of five cases. J Pediatr. 1936;8:600-623 at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from 1990;85;737Pediatrics Elke H. Roland, Olof Flodmark and Alan Hill Thalamic Hemorrhage With Intraventricular Hemorrhage in the Full-Term Newborn Services Updated Information & http://pediatrics.aappublications.org/content/85/5/737 including high resolution figures, can be found at: Citations http://pediatrics.aappublications.org/content/85/5/737#related-urls This article has been cited by 3 HighWire-hosted articles: Permissions & Licensing http://pediatrics.aappublications.org/site/misc/Permissions.xhtml or in its entirety can be found online at: Information about reproducing this article in parts (figures, tables) Reprints http://pediatrics.aappublications.org/site/misc/reprints.xhtml Information about ordering reprints can be found online: Online ISSN: 1098-4275. Copyright © 1990 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005. American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from