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lobar haematoma references to lobar haematoma r e f e r e n c e s n a v i g a t o r < Baram TZ, Butler IJ, Nelson MD Jr., McArdle CB (1988) Transverse sinus thrombosis in newborns: clinical and magnetic resonance imaging findings. Ann Neurol 24(6):792-4.  Bergman, I., Bauer, R.E., Barmada, M.A., Latchaw, R.E., Taylor, H.G., David, R., Painter, M.J. (1985) ‘Intra­cerebral hemorrhage in the full-term neonatal infant.’ Pediatrics, 75, 488–496. Govaert P, Voet D, Achten E, Vanhaesebrouck P, van Rostenberghe H, van Gysel D, Afschrift M (1992b) Noninvasive diagnosis of superior sagittal sinus thrombosis in a neonate. Am J Perinatol 9(3):201-4. Govaert P, Achten E, Vanhaesebrouck P, De Praeter C, Van Damme J (1992c) Deep cerebral venous thrombosis in thalamo-ventricular haemorrhage of the term newborn. Pediatr Radiol 22(2):123-7. Govaert P (1993) Cranial haemorrhage in the term newborn infant. Clinics in Developmental Medicine nr. 129, London: Mac Keith Press, ISBN 0 901260 98 3.Gradnitzer, E, Urlesberger, B, Maurer, U, Riccabona, M and Muller, W (2002). '[Cerebral hemorrhage in term newborn infants--an analysis of 10 years (1989-1999)].' Wien Med Wochenschr, 152:9-13. Haataja, L, Mercuri, E, Cowan, F and Dubowitz, L (2000). 'Cranial ultrasound abnormalities in full term infants in a postnatal ward: outcome at 12 and 18 months.' Arch Dis Child Fetal Neonatal Ed, 82:F128-33. Hanigan, W.C., Powell, F.C., Palagallo, G., Miller, T.C. (1995) ‘Lobar hemorrhages in full-term neonates.’ Child’s Nervous System, 11, 276–280. Hausler, M, Merz, U, Van Tuil, C, Ramaekers, VT (2004). 'Long-term outcome after neonatal parenchymatous brain lesions.' Klin Padiatr, 216:244-51. Hayashi, T., Harada, K., Honda, E., Utsunomiya, H., Hashimoto, T. (1987) ‘Rare neonatal intracerebral hemorrhage. Two cases in full-term infants.’ Child’s Nervous System, 3, 161–164. Holden, KR, Titus, MO and Van Tassel, P (1999). 'Cranial magnetic resonance imaging examination of normal term neonates: a pilot study.' J Child Neurol, 14:708-10. Huang, AH and Robertson, RL (2004). 'Spontaneous superficial parenchymal and leptomeningeal hemorrhage in term neonates.' AJNR Am J Neuroradiol, 25:469-75. Inder TE, Perlman JM, Volpe JJ (2018) Intracranial hemorrhage: Subdural, subarachnoid, intraventricular (term infant), miscellaneous. Chapter 22, 593-622. In: Volpe's Neurology of the Newborn. 6th Ed. Elsevier  Jhawar, BS, Ranger, A, Steven, D and Del Maestro, RF (2003). 'Risk factors for intracranial hemorrhage among full-term infants: a case-control study.' Neurosurgery, 52:581-90; discussion 588-90. King, SJ and Boothroyd, AE (1998). 'Cranial trauma following birth in term infants.' Br J Radiol, 71:233-8. Liu, HY, Huang, LT and Lui, CC (1998). 'Vacuum extraction delivery complicated with acute subdural hematoma and cerebral infarction: report of one case.' Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi, 39:119-22.Pierre-Kahn, A., Renier, D., Sainte-Rose, C., Flandin, C., Hirsch, J-F. (1985) ‘Les hématomes intracrâniens aigus du nouveau-né à terme. A propos de dix-sept cas.’ Annales de Pédiatrie, 32, 419–425. Nikam RM, Kandula VV, Yue X, Krishnan V, Kumbhar SS, Averill LW, Paudyal B, Choudhary AK (2021) Birth-related subdural hemorrhage: prevalence and imaging morphology. Pediatric Radiology 51(6), 939–946. Odita, JC and Hebi, S (1996). 'CT and MRI characteristics of intracranial hemorrhage complicating breech and vacuum delivery.' Pediatr Radiol, 26:782-5. Pettersson, H, McClure, P and Fitz, C (1984). 'Intracranial hemorrhage in hemophilic children. CT follow-up.' Acta Radiol Diagn (Stockh), 25:161-4. Retzius G (1896) Das Menshenhirn: Studien in der Makroskopischen Morphologie. Stockholm: PA Norstedt 1-167. Ries, M., Wölfel, D., Maier-Brandt, B. (1995) ‘Severe intracranial hemorrhage in a newborn infant with transplacental transfer of an acquired factor VIII:C inhibitor.’ Journal of Pediatrics, 127, 649–650. Rooks VJ, Eaton JP, Ruess L, Petermann GW, Keck-Wherley J, Pedersen RC (2008) Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. American Journal of Neuroradiology 29(6),1082–1089. Sandberg, DI, Lamberti-Pasculli, M, Drake, JM, Humphreys, RP, Rutka, JT (2001) Spontaneous intraparenchymal hemorrhage in full-term neonates. Neurosurgery 48:1042-1049. Slovis, T.L., Shankaran, S., Bedard, M.P., Poland, R.L. (1984)'Intracranial hemorrhage in the hypoxic-ischemic infant : ultrasound demonstration of unusual complications.' Radiology, 151, 163-169. Suh, DC, Alvarez, H, Bhattacharya, JJ, Rodesch, G and Lasjaunias, PL (2001). 'Intracranial haemorrhage within the first two years of life.' Acta Neurochir (Wien), 143:997-1004. Tan MA, Miller E, Shroff MM, deVeber GA, Kirton A (2012) Alleviation of Neonatal Sinovenous Compression to Enhance Cerebral Venous Blood Flow. Journal of Child Neurology 28(5) 583-588. Tavani, F, Zimmerman, RA, Clancy, RR, Licht, DJ and Mahle, WT (2003). 'Incidental intracranial hemorrhage after uncomplicated birth: MRI before and after neonatal heart surgery.' Neuroradiology, 45:253-8. Tramonte JJ, Goodkin HP (2004) Temporal lobe hemorrhage in the full-term neonate presenting as apneic seizures. J Perinatology 24:726-729. Tekkok, IH, Ventureyra, EC (1997). ‘Spontaneous intracranial hemorrhage of structural origin during the first year of life.’ Childs Nerv Syst, 13:154-65. Vinchon M, Pierrat V, Tchofo PJ, Soto-Ares G, Dhellemmes P (2005) Traumatic intracranial hemorrhage in newborns. Childs Nerv Syst. [Epub ahead of print]  Wang, LW, Huang, CC and Yeh, TF (2004). ‘Major brain lesions detected on sonographic screening of apparently normal term neonates.’ Neuroradiology, 46:368-73. > algorithm for haemorrhage typical examples: frontal veins and haemorrhage typical examples: occipital  lobar cerebral haematoma typical examples: parietal historical account s u m m a r y pial veins typical examples: temporal Ultrasound aspectsWith US lobar haematomas show as round or elliptic, hyperdense and often clearly delineated zones. Where haematoma borders are irregular, one may be dealing with haemorrhagic conversion of an ischaemic area. US and MR will indicate whether there is still parenchyma between the lesion and the adjacent cranial bone: this allows for a distinction between primary parenchymal and subarachnoid haematoma. The differential diagnosis may vary per lobe.  After a few weeks cystic regression occurs of part (often most) of the affected lobe. The overlying cortex is often necrotic. The absence of mass effect can be striking in cases without extracerebral bleeding. imaging aspects per lobe work-up In a limited number of newborn infants and in the absence of major IVH, one may find haemorrhage in one or more brain lobes, outside basal ganglia and thalamus. Lesions in each region of the cerebrum have been described, mainly with CT or MR. It is common for a lobar haematoma to be associated with a subdural or subarachnoid extra-axial haemorrhage: this raises the question where the primary focus is, in parenchyma or in the extracerebral space. The presenting sign has often been (multi)focal convulsive activity and apnoea but some lobar haematomas are asymptomatic. In most instances the exact mode of genesis remains unknown. There are no reports of well documented sinus thrombosis causing large lobar bleeds in the absence of haemostatic disorders.  Venous anatomy is likely important for many lobar haematomas. These lesions warrant a diligent search for evidence of trauma, haemostatic failure, prothrombotic tendency and vascular malformation.  Saccular arterial aneurysms can present with seizures and meningeal signs in infancy: the MCA is commonly affected but location can be within the posterior fossa or in other supratentorial arteries. Most aneurysms exceede 1 cm in diameter and should be seen on MRA. Non-Galenic arterio-venous malformations present with congestive heart failure (usually large fistulae), haemorrhage (usually small fistulae) or hydrocephalus of the communicating type. Most are supratentorial (9/10). Spontaneous thrombosis of an AVM is exceptional (around 1/10). Cavernous angiomata cause bleeding as a rule, from minor to extensive.  One must always be aware of an underlying tumour in a lobar or subdural or intraventricular haemorrhage: astrocytoma is a known cause of neonatal lobar haematoma. lobar haematoma: summary contusion near fontanel left frontal extensive vit. K deficiency frontal lobar haematoma mesial and subdural complete mesial and basal factor VII def. convexity basal subdural pole + mesial and pole arterial aneurysm up to ventricle pole, SMCV temporal lobar haematoma convexity + mesial parietal lobar haematoma typical giant occipital lobar haematoma Developmental anatomy of the pial cerebral veins The cortical veins of the cerebrum have been examined by upward injection of the internal jugular vein in five fetuses, whose ages ranged from six months to term [O’Connell 1934]. The surface veins are separated into three layers: a superficial, which forms the superficial vessels of the head; an intermediate, which forms the dural sinuses ; and a deep portion which intimately covers the nervous tissue and later forms the cerebral veins. Continuity between the superficial and middle venous strata persists only in the emissary veins. The cerebral veins have important connections with the dural system, firstly in the region where both sets of vessels drain into the primary head vein, and secondly, on the dorsal aspect of the cerebrum close to the midline. In this midline region there is an anastomosis between the vessels of opposite sides which is called the sagittal plexus, and from this the superior and inferior sagittal sinuses and the straight sinus develop. As expected the deepest stratum of the anterior plexus sends some of its anterior branches radiating from the insula to the margin of the hemisphere. This arrangement persists in late fetal and adult life, the superficial middle cerebral vein sends tributaries radiating across the surface of the hemisphere towards its margin.  The radiation of the cortical veins from the region of the insula is very well marked in the fetus and persists in adult life. The superior members of this group of vessels approach the margin of the hemisphere at right angles to the frontal side, but their terminal portions, in most cases, change direction before entering the sinus. From observations on the changes in their direction, which occur between the later months of fetal life and adult life, it is considered that all these vessels originally entered the sinus approximately at right angles to its long axis, but especially posterior (parietal and occipital) veins turn anterior before entering the SS, so that their outgoing flow is against streaming in the SSS. The size of these vessels is inversely proportional to their numbers. In both adult and fetus eight veins were the commonest number present on each side (range 5 to 13). The veins enter the dural wall of the sinus for a short distance posterior to the final entry into the inner sinus wall.  With the growth of the cerebral hemisphere, there is a tendency towards separation of these vessels into (a) a superficial middle cerebral system and (b) a system of veins around the margin of the hemisphere—the superior and inferior cortical veins. In many the continuity of the original channel is not interrupted, and hence the superior anastomotic veins (at least three in number) and the inferior anastomotic veins (usually two in number) persist as evidence of the original arrangement. The direction of the cortical veins of the cerebrum is determined by the growth of the cerebral hemisphere. As a result of the growth anteriorly of the frontal lobe and posteriorly of the main mass of the hemisphere, the direction of the terminal portions of the superior vessels is altered, the anterior veins being directed posteriorly and the posterior veins coursing obliquely anteriorly as they pass to the superior sagittal sinus. The posterior inclination of the inferior veins, as they pass to the transverse sinus, has a similar explanation.  One of the members of the superior cortical series of veins is found in each of the precentral (referred to as vein of Trolard), central and postcentral sulci, and similarly a tributary of the superficial middle cerebral vein is found in each of the sulci which separate the opercula of the insula. The middle cerebral veins drain into cavernous sinus or sphenoparietal sinus. Of tributaries of the superficial middle cerebral vein, some pass anteriorly in the direction of the frontal pole; others pass superiorly, with varying degrees of obliquity, to supero-medial margin of the hemisphere ; while the remainder pass postero-inferiorly to the temporo-occipital region. Of the larger veins radiating from the stem of the lateral fissure the majority, if not all, terminate by passing from the surface of the cerebrum into one of the large venous sinuses—either superior sagittal or transverse.  There are many variations in the number and size of cerebral convexity veins. Most often a large precentral bridging vein (Trolard) connects to the SSS and a large post-insular vein (Labbé) drains into the transverse sinus. These veins are connected in different ways to the superficial and hence deep middle cerebral veins. At birth the lacunae laterales are absent, and later appear and they grow pari passu with the arachnoid granulations after term birth. In adults past middle age the lacunae laterales are two in number—one being placed on each side of the superior sagittal sinus. The "chords of Willis " found in the superior sagittal sinus persist as evidence of its original plexiform character. The lacunae laterales serve as lateral extensions of the lumen of the superior sagittal sinus over the supero-medial margin of the cerebral hemisphere in the posterior frontal, parietal and sometimes also the anterior occipital regions, where the majority of the arachnoid granulations are found. The floor of each lacuna is everywhere carpeted by a layer of these granulations. Cerebral venous thrombosis commonly occurs in the SSS, particularly in its parietal segment. Several anatomical factors have been contributed to this prevalence. One of them is that the BVs drain into the SSS against the blood flow in the sinus, thus causing turbulence in the blood stream. This study found that nearly all the BVs (97%, 561/581) entered the parietal segment of the SSS at an angle opposed to the direction of blood flow in the sinus, with an average angle of 35°. Most importantly, the entrances of these BVs were angled in a three-dimensional way, not simply along the sagittal axis, and before entering the SSS, the veins always adhered or ran parallel to the sinus. Therefore, a shift of the brain in any direction with traction on the BVs may deform the venous wall, inducing thrombosis. Le gros Clark, WE (1920) On the Pacchionian Bodies. Journ. Anat. 55, 40.  0'Connell  JEA (1934) Some observations on the cerebral veins. Brain 57:484-503. Sargent P (1911) Some Points on the Anatomy of the Intracranial Sinuses. Journ. Anat. and Physiol. 46, 69. Schwartz P : Geburtsschaden bei Neugeborenen, Gustav Fisher Verlag, Jena, 1964 Streeter L (1918) The Development of the Venous Sinuses of the Dura Mater in the Human Embryo. Amer. Journ. Anat 18, 145-178. T cerebral pial veins bridging to the SSS < veins and haematomas occipital —> parietal frontal basal vein in imaging temporal for the temporal lobe, venous origin of haematomas can only be understood by study of the dwindling tentorial sinus, the development of the basal vein of Rosenthal and general changes in vein size in the fetal brain brain haemorrhage The possible mechanisms behind extravasation of blood are:  I. within an arterial infarct;  II. within a venous infarct (thrombosis);  III. direct trauma to a vessel;  IV. haemostatic problem with unstoppable bleeding from a small vessel;  V. arterial hypertension;  VI. venous congestion without thrombosis;  VII. vascular anomaly;  VIII. tumor;  IX. other.  polycythaemia Least common are parietal and occipital lobar haematomas.  temporal lobe structures temporal lobe anatomy lobar haematoma: aspects per lobe Frontal lobar haemorrhageCT studies of living term neonates with seizures suggested the existence of a separate clinical entity associating unexplained unilateral frontal parenchymal haemorrhage with a conspicuous extracerebral haemorrhage either between the lobe and the falx, around the frontal lobe or in the Sylvian fissure. All early case histories lack evidence of IVH. The associated extracerebral haemorrhage was either subdural or subarachnoid/pial in location. Against the hypothesis of interfrontal bone displacement due to trauma as the cause is the excellent condition of all infants at birth, the absence of moulding or calvarial damage worthy of note on postnatal clinical examination and absent evidence that this type of displacement can induce direct parenchymal destruction. The exclusion of arterio-venous malformation or angioma on angiographical studies can be important. Typical presentation is with contralateral focal clonic seizures and transient hemiparalysis. If huge, the haemorrhage causes anaemia and a tense fontanelle. Some infants have remained remarkably alert and were fed orally in between convulsions. Seizure control has been reported to be easy. On CT or MRI the lesion presents as an irregular density within the frontal white matter, sparing the cortex but sometimes surrounded by hypoperfused non-haemorrhagic white matter.  Sparing of a rim of mesial cortex renders haemorrhagic infarction of the ACA an unlikely diagnosis. Frank haematoma within a large infarction could mimic these images. If important, the combined lesion displaces the falx and shifts the midline. Severe intracranial hypertension indicates the need for surgical decompression. Despite the obvious sequel of a triangular brain defect, with its basis facing the frontal bone, most children have been reported to recover without cerebral palsy. Posthaemorrhagic hydrocephalus has not been reported. The shape of the brain defect must not be mistaken for regional atrophy following anterior truncal MCA stroke. veins to haematoma basal vein and PCA classification of temporal lobe haematoma temporal veins Temporal lobar haemorrhageThis is a rather common event in term infants. The typical presentation is with apnoea/cyanosis without bradycardia between a few and 24 hours after birth. A clear-cut example of this type of bleeding is depicted by Slovis et al. 1983. A full-term newborn, birthweight 3402 grams, was delivered vaginally after prolonged labour. The Apgar scores, in spite of meconium staining, were eight at one and five minutes. Its neonatal course was complicated by hypoglycaemia, hypocalcaemia and polycythaemia. Seizures prompted investigations on day four: the temporal lobe on the right was completely altered by bleeding on CT scan. Ten days later this lobe had turned into a big cyst. Hyperviscosity - the mother had diabetes mellitus - was the mechanism proposed by the authors.  Though similar in appearance on CT scan, an infant described by Fouché et al. 1982 probably suffered from left subarachnoid haematoma and not lobar parenchymal haemorrhage, as the clinical context was one of disseminated intravascular coagulation in congenital toxoplasmosis. Postmortem details were not present in this case. Baumann et al. 1987 described left temporal lobe haematoma in a thrombocytopenic newborn with subsequent contralateral hemiparesis and hemianiopsia. They considered partial infarction of the area perfused by the middle cerebral artery to be the primary event. These early descriptions clearly illustrate the inhomogeneous character of temporal lobe haematoma, with various types of imaging and some correlation to the causes. Lobar temporal haematoma due to venous ischaemia, haemorrhagic diathesis or other causes has to be differentiated from subarachnoid haematoma and basal subdural haemorrhage with underlying cerebral contusion or arterial infarction.  The outcome of infants with cystic necrosis of one temporal lobe is not well described.  - inspect the scalp - listen for cranial bruits - look for congestive heart failure - look for primary tumors elsewhere - ask complete haemostatic screen, including prothrombotic disorders and platelet function  imaging: - detailed Doppler exam: flow velocity in major veins and arteries, abnormal vessels in and around the haemorrhage - MRI/MRA: in the acute stage: determine location and damage to normal brain, estimate timing of bleeding, document occlusion of large vessels, exclude aneurysms or cavernous haemangiomas, look for AVM in the wall of the haematoma, look for tumor around the haemorrhage; in the subacute stage (after several weeks, typically in the second month after birth): look for vascular anomaly or tumor exclude haemorrhagic diathesis: (1) thrombocytopenia: iso-immune, auto-immune; (2) thrombocytopathy: congenital (von Willebrand disease), by salicylates or non-steroidal anti-inflammatory drugs, congenital amegakaryocytic thrombocytopenia CAMT, thrombocytopenia absent radius TAR, Wiskott-Aldrich; (3) shortage of coagulation factors: congenital (V, VII, VIII, X), due to cumarins, diffuse intravascular coagulation; (4) shortage of anticoagulants: protein C deficiency, FV Leiden, FII mutation; (5)  dysfibrinogenaemia; (6) liver failure: acetaminophen toxicity, perinatal haemochromatosis; (7) glutathion synthetase deficiency.  week 6 no vascular anomaly mitochondrial disorder week 1 work-up for lobar haematoma Like in the adult, on rare occasions a perinatal brain haemorrhage will lodge inside one cerebral lobe, as if it originated in its white matter. If the cortex above it is not affected these lesions are either primary haematomas or lacunar infarctions with secondary haemorrhagic transformation. In association with extensive (grade III) intraventricular haemorrhage they can be periventricular venous infarction. Their striking asymmetry suggests local factors to be generative, like trauma or vascular lesion. The absence of data on this event in the term newborn infant is so striking that an attempt at creating a subdivision similar to the adult counterpart is worth making.  Frontal lobe haemorrhageAnatomical description : Recent CT studies of living term neonates with seizures suggest the existence of a separate clinical entity associating unexplained unilateral frontal parenchymal haemorrhage with a conspicuous extracerebral bleed either between the lobe and the falx or in the Sylvian fissure (Chaplin et al. 1979, Blanc et al. 1982, Pierre-Kahn et al. 1985, Bergman et al. 1985, Welch and Strand 1986, Hayashi et al. 1987). All case histories lack evidence of intraventricular haemorrhage. The associated extracerebral bleed was either subdural or subarachnoid (Hayashi et al. 1987) in location. Incidence : Though not reported in sufficient detail, two such haemorrhages were gathered in a recent prospective NMR study of 100 high-risk newborn infants (Keeney et al. 1991). Its prevalence was two in 25 traumatic parturitional haemorrhages collected by Welch and Strand 1986. Seven cases with sufficient clinical and iconographical detail are summarized in Table I (Chaplin et al. 1979 : cases 1 and 2, Blanc et al. 1982 : case 3, Pierre-Kahn et al. 1985 : case 4, Bergman et al. 1985 : case 5, Hayashi et al. 1987 : cases 6 and 7). Table                 Unilateral frontal intracerebral haemorrhage at term Number                              1         2       3       4       5       6       7  Sex                                     F        M       ?       M       ?       F       F            Birthweight (g)                 3840   3400  1950  3950  3200  2750  3720        Gestational age (w)            42      42      39     42      37     40     38         Delivery mode             . forceps                             +      +  . spontaneous                                                +                 +       +  . caesarean                                            +               + Apgars 1/5 min                 8/9     8/9    5/9  10/10  8/9    9/9   9/10         Interval (h,d)                    36h    13h      ?     <1d     <1d     2d    2d        Focal seizures                     R       L        ?       ?        -        R       R                     Hemiparesis                        +       +       ?        -        -        -       -  Intracranial hypertension     -       -        ?       +        -        +       +   Bleeding side                       L      R       R       L        L        L       L             Associated extra- cerebral haematoma            (interhemispheric)              -      +       +        +       -         +       -                     (in Sylvian fissure)              -       -       -         -      +         -       +         Midline shift                        -       +       -       +       -         +       +           Craniotomy                         -       -       -        +       -         +       +          Normal at 1 year                 +      +       -        +       +         ?       ?         Pathogenesis : These case histories share the absence of definite aetiologies such as mechanical birth trauma (except for case 1 possibly), birth asphyxia or a disturbed clotting mechanism (except for case 3 where disseminated intravascular consumption was recorded, probably secondary to the event and  to intrauterine growth retardation). Hayashi put forward interfrontal bone displacement as the causal factor, based on neurosurgical findings of parenchymal 'contusion' (Hayashi et al. 1987). Although attractive, against this hypothesis are the excellent status of all infants at birth, the absence of moulding or calvarial damage worthy of note on postnatal clinical examination and the non-existence of available evidence that this type of displacement can induce direct parenchymal destruction. The exclusion of arterio-venous malformation or angioma on angiographical studies is very instructive (Hayashi et al. 1987). Future examinations, either by NMR or at postmortem will have to focus on this matter. Clinical setting : As made clear in Table I, typical presentation is with contralateral focal clonic seizures and hemiparalysis. If huge, the haemorrhage causes anaemia and a tense fontanelle. Some infants have remained remarkably alert and were fed orally in between the convulsions (Chaplin et al. 1979). The seizure control has been reported to be easy (Chaplin et al. 1979). Lumbar CSF was haemorrhagic in one report.  Radiological assessment : X ray or ultrasound findings were not considered important in the reports mentioned. On CT scan the lesion presents as an irregular density within the frontal white matter, sparing the cerebral cortex but sometimes surrounded by hypoperfused non-haemorrhagic white matter. Sparing of a rim of cortex renders haemorrhagic infarction of the anterior cerebral artery an unlikely diagnosis. Frank haematoma within a large infarction could mimic these images (Inoue et al. 1980). As already explained, an extensive extracerebral haemorrhage is associated in most, either between the frontal lobe and the falx or within the Sylvian fissure. Although impossible to be certain on CT scan alone, the location and the surgical findings in one report go along with their subarachnoidal location. In an infant not included in the Table, this peculiar extracerebral haemorrhage between mesial frontal lobe and falx, either subarachnoid or pial, was the only finding with CT scan on the third day after severe birth asphyxia at full term (Magilner and Wertheimer 1980). The latter infant presented with clonic seizures, aspiration pneumonia, bilateral retinal haemorrhage and evidence of disseminated intravascular coagulation. Its normal neurological status at the age of 11 months was worthy of note. If important, the combined lesion displaces the falx and shifts the midline. Angiography defines the normalcy of the main related vessels (Hayashi et al. 1987). Management and prognosis : It seems that severe intracranial hypertension indicates the need for surgical decompression (Pierre-Kahn et al. 1985, Hayashi et al. 1987).Ë Despite the obvious sequel of a triangular brain defect, with its basis facing the frontal bone, most children have been reported to recover completely without residual cerebral palsy. Posthaemorrhagic hydrocephalus has not been mentioned. The shape of the brain defect must not be mistaken for regional atrophy following arterial cerebral infarction. Temporal lobe haemorrhageA clear-cut example of this type of bleeding is depicted by Slovis et al. 1983. A full-term newborn, birthweight 3402 grams, was delivered vaginally after prolonged labour. The Apgar scores, in spite of meconium staining, were eight at one and five minutes. Its neonatal course was complicated by hypoglycaemia, hypocalcaemia and polycythaemia. Seizures prompted central nervous system investigations on day four : the temporal lobe on the right was completely altered by bleeding on CT scan. Ten days later this lobe had turned into a big cyst. Hyperviscosity - the mother had diabetes mellitus - was the mechanism proposed by the authors.  Though similar in appearance on CT scan, an infant described by Fouché et al. 1982 probably suffered from left subarachnoid haematoma and not lobar parenchymal haemorrhage, as the clinical context was one of disseminated intravascular coagulation in congenital toxoplasmosis. Postmortem details were not present in this case.  In an article on primary cerebral bleeding at terËm, Bergman et al. 1985 mention a macrosomic neonate without birth asphyxia who presented at two hours with apnoea, tonic seizures and a left abducens palsy; CT scan, not shown in the paper, documented left temporal cerebral haemorrhage. Baumann et al. 1987 described left temporal lobe haematoma in a thrombocytopenic newborn with subsequent contralateral hemiparesis and hemianiopsia. They considered partial infarction of the area perfused by the middle cerebral artery to be the primary event. Case history (VDEC, female, outborn, 37/40, 2100 g) : This firstborn infant was behind in growth on US scan from about 29 weeks on. Oligohydramnios was added to this finding later on. Delivery was spontaneous vaginal at 37 weeks of gestation (first stage two hours, second stage 10 minutes), with meconium stained liquor. Her Apgar scores were four and eight at one and five minutes. She presented with minimal respiratory distress of unspecified nature and hypoglycaemia. Her platelet count dipped at 22,000/mm3 on day three, when her gastric residue became bloodstained. Fetomaternal incompatibility as for  platelet surface antigen PlA1 was subsequently shown without demonstration of specific platelet antibodies. Her platelet count started to rise following IV immunoglobulin treatment, the first normal count achieved on day nine. On day six she was referred with generalized oedema, a tense fontanelle, irritability and a paretic right arm. There were no petechiae or bruises. The initial coagulation screen revealed arguments in favor of disseminated intravascular coagulation. On CT scan in addition to a large left temporal lobe haematoma, were also documented a right occipital parenchymal bleed and a haemorrhage into the left cerebellar hemisphere. The US evolution of the brain lesions: parietal cystic periventricular leukomalacia developed together with cavitary changes in precedent haematomas. At 21 days of age an acute cholestatic episode finally lËed to surgical exploration the next week, after exclusion of hilar angioma on aortography. The proximal bile ducts were obviously dilated because of a hilar scarring proces around the main duct; histological examination excluded a malignant process and confirmed the surgeon's diagnosis of precedent haemorrhage by showing fibrous tissue with siderophages. At two years of age this child is spastic diplegic and squints with a horizontal nystagmus. Our final neurological diagnosis was : multiple parenchymal bleeds in a growth retarded infant with thrombocytopaenia of indefinite cause. The temporal and cerebellar location of haematomas together with the presence of additional (cystic) parietal leukomalacia, militate against a diagnosis of ischaemic white matter disease as a primary event. Lobar temporal haematoma due to venous ischaemia, haemorrhagic diathesis or other causes has to be differentiated from subarachnoid haematoma and basal subdural hemorrhage with underlying cerebËral contusion or arterial infarction (see related chapter). An account of normal sonographic temporal lobe appearance is offered by Sasaki et al. 1989. The outcome of infants with cystic necrosis of one temporal lobe is not well described.  Parietal lobe haemorrhageA search for clear-cut primary parietal bleeding, appearing as a rounded mass on scans and without the cortical involvement and anatomical distribution of arterial infarct, has not been very rewarding. Fenichel et al. 1984 refer to two male newborn infants, both with spontaneous vaginal delivery, one at and one post term. One presented with apnoea and multifocal seizures at 24 hours, the other with focal facial seizures on day seven. The corresponding scans are not shown. Both ended up with cerebral palsy and mental retardation.  Bergman et al. 1985 describe a macrosomic neonate, birthweight 5000 grams, with bilateral intraventricular and right parieto-temporal cerebral haemorrhage at the end of the fiËrst month of life. This infant of a mother with gestational diabetes presented with diarrhoea, fever and seizures on day 27. As her haemoglobin was 180 g/L the suggested cause of this event was hyperviscosity with deep venous thrombosis, impossible to interpret in the absence of related scans. A case history, documented by Cartwright et al. 1979, started with seizures, pallor and intracranial hypertension on the second day after difficult rotational forceps delivery. This boy was born at full term, weighed 3120 grams and had Apgar scores of eight and nine at one and five minutes. His CSF was bloody. CT scan indicated a right posterior parietal haematoma with midline shift. The boy developed contralateral hemiparesis. Case history (MR, male, outborn, 40/40, 2100 g) : This second born child presented with fetal distress, heralded by meconium staining and loss of beat to beat variation on CTG for 30 minutes, at full term. He was delivered in the spontaneous vaginal way with a short second stage. His Apgar score was three at one and three minutes. Before referral he became hypothermic (34˙C) and hypoglycaemic. His respiratory difficulties were thought to result from meconium inhalation and persistent pulmonary hypertension, with an additional left pneumothorax. Haemoglobin on the first day was 140 g/L. The platelet count dipped at 61,000/mm3 on day six. Association of the parietal bleed with a major intraventricular haemorrhage suggested periventricular venous haemorrhagic infarction as our anatomical diagnosis. The sparing of adjacent cortex was striking and excluded arterial stroke. An ipsilateral vitreal haemorrhage accompanied the cerebral lesion. This child developed posthaemorrhagic hydrocephalus but escaped shunting after stabilisation with serial lumbar punctures and diuretics. 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Helvetica paediatrica Acta, 43, 195-202. historical account of lobar haematoma: references from Govaert 1993 temporal lobe haematoma: imaging types polycythaemia temporal lobe structures BVR basal vein of Rosenthal DMCV deep middle cerebral vein SMCV supperficial middle cerebral vein TeS fetal tentorial sinus temporal lobe anatomy basal vein and PCA CUS: SMCV deep veins MRV MRV: branches basal vein imaging CUS: BVR parts CUS: BVR and PCA MRV: MCVs CUS: large lat. mes. v Mechanisms of temporal lobe haemorrhage related to venous developmental anatomy IntroductionVenous congestion during vaginal delivery can be pronounced, leading to striking dilatation of the great cerebral vein and its tributaries (Komiyama et al. 2001, Hunt et al. 2002). This may be so pronounced as to mimick a vein of Galen malformation. Congestion may lead to rupture of fragile proximal veins and may also encourage upstream thrombosis. In both instances haemorrhage surrounds ruptured veins, so that some vascular template should be recognized. This is relevant, since demonstration with ultrasound or MRI of an intravenous thrombus is often but not always possible in the acute stage, unless thrombosis is not complicated by haemorrhage. A particular and not uncommon presentation is that of a term infant with lobar temporal haematoma presenting within hours of birth with apnoea (cyanotic spells) without bradycardia. Although this clinical phenotype is rather uniform, the imaging aspects of the causative lesions are not. Because the haemostatic screen is normal in most and because the lesions do not fit arterial stroke templates and a vascular anomaly is not withheld, the logical step to understand this entity is by the study of the developmental anatomy of veins around the temporal lobe. This report is based on a retrospective illustrative cohort collected in centres organised in a cranial ultrasound network (eurUS.brain). The clinical presentation with apnoea is first explained, then development of the basal vein of Rosenthal and related venous changes in the third trimester of pregnancy are discussed. The lesions in this cohort are defined in relation to temporal substructures before an attempt at classification is produced. Prospective work (with doppler ultrasound and SWI MR imaging) will be needed to clarify the pathogenesis of temporal lobe haematoma around term birth. Hunt RW, Loughnan P, Fink AM, Volpe JJ, Inder TE (2002) Magnetic resonance demonstration in the newborn of generalized cerebral venous dilation with spontaneous resolution. Eur J Paediatr Neurol 6(5):289-92.  Komiyama M, Kitano S, Sakamoto H, Ehara E, Miyagi N, Kusuda S. Rapid normalization of marked dilatation of the cerebral duro-venous system in a newborn infant mimicking a great vein of Galen varix. Pediatr Neurosurg 2001; 35: 149-52. Apnoea in relation to neonatal temporal lobe haemorrhageNeonatal apnoea is common and caused by a myriad of events and diseases. One of the uncommon causes is seizure activity. Although haemorrhagic injury to the temporal lobe in term newborn infants is of different types, they have in common the association of a unilateral temporal lobe lesion with apnoeic seizures (Tramonte and Goodkin 2004, Huang and Robertson 2004, Hoogstraate et al. 2009). In some infants hippocampus and mesial temporal cortex were affected and in others basal temporal cortex alone (Hoogstraate et al. 2009). This suggests that apnoeic seizures might be caused by functional disruption of the hippocampus and the mesial or basal temporal cortex. Clinical reports have indicated the occurrence of neonatal apnoea in relation to other temporal lobe disorders, suggesting respiratory arrest can be caused by seizure discharges from the limbic system (Miyagawa et al. 2007). Respiration is coordinated in centres from mesencephalon to medulla oblongata (Corne et al. 2005, Moss et al. 2005). A dorsal respiratory group of neurons (DRG) lies within the dorsal vagal complex, consisting of dorsal motor and of solitary tract nuclei of the vagal nerve at medullary level. These centres, influenced by visceral afferent information from arteries, larynx and respiratory tract, organize efferent effects needed for breathing (movement of the diaphragm, coordination of pahrynx and larynx muscles). The breathing cycle itself is driven from within the ventral respiratory group (VRG) nested around the ambiguus nucleus in the ventrolateral medullary tegmentum: the ‘noeud vital’ is in the pre-Bötzinger complex of this VRG in its rostral part in pons. Parabrachial and Kolliker-Fuse nuclei in pons bring these respiratory centres in relation to the reticular formation (to sleep/wake states) and in relation to higher influences descending from hippocampus, amygdala and cerebral cortex (orbitofrontal, insular, cingular). At the risk of simplification disorders of breathing control can be subdivided into: (i) anomalies decreasing chemical sensor functions; (ii) anomalies in DRG and/or VRG, the respiratory centre itself; (iii) anomalies interfering with higher descending influences, at mesencephalic level within the temporal lobe or even higher cortical areas.  A prominent role for limbic structures in mediating breathing is suggested (Harper et al. 1998). An important influence on respiration comes from amygdalar fibers descending via the lateral amygdalo-hypothalamic projection system to pons (Fedorchenko et al. 2002). Components of the ascending reticular activating system appear to act as a distributed system to contrive the emotion of ‘‘hunger for air’’; they involve mesencephalic and posterior hypothalamic neuronal groups and elements of phylogenetically ancient areas, allocortex and transitional cortex (including cingulum and insula), together with thalamus, claustrum, and amygdala (Liotti et al. 2001). Structural changes in the insula, temporal lobe or cingulum can therefore induce apnoea through these descending connections. Apnoea as a manifestation of seizure activity is not uncommon in children (Fogarasi et al. 2006). Temporal lobe seizure activity more commonly leads to apnoea than extra-temporal seizures, and seizure apnoea has a predilection for young children. Pure apnoeic seizures have been well documented in infants, commonly without bradycardia and with focal rhytmic discharges preferentially (not exclusively) of temporal location (Ramelli et al. 1998, Hosain et al. 2003).  References in alphabetical order Corne S, Bshouty Z. Basic principles of control of breathing. Respir Care Clin N Am 2005;11:147-72. Fedorchenko ID, Merkulova NA, Inyushkin AN. Amygdalofugal modulation of Hering-Breuer inspiration-inhibiting reflex. Bull Exp Biol Med 2002;133:318-20.  Fogarasi A, Janszky J, Tuxhorn I. Autonomic symptoms during childhood partial epileptic seizures. Epilepsia 2006;47:584-8.  Harper RM, Gozal D, Bandler R, et al. Regional brain activation in humans during respiratory and blood pressure challenges. Clin Exp Pharmacol Physiol 1998;25:483-6. Hoogstraate SR, Lequin MH, Huysman MA, Ahmed S, Govaert PP. Apnoea in relation to neonatal temporal lobe haemorrhage. Eur J Paediatr Neurol. 2009 Jul;13(4):356-61.  Hosain S, La Vega-Talbott M, Solomon G, et al. Apneic seizures in infants: role of continuous EEG monitoring. Clin Electroencephalogr 2003;34:197-200.  Huang AH, Robertson RL. Spontaneous superficial parenchymal and leptomeningeal haemorrhage in term neonates. AJNR Am J Neuroradiol 2004;25:469-75. Liotti M, Brannan S, Egan G, et al. Brain responses associated with consciousness of breathlessness (air hunger). Proc Natl Acad Sci U S A 2001;98:2035-40.  Miyagawa T, Sotero M, Avellino AM, et al. Apnea caused by mesial temporal lobe mass lesions in infants: report of 3 cases. J Child Neurol 2007;22:1079-83. Moss IR. Canadian Association of Neuroscience Review: Respiratory control and behavior in humans: lessons from imaging and experiments of nature. Can J Neurol Sci 2005;32:287-97. Ramelli GP, Donati F, Bianchetti M, et al. Apnoeic attacks as an isolated manifestation of epileptic seizures in infants. Eur J Paediatr Neurol 1998;2:187-91. Tramonte JJ, Goodkin HP. Temporal lobe haemorrhage in the full-term neonate presenting as apneic seizures. J Perinatol 2004;24:726-9. Developmental anatomy of the basal veinThe great cerebral vein of Galen (GCV), bilaterally formed from the internal cerebral and basal veins is a collection of pial veins in contrast to most superficial cerebral veins of comparable size, which are dural in origin. The internal cerebral vein (ICV) is a primary (choroidal) vein, but is late to mature because its definitive tributaries follow predominant expansion of the neopallium. The separate components of the basal vein (vena basalis named after Rosenthal, BVR) appear earlier, but are also not connected by definitive anastomoses until around 14 weeks GA. The BVR is a secondary vessel formed by anastomoses between several primitive veins. These include telencephalic cortical, striatal, diencephalic, mesencephalic, metencephalic and myelencephalic veins. As described by Padget (1956) the primitive telencephalic and diencephalic veins initially drain into the stem of the anterior dural plexus. They later join the newly formed primitive transverse sinus (TS) via a tentorial sinus (TeS). As the stem of the anterior dural plexus withers, the TeS becomes more prominent. When the hemispheres expand posterolaterally and the tentorium moves caudally, this primitive TeS (draining telencephalic, ventral diencephalic and the future ophthalmic veins) is displaced laterally, elongated and circuitous, plexiform near its distal end at the TS. Similarly the primitive mesencephalic vein (MV) is stretched as it passes under the temporal and occipital lobes to enter the emerging TS. The BVR thus develops as a shorter connection from the anterior cerebrum to the TS. This posteromedial and superior drainage of the BVR into the galenic venous system is predominant in primates, especially man. Posterolateral and inferior drainage via the TeS is the primitive variant, persisting in some form in about 1/10 adult brains. Drainage by both may be present on one side, or one type may exist on one side and the other on the opposite side, in any case it is clear that this venous development takes places during fetal life and even after term. The uncal vein (initially connecting the primitive DMCV to TeS, remains as a connection from the first segment of the BVR (BVR I). The uncal vein often ends on the mesial end of the SMCV, near or in the sinus cavernosus. Often a branch develops between the diencephalic segment of the BVR (BVR II) and the primitive ventral metencephalic vein (future petrosal vein), which becomes the anastomotic lateral mesencephalic vein (LMV). Venous drainage may then be directed primarily infratentorial into the superior petrosal sinus via the petrosal vein. A large anterior pontomesencephalic vein can be formed, secondary longitudinal anastomosis between the ventral diencephalic, ventral mesencephalic (peduncular) and ventral metencephalic veins on the anterior aspect of the brainstem. Also late in fetal and early postnatal life secondary anastomoses develop between the TeS, spheno-parietal sinus, ophthalmic vein, cavernous and paracavernous sinuses. Superficial and sometimes deep middle cerebral (Sylvian) veins (SMCVs) drain in the direction of the cavernous sinus. Insular veins (deep middle cerebral veins DMCVs) usually find drainage into the BVR. Later communications develop with the extracranial venous system, through foramina of the middle fossa or through the ophthalmic veins: this is associated with capture of SMCV drainage by the cavernous sinus, in about 1/5 newborns already achieved, in the rest occuring after birth (Tanoue et al. 2006). A facial tributary of the primitive maxillary vein becomes a sphenoidal emissary vein connecting the lateral wing of the cavernous sinus to the extracranial pterygoid plexus; this emissary vein traverses the foramen ovale or occasionally the accessory foramen of Vesalius.  Because of this developmental complexity, numerous variations of the BVR occur (Suzuki et al. 2001). Veins of dural origin, e.g. SMCVs and other major cortical veins, usually do not drain into the BVR. Deep early telencephalic (Sylvian) veins do drain into the BVR. There are often conections between DMCVs and SMCVs, sometimes called uncal veins. There are less than a dozen major stems by which the definitive superior cerebral veins (lateral and medial) of each side enter the superior sagittal sinus (SSS). For some distance before their sinus entrance, these stems veins are either attached to the dura or are in it, or are free in the subdural space as is particularly noticeable in the infant (“bridging veins”). The remainder of the neopallium is drained by the posteroinferior cerebral and SMCVs, emptying primarily into the TS behind the sigmoid sinus. Secondary anastomoses, usually postnatal, transfer some or all of the middle cerebral drainage into the cavernous sinus. The superior and inferior anastomotic veins (of Trolard and Labbé, respectively) appear at earliest in the second trimester of pregnancy. The definitive BVR has several rather constant tributaries (Huang and Wolff 1974, Chung and Weon 2005).  The anterior segment (striatal) stretches from in front of the uncus to the cerebral peduncle, the ambient segment describes a curve around the brainstem to end in the mesencpahlic (posterior or galenic) semgent as the BVR drains into the GCV. The BVR lies between PCA and the brain, but can be crossed above by branches of the anterior choroidal artery. The vein follows the tentorial margin just above it on the mesial side of the gyrus parahippocampalis, in the transverse fissure.  The anterior cerebral (anterior external callosal) vein, is often small. Near their basal junction, the anterior and DMCVs both receive anteroinferior cortical tributaries.  The inferior striate veins of the anterior perforated substance are primary tributaries. A constant inferior ventricular vein, related to the stria terminalis and receiving subependymal vessels from the ventricular walls, results from the constant embryonic ventral diencephalic vein, which corresponds to the anterior choroidal artery.  The uncal vein (UV) is a small vein, known as the anastomotic channel between the cavernous sinus (CS) and the BVR. The UV is located medially to the temporal lobe along the anterior margin of the uncus. The tributaries of the UV communicate with the first segment of the basal vein of Rosenthal, and the UV terminates into the SMCV or CS (Ide et al. 2014). The inferior ventricular vein ends in the BVR at the choroidal point behind the uncus, which tributaries are the inferior choroidal vein, and a hippocampal vein (with rake-like branching on the dentate gyrus and often anastomosing with the proximal end of the basal vein).  An interpeduncular vein emerges from the posterior perforated substance to join the basal vein laterally and form the descending anterior pontomesencephalic vein. Anastomoses across the midline of the interpeduncular and the anterior cerebral veins may form a circle from peduncle to chiasm comparable to the arterial circle.  Often, the largest posterior tributary of the basal vein is the lateral mesencephalic vein.  Other tributaries drain parts of the thalamus (the inferior and posterior thalamic veins) and midbrain, and sometimes a posterior ventricular vein is complementary to the inferior ventricular vein. Anastomoses in thalamus connect the inferior/posterior thalamic veins to the superior thalamic vein which drains into the ICV or GCV (Dorfer et al. 2018).  Any direct anastomoses between the superior striate tributaries of the terminal vein and the inferior striate components of the basal vein are uncommon. In contrast, secondary anastomoses between the superior and inferior choroidal veins are present in the young fetus and the adult. The most constant of the cerebellar venous drainage routes (Galenic, petrosal and tentorial), is the "petrosal vein" (the great anterior cerebellar vein, outlet via the superior petrosal sinus). Developing from the primary metencephalic vein, it drains not only a major part of the cerebellar hemisphere including the dentate nucleus, but often annexes tributaries from pons and medulla. It may thus constitute part (or all) of the caudal outlet of the BVR via the lateral mesencephalic vein in the lateral mesencephalic sulcus. In case of occlusion of the GCV, therefore, deep cerebral drainage can pass into the sigmoid sinus by way of the basal and mesencephalic veins and the superior petrosal sinus. Significant diferences between infant and adult patterns.Apparently seldom at birth do the cavernous and inferior petrosal sinuses drain any veins of the brain. They are a secondary detour through the base of the skull between two extracranial veins, the ophthalmic and the internal jugular. The inferior petrosal sinus enters the internal jugular vein more or less below its bulb. In many, two secondary intradural anastomoses involving the cavernous sinus occur before adult life. One is between the TeS and the anterior end of the cavernous sinus near its junction with the ophthalmic vein. The other anastomosis is between the cavernous sinus and the superior petrosal sinus at the entrance of its primary tributary, the petrosal vein. When well developed in the mature brain, the two distinct anastomoses are remnants of the embryonic TeS.  A persistent tentorial sinus is attached to or lies just within the innermost layer of tentorial dura, after following the edge of the lesser sphenoid wing: it may lie lateral, typically anastomosing  with the middle meningeal sinus (Mizutani et al. 2018). At term birth it typically ends in the transverse sinus just behind its junction with the sigmoid; or sometimes in the superior petrosal sinus. The uncal vein (initially draining the anterior area of the TeS field), remains as a connection of the DMCVs to the sinus cavernosus. A persisting tentorial sinus may drain te SMCVs. The sphenoparietal sinus is partly meningeal and partly diploic,and it is not apparent in the infants. It is derived from the embryonic prootic sinus, specifically from the anteroparietal meningeal sinus. When this meningeal sinus secondarily incorporates a remnant of the embryonic TeS and thus extends to the region of the cavernous sinus, it is properly called the sphenoparietal sinus. The resulting channel that either deeply grooves the bone or partially passes through it (diploic part) constitutes the sinus of Breschet. The emissary veins of the important basal group are all formed as veins that primarily drain extracranial structures medially into the sinuses, and later anastomose with tributaries of the external jugular system. The superior ophthalmic vein and the inferior petrosal vein form a large and relatively constant communication between the external and internal jugular veins by way of the cavernous sinus. The hypoglossal emissary usually comprises several prominent connections with the inferior petrosal sinus just below the skull, the marginal sinus, and the voluminous anterior internal vertebral venous plexus. The equally large sphenoid emissary connects the lateral wing of the cavernous sinus, and also the middle meningeal sinus, with the pterygoid plexus. The sphenoid emissary and the inferior petrosal sinus are not necessarily concerned with drainage of the brain, particularly in the young. References on developmental anatomy of the basal vein in chronological orderPadget DH (1956) The cranial venous system in man in reference to development, adult configuration, and relation to the arteries. Am J Anat 98: 307-55.  Huang YP, Wolff BS (1974). In: Newton TH, Potts DG, eds. Radiology of the Skull and Brain, vol 2, book 3. St Louis: Mosby. Chapter 74: the basal cerebral vein and its tributaries. pp 2111-2154. Matsushima T, Suzuki SO, Fukui M, Rhoton AL Jr, de Oliveira E, Ono M (1989) Microsurgical anatomy of the tentorial sinuses. J Neurosurg 71(6):923-8. Guppy K, Origitano T, Reichman O, Segal S (1997) Venous Drainage of the Inferolateral Temporal Lobe in Relationship to Transtemporal/Transtentorial Approaches to the Cranial Base. Neurosurgery. 41(3):615-620, September 1997.  Suzuki Y, Ikeda H, Shimadu M, Ikeda Y, Matsumoto K (2001) Variations of the basal vein: identification using three-dimensional CT angiography. Am J Neuroradiol 22; 670-676. Chung JI, Weon YC (2005) Anatomic variations of the deep cerebral veins, tributaries of Basal vein of rosenthal: embryologic aspects of the regressed embryonic tentorial sinus. Interv Neuroradiol. 11(2):123-30. Tanoue S, Kiyosue H, Okahara M, Sagara Y, Hori Y, Kashiwagi J, Mori H (2006) Para-cavernous sinus venous structures: anatomic variations and pathologic conditions evaluated on fat-suppressed 3D fast gradient-echo MR images. AJNR Am J Neuroradiol. 27(5):1083-9. Ide S, Kiyosue H, Tanoue S, Okahara M, Sagara Y, Hori Y, Mori H. Anatomical variations in termination of the uncal vein and its clinical implications in cavernous sinus dural arteriovenous fistulas. Neuroradiology. 2014 Aug;56(8):661-8.  Mizutani K, Miwa T, Akiyama T, Sakamoto Y, Fujiwara H, Yoshida K. Fate of the three embryonic dural sinuses in infants: the primitive tentorial sinus, occipital sinus, and falcine sinus. Neuroradiology. 2018 Mar;60(3):325-333. Dorfer C, Khalaveh F, Mallouhi A, Millesi M, Czech T. The Superior Thalamic Vein and its Variations: A Proposed Classification. Oper Neurosurg (Hagerstown). 2018 Jun 1;14(6):675-680. Cerebral sinovenous thrombosis per vesselAlmost all instances of infarction due to sinus thrombosis are of haemorrhagic nature (red infarction)(Govaert et al. 2009, Berfelo et al. 2010). Exceptionally an infarct is purely ischaemic and clearly related to sinus thrombosis, possibly due to reactive arteriospasm. The latter phenomenon could also explain why associated with thrombosis of the SSS, infarction is within the parasagittal cerebral (sub)cortex and not within parenchyma bordering the interhemispheric fissure or deeper down along the convexity. The existence of transmedullary, transnuclear (through basal ganglia) and meningeal collaterals is of importance in avoiding infarction, depending on many factors such as the pace of sinus occlusion, the rheology of the blood, the presence of prothrombotic risk factors. Collateral escape may be prominent on MRI. Tissue damage is often overestimated due to the presence of blood that dissects or displaces tissue. In general red venous infarcts have irregular margins, unlike arterial infarcts. The thrombosed vein can stand out on uncontrasted CT scans (cord sign) or on T2* sequences (as balck cords). Nearby collateral veins may also be changed in intensity on SWI sequences. Knowledge of venous templates is as important in understanding venous infarction as in arterial stroke. Thrombosis can propagate between the superior and transverse sinus and between the superior and straight sinus. In the latter instance further propagation into the internal cerebral vein or basal vein may cause central brain infarction with thalamoventricular haemorrhage, usually on one side in the neonate. In adults on the contrary this sequence leads to bilateral thalamic haemorrhagic infarction in 9/10, only 1/10 is unilateral. Why one side leads to thalamic infarction with thromosis of the GCV or straight sinus probably depends on the patient-specific peculiarities of venous anatomy, e.g. size of the BVR or TS on one or other side.  The visualisation of flow with cranial ultrasound (CUS, either colour or power doppler) can only be done accurately by manipulation of the prf (pulse repetition frequency scale) settings to cover a wide range of velocities and by choice of the appropriate doppler frequency (often the highest possible in the case of sinus thrombosis near the probe). Over a period of a few weeks the clots become less echoic and after a couple of weeks it may be difficult to spot thrombosis, unless absence of flow is confirmed with Doppler. Some weeks later (exact time unclear, but anecdotically experience suggests between 2 to 4 weeks) the vessel may become patent to flow again (recanalized). Insonation with a high frequency probe clearly facilitates recognition of sinus thrombosis. At the moment of diagnosis the affected vein may not be without flow due to recanalisation. Over a period of weeks to months a sinus gradually recanalizes. Straight sinus SS With the convex low frequency probe on the anterior fontanel it is often possible to visualise flow in the sinus rectus. This is imperative to document propagation of thrombosis from the SSS. A better visualisation with the linear high frequency probe is possible from the posterior fontanelle. Oblique mastoid views may also prove useful. More recently, the use of MRI permitted recognition of subtle lesions restricted e.g. to the transverse sinus, in term neonates with a paucity of clinical symptoms and in the absence of obvious precipitating factors (Baram et al. 1988) and with CUS in asymptomatic VLBW preterms (Raets et al. 2013). Basal vein of Rosenthal BVR Basal vein thrombosis can induce haemorrhage with feathered margins in the centre of the temporal lobe and extending upward into infero-lateral hemi-striatum (Govaert et al. 2001). The haematoma does not reach the temporal lobe convexity. The typical endstage BVR runs around the brainstem and drains posteriorly into the Galenic system, in three segments: striate, peduncular and mesencephalic. The BVR is derived around the 11th fetal week from the formation of longitudinal anastomoses between embryonic precursors. Its formation is sensitive to anatomic variation (Chung and Weon 2005). Prospective tributaries may drain almost independently of each other into various sinuses. In about 10 % the BVR does not even connect to the GCV. The sonographic study of the BVR is possible with high-quality Doppler technique, but its horizontal course and variability present sources of difficulty. In many infants the third segment is visualised in coronal sections near the GCV, where the basal veins appear as (upward streaming) short broad vessels meeting the distal ends of the ICVS. In parasagittal sectiosn the striate segment is recognizable between inferior striate veins and the cerebral peduncle, the ambient (peduncular) segment is often seen with its descending lateral mesencephalic vein. Because of limitations of the sensitivity of detecting these veins, to recognize veneous flow with certainty per BVR tributary remains difficult with CUS. Transverse sinus TS and sigmoid sinus SiS In adults cerebellar bleeding has been associated with TS thrombosis (Ushiwata et al. 1989). Temporal lobar haematoma is linked to TS thrombosis (Baram et al. 1988, Huang et al. 2004, Nwosu et al. 2008, Miller et al. 2012), not unexpected given drainage of temporal veins via bridging veins and the vein of Labbé into TS. Peritentorial subdural bleeding has been linked to neonatal transverse sinus thrombosis (Eichler et al. 2007). In adults several patterns of TS bridging veins have been described. Tentorial lakes of type I mainly drain to straight sinus, torcular and mesial/middle TS, of type II to lateral TS and transverse-petrosal junction (Guppy et al. 1997, Muthkumar and Palaniappan 1998). A large draining vein of the cerebral convexity into the TS, the vein of Labbé, is connecting the SMCVs to the vein of Trolard and indirectly to the SSS, but this vein can also be absent, such that its absence alone does not seem robust enough to name its thrombosis as the cause of underlying temporal lobe haematoma.  Young infants are more vulnerable to subdural haematoma because of relatively large venous lakes in the dura around the posterior fossa (Browder et al. 1975). Smooth muscle layers at bridging vein orifices suggest that they are sphincters (Dagain et al. 2009). Variation in end stage anatomy and maturation of these sphincters will codetermine what type of temporal lobe haematoma follows thrombosis of affected veins.  Mastoid high frequency insonation (at various angles from a coronal to an axial plane) permits visualisation of the transverse sinus triangle and - toward the occiput - of the sigmoid sinus along its course. CUS can confirm or refute flow gaps observed with MR venography (Miller et al. 2012). That ultrasound, including color Doppler, can depict sinovenous thrombosis at an early stage, presents therapeutic options prior to parenchymal injury. The transverse to sigmoid transmission may be a developmental, neonatal venous achilles heel because of: (i) relative jugular obstruction in the fetal period; (ii) asymmetrical development of the transverse sinus; (iii) dwindling of the tentorial sinus (summarized in Raets et al. 2015). ECMO is a logical candidate for sinus thrombosis due to jugular vein cannulation (Raets et al. 2013). An infected cephalhaematoma may also lead to TS thrombosis (Chan et al. 2002). Recanalisation of the affected sinus is the rule (Nwosu et al. 2008).  A helpful diagnostic sign may be subarachnoid haemorrhage (SAH) near the thrombosis (Kato et al. 2010). With perfusion CT congestion may present as low perfusion hyperemia, associated with subsequent vessel rupture into the subarachnoid space. This phase, vasogenic edema and SAH, may present with heterogeneously increased ADC values on MRI (contrary to decreased ADC values in arterial stroke). References in alphabetical order Baram TZ, Butler IJ, Nelson MD Jr., McArdle CB (1988) Transverse sinus thrombosis in newborns: clinical and magnetic resonance imaging findings. Ann Neurol 24(6):792-4.  Berfelo FJ, Kersbergen KJ, van Ommen CH, Govaert P, van Straaten HL, Poll-The BT, van Wezel-Meijler G, Vermeulen RJ, Groenendaal F, de Vries LS, de Haan TR. Neonatal cerebral sinovenous thrombosis from symptom to outcome. Stroke. 2010 Jul;41(7):1382-8.  Browder J, Kaplan HA, Krieger AJ. Venous lakes in the suboccipital dura mater and falx cerebelli of infants: surgical significance. Surg Neurol. 1975 Jul;4(1):53-5.  Chan MS, Wong YC, Lau SP, Lau KY, Ou Y (2002) MRI and CT findings of infected cephalhaematoma complicated by skull vault osteomyelitis, transverse venous sinus thrombosis and cerebellar haemorrhage. Pediatr Radiol 32(5): 376-9. Chung JI, Weon YC (2005) Anatomic variations of the deep cerebral veins,tributaries of Basal vein of rosenthal: embryologic aspects of the regressed embryonic tentorial sinus. Interv Neuroradiol 11(2):123-30.  Dagain A, Vignes R, Dulou R, Delmas JM, Riem T, Guerin J, et al. [Study of the junction between the cortical bridging veins and basal cranial venous sinus] Etude anatomique du drainage des veines corticales inferieures dans le sinus transverse. Neurochirurgie. 2009 Feb;55(1):19-24. Eichler F, Krishnamoorthy K, Grant PE (2007) Magnetic resonance imaging evaluation of possible neonatal sinovenous thrombosis. Pediatr Neurol 37: 317-23.  Govaert P, Swarte R, Oostra A, Zecic A, Vanzieleghem B, Van Langenhove P. Neonatal infarction within basal cerebral vein territory. Dev Med Child Neurol. 2001 Aug;43(8):559-62. Govaert P, Ramenghi L, Taal R, Dudink J, Lequin M. Diagnosis of perinatal stroke II: mechanisms and clinical phenotypes. Acta Paediatr. 2009 Nov;98(11):1720-6. Guppy KH, Origitano TC, Reichman OH, Segal S. Venous drainage of the inferolateral temporal lobe in relationship to transtemporal/transtentorial approaches to the cranial base. Neurosurgery. 1997 Sep;41(3):615-9; discussion 9-20. Huang AH, Robertson RL (2004) Spontaneous superficial parenchymal and leptomeningeal haemorrhage in term neonates. AJNR Am J Neuroradiol 25: 469-75.  Hunt RW, Loughnan P, Fink AM, Volpe JJ, Inder TE (2002) Magnetic resonance demonstration in the newborn of generalized cerebral venous dilation with spontaneous resolution. Eur J Paediatr Neurol 6(5):289-92.  Kato Y, Takeda H, Furuya D, Nagoya H, Deguchi I, Fukuoka T, Tanahashi N (2010) Subarachnoid haemorrhage as the initial presentation of cerebral venous thrombosis. Internal Medicine 49:467-470.  Komiyama M, Kitano S, Sakamoto H, Ehara E, Miyagi N, Kusuda S. Rapid normalization of marked dilatation of the cerebral duro-venous system in a newborn infant mimicking a great vein of Galen varix. Pediatr Neurosurg 2001; 35: 149-52. Miller E, Daneman A, Doria AS, Blaser S, Traubici J, Jarrin J, Moineddin R, Moore A, Shroff M (2012) Color doppler US of normal cerebral venous sinuses in neonates: a comparison with MR venography. Pediatr Radiol 42:1070-1079.  Muthukumar N, Palaniappan P. Tentorial venous sinuses: an anatomic study. Neurosurgery. 1998 Feb;42(2):363-71.  Nwosu ME, Williams LS, Edwards-Brown M, Eckert GJ, Golomb MR (2008) Neonatal sinovenous thrombosis: presentation and association with imaging. Pediatr Neurol 39:155-161.  Raets MM, Sol JJ, Govaert P, Lequin MH, Reiss IK, Kroon AA, Appel IM, Dudink J (2013) Serial cranial US for detection of cerebral sinovenous thrombosis in preterm infants. Radiology 269(3):879-86.  Raets MM, Dudink J, Ijsselstijn H, van Heijst AF, Lequin MH, Houmes RJ, Wildschut ED, Reiss IK, Govaert P, Tibboel D (2013) Brain injury associated with neonatal extracorporeal membrane oxygenation in the Netherlands: a nationwide evaluation spanning two decades. Pediatr Crit Care Med 14(9):884-92. Raets M, Dudink J, Raybaud C, Ramenghi L, Lequin M, Govaert P (2015) Brain vein disorders in newborn infants. Dev Med Child Neurol 57:229-40. Ramenghi LA, Govaert P, Fumagalli M, Bassi L, Mosca F. Neonatal cerebral sinovenous thrombosis. Semin Fetal Neonatal Med. 2009 Oct;14(5):278-83.  Ushiwata I, Saiki I, Murakami T, Kanaya H, Konno J, Wada S (1989) Transverse sinus thrombosis accompanied by intracerebellar haemorrhage: a case report. No Shinkei Geka 17:51-55.  Wu YW, Hamrick SE, Miller SP, Haward MF, Lai MC, Callen PW, Barkovich AJ, Ferriero DM (2003) Intraventricular haemorrhage in term neonates caused by sinovenous thrombosis. Ann Neurol 54(1):123-6. temporal lobe venous developmental anatomy the dwindling tentorial sinus and the developing basal vein are major features of third trimester venous development around the temporal lobe frontotemporal haematoma has been reported with rupture of an arterial aneurysm in the perinatal period; for most other haematomas, a venous origin is more likely temporal lobe veins in relation to type of haematoma Mac OS X  2ÖATTRÜ,Ücom.apple.TextEncodingë com.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0081;00000000;;