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term IVH references to term IVH  r e f e r e n c e s Afsharkhas L, Khalessi N, Karimi Panah M (2015) Intraventricular Hemorrhage in Term Neonates: Sources, Severity and Outcome. Iran J Child Neurol. 2015 Summer;9(3):34-9. Fenichel GM, Webster DL, Wong WKT (1984) Intracranial hemorrhage in the term newborn. Archives of Neurology, 41, 30-34. Coplerud JM, Wagerle CL, Delivoria M (1989) Regional cerebral blood flow response during and after acute asphyxia in newborn piglets. Journal of Applied Physiology, 66, 2872-2832. Govaert P (1993) Deep haemorrhage in 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. Jocelyn LJ, Casiro OG (1992) Neurodevelopmental outcome of term infants with intraventricular hemorrhage. American Journal of Diseases of Children, 146, 194-197. Nanba E, Eda I, Takashima S, Ohta S, Ohtani K, Takeshita K (1984) Intracranial hemorrhage in the full-term neonate and young infant : correlation of the location and outcome. Brain Development, 6, 435-443. Szymonowicz W, Walker AM, Cussen L, Cannata J, Yu VYH (1988) Developmental changes in regional cerebral blood flow in fetal and newborn lambs. American Journal of Physiology, 254, H52-H58. Szymonowicz W, Walker AM, Yu VY, Stewart ML, Cannata J, Cussen L (1990) Regional cerebral blood flow after hemorrhagic hypotension in the preterm, near-term and newborn lamb. Pediatric Research, 28, 361-366. Wu YW, Hamrick SE, Miller SP, Haward MF, Lai MC, Callen PW, Barkovich AJ, Ferriero DM (2003) Intraventricular hemorrhage in term neonates caused by sinovenous thrombosis. Ann Neurol. 54(1):123-6. n a v i g a t o r < term IVH Types of intraventricular haemorrhage at term ———————————————————————————— 1) pure intraventricular haemorrhage (from matrix or plexus)  2) associated with subdural/subarachnoid haematoma: this may be due to birth trauma, to haemorrhagic diathesis or to rupture of an intraventricular clot through the occipitotemporal cerebral substance (with secondary basal subdural haematoma formation and a residual ventricular coagulum)   3) associated with primary thalamic or thalamo-ventricular haemorrhage, the most likely cause of which is deep venous thrombosis; there can be a dealy between presentation and the delivery 4) primary lobar cerebral with secondary intraventricular haemorrhage 5) ventricle inondation in case of vascular brain malformation (AVM for instance) or tumor 6) following an endoscopic neurosurgical intervention 7) following acute decompression of hydrocephalus fever congestion > Clinical presentation is with a tense fontanelle and pallor, apnoea, seizures (focal or generalized), irritability, lethargy or fever. Grade 3 leads to PHVD more often (about 50 % versus 5 to 10 % for IVH grade 2). examples of IVH For a fraction of instances originating in residual germinal matrix, near the caudo-thalamic groove, one can - in the term infant - imagine similar mechanisms to be operative in the onset of IVH as in the preterm: acute arterial hyperperfusion of a maximally dilated immature germinal matrix vascular rete, primed by preceding hypoxia and supported by scanty stroma with high fibrinolytic capacity. The complete GMH/IVH/venous infarction sequence can be observed in term neonates. Deep cerebral venous thrombosis, blamed for the majority of IVHs in preterm infants by some authors in the past, is a particular cause of IVH that merits separate description because of its specific association with haemorrhage into thalamus or caudate nucleus (see thalamo-ventricular haemorrhage).  IVH at term often originates in choroid plexus. The amount of blood entering the cavity may be abundant or on the contrary very limited. Older studies suggested prolonged difficult labour could lead to venous congestion and ultimate rupture of small vessels in the mature newborn choroid tissue. Some support for this can still be found in the rare occasion of genuine traumatic subdural haematoma associated with IVH. Though losing 50 per cent of its vascularity from preterm fetal to neonatal age, choroid plexus blood flow is still four times superior to the next best perfused area, the caudate nucleus (Szymonowicz et al. 1988, 1990). Reduction of regional blood flow to choroid tissue occurs following haemorrhagic hypotension in neonatal animals, in contrast to an increase in flow to the other regions.  In acutely asphyxiated neonatal piglets, a redistribution of blood flow was demonstrated during the event with relative overperfusion of the brainstem and reduction of flow to cerebral white matter, gray matter and choroid plexus, the latter possibly by some sympathic nervous influence (Coplerud et al. 1989). Upon recovery there was a uniform slight increase of blood flow to most brain parts. The nervous tools for modulation of vascular tone in the choroid vessels have been illustrated both for ortho- and parasympathic nervous elements (Lindvall et al. 1977).  In line with this, arterial hypertension and postnatal fluid overload were thought to be the causal mechanism of plexus haemorrhage in some term newborns with pure IVH. In adults there seems to be a rich arterial anastomotic network between the feeding branches of the anterior and posterior choroidal arteries facing the occipital horn, for neonates this is not documented. Typical for choroid plexus capillaries is the presence of complex glomeruli, so not surprisingly IVH can complicate a haemorrhagic diathesis. historical account acute (unfibrinated) bleeding into the ventricle on day 2 and day 4 MR of a preterm at 28w GA; notice flaring on US and radial venous accentuation on T2 (dark stripes perpendicular to ventricle wall) vaginal failed breech delivery followed by vacuum extraction of second twin at 33w PMA, congested face and painful head without polycythaemia Preceding venous infarction, veins may be distended by a large GMH or IVH, or by preceding head compression during delivery or high intra-thoracic pressures for instance. There is no definite diagnostic method for congestion. Congested medullary veins, descending from subcortex to lateral or medial subependymal collector veins near the terminal vein, fanning out from the ventricle border, contribute to periventricular flaring by the increased amount of cellular scatterers (Takashima and Tanaka 1978). For this reason it is difficult to evaluate white matter changes near GMH/IVH (Ramenghi et al. 2002). Congestion is expected to releave with time. Distended medullary veins should form a hyperechoic fan near the ventricle; heterogeneous echobright focal change within “flaring" may indicate haemorrhagic diapedesis, frank haemorrhage or infarction. There is a spared subcortical rim of tissue drained towards the pial coverings. Ischaemia (restricted diffusion on DW MRI) with a linear pattern perpendicular to the ventricle lumen, can on occasion be seen along these medullary veins. postmortem scans of twin with twin to twin transfusion at PMA 24w; acceptor with polycythaemia and congestion on top preterm, lethal RDS: parietal flaring reflecting periventricular duskiness and venous distension at postmortem venous congestion Intraventricular haemorrhage at term Anatomical description : Bleeding into the supratentorial ventricle is not exceptional in mature neonates. For practical reasons we will subdivide this group of disease entities according to their presentation on brain imaging pictures (Table I). Fourth ventricle bleeding is discussed together with parenchymal cerebellar haemorrhage. Incidence : Isolated subependymal haemorrhage in the caudo-thalamic groove is surprisingly frequent in healthy term infants, as recognized by the use of five MHz ultrasound sector scanning : an incidence of 3.7 per cent (19/505) has been found within the first three days of life, with 14 bilateral ones, four on the left and one on the right (Hayden et al. 1985). At least one of those was prenatal in origin judging by its central cystic regression. In the absence of postmortem confirmation this incidence may be an overestimate because simple congestion or gliosis of the germinal area might look like haemorrhage on US examination. There were no obvious risk factors in obstetric history or immediate neonatal period to account for these lesions. These findings do show the possibility of germinal matrix injury around term. The location infero-lateral to the foramen of Monro would be in accord with the proposed caudo-rostral regression of germinal matrix (Hambleton and Wigglesworth 1976). During the study period 1980-1991 at Gent University Hospital 18 neonates presented with IVH not related to prematurity : Table II attempts to organize this material from both the anatomical and aetiological point of view. This chapter will concentrate on pure intraventricular haemorrhage and its causes. Various sources point to an intraventricular haemorrhage incidence of at least 1/10,000 liveborn infants at or near term, be it studied at post mortem (Butler and Alberman 1969, Wigglesworth et al. 1976) or in a population of living newborns (Sachs et al. 1987). In a recent centre-based study an incidence of 3.6 per 10,000 live term births was recorded (Jocelyn and Casiro 1992). Towards 36 weeks of gestation the incidence may rise to about one per thousand (Wigglesworth et al. 1976). Average neonatal intensive care units ought to diagnose it at least once a year (Nanba et al. 1984). In obductions of term newborn infants the range of incidence is from two to 25 per cent. Larroche reported 15 instances in over 500 autopsies of term perinates : the source was vascular malformation in five, unknown in four, choroid plexus haemorrhage in three, deep venous thrombosis in two and matrix haemorrhage in one (Larroche 1984). Focusing on clinical signs higher incidences have been found : 7.8 per cent in a prospective study of neonates with 'some neurological sign' (Ludwig et al. 1980), 13 per cent following birth asphyxia with hypoxic-ischaemic encephalopathy (Fitzhardinge et al. 1981) and 10 per cent in persistent pulmonary hypertension of the newborn (Oelberg et al. 1988). Ludwig et al. 1980 did not record any ventricle bleed in 33 control CT scans of asymptomatic children. Pathogenesis and aetiology : From 1978 on pure IVH has been diagnosed regularly by the use of US and CT scan. In a population of 53 diagnoses during life (44 form existing reports and 3 personal observations) we  isolated the pattern of causation (Table III) (Chaplin et al. 1979, Cartwright et al. 1979, Palma et al. 1979, Guekos-Thöni et al. 1980, Flodmark et al. 1980, Mitchell and O'Tuama 1980, Blanc et al. 1982, Scher et al. 1982, Fenichel et al. 1984, Nanba et al. 1984, Bergman et al. 1985, Oelberg et al. 1988, Keeney et al. 1991, Jocelyn and Casiro 1992). Two important necropsy studies have focused on this event. Donat et al. 1978 reported nine choroid plexus bleeds with subsequent dissection to the ventricle cavity, all associated with respiratory distress leading to hypoxia and acidosis in two thirds. Lacey and Terplan 1982 reviewed 32 instances (27 originating in the choroid plexus), unfortunately with limited clinical correlation: at least 24 of those had some respiratory disorder or congenital heart malformation; the association with subdural haemorrhage pointed to birth trauma in three.  Within the CT material referred to above, 13 subependymal haemorrhages were recognized along with 37 ventricle bleeds detailed enough as to allow commenting. Available data thus suggest that at or near term about four in five cases of IVH sprout from the choroid plexus. By the use of CT scan alone prediction of the choroid plexus origin, substantiated by necropsy findings in one child, can be done easily in most cases (Nanba et al. 1984). Excellent descriptions of the nature and evolution of this lesion in the preterm infant give an account of the possible immediate and long-term consequences, which are not up for detailed study here (Larroche 1977, Pape and Wigglesworth 1979, Volpe 1987, Goddard-Finegold and Mizrahi 1987). Even in the preterm the incidence of stromal choroid plexus haemorrhage has been reported to vary from seven to 25 per cent of preterm infants with IVH, but without transependymal rupture in the majority.  For the fraction originating in residual germinal matrix, almost invariably near the caudo-thalamic groove, one can - in the term infant - imagine similar mechanisms to be operative in the onset of bleeding as in the premature neonate : acute arterial hyperperfusion of a maximally dilated immature germinal matrix vascular rete, primed by preceding hypoxia and supported by scanty stroma with increased fibrinolytic capacity (Pape and Wigglesworth 1979). Although not completely forgotten and possibly contributory in selected situations 'venous' hypotheses invoking such mechanisms as prolonged congestion (Sänger 1924, Hausbrandt and Meier 1936, De Courten 1981), rupture of the internal cerebral vein and a stasis-promoting acute angle between the internal cerebral and thalamostriate veins (Larroche 1977), have been replaced by this 'arterial concept'. Association with increased use of NaHCO3-boluses, despite similar acid-base status, supports the causal importance of sudden systemic volaemic changes, although osmolarity changes were originally thought to be contributory as well (Simmons et al. 1974, Hambleton and Wigglesworth 1976). Deep cerebral venous thrombosis, blamed for the majority of IVHs in preterm infants by some authors in the past (Towbin 1969), is an exceptional cause of ventricular haemorrhage that merits separate description because of its specific association with haemorrhage into thalamus or caudate nucleus (see chapter on thalamo-ventricular haemorrhage).  The cause of haemorrhage into the choroid plexus stroma is much less documented but probably not dissimilar (Table IV). Older studies suggested prolonged difficult labour could lead to venous congestion and ultimate rupture of small vessels in the mature newborn choroid tissue (Donat et al. 1978, Lacey and Terplan 1982). Some support for this hypothesis can still be found in the rare occasion of genuine traumatic subdural haematoma associated with IVH  (Ponté et al. 1971, Blank et al. 1978, Flodmark et al. 1980, Fishman et al. 1981, Scotti et al. 1981, Koch et al. 1985). Be it limited in number and depth of observation these case histories seem to suggest that venous congestion, more expected than arterial hyperperfusion in the context of birth trauma, can contribute to germinal matrix or choroid plexus bleeding, leading to mild IVH at full term. Meningeal venous congestion was present in 26/32 of the post-mortem cases reviewed by Lacey and Terplan 1982. The suggested causal role played by birth trauma is further supported in a description of pure IVH at full term presenting with seizures, usually on the second day, after mechanically difficult delivery (Fenichel et al. 1984, Nanba et al. 1984). Donat et al. 1978 introduced the concept that postnatal respiratory distress, hypoxia, acidosis and bradycardia can lead to IVH in some mature newborns . This is analogous to the well-known link between IVH and hyaline membrane disease in the preterm infant. There is some experimental evidence to suggest that the choroid plexus, after regression of the vulnerable germinal matrix, may be next in line to suffer from systemic haemodynamic changes. Choroid tissue, as examined by radioactively labeled microsphere perfusion, is by far the best perfused organ in a study of cerebral blood flow to fetal and newborn lamb brainstem, cerebellum, cerebral cortex, cerebral white matter, caudate nucleus and choroid plexus (Szymonowicz et al. 1988). Though losing 50 per cent of its vascularity from preterm fetal to neonatal age, the choroid plexus blood flow is still four times superior to the next best perfused, the caudate nucleus, in neonatal lamb brains. The same researchers showed isolated reduction of regional blood flow to the choroid tissue following haemorrhagic hypotension in the neonatal animals, in contrast to an increase in flow to the other regions (Szymonowicz et al. 1990). This selective vulnerability seemed to decrease from fetal to neonatal period. Another experimental set-up, using the same investigational method in acutely asphyxiated neonatal piglets, demonstrated a redistribution of blood flow during the event with relative overperfusion of the brainstem and reduction of flow to cerebral white matter, gray matter and choroid plexus, the latter possibly by some sympathic nervous influence (Coplerud et al. 1989). Upon recovery there was a uniform slight increase of blood flow to most brain parts. The nervous tools for modulation of vascular tone in the choroid vessels have been illustrated both for ortho- and parasympathic nervous elements (Lindvall et al. 1977).  Further evidence for systemic 'arterial' factors in the generation of choroid plexus haemorrhage can be found in clinical observations. Maki and Shirai 1975, describing angiographic findings in six full-term infants with intraventricular haemorrhage, documented remarkable hypercaptation and retention of contrast in the choroid plexus well into the venous phase. They further demonstrated early filling of the internal cerebral veins. The latter phenomenon, though normal for the neonatal period, does seems to militate against venous congestion as a primary event in these infants, five of whom had birth asphyxia and two were delivered by the breech. Arterial hypertension and postnatal fluid overload were thought to be the causal mechanism in two full-term newborns with pure intraventricular haemorrhage (one personal observation). Arterial hypertension proximal to an interrupted aortic arch has been considered responsable for hyperdensity of the choroid plexus on CT scan in two neonates (Rand et al. 1990). The observation was strengthened by postmortem findings of normal choroid plexus tissue in one of them who died at three months (CT taken at four weeks), thereby differentiating the striking iconographical findings of hyperperfusion from haemorrhage, haemangioma, calcification or tumor.   The fine structure of the choroid plexus vasculature has hardly been studied in the perinatal period. In adults there seems to be a rich arterial anastomotic network between the feeding branches of the anterior and posterior choroidal arteries facing the occipital horn (Fujii et al. 1980). Typical for choroid plexus capillaries is the presence of vascular glomeruli, the importance of which as fragile sites has yet to be determined (Williams et al. 1989). In the same way the presence of gap junctions in choroid plexus capillary endothelium, unlike tight junctions elsewhere in the brain, has been proposed as a vulnerable site (Armstrong et al. 1980). Thus it would not be surprising to find IVH as a complication of haemorrhagic diathesis. Clinical setting : We are quite far from the ancient descriptions of a piercing, shrill and agonal cry in newborns with a facial expression of torture, rigid truncs and clenched hands as referred to by Craig 1938. Somehow description of the fine neurological features of IVH at full term have been hidden by diversion of the bulk of interest to the same condition in preterm infants. Table V summarizes clinical findings of pure IVH as reported in a limited number of previous reports (Chaplin et al. 1979, Cartwright et al. 1979, Palma et al. 1979, Guekos-Thöni et al. 1980, Mitchell and O'Tuama 1980, Blanc et al. 1982, Scher et al. 1982, Fenichel et al. 1984, Nanba et al. 1984, Bergman et al. 1985). Presentation on the first day of life was recorded in half the cases where IVH was associated with trauma and in only a quarter of those with unknown aetiology. Some less common reported presenting signs have been vomiting (2/43), a high and shrill cry (5/43) or opisthotonus (3/43). Fever was a common sign in a recent series (47 per cent), where unfortunately the clinical findings were not matched with the grading of severity (Jocelyn and Casiro 1992). Seizures were reported to be of easy control in some neonates (Chaplin et al. 1979). If associated with birth trauma the ususal onset of clinical convulsions was on the second day of life (Fenichel et al. 1984). In the series by Ludwig et al. 1980 none of the infants with IVH at full term were asymptomatic. Hypotonia and a short popliteal angle are signs observed in addition (Dubowitz et al. 1981). Both thrombocytopaenia during the acute stage (in association with persistent pulmonary hypertension) and thrombocytosis upon recovery have been linked with IVH at term (Palma et al. 1979). Two EEG patterns associated with  term IVH are worth pointing out: focal ipsilateral epileptic activity (Scher et al. 1982) and the burst suppression type with ulterior normal outcome (Fenichel et al. 1984).   Radiological assessment and relation to prognosis : Soon following introduction of CT scanning in management of sick preterm infants, the importance of grading IVH received appropriate attention and so did its link to immediate and long-term outcome (Papile et al. 1978, Krishnamoorthy et al. 1979, Volpe 1981). Though this link may not exist as clearly in the full-term neonate (Table V), we could not find indication of a need for other discriminative subdivisions. As referred to above, uncontrasted CT scans can allow recognition of posterior IVH around the glomus of the choroid plexus (Nanba et al. 1984). Some impairment in astroglial development and myelination is to be expected even following isolated germinal matrix injury (Evrard et al. 1992). In a minority (6/299) of mentally retarded children subependymal germinolysis was the only recognized macroscopic brain finding (Shaw 1987). It is important to realise that subependymal germinal matrix cysts acquired after birth can be due to haemorrhage as well as ischaemia without preceding bleeding (Takashima et al. 1984). Certainly grade IV haemorrhage carries a gloomy prognosis (Jocelyn and Casiro 1992).  Several authors warned against overdiagnosis of choroid plexus haemorrhage by the use of ultrasound (Hope et al. 1988). The irregularity of density and variable bulk of the healthy plexus is defying accurate recognition of haemorrhage; even asymmetrical hyperdensity can be due to dissipation of clot from the ventricle into the choroid crypts. Venous congestion has been recognized as a cause of false-positive diagnosis in preterm infants (Szymonowicz et al. 1984). In children on extracorporeal membrane oxygenation development of massive IVH may be abrupter than usual but despite huge proportions difficult to sort out at first because of the hypodensity due to systemic anticoagulation (Bowerman et al. 1985). Ultrasound does remain important for follow-up of ventricle size after the acute event. Axial images are especially useful for measurement of third ventricle width and to follow the glial reaction at the ependymal lining (Gaissie et al. 1990).  Case history (CM, female, outborn, 37/40, 2650) : This firstborn girl was delivered at 37 weeks of gestation in a spontaneous vaginal manner. Mild ventricular dilatation had been recognized on US scan at 32 weeks. She weighed 2650 g and had Apgar scores of 9 at 1 and 5 minutes. On the second day she was referred with severe respiratory distress and oedema. Our tentative diagnosis was transient tachypnoea exacerbated by fluid overload. Hematocrit upon admission was 25 per cent. She was suffering from left grade III intraventricular haemorrhage and was in addition found to have complete agenesis of the corpus callosum and hypothyroidoism with ectopic sublingual thyroid gland remnant. Left white matter hyperdensities were suggestive of periventricular leukomalacia. Posthaemorrhagic ventricular dilatation, reaching a maximal third ventricle width of 9 mm, resolved spontaneously within the first month. At six months a mild right hemiplegia was  present. Management : Treatment of posthaemorrhagic hydrocephalus is out of scope in this description. There is no sufficient evidence in favor of early surgical clot removal, but this viewpoint may be altered in the near future (Ritschl and Auer 1987). Attempts at prophylaxis of posthaemorhagic hydrocephalus by intraventricular application of thrombolytic drugs deserve our closest attention (Whitelaw et al. 1992). Some prognostic considerations have been discussed above and were reviewed by Jocelyn and Casiro 1992. Table I    Different types of intraventricular haemorrhage at full term 1) pure intraventricular haemorrhage  2) associated with subdural/subarachnoid haematoma : this may be due to birth trauma, to haemorrhagic diathesis or to rupture of an intraventricular clot through the occipitotemporal cerebral substance with secondary basal  subdural haematoma formation and a relatively small residual ventricular coagulum    3) associated with primary thalamic or thalamo-ventricular haemorrhage, the most likely cause of which is deep venous thrombosis 4) primary cerebral with secondary intraventricular bleeding 5) ventricle inondation in case of vascular brain malformation or tumor Table II     Intraventricular haemorrhage complex at term : Gent 1980-1991                                Trauma        Isolated     Haemorrh.    Sepsis-    Other     Total                                 (a)           asphyxia      diathesis   meningitis    Pure IVH                    1                  2               1 (b)            0            5            9 IVH + SDH (c)             3                  0               0                  0           0             3 IVH + thalamic H        1                  0               0                  1           0             2 IVH + cerebral H        1                   1              0                  1           1            4    Total                         6                  3                1                  2           6           18 a : 4 had birth asphyxia as well; 3 instrumental deliveries, 1 breech, 2 spontaneous vaginalb : maternal salicylate ingestion was the likely causeH haemorrhage   IVH intraventricular haemorrhage  SDH subdural haemorrhage Table III          Aetiology of in vivo diagnosed pure intraventricular haemorrhage at term                       (literature review of 44 cases and 9 from Gent University Hospital) Number                                                   53 -------------------------------------------------------------------- Traumatic delivery (with asphyxia)                11(2)  Isolated birth asphyxia                                    4 Severe respiratory distress                              3   (+- pulmonary hypertension) Haemorrhagic diathesis (a)                              2 Other -dehydration (Mitchell and O'Tuama 1980)           1 -toxaemia (Bergman et al. 1985)                         2 -cardiac arrest (Mitchell and O'Tuama 1980)        1 -hypertension (Guekos-Thöni et al. 1980)            1 -fluid overload with hyponatraemia (b)               1  Unknown                                                        27  --------------------------------------------------------------------- Parenchymal extension                           10 Neonatal death                                        4 Posthaemorrhagic hydrocephalus            14 a : 1 due to maternal salicylate ingestion (personal observation), 1 due to disseminated intravascular coagulation associated with congenital CMV infection (Cartwright et al. 1979)b : personal observation (CE) : 36 week gestation outborn girl, 2950 g at birth, secondary caesarean because of fresh meconium staining; Apgar score 1/10; seizures on day 2, serum Na 122 mmol/L, Ca 1.5 mmol/L; left grade III IVH, right grade II; posthaemorrhagic hydrocephalus, treated conservatively with serial lumbar punctures and acetazolamide-furosemide; hemiplegic cerebral palsy Table IV  Patterns of causation of choroid plexus haemorrhage at full term 1. venous congestion (difficult delivery, asphyxia) 2. systemic, arterial factors  3. vulnerable vascular fine structure Table V               Clinical features of pure intraventricular haemorrhage at full term                                          (58 patients reported in life by 10 authors*) Grading (a)                         Grade 2     Grade 3    Grade 4 Symptoms : number                     22          15          6 - intracranial hypertension            3           3           2 - focal seizures (b)                        7           2           0 - generalized seizures                   3           9           4 - irritability/jitteriness                 9           2           2 - lethargy                                     2           3           0 - fever                                         3           0           2 - apnoea                                      1           3           1 Outcome : number                      27          21         10 - neonatal death                           0           2           2 - shunted hydrocephalus (c)          2           8           7 - cerebral palsy                            4           4           5 a : grade 2 = mild IVH, grade 3 = severe IVH with ventricular dilatation, grade 4 = grade 3 with parenchymal 'extension'b : significantly more focal seizures in mild versus severe IVH by chi-square test (p < 0.02)c : significantly more frequent in severe compared with mild IVH (p < 0.05 by chi-square method)   Abrams, R.M., Ito, M., Frisinger, J.E., Patlak, C.S., Pettigrew, K.D., Kennedy, C. 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Temperature regulation by the dorsomedial effector nucleus in hypothalamus is disturbed from there on.  IVH and fever delayed neonatal plexus clot with PRES antenatal with anaemia preterm asphyxia propagated thrombosis unilateral plexus H due to AVM comparable ultrasound finding in second week of life after term birth asphxyia due to hypertension examples of term IVH with arterial spasm term infant with choroid plexus clot Mac OS X  2ÖATTRÜ,Ücom.apple.TextEncodingë com.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0081;00000000;;