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cerebellar haemorrhage references to cerebellar haemorrhage r e f e r e n c e s < n a v i g a t o r Achiron R, Pinchas OH, Reichman B, Heyman Z, Schimmel M, Eidelman A, Mashiach S (1993) Fetal intracranial haemorrhage: clinical significance of in utero ultrasonographic diagnosis. Br J Obstet Gynaecol 100(11):995-999. Agyemang AA, Sveinsdóttir K, Vallius S, et al. Cerebellar Exposure to Cell-Free Hemoglobin Following Preterm Intraventricular Hemorrhage: Causal in Cerebellar Damage? Transl Stroke Res 2017;8(5):461–73.  Akar ZC, Dujovny M, Gomez-Tortosa E, Slavin KV, Ausman JI (1995) Microvascular anatomy of the anterior surface of the medulla oblongata and olive. J Neurosurg 82: 97-105. Altman J, Bayer SA (2015) Development of the human neocortex: a review and interpretation of the histological record. A Free eBook from the Laboratory of Developmental Neurobiology, Inc. www.neurondevelopment.org © 2015, The Laboratory of Developmental Neurobiology, Inc. 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Pathophysiology, neuropathology, and clinical features. Clin Perinatol 4(1):77-102. Volpe JJ. Cerebellum of the Premature Infant: Rapidly Developing, Vulnerable, Clinically Important. J Child Neurol [Internet] 2009 [cited 2017 Nov 6];24(9):1085–104. Williams RS. Haemorrhage, ischaemia and the perinatal brain (clinics in developmental medicine, nos. 69/70). By Karen E. Pape and J. S. Wigglesworth, with a preface by Gordon B. Avery Spastics International Medical Publications, 1979. Ann Neurol. 1981;9(5):516.  Williamson WD, Percy AK, Fishman MA, Cheek WR, Desmond MM, LaFevers N, Thurber SD (1985) Cerebellar hemorrhage in the term neonate:developmental and neurologic outcome. Pediatr Neurol 1:356-60. Wingate RJ (2001) The rhombic lip and early cerebellar development. Curr Opin Neurobiol 11(1):82-8.  Yoshida S, Hayakawa K, Yamamoto A, Kanda T, Yamori Y. Pontine Hypoplasia in Children with Periventricular Leukomalacia. Am J Neuroradiol. 2008;29(3):425 LP - 430.  Yousefzadeh DK, Naidich TP (1985) US anatomy of the posterior fossa in children: correlation with brain sections. Radiology 156(2):353-61. Yuksel A, Batukan C. Fetal cerebellar hemorrhage in a severely growth-restricted fetus: natural history and differential diagnosis from Dandy-Walker malformation. Ultrasound Obstet Gynecol. 2003 Aug;22(2):178-81. lesion panorama preterm cerebellar haemorrhage: imaging types > Preterm cerebellar haemorrhage was identified with CUS as early as the beginning of the 1980s. Some degree of CBH (macroscopic or microscopic) is observed in around 20 % of neonatal autopsies. It must be admitted that the distance to the fontanel and the normal heterogeneous hyperechogenicity of the cerebellar vermis and foliation make routine detection with CUS difficult.  Different CBH patterns have been described in preterm infants by neuropathology and neuroimaging studies. Hemispheric punctate haemorrhages are usually undetectable by CUS (even when scans are performed through the mastoid fontanel) but they are detected by MRI especially when the Susceptibility Weighted Imaging (SWI) sequence is used. The prognosis of these punctate lesions is debated, but low impact on development is expected (Tam et al. 2011, Steggerda et al. 2012, Steggerda thesis 2014).  Large CBHs are primarily unilateral and located in the hemispheres; the vermis is involved in less than one/third of cases mainly when bleeding occurs within the germinal matrix of the fourth ventricle. Large CBHs may be of limited size (> 4 mm but involving less than 1/3 of the cerebellar hemsiphere). They can be detected with mastoid CUS. Often they are located at the lateral convexity of the hemisphere and on follow up there may be atrophy or irregularity of the affected hemisphere. Extensive haemorrhages involve more than 1/3 of the hemisphere and/or vermis and often lead to clear atrophy. They are already visible in coronal views from the anterior fontanelle. Large CBH are more likely to occur in the youngest and sickest infants and are associated with the worst prognosis.  Massive intracerebellar haemorrhage (destruction of at least one-third of cerebellar tissue) presents in the acute stage with progressive apnoea associated with a falling haematocrit, and motor unrest.   Different ultrasound features of large focal CBHs  accord with timing: - acute phase: globular or less circumscript area of increased echogenicity within the parenchyma; concurrent GMH-IVH and ventricular dilatation might be present - subacute phase: less echoic and even echolucent - chronic phase: focal or extensive atrophy of the cerebellum.  Haemorrhage around the tentorial groove or along a tentorial leaflet is echographically difficult to distinguish from haemorrhage in the superior vermis; a rounded superior delineation in sagittal view suggests the haematoma rests within cerebellar tissue.  Hemispheric haemorrhage may be seen in parasagittal sections adjacent to the midline, having first noticed asymmetry in cerebellar echo­reflections in the coronal plane: only major lesions are US-detectable from the anterior fontanelle (Foy et al 1982, Reeder et al. 1982, Mc Leary et al. 1984, Yousefzadeh and Naidich 1985, Helmke et al. 1987, Ichyama and Hayashi 1991).  The views that provide clear description of the cerebellum are either via the posterior and certainly via the posterolateral fontanelle (at the asterion, mastoid). Only following routine mastoid insonation can the clinically silent or unrecognized lesion be ascertained in cohorts of VLBW infants (Merrill et al. 1998: 3 % below 1500 g birthweight, Limperopoulos et al. 2005: 9 % below 750 g, Muller et al. 2007: 2.9 % below 32 w GA, Steggerda et al. 2009 and 2013). Even here, small intrafolial bleeding can only be detected with flair and susceptibility weighted MR sequences, permitting long recognition. Transnuchal CUS in preterms can provide excellent detail of cerebellar lesions (Muehlbacher et al.2021 and 2025). Larger clinically relevant bleeding can be followed with mastoid insonation. It regresses in a few weeks with cyst formation and focally disturbs the orientation of folia, which is exceptional following peritentorial subdural haematoma..  ELBW infants with IVH who subsequently caused pericerebellar haemorrhage may later develop bilateral hemispheric cerebellar bleeding: subarachnoid haemorrhage may have induced arterial spasm and cerebellar haemorrhagic stroke. Similar effects of posterior fossa subdural haematoma can be expected in neonates irrespective of GA, but this secondary effect is best described in preterms. progression (intra- and extra) examples of cerebellar haemorrhage pericerebellar hygroma limited SAHoma nuchal view ——> dilated v4 lobar sinus thrombosis ++ diaschizis occipital osteodiastasis bilateral DIC: cerebral & cerebellar subarachnoid haematoma in utero diagnosis upward herniation different sizes total destruction Preterm birth is associated with subnormal cerebellar growth even in the absence of obvious cerebellar lesions (Volpe et al. 2009. The disturbance in development is inversely related to gestational age at birth (Limperopoulos et al. 2005). Different mechanisms are involved: hypoxia-ischaemia, inflammation, undernutrition, glucocorticoid exposure, remote effects related to haemosiderin originating from a supratentorial bleeding (Jeong et al. 2016, Agyemang et al. 2017, Sancak et al. 2017).  Development of the cerebellum may also be affected by remote supratentorial parenchymal lesions (e.g. infarction) resulting in trophic (transsynaptic) disturbance of the contralateral cerebellar hemisphere (cerebro-cerebellar diaschizis).  During mastoid CUS the transcerebellar diameter can be measured in the axial and coronal plane to be plotted on maturational nomograms (Swaminatham et al. 1999, Davies et al. 2001, Imamoglu et al. 2013) for detection of hypoplasia or atrophy. This specific cerebellar vulnerability is related to its very prolonged development, from the embryonic period to the end of the first year of life. Some insight in cerebellar development is essential to grasp the importance of perinatal cerebellar destruction by haemorrhage. typical imaging examples lobulation, foliation In preterm infants cerebellar haemorrhage (CBH) occurs under similar circumstances as with cerebral GMH, the latter dominating the clinical picture if associated (Pape and Wigglesworth 1979, Volpe 1987,  Johnsen et al. 2002, Limperopoulos et al. 2005, Muller et al. 2007). Although the precise timing and mode of onset of these lesions is often elusive and because they are pauci-symptomatic, acute and targeted imaging is needed for further study. CBH is not exceptional, especially in very preterm infants: between 1 and 10 %. It originates in the external granular layer or in the germinal matrix in the roof of the fourth ventricle (Biran et al. 2012). Sevral studies point to the densely vascularized region of the emerging internal granule cell layer and adjacent white matter (Haines et al. 20132, Pierson and Sufiani 2016). The pathogenesis of CBH is known to be multifactorial (Limperopoulos et al. 2005). Most preterm CBHs are unilateral. Sometimes preceding cerebellar injury in VLBWs is suspected only later in life, upon recognition of focal cerebellar atrophy on MRI (Mercuri et al. 1997, Johnsen et al. 2002). Such late detected cases of cerebellar “infarction” cannot be classified as arterial stroke because they more likely result from haemorrhage in or on the cerebellum.  A relatively strong association between supratentorial GMH-IVH and CBH has been reported. Parodi et al. in 2013 found that 67.8% of all CBHs were associated with GMH-IVH; similar results were reported by Steggerda et al. in 2009. Dark structures on the cerebellar surface of SWI-MR may represent haemosiderin depositions originating from a supratentorial bleeding and not from primary CBH.  hygroma preterm cerebellar haemorrhage fetal cerebellar haemorrhage imaging description: preterm external granular layer Sequelae related to perinatal cerebellar injury are fine motor incoordination, ataxia, and impaired motor sequencing (Limperopoulos et al. 2005 a,b), although unilateral hemispheric destruction may not be followed by motor disability but by cognitive dysfunction (Merrill et al. 1998, Johnsen et al. 2002) and pervasive disorders (Limperopoulos et al. 2007). In the differential diagnosis are: focal injury with bacterial meningitis, embolic arterial infarction, bleeding associated with transverse sinus or sigmoid sinus thrombosis. postmortem types term cerebellar haemorrhage mechanisms preterm perfusion embryonic cerebellum pericerebellar haemorhage cerebellar expansion cerebellar neurogenesis Cerebellar injury in term infants is associated with a broad spectrum of “typical” neurodevelopmental disabilities, including gross motor delay and hypotonia with truncal taxia, intention treomor and nystagmus, language deficits and behavioural problems.  Independent walking may be delayed beyond 2 years of age. Intellectual performance is moderately or mildly delayed. Some have markedly disordered expressive language. The size of the lesion(s), presence of cerebellar hemispheric atrophy and vermis involvement are associated with the degree of neurodevelopmental impairment.  Cerebellar haemorrhage (CBH) also occurs in (near) term infants, including both small or punctate hemorrhages deep within the cerebellum and large hemispheric or vermian hemorrhages (Limperopoulos et al. 2009). Prenatal and intrapartum risk factors observed in term infants with cerebellar injury include primiparity, advanced maternal age, group B streptococcus-positive mothers, abnormal fetal heart rate, instrumental delivery and urgent caesarean section.  cerebellar haemorrhage in the term newborn Term CBH may be caused by occipital osteodiastasis related to traumatic delivery and/or breech presentation (Hemsath 1934, Ecury-Goossen et al. 2010): in this case the haemorrhages mainly involve the inferior cerebellar areas and have been described as contusions.  Haemorrhagic lesions also occur as a consequence of underlying systemic haemostasis disorders, due to heparinization required for invasive procedures (like ECMO) and/or due to increases in cerebral venous pressure.  Large cerebellar haemorrhages can cause hypertension and mass shift in the posterior fossa, similar to uncal herniation. Indicators of severity are intracranial hypertension with apnoea and/or abnormal breathing patterns such as sighing and gasping. The cushing triad exists in term neonates (hypertension, bradycardia, apnoea). Cranial nerve palsies, of facial and eye musculature, seem to be more common in acutely presenting tentorial damage. Not all symptomatic haemorrhages present with a tense fontanelle.  Drainage of dilated lateral ventricles should not be undertaken when there is ongoing hypertension in the posterior fossa, due to the risk of upward tentorial herniation. By the isthmic organizer, the rhombic lip is induced and produces a number of cerebellar neurons, in addition to the ventricular neuroepithelium. The rhombic lip becomes a defined structure as the roofplate of the fourth ventricle expands, bounded by clear boundaries, which align with gene expression boundaries. Rhombic lip is induced specifically around the edge of the roofplate in both r1/cerebellar territory.  From the fifth week of gestation future GABA-ergic cerebellar neurons proliferate in the ventricular zone of the alar plate of rhombomere 1 at the level of the isthmus: from this (sub)ventricular zone Purkinje cells and before them small inhibitory deep cerebellar nucleus cells migrate radially into the primitive cerebellum between 8 and 13 weeks after conception.  Clustered Purkinje cells form an early layer around 10 weeks. Their GABA-ergic nature will serve to inhibit deep cerebellar nuclei and some vestibular nuclei. Other cortical neurons (basket, stellate, deep cerebellar nuclear interneurons and Golgi cells) develop between week 10 and 23. Basket and stellate cells “loiter’ in the molecular layer by forming a complex 4-stage migration sequence before arriving near the Purkinje cells.  All glutamatergic cells, including glutamatergic neurons in deep cerebellar nuclei, like the dentate nucleus, are derived from the rhombic lip. A transient cell mass, the nuclear transitory zone, lies between the rhombic lip and their final position. Dentate nuclei are formed at stage 23, around 8 weeks after conception. By the end of the embryonic period the superior cerebellar peduncles have been formed.  cerebellar development at the end of the embyronic period Major veins in and around the posterior fossa. Three large drainage systems dominate. Congestion, thrombosis or laceration of veins in any of these systems can explain certain types of cerebellar haemorrhage. venous drainage in the posterior fossa Using an antibody against CD31, specifically reacting with endothelium, vessel density was measured in third trimester human fetuses [Miyawaki et al. 1998]. In the cerebral cortex and subcortical white matter, the vessel density was low at 16–28 w GA, and increased after 36 w. In deep white matter, the vessel density was high in the middle fetal period (16–24w), and then transiently decreased at 28–36 w to again increase after 39 w. In putamen, vessel density was high throughout the fetal period. In basis pontis, the number of vessels increased after 28 w, and after 32 w was higher than in the pontine tegmentum. The transient decrease of vessel density in deep white matter may predispose to periventricular leukomalacia by hypoperfusion. There is some clinical evidence for this. Blood flow distribution in the normal human preterm brain, studied with a radioactive tracer in 12 infants of GA 25-32 weeks, demonstrated comparable flow to cerebellum and basal ganglia, both about four times higher than to subcortical white matter [Borch and Greisen 1998, Greisen and Borch 2001, Borch et al. 2010]. Perturbations in local blood flow are necessary, but not sufficient to explain the distribution of WMI. Borch and Greisen (1998) blood flow distribution in the normal human preterm brain by radioactive tracer: GA 25-32 w, N = 12 flow to cerebellum = to basal ganglia, about x 4 compared to subcortical cerebral white matter cerebral and cerebellar perfusion in the preterm infant In 23 postmortem exams at 23 to 41 weeks of GA, using a barium gelatin injection technique of either carotid artery or jugular vein, the presence of an arterial border zone in cerebral white matter was not confirmed [Nakamura at al. 1994]. On the contrary a hypervascular area of arterioles with plenty anastomoses was seen in preterm deep white matter. Frontal periventricular veins were abundant and mature, clearly different than a vessel-poor outer area with cortical draining venules. In occipital and temporal lobes transcerebral vessels were abundant. Venous factors can play a role in PVL, when venous ischaemia leads to oedema, compression or chemical arteriolar constriction and then focal necrosis [Kuban and Gilles 1985, Nakamura et al. 1994, Anström et al. 2002].   In a study of microvascular development from 14 w of gestation to term, based on staining with CD34 [Chang et al. 2013], a larger percent area was observed in the cerebellar nuclei than in other areas. Vascular density was higher during the early than late fetal stage, with some regional exceptions. Microvascular density must be one of the key players in the genesis of haemorrhage during haemodynamic instability. Vascular density is highest in germinal matrix and cortical plate plus subplate at 23-25 weeks.  postmortem descriptions Postmortem descriptions of cerebellar haemorrhage were abundant in experienced hands (Larroche, Pape et al. 1976, Pape and WIgglesworth 1979, Friede 1989). From early on lesions were not only seen in matrix and in the external granular layer, but also in a folial distribution. In the early days of neonatology a cofactor of venous compression was suspected in preterms with tight compression masks. The idea was that tight caps pushed the occipital bone in the cranium and impeded sinus flow. The impact of masks on compression of emissary veins is not studied.  Pape and Wigglesworth 1979 hemispheric veins cerebellar perfusion in the preterm infant arteries mature cerebellar arteries As in cerebrum, intrinsic vessels penetrate into the parenchyma, but in this case there are vessels from pia mater and from the ependyma of the fourth ventricle from early on (Gillilan 1956). Pia mater around the EGL is rich in immature capillaries, similar to cerebral germinal matrix.  microvascular density Different cerebellar neuron types originate in and migrate from different sources: the rhombic lip, the fourth ventricle neuroepithelium and the external granular layer. Much of the differentiation of cerebellar cortex is a third trimester event. Vermis and hemispheres do not fuse, they develop independently. Before developing dendrites, immature Purkinje cells are bordered outside by a cell free zone, the lamina dissecans, between 20 and around 30 w PMA. As the molecular layer grows with Purkinje cell dendrites, the IGL gradually enlarges due to inward migration of granule cells from the EGL. The EGL remains active until about one year of age. developmental histology of cerebellum timeline the external granular layer Murofushi 1974: at 26 w GA, when crown-rump length is aorund 25 cm, the dentate nucleus is still only partially folded.  mature cerebellar cortex Wingate et al. 2001 After hindbrain segmentation cerebellar rhombic lip gives rise to external granule cell layer precursors (EGL) and neurons in the lateral pons. The medial pontine nuclei and reticulotegmental nuclei derive from a ventrorostral migration from the hindbrain rhombic lip designated as the anterior extramural stream. A posterior extramural stream gives rise to the lateral reticular and external cuneate nuclei, while the vestibulo-acoustic nuclei develop dorsally. The inferior olive is derived from caudal rhombic lip. A deep nucleus, like the dentate nucleus, is in full develooment at early viable preterm age.  migration from EGL to IGL; synaptic pruning Sugihara 2005 At birth, in the rat, each Purkinje cell is innervated by several different climbing fibers. The average number of climbing fibers innervating each cerebellar Purkinje cell decreases gradually as the animal matures until most are singly innervated. Neonatal olivocerebellar axons have much more branches than adult axons and presumably innervate many more Purkinje cells than in adult animals. After complete synaptic pruning, each axon gives rise to ∼7 climbing fibers that each singly innervate a different Purkinje cell Glutamatergic neurons of the EGL proliferate for months at the cerebellar surface; the external granular layer is thus a secondary germinal zone, stimulated by sonic hedgehog, a mitogen secreted by developing Purkinje cells. Mossy fiber contact between 20 and 30 weeks after ovulation parallels presence of the lamina dissecans beneath the Purkinje cell line. The glycoprotein reelin, secreted by the EGL, binds to receptors on Purkinje cell processes, to reduce adhesion between Purkinje cells and to enable cell clusters to elongate into long parasagittal stripes. Purkinje cell maturation concurs in time with granule cell migration. Lemire et al. 1975,Hatten et al. 1997, Vincent et al. 2001, Schilling et al. 2008, Nieuwenhuys et al. 2008 Between 20 weeks gestation and term, the salient feature of cerebellar development is expansion of the external granular layer (EGL) and formation of the internal granular layer (IGL): the external layer reaches a peak thickness around 25 weeks. Only after precursors have divided within the EGL, postmitotic granule cells migrate radially through the cerebellum (using Bergman glia as guide), bypassing outwardly migrating Purkinje cells and settling in the IGL.  ten Donkelaar et al. 2003: Development of the main fissures of occurs the cerebellum in the second trimester of pregnancy. The cerebellar surface increases mainly at the anterior lobe (before the primary fissure) between 15 and 28 weeks of gestation, at the same time the surface of the flocculonocular lobe is relatively reduced (Nowakowska-Kotas et al. 2014).  At later stages the posterior lobe grows relatively stronger (typical of primates with a large neocerebellum due to corticao-pontine influence).  Mitosis is mainly very active at the surface, explaining vulnerability to injurious molecules at the cerebellar surface.  Spreading of the EGL becomes very active in third trimester, such that cerebellar surface increases 40-fold between 24 weeks and term (Lemire et al. 1975).  The relative cerebellum to total brain weight % reverts from a decrease to increase around 20 weeks (from around 4 % at 20 weeks to 6 % at term)(Guihard-Costa and Larroche 1990). At the same time, brainstem becomes relatively smaller. Peak cerebellar growth in % is around 6 fetal months, in grams around term. Where cerebellum is around 5-6 % of brain size around term, it reaches 10 % around 18 months. After term Increasing axonal input further drives neuronal differentiation of the cortex.  cerebellar expansion in the second and third trimester GA 28d, CRL 4 mm: end of diffusion stageICA (from cranial dorsal aorta) bifurcates: anterior (olfactory) division, posterior (mesencephalic) division, intercarotid anastomosis paired longitudinal neural arteries form primitive carotido-basilar anastomoses for hindbrain perfusion (trigeminal, otic, hypoglossal and pro-atlantal)(exist for 4-8 days, vanished at 36 days) GA 29-32d, CRL 5-6 mm, Carnegie 13PCoA develops from connection caudal ICA to longitudinal artery paired longitudinal neural arteries coalesce into basilar artery GA 32-37d, CRL 7-12 mmanterior division forms stem for ACA, MCA, ophtalmic and anterior choroidal artery (largest branch, to diencephalon, metencephalon and plexus) caudal ICA: formation of posterior choroidal and mesencephalic arteries; superior cerebellar artery emerges paired vertebral arteries formed from cervical segmental arteries (C1-7) GA 41d, CRL 12-14 mm (choroid stage)formation of ACoA; primitive ACA is choroidal, MCA is parenchymal branch (striatal) GA 44-48d, CRL 16-18 mmP1 segment of PCA forms from the basilar artery; telencephalic PCA territory forms at expense of AChA; prominent perforant ACA branch (Heubner’s) inferior cerebellar arteries emerge (AICA, PICA) GA 51d, CRL 20-24 mmcircle of Willis completed by ACoA, with median artery of corpus callosum (if persistent referrred to as azygous artery) GA 56d, CRL 40 mmPCoA size inversely related to P1 size: embryonic type of PCoA is large (direct origin from ICA) development of brain arteries (Padget 1948) Though the basic scheme of cell and fiber interaction in cerebellar function is well known, several cell types are present in addition to the Purkinje, granule, stellate and basket cells: - inhibitory Golgi (Go), basket (B), stellate (S);  - inhibitory Lugaro cells (L) in light blue (classical Lugaro cells) or dark blue (globular type) - excitatory granule cells in red, and excitatory unipolar brush cells (U) in orange - candelabra cells. mature cerebellar cortex: cells and functional connections Bayer et al. 1993 and 2004, Altman and Bayer 2015 In the developing midbrain, neurons are generated from the ventricular zone and first migrate radially, with those on the dorsal side forming the tectum and those on the ventral side forming the substantia nigra, red nuclei, and cranial motor nerves 3 and 4. Nuclei in pons and medulla (precerebellar nuclei: pontine nucleus, tegmental pontine reticular formation, external cuneate nucleus and lateral reticular nucleus) are the result of migration streams rostrally from the lower rhombic lip, referred to with the term corpus pontobulbare. Proliferation and migration of these nuclei occurs between weeks 5 and 11. By 15 weeks the inferior olive, developing first and perhaps separate from the inferior rhombic lip, is a C-shaped nucleus that becomes convoluted under the influence of fiber connections between 15 and 22 weeks. timeline of cerebellar neurogenesis The cerebellum consists of the lobus anterior, lobus posterior, and lobus flocculonodulus. These lobes can be subdivided into lobules. Lobes and lobules are separated  by fissures. Each lobule is composed of folia. The lobes, lobules and folia can be followed across the midline from one side of the cerebellum to the other. The cerebellum is also divided into the vermis in the midline, on both sides the paravermes, and more lateral the hemispheres. At the 12th week of development, fissures begin to form transversely to the longitudinal axis of the brain, first on the vermis and then spreading laterally into the hemispheres. The fissura posterolateralis is the first fissure to appear around 50 mm CR (12 weeks gestational age)(Loeser et al. 1972). It divides the cerebellum into lobus flocculonodulus and corpus cerebelli. The second fissure to appear is the fissura prima at 75 mm CR (14 weeks gestational age). This fissure subdivides the corpus cerebelli into the lobus anterior and lobus posterior. The fissura prima and the fissura prepyramidalis demarcate the middle lobe, identifiable by 17 weeks. All nine of the vermis lobules can be identified by the development of the major fissures at approximately 15 weeks of gestation. Later secondary folds appear in the vermis and lobus floccunodularis which eventually extend into the hemispheres and give rise to the adult folia. Shallower fissures subdivide lobus anterior and posterior into a series of transverse lobules which are given specific names. The lobus anterior is divided into three lobules: lingula, lobulus centralis, and culmen. The lobus vermis posterior is divided into five lobules: declive, folium, tuber, pyramis, and uvula. The lobus hemispheri is divided into five lobules as well: simplex, semilunaris, gracilis, biventralis, and tonsilla. The lobulus semiluminaris is further subdivided into superior and inferior. The lobules of the vermis are present at 150 mm CRL (20 weeks postmenstrual age). foliation The vermis cerebelli begins to develop folia by 13-14 weeks gestational age. Each of the lobules vermis except the “middle lobe” (declive, folium and tuber vermis) has at least one sulcus by 14 weeks of gestation. The development of folia continues throughout gestation and is not completed numerically until about two months after term. At this time the number of folia in vermis is nearly the same as in the adult. The gestational age at which each of the lobules has attained half of the adult average number of folia varies between 24 and 37 weeks. Even though the largest lobules (culmen, declive and pyramis) are producing more folia per week, it takes somewhat longer for them to reach the half-way point (28-32 weeks). Smaller lobules (lingula, centralis and nodulus) reach their half-way point earlier (18-28 weeks). The folium vermis and tuber vermis, part of the middle lobe, are the last to reach their half-way point (32-36 weeks). The pattern of folding of the cortex cerebelli is related to the development of the cells within the cortex. The nodulus which is embryologically the first to develop has a higher cell concentration of the internal granular layer than any other lobule at birth but its increase in cell concentration is much slower than the other lobules. The declive is embryologically the last to develop and shows an opposite pattern of cellularity than the nodulus, starting later but ending with a higher cell concentration. The other lobules of the lobus centralis develop between the nodulus and the declive and their cellular postnatal growth apparently reflects a mid-way development. The definite number of foliae is reached a few months after term birth.  The location of cerebellar haemorrhage in the preterm is most likely related to different maturation stage of the different lobes. preterm cerebellar haemorrhage: panorama of preterm cerebellar haemorrhage Ecury-Goossen et al. 2010, based on CUS mechanisms of cerebellar haemorrhage As in the ganglionic eminences, there is developmental fragiltiy in the sinusoids of cerebellar pia mater with the EGL embedded in it, and the molecular layer. This explains common petechial haemorrhage in the preterm cerebellum. Congestion (due to trauma or respiratory distress), thrombosis and haemostatic problems all contribute to the risk of haemorrhage and to the possibility of further expansion of petechial bleeding. In addition intraventricular blood may nest itself in the pericerebellar subarachnoid spaces after outflow in the acute stage from the fourth ventricle outlet foramina. Extensive lobar extension argues against primary pial arterial occlusion of one of the cerebellar arteries as a cause, although extensive subarachnoid bleeding may occlude several pial arteries due to spasm and lead to secondary cerebellar infarction.  cerebellar perfusion in the adult The mature vascular pattern of cerebellum is specific. In sulcal depths veins run a horizontal course along the long axes of folia (Duvernoy et al. 1983, Nonaka et al. 2002). Arteries straddle across these pial veins to run parasagittally, thus perpendicular to veins (straddling them). Arteries end in fork-like ramifications in the sulci. Following penetration of the sulcal depth, arteries either end in the molecular layer, in the Purkinje cell layer, in the IGL or in the subcortical or deep white matter.  Veins leave the folium through its crest. Veins have long side branches at right angles to the parent vessels in a cruciform pattern, that run along the cerebellar sulci; short branches go to the bases of the sulci, terminating in T-shaped bifurcations with numerous tiny branches. In rat cerebellum (as in adult humans), stem vessels branch and terminate at three levels: (1) the molecular layer, (2) the Purkinje cell-granular layer, and (3) the cerebellar white matter (Conradi et al. 1980). All stem vessels are interconnected by the capillary network which is most dense in the Purkinje cell—granular layer.  subdural haematoma However, there are clear ultrasound features of major posterior fossa haemorrhage both on anterior fontanel and mastoid views. CUS detection facilitates early diagnosis and timely intervention: unexplained supratentorial ventricular dilatation, asymmetrical echoic change near the tentorial leaflets, difficulty to delineate the midline posterior fossa structures (cerebellar vermis, pons), an area of increased echogenicity above the vermis in midsagittal plane; mass effect on cerebellum with shift of one or both hemispheres; compression of the fourth ventricle. Extra-axial blood may surround the cerebellar hemisphere(s): acute haemorrhage often has an initial echolucent appearance. In a later chronic stage, hygroma can replace the clot. pericerebellar haemorrhage neurosurgery Minor subdural haemorrhages are often detected by MRI in asymptomatic term infants after vaginal delivery, usually undetectable by CUS (Rooks et al. 2008). Major subdural haemorrhage is typically the result of a traumatic delivery or a disturbance in haemostasis. Major infratentorial hemorrhages can occur after tentorial laceration, with rupture of the straight sinus, vein of Galen, transverse sinus or infratentorial veins, and occipital osteodiastasis with rupture of the occipital sinus. Affected infants show progressive neurologic symptoms related to brain stem compression and dysfunction. Early recognition is crucial because deterioration is often rapid and early therapeutic interventions can be lifesaving. In general CTor MRI are considered superior to CUS to demonstrate the extent of the lesions.  Cerebellar haemorrhage (CBH) may occur in utero, either in isolation or in combination with IVH (Hayashi et al. 2015). Prenatal diagnosis  is with ultrasonography, where depending on timing, the lesion is either hyper- and/or hypoechoic (Ranzini et al. 1998). MRI (T1, T2, DWI and SWI sequences) can be used for confirmation, and assessment of size and localisation. Early diagnosis is of relevance because of long-term consequences. With a systematic review Hortensius et al. 2018 concluded that in children born very preterm (< 32 weeks gestation) with isolated CBH, up to a third are severely impaired in cognitive, motor, linguistic and behavioural domains. Involvement of the vermis and very large bleeding increase the incidence of severe impairment. Hayashi et al. 2015 reported similar impairment in children with prenatal diagnosis of CBH.  Based on neuroimaging the majority of prenatal CBH seems to occur between gestational weeks 21-25.  The underlying mechanisms are insufficiently understood. It has been postulated that CBH often follows bleeding from the germinal matrix (both at the subpial external granule cell layer or the subependymal layer at the roof of the fourth ventricle)(Martin et al. 1976, Grunnet and Shields 1976). However, autopsy studies often reveal no evidence of this (Pierson and Sufiani 2016). The external granular layer region is a zone of rapid angiogenesis with immature, poorly formed capillary beds, which are in a process of remodeling. Because supratentorial IVH often co-exists with CBH, they share overlapping mechanisms (i.e. impaired autoregulation)(Haines et al. 2013). This would explain timing, location, coexistence with IVH and multifocal distribution (Fumagalli et al. 2015). Venous obstruction (e.g. trauma/pressure) might cause blood to pool in well-developed capillary beds in the center of the folia, leading to a central haemorrhagic lesion (venous infarction) involving all layers of the cerebellum (Williams 1979).  Fetal MRI studies suggest a prevalent origin from peripheral caudal portions of the hemispheres (Martino et al. 2016). Maternal risk factors include: coagulopathy (e.g.anti-coagulation medication), thrombophilia, (pre-)eclampsia, septic shock (Hayashi et al. 2015), trauma (increased fetal cerebral venous pressure), seizures, cocaine use (Haines et al. 2013, Nomura et al. 2009). Fetal causes of CBH include: vascular malformation (e.g. capillary telangiectasia), haematological disorders causing thrombosis of the placenta and/or fetal arteries (with secondary haemorrhagic infarction), twin to twin transfusion, anaemia with/without intrauterine transfusion (Aziz et al. 2016), congenital infection [Parvovirus (Glenn et al. 2007) or cytomegalovirus (Ortiz et al. 2017)], congenital tumours (Sharony et al. 1999, Johnsen et al. 2002, Malinger et al. 2006, Castillo et al. 2007).   Postmortem cerebellar examination of infants with CBH documented adjacent cortical changes (reduced thickness due to neuronal loss and gliosis) and an neuronal loss and gliosis in the inferior olivary nuclei and dentate nuclei (Haines et al. 2013).   In contrast to cerebellar haemorrhage, in utero cerebellar arterial ischaemic stroke is rarely reported (Govaert et al. 2009, Ansari et al. 2011).  On postnatal CUS fetal CBH may be detected in the chronic stage as hemispheric volume reduction and surface distortion mimicking a malformation. Data on long-term neurodevelopmental prognosis of disruptive fetal cerebellar haemorrhage are scarce due to the high termination rate. Aziz et al. 2017 reported a favorable short-term prognosis in some affected infants but a high incidence of language disorders has been observed by others as well as cognitive and behavioral impairment. cerebellar haemorrhage in the fetus  Disruptions can be defined as morphological defects resulting from an extrinsic interference with normal development. The human cerebellum has a particular susceptibility to prenatal disruption. Disruptors include maternal illness (e.g. imbalances in vitamin, nutrition or hormonal status,prolonged periods of mental stress),teratogen exposure (e.g. alcohol, cocaine, nicotine, opioid exposure), ischaemic stroke and trauma (e.g. amnion rupture). Most frequent reported are haemorrhage (Hayashi et al. 2015) and infectious agents (e.g. cytomegalovirus, toxoplasmosis, rubella, herpes, zika)(Poretti et al. 2009). Two mechanisms, which may occur simultaneously, and seem to explain this disturbance of cerebellar growth: (1) direct effects on the fast growing cerebellum in the late second and third trimester; (2) remote effects via altered transsynaptic trophic interaction (Volpe et al. 2009). Examples of direct effects on cerebellar development (both intra- and extrauterine) are: inflammation/infection, haemosiderin deposition (iron accumulation, free radical attack), poor nutrition, global hypoxia-ischaemia, severe anaemia requiring intrauterine transfusions (RhD alloimmunization) and glucocorticoids (Volpe 2009, Simonazzi et al. 2016). A well known remote transsynaptic effect is a loss of function in a brain area connected to but remote from a connected lesioned brain area (“diaschisis”). Evidence of diaschisis is prvided by the impressive correlation of cerebellar abnormality in infants with periventricular leukomalacia (Argyropoulou et al. 2003, Shah et al. 2006, Yoshida et al. 2008). Although it might be that the white matter of in cerebellum itself is directly affected similar to supratentorial white matter (cerebellar leukomalacia)(Tsuru et al. 1995), transsynaptic effects are better described. The Cushing reflex is manifested clinically in Cushing's triad: (i) when mean arterial pressure is lower than intracranial pressure: hypothalamus increases sympathetic stimulation of the heart, resulting in vasoconstriction, increased contractility, and increased cardiac output; (ii) increase in blood pressure is detected by baroreceptors in the carotid arteries, triggering a parasympathetic response via vagal stimulation inducing bradycardia; (iii) bradycardia may also be stimulated by impinging on the vagal nerve due to increased intracranial pressure causing a stimulate parasympathetic response. uncal herniation Supratentorial lobar, subdural or subarachnoid haematoma may lead to mass effects that compress the uncus of the temporal lobe into the tentorial notch (Govaert et al. 1993) . This compresses the arterial fork of PCA and superior cerebellar artery, that holds the oculomotor nerve, which results in unilateral mydriasis and ptosis together with anaemia and a tense fontanelle. In advanced cases consciousness may be influenced and a Cushing reflex (bradycardia and hypertension) may follow. This situation requires emergency subdural puncture via the superior or lateral fontanelle. The consequence of this lesion is hemianopsia with or without epilepsy of temporal type (Deonna and Prod’hom 1978). mechanisms behind cerebellar haemorrhage To retin the diagnosis of hygroma evidence has to be present that there is old blood (hemosiderin) in the fluid collection. his is easy with T2 MRI and especially with SWI sequences. Arachnoid cysts of the posterior fossa may appear similar in initial sonograms. posterior fossa hygroma neonatal subdural haematoma surgical intervention for neonatal intracranial haemorrhage one of the intentions of neurosurgery is to stop a mass effect that may lead to several types of tissue herniation, best known is uncal herniation variation in cerebellar perfusion The adult vascular pattern of cerebellum is specific. In sulcal depths veins run a horizontal course along the long axes of folia (Duvernoy et al. 1983, Nonaka et al. 2002). Arteries straddle across these pial veins to run parasagittally, thus perpendicular to veins. Arteries end in fork-like ramifications in the sulci. Following penetration of the sulcal depth, arteries either end in the molecular layer, in the Purkinje cell layer, in the IGL or in the subcortical or deep white matter. Veins leave the folium through its crest. Common variations of cerebellar arteries are described by Krayenbuhl and Yasargil 1957 and 1968, Marinkovic et al. 1995, Tatu et al. 1996, Pekcevik and Pekcevik 2014. The possible patterns of the PICA reflect the variable retention of the primitive lateral vertebrobasilar anastomosis in the trunk of the definitive PICA.  Variations also explain the different perfusion areas described for the typical cerebellar artereis. development of the brain arterial system (Gillilan 1975) vertebro-basilar system mature arteries The brain arterial system is built upon flow from two carotid arteries and one basilar artery [Padget 1948, Gillilan 1975, Menshawi et al. 2015]. - The internal carotid artery (ICA) originates from the dorsal aorta and the third aortic arch at the 4- to 5-mm embryonic stage. The ICA receives contributions from the upper intersegmental and presegmental arteries, connecting the longitudinal neural artery (LNA) on the ventral side of the hindbrain and forming carotid–vertebrobasilar (trigeminal, otic, hypoglossal, and proatlantal intersegmental) anastomoses. The proatlantal intersegmental artery (PIA) supplies the caudal part of the LNAs until this embryonic stage, when the developing vertebral arteries (VAs) take over this function.  - The basilar artery (BA) becomes evident in the 7- to 12-mm stage through the union of the LNAs. The caudal end of every LNA reaches the cervical region and anastomoses with the primitive VAs ascending from the longitudinal anastomotic vessels of cervical intersegmental arteries, branches of the dorsal aorta. At the 11.5-mm stage (34 days), the BA and VA are completely formed.  - At approximately 15- to 17-mm crown rump length, the superior (SCA) and anterior inferior cerebellar arteries (AICA) become prominent. - At 4 mm stage (28 days), the ICA branches off into the anterior and the posterior division. The anterior division initially supplies the optic and olfactory regions through primitive arteries. Later the anterior division of the ICA will give rise to the anterior cerebral artery (ACA), the middle cerebral artery (MCA), and the anterior choroidal artery (AChA), while the posterior division will produce the posterior cerebral artery (PCA) and the posterior choroidal artery (PChA). At this stage the superior cerebellar artery, a branch of the future basilar artery (BA), is the only blood source to the primitive cerebellum. At the 4-5-mm embryonic stage, the hindbrain is supplied by two parallel longitudinal neural arteries. These obtain their blood supply from carotid-vertebrobasilar anastomoses: trigeminal artery (TA), otic artery (OA), hypoglossal artery (HA) and proatlantal artery (ProA).  The BA forms during the 5-8 mm stage from the consolidation of the neural arteries. The lifespan of the TA, OA, and the HA is of approximately a week, and when the posterior communicating artery (PCOMM) develops and connects with the distal BA, the three pre-segmental arteries regress. Unlike the TA, OA, and the HA, the ProA persist until the VA are fully developed, and in fact, a segment of the ProA gets incorporated into the V3 segment of the VA and distal portions of the suboccipital artery. At 7 to 12 mm stage, the VA forms from transverse anastomoses between cervical intersegmental arteries, beginning with the ProA and proceeding downward to the 6th intersegmental artery, which eventually becomes the origin of adult VA from the subclavian artery.  - At 35 days, the development of the MCA is first identified as small buds originating proximal to the ACA on the anterior division of the primitive ICA. Although the MCA is still plexiform, it becomes the major blood source for the cerebral hemispheres. At the16-18 mm stage, the MCA becomes prominent as the plexuses fuse into a single artery and branches pierce the cerebral hemisphere. At the 18-mm stage, the stem of the ACA gives rise to the olfactory artery. The ACA then continues growing medially towards the contralateral ACA, eventually leading to the formation of the ACOMM at the 21-24 mm embryological stage.  - The posterior aspect of the circle of Willis is formed at earlier stages, when the fetal PCA turns into PCoA, the adult PCA connects with the BA as branches from the fetal PCA fuse medially to form the distal end of the BA, and the PChA incorporates into the adult PCA. Consequently, the full development of the ACA and the ACoA mark the shaping of the circle of Willis in the 6-7 weeks embryo. variation Padget 1948 development of the vertebrobasilar system The VA develops as a series of longitudinal anastomoses between the sixth intersegmental artery (ie, the future subclavian artery) and the proatlantal artery of Padget (ProA)(Burger et al. 2007). The VA in its adult form incorporates a portion of the ProA. Initially, the ProA has a typical segmental configuration, with a dorsospinal division that sends a radicular branch along the first cervical nerve root (C1). At the adult stage, this radicular artery of C1 becomes the terminal segment of the VA. It divides into anterior and posterior radicular branches just before entering its intradural course. The anterior radicular branch turns, therefore, into the intradural component of the VA (V4 segment) plus a short extradural segment (distal V3 segment). Distally, it divides into ascending and descending rami that fuse along the midline with their contralateral counterparts to form the BA and the anterior spinal axis, respectively. The descending ramus of the posterior radicular branch of C1 becomes the ipsilateral cranial origin of the posterior spinal artery, whereas its ascending ramus establishes a small connection with the ipsilateral PICA. The first branch of each subclavian artery is the vertebral artery (VA) that courses upward and backward during its first segment (V1) until it enters the transverse foramina of the sixth or fifth cervical vertebra (Caplan 1968, Smith and van der Kooy 1985, Netter 2013). In its second segment (V2) it courses within the intravertebral foramina. The third segment (V3) passes posteriorly behind the articular process of the atlas; it lies in a groove on the upper surface of the posterior arch of the atlas, before piercing the dura mater to enter the foramen magnum. The intracranial portion (V4) ends at or near the medullopontine junction, where the two VAs form the basilar artery. Usually the left vertebral artery is largest and longest (around 6/10), in the remaining the arteries are of equal size or the right is bigger. Absence of one vertebral artery is rare.  The cervical portion of the vertebral arteries gives rise to many muscular and spinal radicular branches. The spinal branches pass through the intervertebral foramina and enter the spinal canal to supply the cervical portion of the spinal cord and the periosteum and bodies of the cervical vertebra. A small anterior and larger posterior meningeal artery originate from the distal extracranial segments (V2, V3). The intracranial vertebral arteries give off posterior and anterior spinal arteries, penetrating arteries to the medulla and the large posterior inferior cerebellar arteries (PICAs) (Mahmood et al. 1991, Akar et al. 1995, Ballesteros et al. 2013). There are two spinal branches forming the anterior spinal artery (ASA) in around 8/10, one from each vertebral artery. In some a double anterior spinal artery exists.   The basilar artery courses rostrally in a groove closely applied to the anterior surface of the pons, in the prepontine cistern behind the clivus. The distal segment enters the interpeduncular cistern, where it is often separated from the basal surface of the brainstem. The distal portion ends at the pontomesencephalic junction, just after passing between the two oculomotor nerves, by dividing into the two posterior cerebral arteries. The basilar artery is often curved and tortuous and may deviate from the midline. The main branches of the artery are the anterior inferior (AICA) and superior (SCA) cerebellar arteries, paramedian arteries that penetrate directly into the pons, and circumferential arteries that course around the pons and give off lateral basal (short) and lateral tegmental (long) penetrating arteries. Between the paramedian branches and the circumferential branches an area of watershed perfusion is present. The PICA is the largest branch of the vertebral artery arising from its intradural portion, just before the vertebral arteries form the basilar artery. The PICA supplies the basal portion of the cerebellar hemispheres, the lower portion of the vermis, part of the cerebellar nuclei, and the choroid plexus of the fourth ventricle, as well as the dorsolateral portion of the medulla. It makes numerous anastomoses with the remaining cerebellar arteries. The size of the PICA territory is inversely related to that of the anterior inferior cerebellar artery (AICA) and the PICA territory may be of different size on the two sides. If one PICA is particularly small, the basal portion of the cerebellum will be supplied by the AICA ipsilaterally and the larger PICA contralaterally (Baehr 2005). A not uncommon congenitally small (“hypoplastic”) vertebral artery may terminate as the PICA and give off no contribution to the basilar artery, which, in such cases, is simply a continuation of the contralateral vertebral artery. The first major branch of the basilar artery is the AICA, which supplies the flocculus and the anterior portion of the cerebellar hemisphere. The AICA also gives off the labyrinthine artery to the inner ear. The superior cerebellar artery SCA arises from the basilar artery below its tip and supplies the rostral portion of the cerebellar hemisphere and the upper portion of the vermis. As it curves around the midbrain, it gives off branches to the tegmentum. cerebellar arteries and branches Mac OS X  2°âATTRâ¼&¼com.apple.TextEncodingËcom.apple.quarantineutf-8;134217984q/0082;6aaea81f;Hype4;