**3. Clinical presentation**

Of all types of ICHs, germinal matrix-intraventricular hemorrhage (GM-IVH) by far is the most common and distinctive pathology in premature infants. The pathogenesis of GM-IVH is multifactorial. It involves a combination of vascular-anatomic immaturity and complex hemodynamic factors. The role of inflammatory and genetic factors is currently under investigation. Germinal matrix (GM) is a highly vascular structure and the source of develop‐ ing brain cells (neuronal and glial cells). The tissue surrounds the fetal ventricular system and gradually involutes to reside over the body of the caudate between 24 and 28 weeks of gestation, at the level of head of caudate nucleus in the caudothalamic groove between 28 and 34 weeks of gestation, and finally completely regresses and converts into normal cerebral parenchyma by the 36th week of gestation. The capillary network of germinal matrix is composed of high-caliber, thin-walled (deficient in muscularis layer) and immature fragile vessels predisposed to rupture. Furthermore, GM lies within an arterial end zone, and is directly connected to the deep galenic venous system, thereby exposing it to insults of arterial ischemic-reperfusion and to venous congestion.[1,2,3] The rupture hemorrhage of the vulner‐ able GM requires the coexistence of several intrinsic and extrinsic hemodynamic factors. Premature infants are believed to have impaired cerebral pressure autoregulation (a major intrinsic factor) that renders these infants susceptible to both cerebral hypoperfusion and ischemia at the border zone GM vessels and hence the rupture of fragile germinal matrix vessels. In term infants, a well developed cerebral pressure autoregulation mechanism maintains a relatively constant cerebral blood flow (CBF) across a range of cerebral perfusion pressures.[4] Various extrinsic hemodynamic factors that potentially interfere with the integrity of the vulnerable GM include low CBF (hypotensive events and frank perinatal asphyxia), high CBF (hypertension, bolus fluid infusion, hypercarbia and low hematocrit), fluctuating CBF, and factors causing increased cerebral venous pressure (respiratory distress syndrome, positive pressure ventilation, pneumothorax, or pulmonary hemorrhage).[1,2] Immature deep galenic system, in a preterm infant, which is prone to venous congestion and stasis is another major factor responsible for development of GM-IVH and its complications. Immature cerebral venous system has several vulnerabilities because (i) development of cerebral venous system occurs late in relation to that of the arteries, (ii) there is sequential remodeling and considerable individual variation in the pattern and size of different veins entering the internal cerebral veins, (iii) immature veins have high caliber and thin wall, they branch parallel to the ventricle, hence tend to collapse, (iv) because of relative paucity of superficial cortical veins between 24 and 28 weeks of gestation, most of the cerebral venous drainage is dependent on the deep galenic system that drains GM and most of the white matter, and (v) the periventricular veins, particularly the terminal (thalamostriate) vein, which is the main vein draining the white matter passes directly through the GM and takes a U-turn to join

In term newborns ICH is relatively uncommon and has a different etiology. ICH in term neonates may be subarachnoid, subdural, intraventricular, parenchymal or epidural in location. In clinical practice, hemorrhage involving multiple compartments is not unusual.[5] Both subdural and subarachnoid hemorrhage in a term newborn is associated with birth trauma either from forceps delivery/vacuum extraction or unassisted vaginal delivery. Vertical moulding of skull causes stretching and tearing of blood vessels of tentorium, falx and dura

the internal cerebral vein.[1,2]

2 Intracerebral Hemorrhage

GM-IVH in premature infant is typically diagnosed during the first week of life, 50% on the first day and 90% within the first 4 days. GM-IVH is usually subependymal and asymptomatic, diagnosed by routine screening cranial ultrasound (CUS) in 25-50% of premature infants less than 1,500 gm birth weight and less than 32 weeks' gestation. Clinically symptomatic cases with large hemorrhage and its complication may present with various degree of altered consciousness, cardiorespiratory deterioration, unexplained drop in hematocrit, acidosis, blood glucose alteration, inappropriate antidiuretic hormone secretion, severe apnea or neonatal seizure, bulging fontanelles, abnormal eye movement or alignment, abnormal pupillary response, and abnormal neuromotor examination (hypotonia, decresased motility, tight popliteal angle). [1,3]

The pattern of hemorrhage also differs from GM hemorrhage common in preterm newborns in having a later onset between the 4th and 10th days after birth. Neurologic manifestations like neonatal seizure, decreased level of consciousness, increased intracranial pressure are the most common presentations of ICH in term newborns. The newborn's history, maternal and family history and perinatal risk factors may suggest the diagnosis of ICH.[5]
