Chapter 3



Germinal matrix hemorrhage (GMH) is a frequent lesion in premature babies who also have hyaline membrane disease and the respiratory distress syndrome.

Bilateral small germinal matrix hemorrhages

Bilateral small germinal matrix hemorrhages.

Grade II germinal matrix

Bilateral germinal matrix hemorrrhage with intraventricular rupture (grade II).

Grade IV IVH.

Grade IV IVH. Bilateral germinal matrix hemorrhage with intraventricular rupture and extension into the periventricular white matter, more prominent on the left side. The infant weighed 1500 gm. Hemoglobin dropped from 15 gm to 9.2 gm.

In the 1970s, the frequency of GMH in premature neonates was 50%. By the 1980s, its incidence in newborns weighing less than 1500 gm dropped to 20% and has not changed. It is much more frequent in babies weighing 500-750 gm. It is a major cause of morbidity and mortality in the newborn period and of cerebral palsy and mental retardation later on.

Germinal matrix

Germinal matrix.Fragile congested vessels in a cellular bed of immature cells.

Prenatal GMH

Bilateral germinal matrix hemorrhage in an 18 week fetus.

GMH usually develops a few hours after birth, but it can occur at any time, including prenatally. The germinal matrix is a thick cellular layer of immature cells (neuronal and glial precursors) under the ependymal lining of the ventricles. The hemorrhage starts usually between the thalamus and the caudate nucleus, adjacent to the foramina of Monro, and is frequently bilateral. If it is large, it ruptures into the ventricles, flooding the lateral, third, and fourth ventricles (intraventricular hemorrhage - IVH). Blood then exits through the foramina of Luschka, causing subarachnoid hemorrhage. Thick clots along the ventral aspect of the brain stem may block the foramina of Luschka. Four grades of GMH are distinguished by imaging: grade I (confined to the germinal matrix), grade II (intraventricular hemorrhage without ventricular dilatatation, grade III (intraventricular hemorrhage with ventricular dilatation), and gade IV (GMH with intraventricular rupture and hemorrhage into the surrounding white matter).

IVH with subarachnoid hemorrhage

Germinal matrix and intraventricular hemorrhage. Blood flowing through the ventricles formed a clot around the foramina of Lushka.

IVH. Intraventricular clots

Clots removed at autopsy from the ventricles of a premature infant. The amount of blood contained in these clots (taking into account the hematocrit) is probably about 30% of the infant's blood volume.


Grade III germinal matrix hemorrhage of several days\' duration. The lateral ventricles are dilated.

Large, bilateral IVH causes fatal acute distention of the ventricles or exsanguination into the ventricles and subarachnoid space. Patients surviving large IVH often develop hydrocephalus due to clots or gliosis of the aqueduct and from obliteration of the foramina of Luschka and subarachnoid space by clots and the fibrous tissue that develops from their organization.

Post-hemorrhagic hydrocephalus

Hydrocephalus following bilateral IVH. The lining of the ventricles has a golden brown color from blood pigment deposition.

Post-hemorrhagic hydrocephalus

Post-hemorrhagic hydrocephalus following bilateral IVH. The cerebral hemispheres are ballooned. The patient was born at 25 weeks and died 10 weeks later.

Periventricular white matter infarction, old

Periventricular white matter infarction, old lesion. Bilateral subependymal porencephalic cysts. The corpus callosum is thin. The lateral ventricles are dilated and their lining is brown.

Another complication is periventricular white matter infarction, which is thought to be a venous infarct of the white matter adjacent to the GMH. This may cavitate, causing porencephaly, and correlates with the spastic hemiparesis that is seen following some cases of GMH. Neurogenesis and neuronal migration are completed by midgestation. Therefore, GMH has little effect on brain development, unless it occurs early in the second trimester, in which case it may potentially deplete the pool of neuronal and glial precursors.

The causes of GMH are multiple. Local anatomical factors include the high vascularity of the germinal matrix, its immature fragile capillary bed with poor stromal support, and the sharp U-turn the thalamostriate veins take at that point, which makes the germinal matrix prone to congestion. Systemic factors include capillary damage from hypoxia, loss of vascular autoregulation, fluctuations in blood flow velocity, and venous congestion. The pathogenesis of GMH probably involves an interaction between the environmental factors listed above and genetic variations affecting inflammatory pathways, coagulation, and vacular structure. Muscle paralysis eliminates fluctuations of cerebral blood flow velocity and reduces the incidence of IVH.

Cerebellar hemorrhage

Diffuse cerebellar hemorrhage in a 23 week gestation infant.

The germinal matrix of the immature cerebellum is the external granular layer. Hemorrhage within this layer, once considered rare, is being increasingly recognized by neonatal ultrasound, especially in extremely low birth weight infants and contributes to their already high morbidity and mortality. The causes of cerebellar hemorrhage include the same systemic factors that are involeved in IVH.

A large proportion of severely premature infants have cerebral palsy and and mental retardation later in life. The neurodevelopmental outcome correlates with the grade of GMH and the presence of white matter abnormalities (probably PVL) on MRI.

Further Reading

Updated: January, 2018

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