Publications Definition Periventricular leukomalacia PVL is characterized by the death of the white matter of the brain due to softening of the brain tissue. It can affect fetuses or newborns; premature babies are at the greatest risk of the disorder. PVL is caused by a lack of oxygen or blood flow to the periventricular area of the brain, which results in the death or loss of brain tissue. Although babies with PVL generally have no outward signs or symptoms of the disorder, they are at risk for motor disorders, delayed mental development, coordination problems, and vision and hearing impairments. PVL may be accompanied by a hemorrhage or bleeding in the periventricular-intraventricular area the area around and inside the ventricles , and can lead to cerebral palsy. The disorder is diagnosed by ultrasound of the head.

Author:Fell Kilabar
Language:English (Spanish)
Published (Last):21 July 2016
PDF File Size:1.28 Mb
ePub File Size:15.98 Mb
Price:Free* [*Free Regsitration Required]

US helps in assessing the neurologic status of the child, since clinical examination and symptoms are often nonspecific. It gives information about immediate and long term prognosis. Ultrasound is a fast and bedside examination which makes it ideal for premature infants.

Try to get all the information you can. Do not limit yourself to only one transducer or only one acustic window figure. Generally the large fontanel is used as acoustic window. The small fontanel however is a good window to the occipital lobes. This can be usefull in patients with borderline hyperechogenicity in these areas. It is a white matter disease that affects the periventricular zones.

In prematures this white matter zone is a watershed zone between deep and superficial vessels. Until recently ischemia was thought to be the single cause of PVL, but probably other causes infection, vasculitis play an additional role. PVL presents as areas of increased periventricular echogenicity. Normally the echogenicity of the periventricular white matter should be less than the echogenicity of the choroid plexus. Detection of PVL is important because a significant percentage of surviving premature infants with PVL develop cerebral palsy, intellectual impairment or visual disturbances.

Regular sonographic examination is mandatory as cysts in PVL can develop as long as 4 weeks after birth especially in prematures Cranial ultrasonographic findings may be normal in patients who go on to develop clinical and delayed imaging findings of PVL. A good protocol is US-examination at least once a week until discharge?

Sagittal image of a child with PVL grade 1 PVL grade 1 PVL is diagnosed as grade 1 if there are areas of increased periventricular echogenicity without any cyst formation persisting for more than 7 days. Suspect PVL if the echogenicity is asymmetric, coarse, globular or more hyperechoic than the choroid plexus. The abnormal periventricular echotexture of PVL usually disappears at weeks.

Transverse and sagittal image of a child with PVL grade 2. The echogenicity has resolved at the time of cyst formation. The severity of PVL is related to the size and distribution of these cysts. Cystic PVL has been identified on cranial ultrasounds on the first day of life, indicating that the adverse event was at least 2 weeks prenatal rather than perinatal or postnatal. This deficiency of neonatal cranial US is important, because noncystic WM injury is considerably more common than cystic WM injury.

Sagittal image demonstarting extensive PVL grade 3 PVL grade 3 PVL is diagnosed as grade 3 if there are areas of increased periventricular echogenicity, that develop into extensive periventricular cysts in the occipital and fronto-parietal region. Coronal and transverse images demonstrating PVL grade 4 PVL grade 4 PVL is diagnosed as grade 4 if there are areas of increased periventricular echogenicity in the deep white matter developing into extensive subcortical cysts.

PVL grade 4 is seen mostly in fullterm neonates as opposed to PVL grade , which is a disease of the preterm neonate.

Flaring persisting beyond the first week of life is by definition PVL garde 1. Flaring Transverse and sagittal images demonstrating flaring in a premature infant. The term flaring is used to describe the slightly echogenic periventricular zones, that are seen in many premature infants in the first week of life.

During this first week it is not sure if this is a normal variant or a sign of PVL grade 1. Flaring persisting beyond the first week of life is by definition PVL grade 1. LEFT: Initial examination shows flaring. Follow up is needed to differentiate flaring from PVL grade I. The case on the left shows a premature infant with flaring. At follow up no cyst formation was found and after the first week a normal periventricular white matter was seen.

Germinal Matrix Hemorrhage Germinal matrix hemorrhage GMH is also known as periventricular hemorrhage or preterm caudothalamic hemorrhage. These germinal matrix hemorrhages occur in the highly vascular but also stress sensitive germinal matrix, which is located in the caudothalamic groove. This is the subependymal region between the caudate nucleus and thalamus.

The germinal matrix is only transiently present as a region of thin-walled vessels, migrating neuronal components and vessel precursors It has matured by 34 weeks gestation, such that hemorrhage becomes very unlikely after this age. Most GMHs occur in the first week of life Most common in infants These hemorrhages start in the caudothalamic groove and may extend into the lateral ventricle and periventricular brain parenchyma. Most infants are asymptomatic or demonstrate subtle signs that are easily overlooked.

These hemorhages are subsequently found on surveillance sonography. Grade 1 intracranial hemorrhageSagittal and coronal US of subependymal hemorrhage located in the groove between the thalamus and the nucleus caudatus. Grade 1 intracranial hemorrhage On the left an intracranial hemorrhage confined to the caudothalamic groove. It is staged as grade 1 hemorrhage. In the acute phase these bleedings are hyperechoic, changing to iso- and hypo-echoic with time.

Sagittal and coronal US of a grade 2 hemorrhage Grade 2 intracranial hemorrhage On the left a grade 2 intracranial hemorrhage. On the coronal image only the cavum septi pellucidi is seen. Both lateral ventricles are filled with blood, but there is no ventricular dilatation. On the left the same patient after 3 days.

The ventricles are dilated and clot formation is seen. Secondary hydrocephalus occuring several days after a grade 2 bleed should not be mislabeled as grade 3 hemorrhage. Grade 3 intracranial hemorrhage On the left a grade 3 intracranial hemorrhage filling the left lateral ventricle. Also note the wedge shaped hyperechoic area on the laterosuperior side of the ventricle. This represents a small venous infarction. Yellow arrow indicating cyst formation within venous infarction.

Same patient as above. Two weeks later the venous infarction has developed into a hypoechoic area with cyst formation. Intracranial hemorrhage grade 4 Grade 4 intracranial hemorrhage Originally these grade 4 hemorrhages were thought to result from subependymal bleeding into the adjacent brain. Today however most regard these grade 4 hemorrhages to be venous hemorrhagic infartions, which are the result of compression of the outflow of the veins by the subependymal hemorrhage.

On the left a grade 4 hemorrhage. There is a large subependymal bleeding but also a large area with increased echogenicity in the brain parenchyma lateral to the ventricle. This is probably the result of a venous infarct. These venous infarctions resolve with cyst formation. These cysts can merge with the lateral ventricle, finally resulting into a porencephalic cyst.

On the left a different patient with a grade 4 hemorrhage at a later stage with extensive cyst formation. Grade 1 and 2 bleeds generally have a good prognosis. Grade 3 and 4 bleeds have variable long-term deficits, but outcome in grade 3 hemorrhages is usually good when no parenchymal injury has occurred. Hydrocephalus is a common complication and many infants require ventriculoperitoneal shunting.

The mechanisms by which hydrocephalus develop include: Communicating hydrocephalus: decreased absorption of cerebral spinal fluid CSF secondary to obstruction of arachnoid villi by blood and debris or the development of arachnoiditis Obstructive hydrocephalus: obstruction to CSF circulation.

Normal Variants Common variants are listed in the Table on the left. LEFT: Coronal image. Cavum septi pellucidi is seen in between the lateral ventricles. Cavum septi pellucidi, cavum vergae and cavum of the velum interpositum Well known variants are the cavum of the septum pellucidum and the cavum vergae. The more premature the baby, the more frequently these cavities are present. They can persist until adulthood.

A less frequently seen variant is the cavum of the velum interpositum. This presents as a cyst-like structure in the region of the tectum.

It can easily be confused with a subarachnoid cyst or a cyst of the pineal gland. At prenatal US these cysts can be predictive of trisomy About half of babies with Trisomy 18 show a CPC on ultrasound, but nearly all of these babies will also have other abnormalities on the ultrasound, especially in the heart, hand, and feet.

An exeption must be made for cysts that arise close to the foramen of Monro. Although these cysts often disappear spontaneously, follow up US is necessary to ensure disappearance. Some may produce symptoms of raised intracranial pressure due to obstruction to the cerebrospinal fluid CSF flow. Benign macrocrania Benign macrocrania is also known as extraventricular obstructive hydrocephalus. This is seen in children between 6 months and 2 years. The head circumference is above the 97th percentile.

After the age of 2 years the head size normalizes. Often the mother or father of the child had large heads at that age. The cause is not known. Most state that it is a normal condition, although some state that these children have a slight developmental delay. When children with a large head are presented for US, examine the superficial subarachnoid space and the ventricles.

Normal subarachnoid space measures The ventricles are often slightly enlarged. Thes prominent subarachnoid space and ventricular system in these children should not be interpreted as cerebral atrophia, as in atrophia there is a small head circumpherence.

Mineralizing vasculopathy Mineralizing vasculopathy can be seen in the thalamostriatal and lenticulostriatal arteries and is caused by calcification of the arterial wall. A wide range of perinatal, acquired, and nonspecific clinical conditions may result in this sonographic finding.

Germinolytic cysts Are located at the caudothalamic groove. They are tear shaped.


Neonatal Brain US

The condition involves the death of small areas of brain tissue around fluid-filled areas called ventricles. The damage creates "holes" in the brain. Causes PVL is much more common in premature infants than in full-term infants. A major cause is thought to be changes in blood flow to the area around the ventricles of the brain. This area is fragile and prone to injury, especially before 32 weeks of gestation. Infection around the time of delivery may also play a role in causing PVL.


Leucomalacia periventricular

The white matter in the periventricular regions is involved heavily in motor control, and so individuals with PVL often exhibit motor problems. However, since healthy newborns especially premature infants can perform very few specific motor tasks, early deficits are very difficult to identify. The extent of signs is strongly dependent on the extent of white matter damage: minor damage leads to only minor deficits or delays, while significant white matter damage can cause severe problems with motor coordination or organ function. Some of the most frequent signs include delayed motor development, vision deficits, apneas , low heart rates , and seizures. Delayed motor development[ edit ] Delayed motor development of infants affected by PVL has been demonstrated in multiple studies. Those with white matter injury often exhibit "tight coupling" of leg joints all extending or all flexing much longer than other infants premature and full-term. Vision deficits[ edit ] Premature infants often exhibit visual impairment and motor deficits in eye control immediately after birth.


Periventricular Leukomalacia Information Page

Pathology It likely occurs as a result of hypoxic-ischemic lesions resulting from impaired perfusion at the watershed areas, which in premature infants are located in a periventricular location. It is likely that infection or vasculitis also play a role in pathogenesis. Radiographic features Ultrasound Cranial ultrasound provides a convenient, non-invasive, relatively low-cost screening examination of the haemodynamically-unstable neonate at the bedside. The examination also imparts no radiation exposure. Sonography is sensitive for the detection of hemorrhage, periventricular leukomalacia, and hydrocephalus.


Leucomalácia periventricular

Periventricular leukomalacia Periventricular leukomalacia Periventricular leukomalacia PVL is a type of brain injury that is most common in babies born too soon premature or at low birthweight. The white matter leuko surrounding the ventricles of the brain periventricular is deprived of blood and oxygen leading to softening malacia. The white matter is responsible for transmitting messages from nerve cells in the brain so damage to the white matter can cause problems with movement and other body functions. What causes periventricular leukomalacia?

Related Articles