Periventricular Leukomalacia (PVL): Difference between revisions
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== Clinically Relevant Anatomy | == Introduction == | ||
In the United States, about 57,000 infants are born every year with a birth weight below 1500g (Very Low Birth Weight). While 90% of these infants will survive, approximately 10% will exhibit [[Cerebral Palsy Aetiology and Pathology|cerebral palsy]] later on and a further 25-50% will demonstrate cognitive or behavioral deficits. '''Periventricular Leukomalacia''' (PVL) has been cited as one of the leading causes of brain injury leading to such deficits.<ref name=":0">Volpe JJ. [https://www.nature.com/articles/pr2001219 Neurobiology of periventricular leukomalacia in the premature infant]. Pediatric research. 2001 Nov;50(5):553-62.</ref> | |||
== Clinically Relevant Anatomy == | |||
add text here relating to '''''clinically relevant''''' anatomy of the condition<br> | add text here relating to '''''clinically relevant''''' anatomy of the condition<br> | ||
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== Mechanism of Injury / Pathological Process<br> == | == Mechanism of Injury / Pathological Process<br> == | ||
Incidences of PVL have been linked to neonatal hypocarbia, hypotension, prolonged cardiac surgery as well as sick infants where events led to the failure of areolar autoregulation of cerebral perfusion.<ref name=":1">Deng W, Pleasure J, Pleasure D. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898886/ Progress in periventricular leukomalacia]. Archives of neurology. 2008 Oct 13;65(10):1291-5.</ref> | |||
At 32 weeks and less (gestation age), the germinal matrix (GM) of the neonate is particularly sensitive to bleeding. <ref name=":1" /> | |||
Hemorrhages confined to the GM generally do not have a major effect on the prognostic outcome. When bleeding extends into the ventricles, hydrocephalus may result. If this is severe, distortion of the corticospinal tracts ensues. This has been linked to more severe [[Cerebral Palsy Introduction|spastic diplegic]] presentation in those affected.<ref name=":1" /> | |||
'''There are 2 components of a PVL injury.'''<ref name=":0" /> | |||
# The first component is the '''focal component'''. This is characterized by localized necrosis of all cellular elements. This then leads to '''cyst formation'''. | |||
# The second component is the '''diffuse component'''. This is cell-specific death of oligodendroglia - those cells which will mature into oligodendrocytes (forming the myelin of the cerebral white matter). | |||
When a PVL insult occurs, microglia become activated leading to a release of toxic products thought to lead to the death of premylinating [[Glial Cells|oligodendroglia]] in the periventricular area. There is also the death of [https://www.frontiersin.org/articles/10.3389/fnana.2020.00008/full subplate neurons] (susceptible to ischemia). These subplate neurons are important in the formation of mature thalamocortical connections.<ref name=":1" /> | |||
== Epidemiology == | |||
== Clinical Presentation == | == Clinical Presentation == | ||
The presentation of spastic diplegia is most often linked to an incidence of PVL.<br> | |||
== Diagnostic Procedures == | == Diagnostic Procedures == | ||
=== Brain imaging === | |||
[[Ultrasound Scans|Ultrasonography]] - Can be used in utero and postnatally. Cystic changes and increased echogenicity are indicators of PVL. After 1 week of birth, ultrasonography which yields no abnormalities can exclude PVL as a diagnosis.<ref name=":1" /> | |||
[[MRI Scans|MRI]] - Can be used earlier than ultrasonography. Repeated MRIs and [https://radiopaedia.org/articles/diffusion-tensor-imaging-and-fibre-tractography-1 diffuse tension imaging] can be used to determine prognostic information by tracking grey matter atrophy and tract degeneration.<ref name=":1" /><br> | |||
== Outcome Measures == | == Outcome Measures == | ||
| Line 30: | Line 49: | ||
== Management / Interventions<br> == | == Management / Interventions<br> == | ||
Prevention is the best form of treatment. An important aspect in this regard is ensuring arterial CO2 (PCO2)does not fall below 35mmHg. <ref name=":1" /> | |||
In low-birth-weight infants inhalation of NO has seen to decrease the incidence of PVL. <ref name=":1" /> | |||
Cooling, as done for HIE has had little attention in the research and thus has no definable outcomes.<ref name=":1" /><br> | |||
== Differential Diagnosis<br> == | == Differential Diagnosis<br> == | ||
Revision as of 11:26, 19 September 2023
This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (19/09/2023)
Introduction[edit | edit source]
In the United States, about 57,000 infants are born every year with a birth weight below 1500g (Very Low Birth Weight). While 90% of these infants will survive, approximately 10% will exhibit cerebral palsy later on and a further 25-50% will demonstrate cognitive or behavioral deficits. Periventricular Leukomalacia (PVL) has been cited as one of the leading causes of brain injury leading to such deficits.[1]
Clinically Relevant Anatomy[edit | edit source]
add text here relating to clinically relevant anatomy of the condition
Mechanism of Injury / Pathological Process
[edit | edit source]
Incidences of PVL have been linked to neonatal hypocarbia, hypotension, prolonged cardiac surgery as well as sick infants where events led to the failure of areolar autoregulation of cerebral perfusion.[2]
At 32 weeks and less (gestation age), the germinal matrix (GM) of the neonate is particularly sensitive to bleeding. [2]
Hemorrhages confined to the GM generally do not have a major effect on the prognostic outcome. When bleeding extends into the ventricles, hydrocephalus may result. If this is severe, distortion of the corticospinal tracts ensues. This has been linked to more severe spastic diplegic presentation in those affected.[2]
There are 2 components of a PVL injury.[1]
- The first component is the focal component. This is characterized by localized necrosis of all cellular elements. This then leads to cyst formation.
- The second component is the diffuse component. This is cell-specific death of oligodendroglia - those cells which will mature into oligodendrocytes (forming the myelin of the cerebral white matter).
When a PVL insult occurs, microglia become activated leading to a release of toxic products thought to lead to the death of premylinating oligodendroglia in the periventricular area. There is also the death of subplate neurons (susceptible to ischemia). These subplate neurons are important in the formation of mature thalamocortical connections.[2]
Epidemiology[edit | edit source]
Clinical Presentation[edit | edit source]
The presentation of spastic diplegia is most often linked to an incidence of PVL.
Diagnostic Procedures[edit | edit source]
Brain imaging[edit | edit source]
Ultrasonography - Can be used in utero and postnatally. Cystic changes and increased echogenicity are indicators of PVL. After 1 week of birth, ultrasonography which yields no abnormalities can exclude PVL as a diagnosis.[2]
MRI - Can be used earlier than ultrasonography. Repeated MRIs and diffuse tension imaging can be used to determine prognostic information by tracking grey matter atrophy and tract degeneration.[2]
Outcome Measures[edit | edit source]
add links to outcome measures here (see Outcome Measures Database)
Management / Interventions
[edit | edit source]
Prevention is the best form of treatment. An important aspect in this regard is ensuring arterial CO2 (PCO2)does not fall below 35mmHg. [2]
In low-birth-weight infants inhalation of NO has seen to decrease the incidence of PVL. [2]
Cooling, as done for HIE has had little attention in the research and thus has no definable outcomes.[2]
Differential Diagnosis
[edit | edit source]
add text here relating to the differential diagnosis of this condition
Resources
[edit | edit source]
add appropriate resources here
