Cerebral softening

Encephalomalacia

Stroke Brain (Similar to Cerebral Softening)

Classification and external resources
ICD-9-CM
MeSH

348.89
D004678

In medicine, cerebral softening (encephalomalacia) is a localized softening of the brain substance, due to
hemorrhage or inflammation. Three varieties, distinguished by their color and representing different stages of
the morbid process, are known respectively as red, yellow, and white softening. [1][2]

Causes
Stroke
Main article: Ischemia
Ischemia: A decreased or restriction of circulating blood flow to a region of the brain which deprives neurons
of the necessary substrates (primarily glucose); represents 80% of all strokes. A thrombus or embolus plugs an
artery so there is a reduction or cessation of blood flow. This hypoxia or anoxia leads to neuronal injury, which
is known as a stroke. The death of neurons leads to a so-called softening of the cerebrum in the affected area.
Hemorrhage: Intracerebral hemorrhage occurs in deep penetrating vessels and disrupts the connecting
pathways, causing a localized pressure injury and in turn injury to brain tissue in the affected area.
Hemorrhaging can occur in instances of embolic ischemia, in which the previously obstructed region
spontaneously restores blood flow. This is known as a hemorrhagic infarction and a resulting red infarct occurs,
which points to a type of cerebral softening known as red softening.[1][3]

The relation of the Circle of Willis

In a study on the Circle of Willis and its relation to cerebral vascular disorders, a comparison on various
anomalies between normal brains (those without the condition of cerebral softening) and brains with cerebral
softening were looked at to observe trends in the differences of the anatomical structure of the Circle of Willis.
Statistically significant results were found in the percentage of normal brains that had a normal Circle of Willis
and those that had cerebral softening and had a normal Circle of Willis. The results yielded 52% of normal
brains having a normal Circle of Willis, while only 33% of brains with cerebral softening had a normal Circle of
Willis. There were also a higher number of string-like vessels in brains with cerebral softening (42%), than there
were in normal brains (27%). These results point to an assumption of a higher incidence rate of anomalies in
brains with cerebral softening versus those that do not have cerebral softening. [4]

Types of softening
Red softening
Red softening is one of the three types of cerebral softening. As its name suggests, certain regions of cerebral
softening result in a red color. This is due to a hemorrhagic infarct, in which blood flow is restored to an area of
the brain that was previously restricted by an embolism. This is termed a "red infarct" or also known as red
softening.[1]
Upon autopsy of several subjects, Dr. Cornelio Fazio found that the most common areas of this type of
softening occurred where there was a hemorrhage of the middle cerebral artery or the superior or deep
branches to it. The subjects' softened area was not always near the arteries but where the capillaries perfused
the brain tissue. The symptoms were similar to that of a stroke.[5]

White softening
White softening is another form of cerebral softening. This type of softening occurs in areas that continue to be
poorly perfused, with little to no blood flow. These are known as "pale" or "anemic infarcts" and are areas that
contain dead neuronal tissue, which result in a softening of the cerebrum.[1]

Yellow softening
Yellow softening is the third type of cerebral softening. As its name implies, the affected softened areas of the
brain have a yellow appearance. This yellow appearance is due to atherosclerotic plaque build-up in interior
brain arteries coupled with yellow lymph around the choroid plexus, which occurs in specific instances of brain
trauma.[2]

Stages
Early life
Newborn cerebral softening has traditionally been attributed to trauma at birth and its effect on brain tissue
into adulthood.[6] However, more recent research shows that cerebral softening in newborns and the
degeneration of white matter is caused by asphyxia and/or later infection. There is no causal evidence to
support the hypothesis that problems in labor contribute to the development of softening in infant white
matter.[7] Also, further evidence shows a possible connection between low sugar and high protein levels in
cerebral spinal fluid that can contribute to disease or virus susceptibility leading to cerebral softening. [8]

Later life

Cases of cerebral softening in infancy versus in adulthood are much more severe due to an infant's inability to
sufficiently recover brain tissue loss or compensate the loss with other parts of the brain. Adults can more
easily compensate and correct for the loss of tissue use and therefore the mortality likelihood in an adult with
cerebral softening is less than in an infant.[9]

Encephalomalacia
Encephalomalacia is term given to describe softening or loss of brain parenchyma with or
without surrounding gliosis, as a late manifestation of injury.
Clinical presentation

asymptomatic

serve as a focus of seizure

Pathology

Encephalomalacia is the end result of liquefactive necrosis of brain parenchyma following

insult, usually occurring after cerebral ischaemia, cerebral infection, haemorrhage,
traumatic brain injury, infection, surgery or other insults. It is not synonymous with gliosis,
with is the proliferation of glial cells in response to injury.
Subtypes

multicystic encephalomalacia

Radiographic features
CT

region of hypoattenuation

volume loss

can occur anywhere however has characteristic locations are anteroinferior, frontal and
temporal lobes

is often associated with gliosis and wallerian degeneration