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. 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. Stages
Early life
Newborn cerebral softening has traditionally been attributed to trauma at birth and its effect on brain tissue into adulthood. 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. 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. Later life
Cases of cerebral softening in infancy versus in adulthood are much more severe due to an infants 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. Documented cases
In this late 19th-century case study, a 10-year-old boy was found to have cerebral softening in specific parts of the brain, limiting specific sensory function. The identifiable softening enabled researchers to detect and partition cerebral areas related to different sensory perceptions.Another case in the late 19th century showed that cerebral softening, when caused by hemorrhaging, can affect various neural pathways leading to convulsions, spasms, coma and death.A third case in 1898 followed the ten-day decline of a 66-year-old woman with cerebral softening. She had yellow softening which led to symptoms that started slowly with transient facial paralysis on the right side of the face. The limbs later became cold and the right side of the body transiently progressed between semi-paralysis and tetanus. Her heart rate and respiration rate became slow by days three and four. Later she developed a yellow jaundiced appearance in the sclera and skin that the doctor proposed as paroxysmal hemoglobinuria upon autopsy. On the last days, the paralysis became more frequent, respiration rose and she developed tachycardia. She died on the evening of the tenth day. The autopsy revealed that the top of the brain down to the lateral ventricle were healthy, but below that there was a 2.5 × 2 × 1 inch area on the left side of the brain that was softened and yellow.