Table 1.

Summary of the role of postmortem brain cell decomposition mechanisms.

Mechanism or associated outcome	Role in postmortem brain decomposition
Cell death by oncotic necrosis	The main cell death pathway in the postmortem brain, wherein the loss of ATP leads to a sequence of morphological changes and eventual necrosis
Autolysis	Primary role in the early postmortem decomposition of brain cells
Apoptosis	Not a substantial contributor to postmortem decomposition, because this cell death pathway requires ATP
Compacted neurons (a.k.a. dark neurons)	May become more common after short periods of PMI, but less common with longer periods of PMI; is not thought to contribute to postmortem decomposition
Temporary ischemia	Temporary cerebral ischemia followed by reperfusion has much different mechanisms of decomposition (e.g. requiring ATP) than the permanent global cerebral ischemia that occurs postmortem
Postmortem fluid shifts	Biomolecular breakdown and blood extravasation leads to dramatic fluid shifts in the early postmortem brain; eventually, the brain is transformed to a paste- or fluid-like consistency
Perivascular and pericellular rarefactions	These areas expand and become more frequent in the PMI, which appears to be due to the swelling of astrocyte processes and other cells, causing those areas to not stain on light microscopy
Vacuolization	Common finding in postmortem brain cells and tissue spaces such as the neuropil that evolves throughout the PMI and can cause alteration of cell morphometry or compression of other structures
Biomolecule degradation	Largely driven by enzymes, biomolecule breakdown is a key driving force of postmortem decomposition, varying in rate based on many factors, such as the substrate and the temperature
Biomolecule redistribution	The breakdown of the factors stabilizing biomolecules in place in vivo leads them to eventually diffuse away from their original locations, with degrees of both Gaussian and non-Gaussian spread