= Solution
\b[“Softening” describes disintegration of nervous tissue; it does not identify one cause.] The 1865 colour categories were chiefly red, yellow and white softening. They must be distinguished from the causal classification into vascular injury, <inflammation>, pressure-related injury, trauma and post-mortem change. Historical observers sometimes interpreted pale ventricular softening as a consequence of <oedema>; modern <pathology> requires evidence of tissue death before calling such a region <encephalomalacia>.<Pathological Anatomy of Insanity in the American Journal of Insanity (1865)>[Volume 22, p. 177: white, yellow and red brain softenings]{ref}
Red softening contains conspicuous extravasated <blood>, sometimes with vascular engorgement. It may occur in a haemorrhagic <cerebral infarction>, a contusion or destructive <inflammation>. Yellow softening is a later discoloured, friable focus containing products of tissue and blood breakdown, often with lipid-laden <macrophages>. White or pale softening has little visible <haemorrhage>; an ischaemic focus in the <white matter> can be pale, as can waterlogged tissue around a <ventricular system>[cerebral ventricle]. These appearances overlap through time. Neither red colour proves primary <encephalitis> nor white colour proves absence of vascular disease.
In the <cerebral hemispheres>, a major cause of genuine destructive softening is interruption of arterial <blood flow>: <thrombosis> on diseased arteries, an <embolus> from the <heart> or another artery, or inadequate perfusion during severe systemic circulatory failure. The territory supplied by the obstructed vessel helps explain a focal lesion; prolonged global failure particularly injures vulnerable neurons and boundary zones between arterial territories. Cortical lesions and deep lesions involving the <basal ganglia> or internal pathways can therefore have different distributions. <Cerebral infarction> evolves through neuronal injury, removal of dead tissue by <microglia> and <macrophages>, and <liquefactive necrosis>; a chronic lesion may leave a fluid-filled cavity with surrounding <gliosis>.<Central Nervous System Pathology by the National University of Singapore>[Cerebral infarction: gross and microscopic progression from acute injury to liquefaction]{ref}
In the <cerebellum> and <brainstem>, interruption of the vertebrobasilar circulation is likewise an important vascular cause; local <haemorrhage>, trauma and infection are alternatives. Suppuration can cause destructive softening in any region, and a nearby <tumour> can injure tissue by compression, interference with its blood supply or associated <oedema>. These mechanisms must be investigated rather than inferred from consistency alone.
In the <spinal cord>, destructive <myelomalacia> can follow vascular interruption, severe compression, direct trauma or inflammatory <myelitis>. Vertebral disease or an epidural mass may compress both the <spinal cord> and its vessels. Infarction often involves the territory of the <anterior spinal artery>; reduced perfusion can preferentially damage the vulnerable central <gray matter>. <Myelitis> can also disrupt tissue without a primary arterial obstruction. It would be misleading to transfer the relative frequency of cerebral embolism unchanged to every spinal lesion.<Spinal Cord Infarction by Merck Manual Professional Edition>[Causes and anterior spinal artery territory]{ref}
At examination, record the location, vascular territory, firmness, colour and adjacent membranes; inspect the arteries and search for an embolic source or compression. <Microscopy> asks whether there is <necrosis>, <inflammatory exudation>, <haemorrhage>, myelin debris, cellular clearance or repair. Finally exclude simple post-mortem <autolysis>.
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