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A sudden spinal syndrome—often pain followed rapidly by weakness, a sensory level and sphincter disturbance—would raise suspicion of haematomyelia. Symptoms can localise injury to the spinal cord, but cannot prove that the material within it is blood.

The classical presentation is abrupt severe spinal or radicular pain followed by rapid loss of motor power below the affected level. A thoracic lesion can produce paraplegia; a cervical lesion can affect all four limbs, and a high cervical lesion can impair breathing. Bladder retention or loss of control and bowel disturbance support interruption of descending spinal pathways. Sensory examination may show a sensory level below which sensation is altered; the distribution need not be perfectly symmetrical.

A centrally placed haemorrhage can especially injure crossing spinothalamic pathways and the anterior horns. There may therefore be disproportionate loss of pain and temperature with relative preservation of some other modalities, together with segmental weakness, reduced reflexes or later wasting at the level of the lesion. Damage to descending motor pathways produces weakness below it. Acute spinal shock can initially suppress reflexes below the lesion; later reflex behaviour depends on the pathways destroyed and should not be predicted from the first examination alone.^[ref]

The history should look for trauma, a bleeding disorder or anticoagulant exposure, a vascular malformation or an underlying spinal lesion. In a modern assessment these are possible causes, not prerequisites. A haemorrhage can also develop subacutely or recur, so the apoplectic onset is suggestive rather than universal.^[ref]

Important alternatives are spinal cord infarction, acute inflammatory myelitis, traumatic injury without intramedullary bleeding, and an epidural or other extramedullary collection compressing the spinal cord. A spinal meningeal bleed is anatomically different from haematomyelia, even if pain and weakness overlap. Preserved consciousness and absence of cranial signs may support spinal localisation, but neither is an absolute rule.

Modern magnetic resonance imaging is required to demonstrate the location and nature of the lesion; it can distinguish intramedullary blood from external compression and guide investigation of an underlying vascular or neoplastic cause.^[ref] In an 1864 answer, sudden onset and anatomical localisation justify a suspected diagnosis; they do not justify claiming certainty from symptoms alone.

“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.^[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 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.^[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.^[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.