Eight patients died after traumatic spinal cord injuries. At autopsy, neuropathological examination revealed longitudinal spreading of cord lesions in two of these patients. One developed progressive paralysis 43 h after fracture of the fifth cervical (C5) vertebra and died 38 days after injury. Necrotic lesions extended upward to the medulla oblongata and downward to the C7 cord segment. Pencil-shaped necrosis (C7-T4) and marginal spongiosis (C7-T2) were also found. A second patient died 5 months after C5 subluxation with tetraplegia. His spinal cord was severely compressed at C4/5 and pencil-shaped necrosis, which had become partially cystic, extended upward to C3 and downward to T1; marginal spongiosis was also found in C4-C5. In both cases, complete necrosis without cell reaction was found in several cord segments, including the initially impacted segment. These findings suggest that intra- and extramedullary circulatory impairment occurred not only at the initial impact level, but also in the adjacent levels. Increased intramedullary pressure, resulting from this circulatory disturbance, in combination with a narrowed spinal canal, may induce the upward and downward spreading of the lesion.