Radiculomyelitis following acute haemorrhagic conjunctivitis.

The clinical manifestations and natural history of radiculomyelitis following a newly reported disease--acute haemorrhagic conjunctivitis (AHC)--have been studied in 33 patients in Taiwan, and the following observations made: All the patients in this series were adults at ages ranging from 21 to 55 years; the salient initial neurological manifestations were radicular pains and acute flaccid paralysis which developed from five to thirty-seven days after the onset of AHC. In some patients, signs and symptoms indicating involvement of the meninges, cranial nerves and the white matter of the cord were observed; motor paralysis was the most striking feature during the whole clinical course; it consisted of flaccid asymmetrical weakness in one or more limbs, usually being more severe in the lower limbs than in the upper, and often more proximal than distal. Atrophy in the severely affected muscles usually became apparent in the second or third week of the weakness; the prognosis regarding the return of function in the affected muscles was dependent on the severity of the involvement. Permanent incapacitation due to paralysis and muscular atrophy in the affected proximal muscles of lower limbs was the main sequel in severe cases. The pattern and prognosis of flaccid motor paralysis were reminiscent of acute poliomyelitis in which the anterior horn cells of the spinal cord are mainly involved. Pleocytosis ranging from 11 to 270 per mm3 was noted in the majority of the patients when the cerebrospinal fluid was examined within the first three weeks from the onset of neurological symptoms; the total protein level was raised invariably from the second week onwards in all specimens, and remained so throughout the subsequent course as long as the seventh week or later. Tissue culture neutralization tests were performed on the sera from 9 patients; significant rises in the antibody titres (greater than or equal to 1:16) to AHC virus antigens were found in 8 cases, and in 2 of them a fourfold rise in the paired sera was noted. The differentiation of this syndrome from poliomyelitis and from Guillain-Barré syndrome, the relative freedom of children from neurological complications of AHC and the aetiological relationship of AHC virus to the syndrome have been discussed. It is concluded that this unusual neurological syndrome is caused by the neurovirulent properties of the AHC virus.