Can periventricular leucomalacia cause spastic diplegia in premature infants?

Abstract

Sir: Blumenthal [3] claims that periventricular leucomalacia (PVL) is the most common cause of cerebral palsy. He notes that Banker and Larroche [1] coined this term in 1962. Shuman and Selednik [9] found that lesions at post mortem were present in restricted sites and always in the collateral trigone. This site, however, is in the optic radiation and a considerable distance from the cortico-spinal pathways, which run in the posterior limb of the internal capsule [6]. If PVL lesions do cause permanent nerve damage, it is surprising that cortical blindness is rare. Even if ‘white matter injury is both generalised and more common than previously realised’ [3], it is difficult to understand why the pathology is confined to the pyramidal tracts. As Polani has emphasised [4], spastic diplegia associated with prematurity is a ‘striking clinical entity, striking for the symmetry of the neurological signs, striking for the relatively good intelligence of the patients, and for their comparative freedom from seizures’. There is thus little evidence for a ‘neurocognitive deficit’ [3]. An alternative hypothesis has been presented, in which a ‘dying back neuropathy’ may be responsible for the nerve damage in diplegia in premature infants. The lesions may therefore lie in the distal endings of the cortico-spinal axons, in the caudal part of the spinal cord. Evidence to support this hypothesis has been presented previously [6,8]. It is also interesting that Kinnier-Wilson [7] remarked ‘I have often noticed integrity of the abdominals—a curious point’. Their preservation would be consistent with a lesion in this part of the spinal cord. Interferon a has been found to cause spastic diplegia in children treated therapeutically [2], but without any apparent structural damage to the cerebral hemispheres, so it is possible that this cytokine is acting selectively on the distal endings of the cortico-spinal axons. It is unfortunate that levels of interferon a in premature infants who subsequently developed cerebral palsy could not be measured for technical reasons [5].