Mineralizing angiopathy and minor head trauma


SIR–We read with interest the article by Lingappa et al.[1] and the commentary by deVeber[2] on the relationship between acute basal ganglia stroke, mineralizing angiopathy, and minor head trauma. deVeber notes the very strong association of head and neck trauma in the week preceding childhood stroke, and discusses a mechanism involving mechanical stretching of arteries during trauma.

The pathophysiology of human traumatic brain injury is highly complex; following primary mechanical stress, a complex secondary cascade (including release of neurotransmitters, neurogenic inflammation, and cortical spreading depression), occurs.[3, 4] These may lead to changes in brain perfusion, mediated through autonomic and trigeminovascular responses.[5]

deVeber proposes that mineralized arteries would be more rigid than normal vessels and predisposed to shear injury. Mineralized vessels will, however, not only be rigid and likely to shear, but their contractility and barrier properties are likely to be affected as well. We do not as yet know which cells are involved in vascular calcification, but there is evidence to implicate pericytes[6] (including unpublished results from the present author) which derive from the mesoderm and have osteogenic properties.[7] Basal ganglia vascular calcification appears to involve adventitial or subendothelial cells, where pericytes are found,[8] and in adults basal ganglia calcification is associated with bone matrix proteins.[9] These observations suggest that pericytes may be responsible for basal ganglia vascular calcification, but much more study is required.

Pericytes are critical in the developing brain for formation and stabilization of blood vessels,[10] and for regulation of capillary blood flow in normal and pathological states.[11] If their function is impaired by calcification then they may be unable to participate in these roles and mount an appropriate response to trauma.

We suggest that mechanisms other than primary mechanical stress, which is not treatable, should be considered in paediatric head trauma as some of these secondary mechanisms may eventually be amenable to therapy.