A systematic autopsy survey of human infant bridging veins

In the first years of life, subdural haemorrhage (SDH) within the cranial cavity can occur through accidental and non-accidental mechanisms as well as from birth-related injury. This type of bleeding is the most common finding in victims of abusive head trauma (AHT). Historically, the most frequent cause of SDHs in infancy is suggested to be traumatic damage to bridging veins traversing from the brain to the dural membrane. However, several alternative hypotheses have been suggested for the cause and origin of subdural bleeding. It has also been suggested by some that bridging veins are too large to rupture through the forces associated with AHT. To date, there have been no systematic anatomical studies on infant bridging veins. During 43 neonatal, infant and young child post-mortem examinations, we have mapped the locations and numbers of bridging veins onto a 3D model of the surface of a representative infant brain. We have also recorded the in situ diameter of 79 bridging veins from two neonatal, one infant and two young children at post-mortem examination. Large numbers of veins, both distant from and directly entering the dural venous sinuses, were discovered travelling between the brain and dural membrane, with the mean number of veins per brain being 54.1 and the largest number recorded as 94. The mean diameter of the bridging veins was 0.93 mm, with measurements ranging from 0.05 to 3.07 mm. These data demonstrate that some veins are extremely small and subjectively, and they appear to be delicate. Characterisation of infant bridging veins will contribute to the current understanding of potential vascular sources of subdural bleeding and could also be used to further develop computational models of infant head injury

Peripheral Nerve Grafts Support Regeneration after Spinal Cord Injury

Traumatic insults to the spinal cord induce both immediate mechanical damage and subsequent tissue degeneration leading to a substantial physiological, biochemical, and functional reorganization of the spinal cord. Various spinal cord injury (SCI) models have shown the adaptive potential of the spinal cord and its limitations in the case of total or partial absence of supraspinal influence. Meaningful recovery of function after SCI will most likely result from a combination of therapeutic strategies, including neural tissue transplants, exogenous neurotrophic factors, elimination of inhibitory molecules, functional sensorimotor training, and/or electrical stimulation of paralyzed muscles or spinal circuits. Peripheral nerve grafts provide a growth-permissive substratum and local neurotrophic factors to enhance the regenerative effort of axotomized neurons when grafted into the site of injury. Regenerating axons can be directed via the peripheral nerve graft toward an appropriate target, but they fail to extend beyond the distal graft–host interface because of the deposition of growth inhibitors at the site of SCI. One method to facilitate the emergence of axons from a graft into the spinal cord is to digest the chondroitin sulfate proteoglycans that are associated with a glial scar. Importantly, regenerating axons that do exit the graft are capable of forming functional synaptic contacts. These results have been demonstrated in acute injury models in rats and cats and after a chronic injury in rats and have important implications for our continuing efforts to promote structural and functional repair after SCI