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Tendon transfer of the flexor digitorum longus tendon (FDLT) or the flexor hallucis longus tendon (FHLT) into the tibialis posterior tendon is carried out in patients with tibialis posterior dysfunction. FDLT and FHLT are connected in the region of the knot of Henry. The present study has investigated the anatomical variations of this tendinous interconnection. The results could be used to determine which of the two tendons should be transected proximal to the region of the knot of Henry in the surgical treatment of tibialis posterior dysfunction. In over two-thirds of cadaver specimens investigated, tension applied solely to FHLT resulted in flexion of all digits and the hallux. On the basis of these results, we propose that identification of the tendon to be transected should be decided at the time of surgery depending on the anatomical pattern. Based on the evidence provided by 16 cadaveric dissections, transection of FDLT proximal to the region of the knot of Henry for the repair of tibialis posterior dysfunction would result in retention of function of the hallux and lesser digits in the majority of cases.

Epidemiological evidence indicates that the severity of many human neuropathologies is often age-related, and this also appears true in rodent models of human disease. In this study, we examined the inflammatory response within the brain to the archetypal pro-inflammatory cytokines interleukin-1beta (IL-1beta) or tumour necrosis factor-alpha (TNF-alpha). We assessed how the cerebral vasculature changes with age and whether any structural alterations are associated with altered cytokine sensitivities. Six hours after equivalent microinjections of IL-1beta or TNF-alpha, 3-week-old juvenile and 18-month-old aged rats displayed increased leucocyte recruitment, blood-brain barrier (BBB) breakdown, and a loss of specificity in the populations of leucocytes recruited when compared with the restricted profile observed in 2-month-old young adult rat brain. The expression of the tight junction protein claudin-1 was absent in those vessels where neutrophils were being actively recruited. To determine whether changes in the structure of the BBB might be responsible for the increased susceptibility observed at either end of the age spectrum, we compared the number of claudin-1 positive vessels in the unchallenged brain to the total number of vessels. Virtually all vessels in the young adult brain express claudin-1, but a significant proportion of vessels are claudin-1 negative in the juvenile rat brain. In the aged rat brain, the overall number of vessels is markedly reduced, but the majority of these still appear to be claudin-1 positive. The pattern of claudin-1 expression together with the change in vessel density indicates that the properties of the BBB change with age, and, despite similarities, the underlying cause of the heightened inflammatory response in the juvenile and in the aged brain is likely to differ. Indeed, the spatial characteristics of the cytokine-induced BBB breakdown are different at either end of the age spectrum. These studies identify two periods within the lifespan of a rat where susceptibility to pro-inflammatory mediators is dramatically increased.

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