The bifurcation and topography of the posterior tibial artery within the tarsal tunnel.

PURPOSE: The tarsal tunnel (TT) is a fibro-osseous anatomical space coursing from the medial ankle to the medial midfoot. This tunnel acts as a passage for both tendinous and neurovascular structures, including the neurovascular bundle containing the posterior tibial artery (PTA), posterior tibial veins (PTVs) and tibial nerve (TN). Tarsal tunnel syndrome (TTS) is the entrapment neuropathy that describes the compression and irritation of the TN within this space. Iatrogenic injury to the PTA plays a significant role in both the onset and exacerbation of TTS symptoms. The current study aims to produce a method to allow clinicians and surgeons to easily and accurately predict the bifurcation of the PTA, to avoid iatrogenic injury during treatment of TTS. METHODS: Fifteen embalmed cadaveric lower limbs were dissected at the medial ankle region to expose the TT. Various measurements regarding the location of the PTA within the TT were recorded and multiple linear regression analysis performed using RStudio. RESULTS: Analysis provided a clear correlation (p < 0.05) between the length of the foot (MH), length of hind-foot (MC) and location of bifurcation of the PTA (MB). Using these measurements, this study developed an equation (MB = 0.3*MH + 0.37*MC - 28.24 mm) to predict the location of bifurcation of the PTA within a 23° arc inferior to the medial malleolus. CONCLUSIONS: This study successfully developed a method whereby clinicians and surgeons can easily and accurately predict the bifurcation of the PTA, to avoid iatrogenic injury that would previously lead to an exacerbation of TTS symptoms.

The effect of hypothermia on transient focal ischemia in rat brain evaluated by diffusion- and perfusion-weighted NMR imaging.

The effect of moderate whole-body hypothermia (30 degrees C) on transient middle cerebral artery (MCA) occlusion in the rat was evaluated using diffusion- and perfusion-weighted magnetic resonance imaging. Two hours of transient MCA occlusion was induced by intracarotid insertion of a nylon filament under normothermic (n = 14) and hypothermic (n = 7) conditions. Diffusion- and perfusion-weighted imaging were performed before, during, and after focal ischemia from 30 min up to 7 days. In hypothermic animals, scattered neuronal necrosis was localized to select areas of the caudate putamen and the parietal and insular cortex. In contrast, the normothermic ischemic animals exhibited pan-necrosis and infarct encompassing the damaged area. The diffusion and perfusion data measured from caudate putamen indicate that hypothermia causes a significant reduction in the apparent diffusion coefficient of water (ADCw) and CBF values from normothermic control values (p < 0.01). In both normothermic and hypothermic animals after onset of MCA occlusion, ADCw and CBF values in the core of the ischemic region (striatum) significantly declined from the preischemic and homologous contralateral control ADCw and CBF values (p < 0.05). However, ADCw and CBF in the hypothermic group returned toward control more rapidly than in the normothermic group. These results suggest that the protective effect of hypothermia on ischemic cell damage is reflected in the early return of ADCw during reperfusion and the reduction of ischemic cell damage by hypothermia may be mediated by the improved CBF during acute reperfusion.

Temporal evolution and spatial distribution of the diffusion constant of water in rat brain after transient middle cerebral artery occlusion.

The regional distribution and temporal evolution of the diffusion coefficient (Dw) of water in rat brain was measured during and after transient middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 14) were subjected to 2 h of middle cerebral artery occlusion, induced by intracarotid insertion of a filament. Diffusion (n = 14) and perfusion (n = 7) weighted magnetic resonance imaging were performed before, and at various time points after MCA occlusion, ranging from 30 min up to 7 days. Our data demonstrate that the temporal profiles of Dw differ between the severely and the least damaged regions of tissue. In the core of the lesion, where the tissue evolved to necrosis, Dw declined significantly (P < 0.001) within 0.5 h after onset of ischemia, and remained depressed until 24 h after withdrawal of the suture. However, no statistically significant decline in Dw was found in the perifocal regions containing morphologically intact cells. Perfusion MRI qualitatively exhibited a hypoperfusion and reperfusion during, and after 2 h MCA occlusion, respectively. A significant (r > or = 0.71, P < 0.01) correlation was found between delta Dw (the difference in Dw between the ipsilateral ischemic and homologous contralateral control regions) obtained immediately before withdrawal of the suture (2 h of ischemia) and at specific early time points after withdrawal of the suture, and the degree of ischemic cell damage. No significant (P > 0.01) correlation was detected at an early time points of ischemia or at other time points after withdrawal of the suture.(ABSTRACT TRUNCATED AT 250 WORDS)