Diffusion tensor imaging (DTI) has been proposed as a sensitive biomarker of traumatic white matter injury, which could potentially serve as a tool for prognostic assessment and for studying microstructural changes during recovery from traumatic brain injury (TBI). However, there is a lack of longitudinal studies on TBI that follow DTI changes over time and correlate findings with long-term clinical outcome. We performed a prospective longitudinal study of 30 adult patients admitted for subacute rehabilitation following severe traumatic brain injury. DTI and conventional MRI were acquired at mean 8 weeks (5–11 weeks), and repeated in 23 of the patients at mean 12 months (9–15 months) post-trauma. Using a region-of-interest-based approach, DTI parameters were compared to those of healthy matched controls, scanned during the same time period and rescanned with a similar interval as that of patients. At the initial scan, fractional anisotropy was reduced in all the investigated white matter regions in patients compared to controls (P ≤ 0.01) due to decreased diffusivity parallel (λ_∥) and increased diffusivity perpendicular (λ_⊥) to axonal fibre direction. Fractional anisotropy in the cerebral peduncle correlated with ∼1 year Glasgow outcome scale score (r = 0.60, P<0.001) and in this sample predicted dichotomized outcome with 76% accuracy when taken alone, and with 100% accuracy in combination with clinical evaluation by functional independence measure at the time of the first scan. At follow-up DTI, fractional anisotropy in patients had increased in the internal capsule and in centrum semiovale (P ≤ 0.01) due to an interval increase of λ_∥ with unchanged λ_⊥. In these regions, fractional anisotropy and λ_∥ reached normal or supranormal levels, primarily in patients with favourable outcome. In the cerebral peduncle and in corpus callosum, λ_∥ and λ_⊥ both increased during the scan interval and, particularly in patients with unfavourable outcome, fractional anisotropy remained depressed. No significant DTI parameter changes over time were found in controls, or in CSF of patients. These findings support that DTI is a clinically relevant biomarker in TBI, which may have prognostic value and also might serve as a tool for revealing changes in the neural tissue during recovery.

The regional cerebral blood flow can be calculated from the initial slope of the logarithmically displayed clearance curve following intra-arterial injection of ¹³³ Xe (rCBF _initial ). The relationship between this parameter and the values resulting from stochastic (height over area) and compartmental analyses is extensively discussed. Experimental results demonstrate the theoretically expected close relationship between rCBF _initial and flow of gray substance (rCBF _initial 20% to 30% lower than F _g ). It is shown how the cerebral clearance curve (normally biexponential) with low flow values becomes gradually monoexponential. Thus only flow of gray substance changes, whereas flow of white substance is independent of CBF _∞ . CBF ₁₀ was shown to overestimate CBF _∞ with about 15% independent of the flow level. Correlation between CBF _initial and CBF ₁₀ was linear (r=0.98) at CBF ₁₀ values above 20 ml/100 gm/min. The CBF _initial normal value is found to be 64±9 ml/100 gm/min, and the interchannel coefficient of variation is 8.2%. A correction for remaining radioactivity from previous measurements is described. Using this, no significant difference was found between repeated resting state measurements. The CBF _initial -Paco ₂ relationship was found to be best described as exponential. In a group of patients with various intracranial diseases, 1 mm Hg change in Paco ₂ resulted in 4% change of CBF _initial quite independent of the CBF _initial level.

Local increases in neuronal activity within the brain lead to dilation of blood vessels and to increased regional cerebral blood flow. Increases in extracellular potassium concentration are known to dilate cerebral arterioles. Recent studies have suggested that the potassium released by active neurons is transported through astrocytic glial cells and released from their endfeet onto blood vessels. The results of computer simulations of potassium dynamics in the brain indicate that the release of potassium from astrocyte endfeet raises perivascular potassium concentration much more rapidly and to higher levels than does diffusion of potassium through extracellular space, particularly when the site of a potassium increase is some distance from the vessel wall. On the basis of this finding, it is proposed that the release of potassium from astrocyte endfeet plays an important role in regulating regional cerebral blood flow in response to changes in neuronal activity.