P eriventricular lucency (PVL) refers to the decreased attenuation level, or "blurring," around the periventricular area on CT, or T2 hyperintensity on MRI. This radiological phenomenon is a common finding not only in various neurological or cardiovascular disorders, but also in the general elderly population. 21,22,29,47 Although widely researched and documented, the pathogenesis and clinical significance of PVL are still inconclusive, especially for PVL associated with hydrocephalus. Hydrocephalus is defined as the excessive accumulation of CSF in the brain due to various causes. The disease is considered to be caused by an imbalance between the formation and reabsorption of CSF, due to the disturbance in CSF dynamics. 28 Considering the site of the obstruction in the flow of CSF, two types of hydrocephalus have been defined: communicating and noncommunicating. PVL in hydrocephalus was first documented by Naidich et al. 27PVL and enlarged ventricles are typical radiological signs of acute or noncommunicating hydrocephalus.30 However, these two signs also exist in chronic or communicating hydrocephalus, although the prevalence is relatively lower. 25,34 In either case, the pathogenesis of PVL remains abbreviatioNs FE = finite element; ICP = intracranial pressure; ISF = interstitial fluid; PVL = periventricular lucency; TPG = transmantle pressure gradient. obJective Periventricular lucency (PVL) is often observed in the hydrocephalic brain on CT or MRI. Earlier studies have proposed the extravasation of ventricular CSF into the periventricular white matter or transependymal CSF absorption as possible causes of PVL in hydrocephalus. However, there is insufficient evidence for either theory to be conclusive. methods A finite element (FE) model of the hydrocephalic brain with detailed anatomical geometry was constructed to investigate the possible mechanism of PVL in hydrocephalus. The initiation of hydrocephalus was modeled by applying a transmantle pressure gradient (TPG). The model was exposed to varying TPGs to investigate the effects of different geometrical characteristics on the distribution of PVL. The edema map was derived based on the interstitial pore pressure. results The model simulated the main radiological features of hydrocephalus, i.e., ventriculomegaly and PVL. The degree of PVL, assessed by the pore pressure, was prominent in mild to moderate ventriculomegaly. As the degree of ventriculomegaly exceeded certain values, the pore pressure across the cerebrum became positive, thus inducing the disappearance of PVL. coNclusioNs The results are in accordance with common clinical findings of PVL. The degree of ventriculomegaly significantly influences the development of PVL, but two factors were not linearly correlated. The results are indicative of the transependymal CSF absorption as a possible cause of PVL, but the extravasation theory cannot be formally rejected.

Microcellular polylactide (PLA)/modified-silica (m-silica) nanocomposite foams were prepared in a batch process using supercritical carbon dioxide as physical blowing agent. To enhance the dispersion in the PLA matrix, silica nanoparticles were modified by dodecyltrichlorosilane) and were melt compounded with PLA using a twin-screw extruder. PLA/m-silica nanocomposites with msilica contents of 0.5, 1, 2, 3, and 5 wt % were obtained. The incorporation of m-silica nanoparticles in PLA enhanced the thermal and mechanical properties of PLA. The resultant foams were observed by scanning electron microscopy (SEM) and average cell diameter and cell density were calculated using SEM micrographs. The incorporation of m-silica nanoparticles into the PLA matrix had the effect of decreasing the cell diameter and increasing the cell uniformity and cell density.

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Spinal stenosis is a common degenerative condition. However, how neurogenic claudication develops has not been clearly elucidated. Moreover, cerebrospinal fluid physiology at the lumbosacral level has not received adequate attention. This study was conducted to compare cerebrospinal fluid hydrodynamics at the lumbosacral spinal level between patients with spinal stenosis and healthy controls. Twelve subjects (four patients and eight healthy controls; 25-77 years old; seven males) underwent phase-contrast magnetic resonance imaging to quantify cerebrospinal fluid dynamics. The cerebrospinal fluid flow velocities were measured at the L2 and S1 levels. All subjects were evaluated at rest and after walking (to provoke neurogenic claudication in the patients). The caudal peak flow velocity in the sacral spine (À0.25 AE 0.28 cm/s) was attenuated compared to that in the lumbar spine (À0.93 AE 0.46 cm/s) in both patients and controls. The lumbar caudal peak flow velocity was slower in patients (À0.65 AE 0.22 cm/s) than controls (À1.07 AE 0.49 cm/s) and this difference became more pronounced after walking (À0.66 AE 0.37 cm/s in patients, À1.35 AE 0.52 cm/s in controls; p ¼ 0.028). The sacral cerebrospinal fluid flow after walking was barely detectable in patients (caudal peak flow velocity: À0.09 AE 0.03 cm/s). Cerebrospinal fluid dynamics in the lumbosacral spine were more attenuated in patients with spinal stenosis than healthy controls. After walking, the patients experiencing claudication did not exhibit an increase in the cerebrospinal fluid flow rate as the controls did. Altered cerebrospinal fluid dynamics may partially explain the pathophysiology of spinal stenosis. ß