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CSF Pulsatility, Ventricular Reflux and Periventricular Changes

Although there appears to be clear evidence linking increased pulsatility in the cerebral vascular bed with WM changes, the link between increased CSF pulse amplitude in the AoS and neuropathology appears more tenuous. Increased aqueductal CSF pulsatility has been shown to be a feature of MS [97-99] and NPH [100-105]. However, the extent to which this phenomenon contributes to any pathology is unclear. T1 and T2 lesion volumes have been found to be positively correlated with the aqueductal pulse in MS patients [97]. However, this might be indicative of increased lateral ventricle size, rather than any causal relationship linking altered CSF dynamics with lesion formation. Notwithstanding this, it has been shown that increased aqueductal CSF pulsatility is associated with early-stage microstructural

WM changes in healthy adults [106] and elderly subjects [92] with no neurologic condition. This raises questions as to whether or not ventricular reflux, the resorption of CSF through the ependymal wall, might be a feature of some neurodegenerative disease. MS lesions are often observed around the subependymal veins at the edge of the lateral ventricles [18, 20]. Likewise, demyelinated lesions associated with other WM disorders such as Binswanger’s encephalopathy and leukoaraiosis often occur in the vicinity of the periventricular veins [39, 107, 108]. This has led several investigators to suggest that CSF leakage through the ependymal wall might be a contributory factor in periventricular lesion formation in MS patients [109]. Recently, Liu et al. [110] demonstrated that in MS patients, tissue structural abnormalities in the normal-appearing WM and WM lesions were greatest near the ventricles, with the magnetisation transfer ratio being abnormally low (compared with healthy controls) adjacent to the ventricles and increasing with distance from the ependymal wall. This they interpreted as being consistent with CSF or ependymal mediated pathogenesis.

NPH is associated with significantly reduced CSF absorption into the superior sagittal sinus (SSS) [111, 112], and this has led to speculation that CSF resorption might be occurring in the subependymal brain parenchyma [75]. Ventricular reflux of fluid has been shown to be a characteristic of communicating hydrocephalus [113, 114], with the periventricular tissue characterised by disruption of the ependyma, oedema, neuronal degeneration and ischemia [115]. Animal studies have also shown that in hydrocephalus, part of the CSF flow is cleared via a trans-parenchymal route into the cerebral vasculature [116-118], suggesting that a similar phenomenon may also be present in NPH [119]. If ventricular reflux of CSF is breaching the ependymal wall in NPH, then this might result in oedemas in the periventricular parenchyma, something which could inhibit CBF in this region [120]. CBF has been found to be generally lower in NPH patients than in normal controls [120-123], mirroring a similar phenomenon in MS patients [57-59]. However, after shunting, cerebral metabolism is increased [124], suggesting that in NPH reduced perfusion in this region is reversible and associated with CSF disturbances. Indeed, it has been postulated that CSF shunting in patients with NPH leads to a reversed flow of extracellular fluid from the periventricular WM into the ventricles, reducing the amount of extracellular water in the subependymal brain parenchyma [119].

 
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