A hypothesis of cerebral venous system regulation based on a study of the junction between the cortical bridging veins and the superior sagittal sinus

Vignes, Jean‐Rodolphe; Dagain, Arnaud; Guérin, J.; Liguoro, Dominique

doi:10.3171/jns-07/12/1205

Cited by 66 publications

(49 citation statements)

References 41 publications

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“…120,121 These are not only the most common sites of SDH identified in healthy neonates, but also are the characteristic sites of SDH in infants diagnosed as SBS/abusive head trauma. [123][124][125][126] As there are no such sphincters on the small intrinsic dural vessels draining into the dural sinuses, 127,128 increased pressure within the sinuses likely results in preferential flow into these small dural vessels. Dural venous sinus pressure is increased by pressure on the head, altered head position, obstruction of the jugular veins, and also by positive pressure ventilation.…”

Section: Prolonged Hypoxia and Advanced Resuscitationmentioning

confidence: 99%

Infants dying suddenly and unexpectedly share demographic features with infants who die with retinal and dural bleeding: a review of neural mechanisms

Squier

Mack

Jansen

2016

Develop Med Child Neuro

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The cause of death in infants who die suddenly and unexpectedly (sudden unexpected death in infancy [SUDI]) remains a diagnostic challenge. Some infants have identified diseases (explained SUDI); those without explanation are called sudden infant death syndrome (SIDS). Demographic data indicate subgroups among SUDI and SIDS cases, such as unsafe sleeping and apparent life-threatening events. Infants dying suddenly with retinal and dural bleeding are often classified as abused, but in many there is no evidence of trauma. Demographic features suggest that they may represent a further subgroup of SUDI. This review examines the neuropathological hypotheses to explain SIDS and highlights the interaction of infant oxygen-conserving reflexes with the brainstem networks considered responsible for SIDS. We consider sex- and age-specific vulnerabilities related to dural bleeding and how sensitization of the dural innervation by bleeding may influence these reflexes, potentially leading to collapse or even death after otherwise trivial insults.

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Section: Prolonged Hypoxia and Advanced Resuscitationmentioning

confidence: 99%

Infants dying suddenly and unexpectedly share demographic features with infants who die with retinal and dural bleeding: a review of neural mechanisms

Squier

Mack

Jansen

2016

Develop Med Child Neuro

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“…The inconclusive clinical effect of aminergic stimulation and the general histological lack of smooth muscle cells in cerebral veins (Cervós-Navarro and Roggendorf 1983) rendered the hypothesis of active venous cerebral volume control unlikely until recently. The discovery of a venous cuff mechanism consisting of collagen fibres (Pang et al 2001) and smooth muscle cells (Vignes et al 2007;Dagain et al 2009) at the entrance of the bridging veins to the sinuses revived the hypothesis of active venous volume control.…”

Section: Introductionmentioning

confidence: 97%

Active regulation of cerebral venous tone: simultaneous arterial and venous transcranial Doppler sonography during a Valsalva manoeuvre

et al. 2010

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The aim of this study was to analyse the cerebral venous outflow in relation to the arterial inflow during a Valsalva manoeuvre (VM). In 19 healthy volunteers (mean age 24.1 +/- 2.6 years), the middle cerebral artery (MCA) and the straight sinus (SRS) were insonated by transcranial Doppler sonography. Simultaneously the arterial blood pressure was recorded using a photoplethysmographic method. Two VM of 10 s length were performed per participant. Tracings of the variables were then transformed to equidistantly re-sampled data. Phases of the VM were analysed regarding the increase of the flow velocities and the latency to the peak. The typical four phases of the VM were also found in the SRS signal. The relative flow velocity (FV) increase was significantly higher in the SRS than in the MCA for all phases, particularly that of phase IV (p < 0.01). Comparison of the time latency of the VM phases of the MCA and SRS only showed a significant difference for phase I (p < 0.01). In particular, there was no significant difference for phase IV (15.8 +/- 0.29 vs. 16.0 +/- 0.28 s). Alterations in venous outflow in phase I are best explained by a cross-sectional change of the lumen of the SRS, while phases II and III are compatible with a Starling resistor. However, the significantly lager venous than the arterial overshoot in phase IV may be explained by the active regulation of the venous tone.

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“…Blood flow through these compliant vessels is controlled by sphincters, which regulate discharge into the SSS [158,159]. This means that these vessels possess characteristics similar to those of a Starling resistor [160-163], and these collapse, occluding the blood flow, when the transmural pressure reaches a certain threshold [164].…”

Section: Introductionmentioning

confidence: 99%

“…Although the physiology associated with this mechanism is not well understood, it seems likely that much of this blood is stored during diastole in the cortical bridging veins that transverse the SAS. Discharge from these veins is controlled by regulatory sphincters [158,159]. Constriction of these sphincters results in an increase in the transmural pressure of the bridging veins, causing them to engorge and ‘puff out’, before periodically discharging into the SSS.…”

Section: Introductionmentioning

confidence: 99%

Venous hemodynamics in neurological disorders: an analytical review with hydrodynamic analysis

Beggs

2013

BMC Med

105

102

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Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.Venous hypertension in the dural sinuses can alter intracranial compliance. Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.

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A hypothesis of cerebral venous system regulation based on a study of the junction between the cortical bridging veins and the superior sagittal sinus

Abstract: The point of convergence between the cortical veins and the SSS is a key area. The authors also hypothesize that the myoendothelial junction acts as a smooth sphincter and that it plays a role in cerebral venous hemodynamics and pathological conditions.

Cited by 66 publications

References 41 publications

Infants dying suddenly and unexpectedly share demographic features with infants who die with retinal and dural bleeding: a review of neural mechanisms

Infants dying suddenly and unexpectedly share demographic features with infants who die with retinal and dural bleeding: a review of neural mechanisms

Active regulation of cerebral venous tone: simultaneous arterial and venous transcranial Doppler sonography during a Valsalva manoeuvre

Venous hemodynamics in neurological disorders: an analytical review with hydrodynamic analysis

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