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Introduction: Chronic overdrainage affects shunted patients producing a variety of symptoms that may be misdiagnosed. The best known symptoms are so-called shunt-related headaches. There is mounting evidence that changes in cerebrospinal venous system dynamics are a key factor to the pathophysiology of chronic overdrainage syndrome.Clinical presentation: We report the case of a 29-year-old woman with a shunt since the postnatal period suffering from chronic but the most severe intermittent headache attacks, despite an open shunt and with unchanged ventricular width during attacks. Intracranial pressure (ICP) recordings were performed during headache attacks and thereafter.Diagnosis and managment: Massively increased ICPs, a continuous B wave “storm,” and severely compromised intracranial compliance despite an open shunt were found, a scenario that was always self-limiting with the resolution of symptoms after several hours. When mobilized to the upright position, her ICPs dropped to − 17 mm Hg, proving shunt overdrainage.Outcome and conclusions: Symptomatology can only be explained by sudden venous entrapment following chronic venous distention as a result of chronic overdrainage. Subsequent therapeutic management with an overdrainage preventing shunt and satisfying clinical outcome with complete ceasing of headache attacks adds insight into the pathophysiology of chronic overdrainage syndrome. [ABSTRACT FROM AUTHOR]

Loss of cerebrospinal fluid (CSF) occurs commonly in daily neurosurgical practice. Understanding the altered physiology following CSF loss is important for optimization of patient care and avoidance of complications. There is overwhelming evidence now that the cerebral venous system plays a major role in intracranial pressure (ICP) dynamics especially when one takes into account the effects of postural changes, atmospheric pressure, and gravity on the craniospinal axis as a whole. The CSF and cerebral venous compartments are tightly coupled in two important ways. CSF is resorbed into the venous system, and there is also an evolved mechanism that prevents overdrainage of venous blood with upright positioning known as the Starling resistor. With loss of CSF pressure, this protective mechanism could become nonfunctional which may result in posture-related venous overdrainage through the cranial venous outflow tracts leading to pathologic states. This review article summarizes the relevant anatomic and physiologic basis of the relationship between the craniospinal venous and CSF compartments in the setting of CSF diversion. It is hoped that this article improves our understanding of ICP dynamics after CSF loss, adds a new dimension to our therapeutic methods, stimulates further research into this field, and ultimately improves our care of these patients. [ABSTRACT FROM AUTHOR]

In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation. We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa. A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP = 1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces. [ABSTRACT FROM AUTHOR]