An anti-siphoning valve for use in hydrocephalic shunt systems is described. The addition of this valve to the system effectively reduces the hazard of negative intraventricular pressure when the patient is sitting or standing. The formation of post-shunt subdural hematomas was prevented by temporary postoperative occlusion of the shunt using a percutaneously reversible occlusion valve, which is also described. KEY WORDShydrocephalie shunts hypotension subdural hematoma 9 reversible occlusion valve siphon effect ventricular anti-siphon valve 1.

Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.

Systems analysis is explored as a method of evaluating intracranial pressure (ICP). The intracranial cavity is characterized by a transfer function that is evaluated by the blood pressure pulse acting as the system input and the ICP pulse acting as the output. A comparison is made of the ability of systems analysis, volume-pressure test (VPT), and cerebrospinal fluid-pulse amplitude analysis (CSFPAA) to distinguish between an epidural balloon inflation (EBI) and an intraventricular infusion (IVI) at various steady state levels of ICP. The VPT could not distinguish between EBI and IVI at any level of ICP, and above 30 mm Hg the volume-pressure response decreased. Spectral analysis was able to distinguish EBI from IVI above 30 mm Hg, and CSFPAA was demonstrated to be a simplified spectral analysis. Changes in ICP waveform generated during each cardiac cycle appear to be related to changes in vasomotor reactivity and may have value in the clinical monitoring of ICP.

Little is known about intracranial venous pressure in hydrocephalus. Recently, we reported that naturally occurring hydrocephalus in Beagle dogs was associated with an elevation in cortical venous pressure. We proposed that the normal pathway for cerebrospinal fluid (CSF) absorption includes transcapillary or transvenular absorption of CSF from the interstitial space and that the increase in cortical venous pressure is an initial event resulting in decreased absorption and subsequent hydrocephalus. Further analysis, however, suggests that increased cortical venous pressure reflects the effect of the failure of transvillus absorption with increase in CSF pressure on the venous pressure gradient between ventricle and cortex. Normally, the cortical venous pressure is maintained above CSF pressure by the Starling resistor effect of the lateral lacunae. A similar mechanism is absent in the deep venous system, and thus the pressure in the deep veins is similar to that in the dural sinuses. Decreased CSF absorption causes an increase in CSF pressure followed by an increase in cortical venous pressure without a similar increase in periventricular venous pressure. The periventricular CSF to venous (transparenchymal) pressure (TPP) gradient increases. In contrast, cortical vein pressure remains greater than CSF pressure (negative TPP). The elevated periventricular TPP gradient causes ventricular dilatation and decreased periventricular cerebral blood flow (CBF), a condition that persists even if the CSF pressure returns to normal, particularly if tissue elastance is lessened by tissue damage. If deep CBF is to be maintained, periventricular venous pressure must increase. Since the veins are in a continuum, cortical venous pressure will further increase above the CSF pressure.(ABSTRACT TRUNCATED AT 250 WORDS)