The aforementioned recent observations demonstrating a much greater prevalence of venous sinus obstruction in patients with PTS raise the question of what role venous sinus obstruction occupies in the aetiology of PTS. Clearly, in cases of cerebral venous sinus thrombosis the role has been defined. However, the nature of venous sinus obstruction in PTS is different. Both intrinsic and extrinsic lesions have been identified and both characteristically are found in the region of the junction of the middle and dis tal thirds of the transverse sinus close to the asterion of the skull. Before attempting to answer the question of whether the lesions are the cause or effect of raised intracranial pressure, the effects of primarily raising venous pressure on CSF pressure, and the reverse, will be examined in both the experimental and clinical settings.
Effects of Raised Venous Pressure in Adults and Children
Experimentally, early studies aimed not to produce PTS but rather hydrocephalus by increasing venous sinus pressure. Attempts to produce sustained increases in venous sinus pressure, particularly by occluding large venous conduits, usually failed [8, 32]. Dixon & Halliburton  increased venous sinus (torcular) pressure acutely in the dog and found a small increase in CSF pressure (approximately 25% of the increase in venous pressure). The difficulties in these earlier experiments probably related to the difficulties in isolating the venous circulation in most species of laboratory animals, the propensity for the development of venous collaterals and the existence of alternative routes of CSF drainage by pathways such as the cribriform plate .
The first study in which adequate occlusion of cranial venous outflow was achieved was that of Bering & Salibi  in dogs. The external and internal jugular veins were ligated in the neck proximal to the facial vein. The condyloid foramen was also occluded. After one week, a neck dissection was performed and any collateral venous drainage was ligated. Of the 21 dogs subject to this procedure 13 developed hydrocephalus. In almost all animals both the CSF and SSS pressures were elevated. In dogs that developed hydrocephalus, CSF pressure fell after a few days and remained below the SSS pressure. However SSS pressure also fell with time and was associated with the development of collaterals as demonstrated using sinography. Of the 8 animals that did not develop hydrocephalus, ligation was incomplete in one while another was killed the day of completion of the surgery. In the remaining six animals both the CSF pressure and SSS venous pressures increased. Also examined were the pulse pressures of the CSF and SSS. In the eight animals so examined, 3 developed hydrocepha-lus and these animals had higher pulse pressures than those that did not. The results were taken as evidence of a long suspected link between hydro-cephalus and venous sinus obstruction. However later studies did not confirm Bering and Salibi's findings. Guthrie et al.  obstructed the torcular and transverse sinuses of 10 adult dogs using cotton pledgelets in an attempt to produce hydrocephalus. Over a period of up to 29 weeks SSS pressure increased significantly as did CSF pressure. However both pressures fell towards 5 weeks and was associated with the development of venous collaterals around the torcular. There was no difference in ventric ular size at post-mortem. The result of the experiment, at least initially, was thus not hydrocephalus but PTS. It has also been suggested that the extent of dissection required to isolate the venous circulation in the animals of Bering and Salibi's study was so great that alterative routes of CSF drainage including the lymphatics were also compromised.
Clinically, venous sinus hypertension due to obstruction is known to result in PTS. The most common clinical example of this is the venous obstruction of the cerebral sinuses that occurs in cerebral venous sinus thrombosis (CVT). Cerebral venous thrombosis is the most well recognized cause of venous sinus hypertension and when venous sinus thrombosis is limited to the lumen of the sinus and does not involve cortical veins the clinical picture may be identical to PTS [18, 147]. The acknowledgement of venous sinus thrombosis as a cause of PTS syndrome is evident in the need to exclude venous sinus thrombosis in cases of PTS . This distinction between CVT and PTS is justified by the differences in management and prognosis of the two conditions . These issues aside CVT does demonstrate the clinical effects of venous sinus obstruction on CSF and intracra-nial pressures.
Venous sinus obstruction may also occur from non-thrombotic venous sinus obstruction. There are a few small series and a large number of case reports documenting PTS due to mass lesion both intrinsic and extrinsic to the venous sinuses that result in PTS. A non-exhaustive list of these published cases are presented in Table 1. Furthermore relief of the obstruction by removal of the offending lesion usually results in a reduction in CSF pressure and relief of clinical symptoms.
Venous sinus obstruction causes an increase in venous sinus pressure proximally. The effects of this raised cranial venous outflow pressure on the brain and CSF do not occur in isolation and so need to be considered together. Elevated venous sinus pressure affects both CSF absorption and production. The main site of CSF absorption is thought to be the arachnoid villi of the lateral lacunae and SSS's. The absorption process is a pressure-dependent process. Davson  demonstrated that the absorption of CSF depends on a pressure gradient between the subarachnoid space and the venous sinus of approximately 3 mmHg in health. Thus when venous sinus pressure is raised, CSF pressure must also rise in order for CSF absorption to continue. This explains why CSF pressure is usually a few millimetres of mercury higher than venous sinus pressure in cases where both pressures are monitored simultaneously. In addition to causing an increase in CSF pressure, venous sinus hypertension may also effect production. CSF production is for the most part a pressure-independent process in respect to CSF pressure. However, venous sinus hypertension will affect venous outflow from the site of CSF production, that is, the choroid plexus. As part of the mechanism of CSF production is filtration of plasma
Table 1. Case Reports and Series of Patients with a Pseudotumor Syndrome Secondary to Venous Sinus Obstruction of Various Aetiologies
across the choroid, the increase in venous sinus pressure, if the deep system is affected, might increase the hydrostatic pressure in the capillaries of the choroids plexus and increase CSF production. Kollar et al.  reported a case of PTS in a 5 year-old boy who had undergone embolisation of a deep temporal lobe AVM that drained via large venous varix into the vein of Galen. After embolisation a cerebral angiogram demonstrated that the vein of Galen did not fill and only sluggish flow in the straight sinus. The other dural sinuses were patent. The authors speculated that the venous outflow of the deep venous system would increase transcapillary CSF production in the choroid plexus. If this production was in excess of absorptive capacity, as may be the case if the system was underdeveloped, then PTS might result.
The other effect of raising venous sinus pressure is on venous outflow from the brain itself. Apart from perhaps the lumbar subarachnoid space, the cerebral venous system contributes most to the compliance of the intra-cranial space. Therefore, an increase in venous sinus and cerebral venous pressure increases the volume of the venous system proximal to the obstruction and reduces the compliance of the craniospinal axis. When venous sinus obstruction occurs, the high compliance cerebral venous system should increase in size and should be reflected in the observation of increased cerebral blood volume (CBV). In fact, Dandy  hypothesised that PTS was a result of increased CBV. Mathew et al.  calculated cerebral blood flow (CBF) and CBV before and after treatment using carotid injections of Xe133 and Tc99m. Both patients demonstrated increased CBV and this decreased towards normal when CSF pressure had been reduced. CBF was also slightly reduced in both cases prior to treatment and increased after CSF pressure reduction. Mathew et al.  stated that the cases provide evidence of venous engorgement. Raichle et al.  studied CBF, cerebral metabolic rate oxygen (CMRO2) and CBV using carotid injection of 15O-labelled water, oxyhaemoglobin and carboxyhaemoglobin. Compared to normal values there was a small but significant reduction in CBF of 18.5% (n = 9) and an increase in CBV of 33% (n = 8). In 3 patients, the studies were repeated after CSF was removed to lower ICP. CBF remained unchanged but there was a 10% reduction in CBV. Most patients had undergone cerebral angiography and no evidence of venous outflow obstruction was reported. In contrast, Brooks et al.  used positron emission tomography and steady-state inhalation of C15O2, 15O2 and 11 CO to study regional CBF, CMRO2 and CBV. No difference in any of these variables could be demonstrated between the 5 patients and 15 controls. In one patient, the study was repeated after lumbo-peritoneal shunting. CBF and CMRO2 appeared improved, at least in white matter. There was no change in CBV. Thus there is at least tentative evidence in a limited number of studies for an increase in CBV in PTS. Modern imaging techniques have yet to be applied to the study of CBV in PTS.
An increase in cerebral venous pressure will alter the Starling equation across the capillary bed as the venous outflow pressure and therefore capillary hydrostatic pressure is increased. This would normally result in an increase in ultrafiltrate and vasogenic oedema. There is little direct evidence for brain oedema in PTS. Although Sahs, Hyndman and Joynt [149, 150] provided histological evidence of brain oedema at post-mortem, their findings have been questioned on the basis of tissue preparation and artefact. Wall  could find no evidence of brain oedema in 2 patients with non-active PTS at post-mortem. However it should be clear that although there is no histological evidence supporting the finding of brain oedema there is no good evidence to refute such a claim.
More information has become available using MR imaging which has the ability to detect increased brain water. Early studies using low strength magnets without the benefits of diffusion weighted scans were contradictory. Connolly et al.  using qualitative examination of images obtained on a 0.15 Tesla magnet reported no signal change in 7 children with PTS. The same finding was reported by Silbergleit et al.  in 6 patients with PTS using a 0.35 Tesla magnet. Benefiting from improved technology, Moser et al.  used a heavily-weighted T2 MR technique (1.5 Tesla) to investigate the brain water content in 10 patients with PTS. They found an increase in the signal white matter free water content as reflected in prolongation of the T2 relaxation time. The authors concluded that this represents a diffuse low level of oedema. In addition, a triple-echo sodium MR technique was used to study 5 patients. Three demonstrated no change in their sodium signal. However, two patients who were clinically the most severely affected demonstrated increases in their sodium signal. As most sodium is extracellular, the authors concluded that the increase in brain water was likely to represent a vasogenic oedema. Sorenson et al. [161, 162] using diffusion sensitive sequences at 1.5 Tesla found that self-diffusion of white matter was increased. In some cases this was restricted to the periventricu-lar region while in others it was distributed throughout the brain.
Gideon et al.  investigated a group of patients with PTS using diffusion-weighted MR imaging. They applied a diffusion gradient in one direction only and found that diffusion was increased in 10 patients with PTS. These studies indicate that there is a small but significant amount of brain oedema in PTS. In contrast, a more recent study by Bastin et al.  in 10 patients could demonstrate no evidence of brain oedema in PTS. These authors also used diffusion-weighted imaging (1.5 Tesla) but obtained their images using diffusion gradients in three orthogonal directions and used echo planar imaging. This allows very short acquisition times and minimises the effects of bulk brain motion. Using echo-planar imaging and diffusion tensor imaging at 3 Tesla we performed a regional analysis of the brains of 5 patients with PTS and 6 normal healthy controls . Apart from small focal decreases in trace (diffusivity) in some grey matter regions, there were no differences in trace or the anisotropy of white matter regions between the two groups.
The effects of an increase in venous sinus pressure are therefore several although competing. Obstruction to cranial venous outflow appears to produce a balance between an increase in CSF pressure, capillary hydrostatic pressure, intraparenchymal pressure and CBV. This is brought about by these components being enclosed within the rigid cranium (the Munro-Kellie hypothesis). Although there is possibly a small increase in CBV, the pressure exerted on the parenchyma by an increased CSF pressure increases intraparenchymal pressure and so negates the ability of the increased capillary hydrostatic pressure to produce brain oedema. Thus the morphology of the brain does not appear to change although the intracra-nial pressure is increased and the compliance significantly reduced. A disturbance of this balance may be the reason for an increase tendency to wards slit ventricle syndrome in PTS after ventricular shunting and the formation of the acquired Chiari syndrome after lumboperitoneal shunting in PTS. That is to say, reducing CSF pressure in the presence of continued raised venous pressure will leave the increased capillary hydrostatic pressure unbalanced resulting in brain oedema and an increase in cerebral volume.
In neonates and infants the effects of raised venous sinus pressure are different from those in adults and children. Haar and Miller  as well as Rosman & Shands  catalogued a handful of cases of venous sinus obstruction with CSF circulation disorders. In patients under 18 months of age hydrocephalus developed while in those over 3 years of age PTS resulted. Both groups concluded that whether venous sinus obstruction results in hydrocephalus or PTS depends on the state of the cranial sutures [60, 146]. This difference in clinical expression of venous sinus hypertension was demonstrated experimentally by Olivero & Asner . Occlusion of the posterior sagittal sinus in 10 craniectomised rabbits caused a moderate but significant increase in ventricular size compared to 5 animals that had undergone sinus occlusion but not craniectomy (distance from head of caudate to junction of septum pellucidum and corpus callosum: 7.2 +/— 0.7 mm compared to 4.6 +/— 0.5 mm).
Clinically, like in adults and older children, there are a large number of case reports in which various problems have caused venous hypertension (Fig. 1). However, instead of PTS, these cases develop hydrocephalus. These case series and reports are presented in Table 2. Although in some reports or series the age of the patients is greater than 18 months almost all cases had evidence of increasing head circumference from in the neonatal period. In some cases relief of the obstruction may produce relief of hydrocephalus and/or megalencephaly.
Due to these observations, there has been a gradual recognition of the role of venous sinus hypertension in the aetiology of some forms of infantile hydrocephalus and megalencephaly that have previously been thought to occur through other mechanisms. This is particularly true in achondro-plasia  and patients with myelomeningoceles. More recently, venous outflow obstruction has been implicated in the aetiology of ventriculome-galy commonly seen in various forms of osteopetrosis .
Achondroplasia is frequently associated with hydrocephalus and mega-lencephaly. Growth in head circumference is most prominent in the first few months of life and is followed by a period of stabilisation between the 4th and 24th months. Pierre-Kahn et al.  found clinical evidence of increased prominence of venous collateral circulation in 17 of 18 patients with achondroplasia. One patient underwent angiography that depicted
Table 2. Case Series and Reports of Hydrocephalus Resulting from Venous Sinus Obstruction of Varying Aetiology
Agenesis of arachnoid granulations 2 (children)
CCF/Glenn procedure 1 (infant)
Congenital abnormality SSS 2 (children)
SVC syndrome 3 (infants)
Cystic Fibrosis 3 (infants)
Posterior fossa tumour compressing lateral 4 (children) sinus
Craniostenosis and achondroplasia 4 (children)
Achondroplasia and jugular foramen stenosis 10 (children)
SVC syndrome 1 (infant)
SVC syndrome (thymic hyperplasia) 1 (infant)
AVM draining to both lateral sinuses 1 (16 years)
Cerebral AVM 2 (infants)
Cerebral AVM - vein of Galen 1 (infant)
Jugular vein thrombosis - TPN 4 (infants)
severe bilateral sigmoid sinus stenosis at the level of the jugular foramen. Friedman & Mickle  also reported a case with bilateral venous outflow obstruction at the level of the jugular bulb. Steinbok et al.  studied four achondroplastic children with active hydrocephalus using retrograde venography and documented significant venous hypertension in at least 2 patients associated with jugular vein stenosis and superior vena caval obstruction at the level of thoracic outlet. Furthermore, Lundar et al.  reported a case of achondroplasia with active hydrocephalus. Digital subtraction angiography demonstrated severe bilateral venous outflow obstruction at the foramen magnum. Operative decompression of the right sigmoid sinus and its junction with the jugular vein at the foramen was undertaken. A bony spur was found to be kinking the vein. Improved venous outflow was confirmed radiologically. Head circumference decreased and growth normalised.
Venous sinus obstruction is also common in craniosynostosis. Rollins et al.  using MRV studied 17 patients with craniosynostosis and a mean age of 7.3 years (4 months-34 years). The authors concentrated on the patency of the sigmoid sinus and jugular veins. No comments were made on the transverse sinuses. In 12 patients the MRV was abnormal. In 9 patients there was venous outflow obstruction at the sigmoid sinus and/or jugular bulb while in 3 patients there was jugular vein obstruction. Of these patients 9 had hydrocephalus. Venous sinus obstruction was associated with enlargement of collateral venous drainage particularly via the posterior condylar veins. Two of 11 patients with hydrocephalus had a normal MRV. However, the results of this study are difficult to interpret given the age of the patients and the time since the initial surgery in most cases. Taylor et al.  studied 23 such patients with digital subtraction angiogra-phy. ICP monitoring confirmed raised pressure in 21 cases and in 2 cases plain X-ray suggested the presence of large transcalvarial venous collateral drainage. In a total of 24 angiograms there was a greater than 50% stenosis or no flow in the sigmoid-jugular venous complex in 18 patients; in 7 unilateral and 11 bilateral. Of these 18 angiograms, florid transcalvarial collateral venous flow via a large stylomastoid emissary vein was observed in 11 cases. The severity of the stenosis did not correlate with ICP but did appear age-related. The mean age of patients with bilateral stenosis was 20.4 months, unilateral stenosis 25 months and 54 months in those with mild or no stenosis. The authors conclude that patients with more severe venous outflow obstruction tend to present with raised ICP earlier.
The importance of the state of the cranial sutures for the clinical manifestation of venous sinus obstruction is exemplified by the condition of cra-niosynostosis. If ICP is raised, this may manifest itself in several ways. Most commonly, raised ICP is noted after investigation for behavioural alteration or papilloedema. In the presence of normal or small sized ventricles, raised ICP is frequently attributed to inadequate intracranial volume and craniostenosis. However hydrocephalus is also recognised as occurring in association with craniosynostosis, particularly in syndromic cases where multiple sutures and the skull base are involved . Hydrocephalus may occur with or without head enlargement . Hydrocephalus with head enlargement may occur in the presence of sufficient uninvolved sutures or after the surgical suture release or cranial vault remodelling.
Cinalli et al.  reviewed 1727 cases of craniosynostosis. Of the 1447 cases of non-syndromic craniosynostosis, the prevalence of hydrocephalus at presentation requiring shunt insertion was just 0.28%; similar to the normal population. Two of these cases with complex craniosynostosis exhibited bilateral jugular foraminal narrowing. In comparison, syndromic cases of craniosynostosis (280) had a prevalence of hydrocephalus requiring a shunt of 12.1%. Non-progressive ventriculomegaly was seen in 15.7%. Hydrocephalus was most common in patients with Crouzon's disease (54%) and all of these patients had either their coronal, sagittal or both sutures open at the time of ventricular enlargement. In the other patients hydrocephalus occurred after surgical correction and all of these had had more severe craniosynostosis with fusion of both the coronal and sagittal sutures. Angiography demonstrated bilateral jugular vein stenosis in 13/16 patients (81.3%) examined. Of the patients with Apert's syndrome, progressive hydrocephalus requiring shunting was less common (6.5%) al though 18 (23.7%) had non-progressive ventriculomegaly at presentation and another 12 developed ventriculomegaly not requiring shunting after surgery. Thirteen patients underwent angiography and 7 demonstrated jugular venous obstruction (53.8%).
To summarise, venous sinus hypertension produces an increase in CSF pressure. Whether hydrocephalus or PTS results depends on the state of the cranial sutures. Where the cranial sutures are fused, such as in adults, older children and infants with severe forms of craniosynostosis, raised venous pressure causes a PTS syndrome. There is an increase in CSF pressure and a reduction in intracranial compliance. Available evidence suggests that brain oedema does not occur and that there may be either a small or no increase in CBV. If the cranial sutures are patent, such as in the infant, hydrocephalus results as the raised CSF pressure is allowed to act on the cerebral mantle and cranium.
In conditions that affect the CSF circulation and raise CSF pressure there are secondary effects on the cerebral veins and the dural venous sinuses. The cerebral veins must cross the subarachnoid space in order to reach the sinuses or lateral lacunae. At this point they are prone to compression by raised CSF pressure. The lateral lacunae, because of their wide surface area, are even more prone to compression and may assist in maintaining the patency of the cerebral venous outflow. It is also proposed that in health, these structures act as Starling resistors regulating CSF absorption according to changes in CSF pressure. That is when CSF pressure is high, the lacunae collapse, decreasing venous flow, dropping sinus pressure, increasing the gradient across the arachnoid villi and increasing CSF absorption.
The dural sinuses are enclosed between the two layers of the dura. The SSS and the transverse sinuses are triangular in cross section with their base on the dura lining the skull. At the apex of the triangle the other dural leaves fuse such that the walls of these sinuses are held open by the falx cerebri and tentorium cerebelli. The sigmoid sinus also appears protected as it usually runs in a deep groove to the jugular foramen. The assumption usually made is that the sinuses are not compressible due to the structures that maintain their shape. However, the sinuses, particularly the transverse sinuses, may be compressed due to significantly raised intracranial pressure as demonstrated by a number of experimental and clinical studies (vide infra).
Cushing  studied the effects of raised CSF pressure on the SSS of the dog and reported that increased CSF pressure resulted in SSS collapse. Wright  later repeated the study, again in the dog, but found that this collapse only occurred when the dura surrounding the sinus had been incised. He did however demonstrate that pressures within the SSS were af fected by CSF pressure in the subarachnoid space. Both Becht  and Weed & Flexner  reported that venous sinus pressures were not influenced by changes in CSF pressure. In contrast Dixon & Halliburton  reported that increases in CSF pressure were accompanied by increases in torcular venous pressure. However, Wright  and Bedford  noted that increases in CSF pressure caused a small decrease in venous sinus pressure. This effect was usually seen as CSF pressure was initially being increased and most likely represented a compressive effect on the cerebral veins in the subarachnoid space and a decrease in venous return to the SSS. In terms of the relationship between the venous sinuses and CSF pressure, the arrangement of venous sinuses in the dog is different from that in humans in that the torcular and lateral sinuses are encased in bone and thus protected from any compressive effects. The applicability of these early studies to human physiology is therefore questionable.
Langfitt et al.  reported the effects of increasing ICP using a sub-dural balloon in the rhesus monkey. Initially, SSS pressure decreased, increased or was unchanged. When ICP approached 30 mmHg SSS pressure began to rise. The transverse and sigmoid sinus pressures were influenced far less by changes in ICP. The authors reported that a gradient was demonstrated in some instances between the SSS and distal transverse sinus. In an extension of that study, Shapiro et al.  described the morphological changes of the cerebral venous system that took place in the rhesus monkey during fatal increases in ICP due to brain oedema. These animals demonstrated collapse of the SSS and straight sinuses presumably secondarily to compression. However, as ICP approached arterial pressure in these animals the implications of the results are not clear. Johnston & Rowan's  study of the effects of raised intracranial pressure on cerebral venous blood flow in baboons also demonstrated that the sinuses may collapse with increasing ICP. Using saline infusion into the cisterna magna of 6 baboons to raise ICP, cortical venous pressure was noted to rise linearly with ICP and remained above subarachnoid CSF pressure at all times. Animals demonstrated two distinct patterns of SSS pressure response. In 3 animals SSS pressure remained less than 20 mmHg while in the other 3 animals SSS pressure rose linearly once ICP reached 40 mmHg and remained just below cortical venous pressure.
In man, Greenfield & Tindall  performed cerebral angiography on 3 patients at normal and raised CSF pressures and found compression of the cerebral veins in the subarachnoid space or of the venous sinuses. Kinal  performed sinography on 4 patients (age 7 months-15 years) who presented with evidence of a posterior fossa lesion. In all patients the lesions had resulted in obstructive hydrocephalus with raised pressure. Sinography revealed bilateral transverse/sigmoid sinus stenosis with development of venous collateral circulation. Removal of the posterior fossa lesions resulted in improvement in venous sinus flow demonstrated by opacification of the transverse/sigmoid sinuses and the disappearance of venous collaterals on sinography.
Osterholm  performed antegrade cerebral venography in patients with subdural (4 patients) or extradural (1 patient) haematomas. SSS pressure was measured and venography was performed immediately prior to operative decompression. Venous sinus pressure was 21-46 cm saline and venography demonstrated bilateral transverse sinus stenosis with opacifica-tion of venous collaterals. Cerebral decompression resulted in a fall in venous pressure to 0-4 cm saline and venography showed normally filling transverse sinuses without opacification of venous collaterals. To further examine the secondary collapse of the venous sinuses as a result of increasing ICP, Osterholm  also performed experiments on 3 fresh human cadavers. Into the anterior SSS was perfused 600 ml/min of saline. Distally the SVC was open. Ventricular and cisterna magna CSF pressures were monitored. Infusion of normal saline into the cisterna magna allowed ICP to be raised in 10 mmHg increments. No change in SSS flow was appreciable below 20 mmHg. At 50 mmHg there was a 30% flow reduction, at 70 mmHg there was a 60% SSS flow reduction and at 200 mmHg SSS flow was arrested.
Martins et al.  monitored CSF pressure and SSS pressure simultaneously in 12 patients undergoing ventriculography who were subsequently found to have cerebral tumours. In 9 patients SSS pressure was not related to CSF pressure and remained below 14 mmHg in the presence of spontaneous or artificial increases in CSF pressure up to 75 mmHg. On venogra-phy performed in 2 of these patients there was no change in CSF pressure while in the third patient there was a partial collapse of the transverse sinus at 40 mmHg despite there being no change in SSS pressure when CSF pressure was higher. In 3 patients, SSS pressure changed with ICP. In 2 patients it increased but to a lesser extent than CSF pressure while in another patient CSF pressure and SSS pressure remained closely related throughout. In one patient who demonstrated an increase in SSS pressure with increased CSF pressure there was partial collapse of the sagittal and transverse sinuses at 40 mmHg. In addition Martins et al.  noted that 3 patients had pressure waves during recording. In 2 patients the duration was less than 1 minute. These patients had no change in SSS pressure during the pressure wave. In contrast, the third patient experienced a pressure wave of 5 minutes and this was associated with an increase in SSS pressure.
The ability of increased CSF pressure to cause venous sinus obstruction is also seen in infants with hydrocephalus. Shulman and Ranshoff  measured CSF and SSS pressures of 15 such cases of varying causes and included both communicating and non-communicating forms of hydroce-phalus. They found a close relationship between the SSS pressure and CSF
pressure and the ratio of the former to latter was 1.08. By plotting the SSS pressure versus the CSF pressure they found a regression co-efficient of 0.95 with a standard error of 0.08 indicating that SSS pressure and CSF pressure were closely related in these patients. In some patients CSF was allowed to drain while CSF pressure and SSS pressure were recorded simultaneously. The regression slop of this curve was 1 and bisected the SSS pressure axis at approximately 30 mmH2O (probably reflecting the venous outflow pressure). The authors postulated that the increase in SSS pressure was secondary to increased CSF pressure collapsing the sinus near the point of outflow from the skull. In 3 infants antegrade venography was performed. In 2 infants the sinuses appeared normal while in a third the lateral sinuses appeared to taper on each side and end in the jugular foramen. Collateral drainage was provided by enlarged parietal and mas-toid emissary veins.
Norrell et al.  studied SSS and CSF pressures in 30 infants with hydrocephalus. Eleven patients had myelomeningoceles. CSF pressure exceeded SSS pressure in 12 patients, SSS pressure exceeded CSF pressure in 8 cases and the pressures were equal in 10 cases. SSS pressure was elevated more frequently in patients with myelomeningoceles (9/11) compared to those without (9/19). Of the non myelomeningocele group none of the patients with aqueduct stenosis had elevated sinus pressures compared to 9 of the 14 patients with communicating hydrocephalus. Adequate venog-raphy was performed in 28 patients. In 18 cases both lateral sinuses were opacified whereas only one sinus opacified in 10 cases. In the 17 patients without myleomeningoceles, the anatomical position and arrangement was considered normal. In one case there was stenosis of the lateral sinus. In 11 patients with myelomeningoceles, anatomical arrangement of the venous system was abnormal and consisted of a low lying torcular with the transverse/sigmoid sinuses running directly forward around the foramen magnum to the jugular bulb. Four of these patients had venography performed at CSF pressures of 10 and 60 cmCSF. This increase in ICP caused a partial or complete collapse of the lateral sinuses, an increase in opacifi-cation of emissary collateral veins, delayed sagittal sinus emptying time and a parallel rise in SSS pressure in all cases. Lateral sinus obstruction was not seen when the CSF pressure was elevated in hydrocephalic infants without myelomeningoceles and there was no change in emptying time.
These findings demonstrate that the falx cerebri and tentorium cerebelli do not afford protection of the cerebral venous sinuses from increased CSF pressure. There also appears to be considerable differences between individuals as to when secondary collapse of the sinuses occurs. The most common site of secondary compression of the venous sinuses is the distal transverse sinus; the same site that venous sinus obstruction is observed in PTS. It is possible that secondary venous sinus compression may be important in maintaining the patency of more proximal venous channels and or have some other important role. In addition, it appears that in some conditions such as myelomeningocele with Chiari malformations, abnormally positioned venous sinuses may be more exposed to CSF pressure elevations.
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