Venous Sinus Obstruction in Pseudotumor Cerebri Syndrome Cause or Effect

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Whether venous sinus obstruction in PTS is cause or effect remains unresolved. The experimental and clinical evidence discussed above indicates that there is potential for primary venous sinus pathology to cause PTS and there is also potential for secondary venous sinus obstruction due to raised intracranial pressure. We discuss below the available evidence and also present a unifying theory based on the establishment of a disordered positive feedback cycle. The discussion will centre on the site of venous obstruction, the morphology of venous sinus obstruction and the effects of removing venous sinus obstruction.

Venous sinus obstruction in PTS is most commonly, although not exclusively, seen in the transverse sinus. This is very commonly at the junction of the distal and middle thirds of the sinus. It co-incides with the area of the skull at which a number of bony sutures meet called the asterion. Other regions that may demonstrate stenosis are the other portions of the transverse sinus, posterior third of the SSS, sigmoid sinuses and jugular bulb. This point appears to be the same site at which compression of the venous sinuses takes place when CSF pressure is raised in experimental and clinical studies. If the venous sinuses are considered as a series of collapsible tubes then collapse of the tubes in such a system tends to occur at its distal end. However, it is also the most common site for the location of large arachnoid granulations that are known to cause obstruction of the transverse sinuses.

The symmetrical bilateral nature of the obstructions is also a consistent finding. This is important because, although the right transverse sinus is dominant in most cases, there is usually sufficient communication through the torcular Herophili to overcome a unilateral obstruction. The exception occurs in cases where one sinus is atretic or hypoplastic; usually the left. In these cases unilateral venous sinus obstruction may be sufficient to compromise venous outflow sufficiently to produce symptoms.

Morphologically, there are four basic types of lesions that obstruct the venous sinuses: extrinsic compression and intrinsic lesions of three main forms (Fig. 2). Extrinsic compression may be implied from the appearance of a smooth tapering of the sinus. This appearance tends to indicate that increased CSF pressure may be secondarily collapsing the venous sinus. Intrinsic lesions are of three main types: 1) broad-based lesions with an undu-

Arachnoid Granulation Mrv

Fig. 2. Various forms of focal venous sinus obstruction in the transverse sinuses of 4 patients. Intrinsic filling defects are obvious in the top two radiographs being an arachnoid granulation (A) and a broad based undulating lesion (B). Of the lower two, the radiograph on the left (C) could be a focal stricture or extrinsic compression while the radiograph on the right (D) appears to indicate secondary venous sinus compression or irregularity due to old thrombus

Fig. 2. Various forms of focal venous sinus obstruction in the transverse sinuses of 4 patients. Intrinsic filling defects are obvious in the top two radiographs being an arachnoid granulation (A) and a broad based undulating lesion (B). Of the lower two, the radiograph on the left (C) could be a focal stricture or extrinsic compression while the radiograph on the right (D) appears to indicate secondary venous sinus compression or irregularity due to old thrombus lating surface that are of unknown aetiology. These may be difficult to distinguish from extrinsic compression but may require significant pressure application during stent deployment indicating the presence of a focal sten-otic lesion (Fig. 3); 2) Abnormally large arachnoid granulations forming a round well defined filling defect in the venous sinus (Fig. 4), and; 3) Irregular lesions suggesting old thrombus.

Arachnoid granulations are most frequently reported as incidental findings on angiography, contrast enhanced CT or MR imaging [22, 142]. The true incidence and range of variation of 'normal' arachnoid granulations in a large series of asymptomatic individuals is yet to be established. On angiographic studies, arachnoid granulations of small to moderate size are frequently seen as filling defects of the sagittal and transverse sinuses. An example of a likely arachnoid granulation causing venous sinus obstruction

Dural Sinus Stenosis Stent
Fig. 3. Bilateral venous sinus obstruction. During the deployment of the stent, significant pressure was required in order to overcome this focal venous sinus stenosis

was provided by Arjona et al. [4] who reported a case of PTS in a 51 year-old man where the venous phase of cerebral angiography demonstrated the lesions protruding into the transverse sinus. On contrast enhanced CT arachnoid granulations are usually seen as round or oval hypodense lesions within the dural sinuses. They are best appreciated on fine slice contrast enhanced CT which may be more sensitive than MR for small lesions [96]. On MR, arachnoid granulations are of variable signal on T1-weighted images and hyperintense on T2 weighted images. Compared to CSF, arachnoid granulations are usually isointense to CSF on T1 weighted, T2 weighted and FLAIR MR imaging but may also have signal characteristics suggesting fat content. Their appearance is variable on proton density images [70] and may be altered by the presence or absence of calcification [142]. Oblique views on MR venography may give the impression of elongated lesion that may be mistaken for thrombus [142].

Roche & Warner [142] reported 41 arachnoid granulations in 32 patients (17 males and 15 females) on either CT or MR imaging in a 5 year period. Thirty-five (85.4%) of the arachnoid granulations were found in the distal or middle thirds of the transverse sinus. One or more vessels were closely associated with the granulation in 16 cases and appeared to enter 4 granulations. There were 2 arachnoid granulations located at the torcular and 4 in the sigmoid sinuses. Leach et al. [96] found 168 arachnoid granulations in 138 patients (24%) on reviewing 573 contrast enhanced CT scans; 92% of the granulations were found in the transverse sinus, especially in the middle and lateral parts. A vein entered the sinus adjacent to the granulation in 62% of cases and there was a tendency to increased incidence with age. There was no difference in the male to female distribution. On reviewing 100 MR scans there were 14 granulations identified in 13

Superior Sagittal Sinus Lesion Scan

rt rt cr

Fig. 4. A Patient with PTS with an intrinsic lesion on venography with a pressure gradient. On review of the MR images focal lesions were demonstrated in the transverse sinuses of both sides. These may represent either large arachnoid granulations or fat within the sinuses

Fig. 4. A Patient with PTS with an intrinsic lesion on venography with a pressure gradient. On review of the MR images focal lesions were demonstrated in the transverse sinuses of both sides. These may represent either large arachnoid granulations or fat within the sinuses

patients; 85% were closely associated with a vein draining into the sinus. Ikushima et al. [70] reviewed static MR images of 1118 patients. Arachnoid granulations were present in 8.3% of males and 12.2% of females. A total of 134 arachnoid granulations were found with an overall incidence of 10%. In 14 patients there were was more than one granulation. The most common site of the granulations was the transverse sinus (85.8%).

In Browder et al.'s. [20] report arachnoid granulations were described as benign tumours of the cerebral venous sinuses. In an anatomical study of 295 sinuses, 25 arachnoid granulations were identified; all but 2 were in the transverse sinuses. Of those in the transverse sinuses they were almost always associated with the vein of Labbe as it entered the sinus. Mamour-ian & Towfighi [107] studied 10 patients without known venous sinus disease, 2 patients were found to have giant arachnoid granulations of the distal transverse sinus. In one patient there were bilateral lesions. Leach et al. [96] reported on the inspection of the sinuses of 29 cadavers for the presence of focal intraluminal protuberances. Ninety-one protuberances were observed in 19 cases (66%) and ranged in size from less than 1 mm to 8 mm diameter. Ninety-five percent were located in the transverse sinus -predominantly the left. In Rosenberg et al.'s [145] report of 4 cases of giant arachnoid granulations presenting as osteolytic skull lesions, histological examination demonstrated loss of the normal stromal organisation. Instead large CSF filled cystic spaces were seen. Upton et al. [175] reported on the structure of arachnoid granulations obtained from 23 autopsies. There was a tendency for the granulations to become larger and more complex with age.

Given the typical site and the correspondence with intrinsic lesions seen on MRV or DRCV, arachnoid granulations may represent a proportion of the obstructing lesions in PTS. While the natural occurrence suggests a primary role for these lesions, they may increase in size secondary to increases in CSF pressure for a number of reasons. In animals, arachnoid granulations may increase in size with increases in CSF pressure [54, 100]. It may also be that increased CSF pressure increases the CSF component of the arachnoid granulation which becomes incarcerated in the lumen of the sinus further exacerbating the increased CSF pressure. An increase in the size of the collagenous core of the granulation may also increase its size. Chronic inflammation of this core may result in such an increase [175]. Hayes et al. [62] studied the effects of dietary vitamin A deficiency in calves and rats and confirmed Eaton's [39] finding that it resulted in increased CSF pressure. Histological examination of the arachnoid granulations in rats and calves revealed the granulations to be larger in the vitamin A deficient animals compared to controls. This was particularly so along the transverse sinuses of the calves. The increase in size of the granulations was associated with an increase in collagen with stimulation of fibroblasts with an increase and extreme dilation of the golgi endoplasmic reticulum of these cells. Hernias of brain tissue into the core of arachnoid granulations may also result in enlargement of the granulation. Kollar et al. [87] reported a case of where an abnormally large arachnoid granulation was removed and the histological sections published clearly demonstrate a hernia of brain into the granulation. The authors at the time described this as 'ectopic' brain tissue but the true nature of the lesion is evident. Small hernias of brain tissue are frequently seen in the bases of arachnoid granulations at craniotomy (M Besser; personal communication).

There are various other pathological entities that may be represented in the spectrum of obstructive intrinsic venous sinus lesions. Fat deposits in the dural sinuses on CT was reported by Tokiguchi et al. [173]. These authors reported 8 cases in which macroscopic, non-obstructing fat deposits were demonstrated in the walls of the sinuses. In 5 cases fat was located at the torcular while in 3 it was located in the SSS. Anatomical proof that these lesions did indeed consist of fat was supplied in a later report where 2 of these patients had later undergone autopsy [174]. Finally, nodules of cavernous tissue have been identified in the sinuses, especially at the junction of the straight sinus and vein of Galen [13, 95]. The nodules, distinct from arachnoid granulations, were common at autopsy and were composed of endothelium lined sinusoids resembling erectile tissue.

Cerebral venous sinus thrombosis (CVT) may also contribute a proportion of the cases of PTS. Acute CVT should be distinguished from chronic CVT. In the former, provided the thrombus does not involve the cortical veins, the condition may certainly cause a pseudotumor syndrome [14, 99, 159]. The approach to management of these patients is quite different. The prevention of thrombus propagation and dissolution of the thrombus are important in the management [12]. Thus anticoagulation either sys-temically or locally via the endovascular route are used. Persistence of thrombosis with reorganisation and recanalisation may result in improved cerebral venous outflow. In such cases intrinsic venous sinus obstructive lesions may represent old thrombus. However, more frequently such chronic CVT cases appear to have less focal stenosis and may be difficult to treat.

There is also significant circumstantial evidence for a role of occult CVT in PTS from the association of a large number of prothrombotic states. These associations include the thrombophilias [81, 101, 112, 119] as well as other prothrombotic states such as essential [118] and iron deficiency anaemia [69]. This association between prothrombotic conditions and PTS was reviewed by Sussman et al. [169]. A mixed group of 38 retrospectively and prospectively accumulated patients. Eighteen patients were subject to angiography and three patients were found to have venous sinus thrombosis although the location and other details were not given. Each of these patients had a prothrombotic disorder.

In order to test whether the venous obstruction is primary or secondary one may either relieve the obstruction and observe the effects on CSF pressure or, reduce CSF pressure and observe the effects on venous obstruction. However even these measures may not produce a conclusive result due to the nature of positive feedback loops which can be interrupted without producing conclusive information on causation. For example, stopping chickens breeding does not determine whether the chicken or the egg came first.

King et al. [85] reduced CSF pressure in a total of 21 patients with PTS for which no obvious cause was found (for example minocycline) were examined using venography and manometry. With the exception of 2 patients, SSS and CSF pressures followed each other closely. In these patients there were transverse sinus stenoses with significant pressure gradients. Of these patients 8 underwent C1-2 puncture with removal of 2025 mls CSF. Manometry was then repeated. The procedure was also performed on 3 patients with so-called non-idiopathic PTS. The drop in CSF pressure produced by C1-2 puncture was measured in only 3/11 patients. The reductions were 40, 23 and 10 cm CSF. All patients had a reduction in the proximal venous sinus pressures. In 5/8 idiopathic PTS patients, the pressure gradient in the transverse sinus disappeared. In 2 other patients in this group the gradient remained although it was reduced. One patient had no transverse sinus obstruction or gradient before C1-2 puncture. Of the 3 patients with so-called non-idiopathic PTS who were examined after C1-2 puncture, two patients had no venous pressure gradient to begin prior C1-2 puncture. The results of the patient with a high CSF pressure and a transverse sinus pressure gradient prior to C1-2 puncture are difficult to interpret as although proximal venous pressure fell to 10 mmHg, the distal sinus pressure was not recorded.

Given the reduction in venous sinus pressures and associated pressure gradients after C1-2 puncture and the CSF pressure reduction, the authors [85] and others [25] concluded that transverse sinus obstruction in PTS was a result of raised CSF pressure but not the cause. However, such a conclusion is difficult to justify on the basis of these results. First, although no normal healthy controls were examined, venography and manometry were performed on 10 patients with diseases other than idiopathic PTS. CSF pressure was raised in 7 patients (20-50 cmCSF) but venography and man-ometry demonstrated transverse sinus gradients in only 3 (43%) of these patients. In the other four there was no evidence of venous sinus hypertension. In comparison, of the 21 patients with idiopathic PTS venous sinus hypertension with transverse sinus pressure gradients were found in 19 (90%). Although the average CSF pressure was higher in the idiopathic PTS group, the higher incidence of venous sinus hypertension indicates that it may be an aetiological factor. Second, the results indicate that venous sinus pressure fell almost universally after C1-2 puncture. This is an expected outcome even in the presence of a fixed venous sinus stenosis. In at least 2 patients, the venous sinus gradient remained although reduced. Finally, the authors avoided the issue of morphological change in the stenoses after C1-2 puncture. Although they allude to the presence of either tapering or intraluminal filling defects on pre-C1-2 puncture venograms they were unable to state whether these lesions were present or absent after CSF pressure reduction. The heterogeneous nature of the stenosing or obstructing lesions means that the conclusions of the authors may only be valid for one subtype of obstructing lesion, in particular extrinsic compression.

In support of King et al. is a case report by McGonigal et al. [115] who document a case of bilateral transverse sinus obstruction in a 19 year old with quite severe PTS. The obstructions had the appearance of a smooth tapering on CT venogram. After insertion of a lumboperitoneal shunt symptoms resolved and there was marked improvement in the degree of narrowing bilaterally. Higgins and Pickard [66] also reported resolution of venous sinus obstruction in a very similar case after lumboperitoneal shunting. We have also observed this phenomenon after ventriculoperiteo-neal shunting in one case. In contrast, morphological and functional venous sinus obstruction in the presence of a functioning shunt has been observed in 2 of 8 cases from our series and in 2 patients in the series of Higgins et al. [63].

Sainte-Rose et al. [151] studied the relationship between CSF and venous pressures in 31 infants (age 1-23 months). These patients consisted of 6 cases of communicating hydrocephalus, 6 cases of hydrocephalus associated with a myelomeningocele, 14 cases of craniostenosis, 3 cases of achondroplasia and a case each of aqueduct stenosis and subdural haema-toma. In the first part of the study, consisting of a group of 11 infants mainly with craniostenosis, intraventricular CSF and SSS venous pressures were recorded simultaneously. In all patients the difference between CSF and SSS venous pressures were small (< 3 mmHg). CSF pressure was elevated (15-25 mmHg) in 8 patients but there was no relationship between underlying pathology and pressure recordings. In the second part of the study, a second ventricular catheter was also introduced to allow CSF pressure reduction via CSF withdrawal. The jugular venous pressure was also monitored. In 16 of 20 patients, after withdrawal of CSF to reduce CSF pressure to zero, SSS venous pressure also fell to the jugular venous pressure. Re-injection of the same volume of CSF usually restored CSF pressure to the same or a slightly higher CSF pressure than at baseline. SSS venous pressure also increased to baseline. In these patients there was no evidence of sigmoid sinus compression on sinography. In the remaining 4 patients; two with achondroplasia and two with craniostenosis; SSS did not decrease to the jugular venous pressure when CSF pressure was reduced to zero. Instead illustrated traces demonstrate a modest fall in SSS pressure.

Also suggestive of a fixed obstruction was the finding that reinjection of CSF produced a rise in SSS pressure above baseline. Fixed venous sinus obstruction of the transverse or sigmoid sinus was confirmed on sinography.

The effects of relieving the venous sinus obstruction in PTS have also been studied. The results of these studies will be considered fully in the section on treatment (vide infra). However, it is clear that reduction of venous sinus hypertension in PTS may result in rapid clinical resolution and a reduction in CSF pressure. Of the cases reported to date, significant clinical improvement was apparent in 4 of 4 cases in our series [130] and in 8 of 12 cases in the series from Cambridge [63]. These results, along with the observation that some obstructions are intrinsic, indicate that venous sinus obstruction in PTS may have a primary aetiological role, possibly exacerbated by raised ICP due to disordered positive biofeedback.

It is clear that arguments exist for primary and secondary aetiological roles for venous sinus obstruction in PTS. Certainly there are cases in which either may exist. Failure of treatment of venous sinus obstruction in a handful of cases indicates that it may be important to differentiate between the two. However, there may be a role for treatment of the obstruction whether the obstruction is primary or secondary. The argument for treatment of primary lesions is intuitive; however secondary venous sinus obstruction may exacerbate any underlying CSF circulation disorder; an argument supported by King [85] and Quattrrone et al. [137]. When CSF pressure becomes increased and venous sinus obstruction ensues, the compliance of the craniospinal axis is reduced because of engorgement of the cerebral venous compartment. Therefore small increase in CSF or blood volume will cause rapid increases in CSF pressure. More importantly though, if CSF pressure is increased sufficiently to overcome venous pressure and collapse the sinuses, venous pressure must increase in order to overcome the obstruction and maintain adequate cranial venous outflow. Venous sinus hypertension therefore becomes increased. Ifthe primary problem is one of CSF absorption and raised Rcsf, then in order for CSF absorption to continue, the pressure gradient between the subarachnoid CSF must be even higher than the normal gradient of 3 mmHg. CSF pressure must rise further and thus a vicious circle of rising CSF pressure, venous sinus obstruction and rising venous sinus pressure is established. Treatment of the venous sinus obstruction may interrupt this positive feedback loop and restore the normal compliance of the cerebral venous compartment.

We therefore propose the following unifying hypothesis. Normally, increased CSF pressure leads to increased CSF drainage and restoration of normal CSF pressure, representing classical physiological biofeedback control where the response of the system has a negative effect on the stimulus (Fig. 5) [59]. In PTC, with venous abnormalities, the presence of the lesion in the venous outflow system creates a possibility for an abnormal

CSF pressure

Cerebral venous pressure (not recruited into system)

Fig. 5. Normal negative feedback. Increases in CSF pressure are controlled by an increase in the rate of CSF absorption as it is a pressure dependent process positive biofeedback to develop as increases in CSF pressure can worsen the degree of venous compromise leading to a further increase in CSF pressure, a further increase in venous obstruction, and so on (Fig. 6). The degree to which cerebral venous pressure is recruited into the control system could determine the extent to which CSF pressure rises until other negative feedback mechanisms (for example, CSF absorption through other routes) become significant and re-establish control of CSF pressure at a higher level. Recruitment of cerebral venous pressure into this control system is variable, and due to a variety of factors, potentially explaining the variability of PTC symptoms over time. The prolonged benefit produced by a single CSF tap in PTC patients may be understood in this way if one postulates that removal of CSF reduces secondary venous compression and improves CSF drainage due to uncoupling of cerebral venous pressure from the control system for a period much greater than that required to re-

CSF pressure

CSF Drainage

Cerebral venous pressure (recruited into system)

Degree of symptoms

Fig. 6. Disordered positive feedback. Recruitment of the cerebral venous sinuses into the feedback loop due to venous sinus collapse, secondary to increased CSF pressure, causes venous sinus pressure ( particularly SSS pressure) to increase. This inhibits CSF drainage and results in further increases in CSF pressure and so on place the volume of CSF removed. Permanent decoupling of cerebral venous pressure by stenting an obstructive cause may be therapeutic, regardless of the initial cause.

Non Obstructive Venous Hypertension

Venous sinus hypertension also occurs in the absence of venous sinus obstruction. Karahalios et al. [78] drew attention to systemic venous hypertension in their series of patients studied with venography. There are several case reports in which cardiac lesions have been associated with PTS [72] or hydrocephalus [134]. However, the most well-studied scenario is that of morbid obesity and its association with venous sinus hypertension and PTS.

Obesity is strongly associated with development of PTS in both men and women [36, 51, 178]. Johnston & Paterson [75] found that of 110 patients with PTS, 35 were moderately or grossly obese. These patients were all female and 27 of them had no recognisable aetiology. Foley [45] found that only 1 of 46 cases with 'otitic hydrocephalus' compared to 20 of 60 cases with 'toxic hydrocephalus' were obese. In a prospective study of 50 patients with PTS by Wall & George [177] 94% were noted to be overweight.

Corbett & Mehta [26] investigated CSF pressure in 116 acute PTS patients, 8 chronic PTS patients, 41 normal obese volunteers and 15 normal non-obese volunteers. CSF pressure was only slightly higher in the normal obese subjects compared with normal non-obese subjects. There was no correlation with the degree of obesity and CSF pressure in this study. Patients with acute PTS all had CSF pressures markedly higher than both patients with chronic papilloedema and normal subjects. In a study of 19 patients (mean BMI 39.3 kg/m2) randomly selected from an obesity clinic CSF pressure was recorded during lumbar puncture [61]. CSF pressure was elevated (> 20 mmHg) in 15 patients (79%); in 8 patients it was greater than 25 mmHg and in 2 patients it was greater than 30 mmHg. The authors could not find any correlation between CSF pressure and BMI. No patient reported headaches and no patient had papilloedema.

There has been much speculation on the relationship between obesity and PTS. Numerous hormonal and metabolic links between obesity and raised CSF pressure have been proposed. In some cases a weight reduction can result in clinical improvement. There are reports of dramatic clinical improvement in patients with extreme obesity and PTS who have undergone surgically induced weight loss. Noggle & Rodning [122] reported a case of PTS in a morbidly obese patient who was successfully treated (weight reduction from 150 to 86 kg; resolution of clinical PTS) with gastric exclusion surgery. Furthermore symptoms recurred 3 years later with failure of the gastroplastic stapling line and recurrent weight gain. After revision of the gastric surgery, significant weight loss and clinical PTS resolved. At around the same time Amaral et al. [2] reported a similar case (138 kg) in whom surgically induced weight loss resulted in clinical resolution of PTS and a reduction in CSF pressure.

In 1995 Sugerman et al. [167] reported resolution of symptoms of PTS in morbidly obese patients (BMI 49 +/— 3 kg/m2) following surgically induced weight loss. At mean follow-up of 34 months average CSF pressure had reduced from 35.3 +/— 3.5 to 16.8 +/— 1.2 cmH2O. These initial results were confirmed in a second study of 24 severely obese patients (mean BMI 47 +/— 6 kg/m2) previously diagnosed with PTS [168]. Mean CSF pressure was 32.4 +/— 8.3 cmH2O. Twenty three patients underwent gastric bypass and one had laproscopic gastric banding. Follow-up was 62 +/— 52 months. At the time of the report, one year follow-up was available in 19 patients who had lost an average of 71 +/— 18% of their excess weight (45 +/—12 kg). Headache and pulsatile tinnitus resolved within 4 months of surgery with the exception of one patient. Papilloedema and cranial nerve dysfunction improved in all patients. Interestingly, 2 patients who had initially lost weight and experienced resolution of their symptoms developed recurrent PTS on regaining weight. As a non-surgical solution, Sugerman et al. [165] designed a counter-traction mechanism to reduce intra-abdominal pressure and central venous pressures. Improvement in headache and pulsatile tinnitus was reported with the nocturnal application of this external negative abdominal pressure device to the abdomen of 5 patients with severe obesity and PTS.

Sugerman et al. [166] studied 6 obese patients (mean BMI 45 +/— 3 kg/ m2) with PTS undergoing gastric banding. Mean ICP was 29.3 +/— 8.0 cm H2O. Intra-abdominal pressure (22 +/— 3 cmH2O), central venous pressure (20 +/— 6 mmHg; n = 5) and transoesopohageal pleural pressure (15 +/ — 10 mmHg; n = 3) were all elevated in these patients. The authors concluded that central obesity raises intra-abdominal, pleural and cardiac filling pressures. The later impedes cranial venous outflow and causes PTS. Gastric bypass or laproscopic gastric banding in these patients resulted in significant weight loss. At the time of the report 5 of the 6 patients had resolution of their PTS symptoms, including pulsatile tinnitus. One patient had only recently undergone their surgery. Although the right atrial pressures demonstrated using venography and manometry in the study of Kar-ahalios et al. [78], the mechanism that these authors propose may still be plausible. However, as Sugerman and colleagues themselves noted, there remains no satisfactory explanation for why some obese individuals develop PTS but most do not. In addition, why are women more commonly affected than males given that the proposed mechanism is increased intraabdominal pressure and males tend to have more central obesity compared to females.

Experimentally, Luce et al. [104] demonstrated that in anaesthetized dogs, an increase in pleural pressure increases lumbar and intracranial CSF pressure. This increase in CSF pressure was secondary to elevation of venous pressure in the superior vena cava. In the swine, Bloomfield et al. [16] demonstrated that elevation of intraabdominal pressure 25 mmHg above baseline caused an increase in central venous and intracranial pressures (7.6 +/— 1.2 to 21.4 +/— 1.0 mmHg). In addition there was a reduction in cardiac index and CPP decreased. Expansion of intravascular volume returned cardiac index and CPP to normal and also resulted in a further increase in ICP (27.8 +/— 1.0 mmHg). Decompression of the abdomen returned ICP to normal. The effects on central venous pressure and ICP were negated by sternotomy and pleuropericardotomy [16]. Even when ICP was already artificially elevated (mean 25.8 mmHg) increases of 15-25 mmHg in intra-abdominal pressure resulted in significant increases in intra-thoracic pressure and ICP (25.8 to 33.8 and 39.0 mmHg, respectively) [148].

There exists, therefore, a co-hort of patients with systemically increased venous sinus pressure without focal obstruction. These patients appear to be those with morbid obesity. It should be stressed that the degree of obesity in the patients that Sugerman et al. have dealt with surgically is much greater than that in the average overweight patient with PTS. In addition, it should also be noted that venous sinus obstruction, from both intrinsic lesions and extrinsic compression does also occur in obese patients. Non-obstructive venous sinus hypertension are a particularly difficult group to diagnose as there are no static CT or MR examinations that will demonstrate this aetiology. Instead cerebral venography with manometry including right atrial pressures, preferably in the awake patient, should be performed. These patients are also difficult to distinguish from a co-hort of patients with normal veins, normal venous pressures and increased CSF pressure possibly due to disordered function of the arachnoid granulations.

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