Cranial Venous Outflow Obstruction Research Articles

Cranial venous-outflow obstruction promotes neuroinflammation via ADAM17/solTNF-α/NF-κB pathway following experimental TBI

Traumatic brain injury (TBI) is a global public health problem. As an important cause of secondary injury, cerebrovascular reaction can cause secondary bleeding, venous sinus thrombosis, and malignant brain swelling. Recent clinical studies have confirmed that intracranial venous return disorder is closely related to the prognosis of patients, yet the specific molecular mechanism involved in this process is still unclear. This study used an acute subdural hematoma (ASDH) model with cranial venous outflow obstruction (CVO) to explore how CVO aggravates the pathological process after TBI, especially for inflammation and tissue damage. The results suggest that intracranial venous return disorder exacerbates neurological deficits and brain edema in rats with ASDH by aggravating the destruction of endothelial cell tight junctions (TJs) proteins and promoting the expression of inflammatory factors, the activation of microglia and expression of recombinant A disintegrin and metalloprotease 17 (ADAM17) as well as the secretion of solTNF-α, a soluble form of tumor necrosis factor-alpha (TNFα), which in turn increase IκB-α ((inhibitor of the transcription factor nuclear factor-κB) and NF-κB p65. Our study revealed a molecular basis of how CVO aggravates inflammation and tissue damage.

A paradigm for chronic fatigue syndrome: caught between idiopathic intracranial hypertension and spontaneous intracranial hypotension; caused by cranial venous outflow obstruction

ABSTRACT Background Clinical similarities between chronic fatigue syndrome and idiopathic intracranial hypertension, supported by measurements of intracranial pressure, invite suggestions that they may be connected, the first representing a mild version of the second. Yet, if this is to be the basis for a structural explanation for chronic fatigue syndrome, it already seems incomplete, failing to explain cases where disability seems disproportionate. Is there some other confounding variable? Purpose To refine, in this theoretical paper, an earlier model connecting chronic fatigue syndrome with idiopathic intracranial hypertension to allow for a cerebrospinal fluid (CSF) leak. Model In this model, the primary structural problem is acquired obstruction to cranial venous outflow. This obstruction can take different forms, may be intermittent and subtle, and even be mistaken for normal venous anatomy, yet would be the driving force behind a tendency towards increased intracranial pressure. This chronic elevation of intracranial pressure stresses the dural membrane maintaining the integrity of the subarachnoid space, which can rupture at a weak point, allowing CSF to leak away and intracranial pressure to fall. The clinical manifestation of this disorder is the product of the severity of cranial venous outflow compromise and of the competing forces on intracranial pressure. In some instances, a CSF leak will mitigate the effects of venous compromise, in others it will compound it, producing a disease spectrum ranging through idiopathic intracranial hypertension, chronic fatigue syndrome, fibromyalgia, and spontaneous intracranial hypotension. Conclusion In chronic fatigue syndrome a normal intracranial pressure does not exclude significant physiological disturbance.

Spontaneous Intracranial Hypotension Complicated by Subdural Effusions Treated by Surgical Relief of Cranial Venous Outflow Obstruction

Spontaneous intracranial hypotension describes the clinical syndrome brought on by a cerebrospinal fluid (CSF) leak. Orthostatic headache is the key symptom, but others include nausea, vomiting, and dizziness, as well as cognitive and mood disturbance. In severe cases, the brain slumps inside the cranium and subdural collections develop to replace lost CSF volume. Initial treatment is by bed rest, but when conservative measures fail, attention is focused on finding and plugging the leak, although this can be very difficult and some patients remain bedbound for months or years. Recently, we have proposed an alternative approach in which obstruction to cranial venous outflow would be regarded as the driving force behind a chronic elevation of CSF pressure, which eventually causes dural rupture. Instead of focusing on the site of rupture, therefore, investigation and treatment can be directed at locating and relieving the obstructing venous lesion, allowing intracranial pressure to fall, and the dural defect to heal. The case we describe illustrates this idea. Moreover, since there was a graded clinical response to successive interventions relieving venous obstruction, and eventual complete resolution, it also provides an opportunity to consider particular symptoms in relation to cerebral venous insufficiency in its own right.

Headache, Cerebrospinal Fluid Leaks, and Pseudomeningoceles after Resection of Vestibular Schwannomas: Efficacy of Venous Sinus Stenting Suggests Cranial Venous Outflow Compromise as a Unifying Pathophysiological Mechanism.

Background Regardless of the operative approach, headache, cerebrospinal fluid (CSF) leaks, and pseudomeningoceles remain disproportionately common problems after surgery for vestibular schwannomas and have a significant negative impact on quality of life and potential to return to full employment. Recent work has raised the possibility that these problems may, in part, be related to acquired obstruction of cranial venous outflow. This article explores this idea further with respect to a group of patients with severe and intractable symptoms. Objective The main objective of this article is to describe our experience diagnosing, investigating, and treating cranial venous outflow obstruction following translabyrinthine resection of vestibular schwannomas. Methods Retrospective review of all patients ( n = 9) at our institution referred for sigmoid sinus stenting following translabyrinthine surgery. Results Headache resolved or improved after sigmoid stenting in all five patients in whom it was the primary symptom. CSF leak was the primary problem in two patients. In one, the leak was unchanged, but headache improved. In the other, the leak resolved, and headache improved. Two patients had symptomatic pseudomeningoceles and both resolved Conclusion Assuming a meticulous approach to wound closure, a CSF leak following surgery for vestibular schwannoma can be viewed as a pathological, but essentially homeostatic, response to raised intracranial pressure caused by acquired obstruction to cranial venous outflow. Postoperative headache (from high or low intracranial pressure) and CSF leaks, therefore, may all respond to measures aimed at eliminating the obstructing lesion.

MR Imaging Findings in Patients with Secondary Intracranial Hypertension

IH can alter the configuration of anatomic structures of the central nervous system. We determined the sensitivity and specificity of MR imaging to detect these changes in patients with secondary IH. Patients (n = 36) with IH were prospectively investigated with MR imaging and were matched to 36 controls. MR images were evaluated for elongation and edema of the optic nerves, protrusion of the optic disc, flattening of the posterior sclera, height of the pituitary gland, and width of the optic nerve sheath. On MRV, we recorded venous sinus abnormalities and measured the luminal width of the superior ophthalmic veins. A grading score was introduced to define cranial venous outflow obstruction. Cranial venous outflow obstruction and ONS hydrops were the most valid signs indicating IH with a sensitivity of 94% and 92% and a specificity of 100% and 89%, respectively. Sensitivities and specificities were 56% and 97% for reduced pituitary height, 64% and 78% for flattening of the posterior sclera, 31% and 97% for widening of the superior ophthalmic veins, 33% and 100% for optic disc protrusion, 14% and 100% for optic nerve edema, and 6% and 100% for elongation of the optic nerve. At least 2 MR imaging findings could be demonstrated in each patient but in none of the controls. The number of positive MR imaging findings correlated with CSF pressure (r = 0.62, P = .01). The combination of cranial and orbital MR imaging and MRV can be highly sensitive and specific in the diagnosis of patients with IH.

The entire dural sinus tree is compressed in patients with idiopathic intracranial hypertension: a longitudinal, volumetric magnetic resonance imaging study

The objective of this study was to explore the volumetric alterations of dural sinuses in patients with idiopathic intracranial hypertension (IIH). Standardized cranial magnetic resonance imaging (MRI) was used in 17 patients prior to and following treatment of IIH and in seven controls. Magnetic resonance venographies (MRV) were employed for (a) judgement of circumscript dural sinus stenoses and (b) computation of sinus volumes. Cross-sectional areas (CSA) of the superior sagittal sinuses (SSS) were measured on T2-weighted images. Results of the initial MRIs were compared to those on follow-up MRIs and to results of controls. Stenoses of the transverse sinuses (TS) resulting in cranial venous outflow obstruction (CVOO) were present in 15/17 (88%) patients, normalizing in 7/15 cases (47%) after treatment of IIH. CVOO was not detected in the control group. Segmentation of MRV revealed decreased dural sinus volumes in patients with IIH as compared to controls (P = 0.018). Sinus volumes increased significantly with normalization of intracranial pressure independent from disappearing of TS stenoses (P = 0.007). The CSA of the SSS were normal on the initial MRIs of patients with IIH and increased on follow-up after treatment (P < 0.001). However, volumetries displayed overlap in patients and controls. Patients with IIH not only exhibit bilateral stenoses of the TS as has been reported, but volume changes of their entire dural sinus system also occur. The potential etiopathological and diagnostic roles of these changes are discussed.

Cranial venous outflow obstruction in the pseudotumour syndrome: incidence, nature and relevance

This study reports a retrospective analysis of the evidence of cranial venous outflow pathology in 188 patients with pseudotumour syndrome (PTS) investigated over the period 1968–1999. Standard methods of investigation appropriate to the period were used, i.e. cerebral angiography, CT and MR scanning. Recently, some patients had specific venous studies including intraluminal cranial venous sinus pressure measurements. A sub-group (25 patients) was investigated for haematological abnormalities. The overall incidence of cranial venous outflow abnormality was 19.7% (37 cases). In decades, related to the predominant investigative method, the figures were: to 1979, 4.2% (2 cases); to 1989, 15.0% (8 cases); to 1999, 31.0% (27 cases). A cause of the venous abnormality was identified in 20 cases, most commonly haematological and iatrogenic. In 17 patients (all females) no cause was identified. Fifteen of the 25 patients (60%) tested specifically were found to have a haematological abnormality, although no correlation was shown between this and a demonstrable venous outflow abnormality. The conclusion was drawn that there is a high incidence (close to one-third) of venous outflow abnormalities in PTS with detailed investigation. Issues of mechanism and therapy are discussed.

Dural sinus thrombosis: a mechanism-based classification and review of 42 cases

Cranial venous outflow obstruction due to dural sinus thrombosis may result in venous hypertension, cerebral infarction, cerebral haemorrhage or impaired cerebrospinal fluid (CSF) absorption with consequent pseudotumour syndrome. We propose a mechanism based classification of dural sinus thrombosis from these four outcomes. Forty two cases of dural sinus thrombosis presenting to Royal Prince Alfred Hospital between 1986–1997 were retrospectively reviewed. These cases were classified according to mechanism of presentation and relevance of this to site of thrombosis, treatment and prognosis. This study shows that the superior sagittal sinus and transverse sinus are the commonest sites of thrombosis, and multiple sites of thrombosis (69%) are more frequent than a single site. Magnetic resonance imaging (MRI) with venous flow studies is the investigation of first choice for diagnosis but angiography remains the gold standard. A pseudotumour syndrome is the commonest presentation (43%) followed by cerebral haemorrhage (31%). The overall prognosis for sinus thrombosis is good, with 71% of cases recovering to normal function.

The Pseudotumor Syndrome

We report a series of eight cases that show a close resemblance to, but are not identical with, pseudotumor cerebri (PTC) as normally defined. The majority of these cases are characterized by raised intracranial pressure without ventriculomegaly. They include two cases of cranial venous outflow obstruction in which clinical or radiologic abnormalities precluded the diagnosis of PTC proper (cases 1 and 2); one case of chronic meningitis in which an abnormal cerebrospinal fluid (CSF) composition precluded the diagnosis of PTC (case 3); two cases without either papilledema or a measured increase of CSF pressure, which in other respects, particularly in response to treatment, resembled PTC (cases 4 and 5); and three cases of what is thought to represent an infantile form of PTC (cases 6 through 8). The purpose of the analysis of these cases is twofold. First, it is argued that these cases throw light on the mechanism of PTC itself, supporting a concept of a disturbance of CSF circulation in this condition, and that they are themselves illuminated by considerations of typical PTC. Second, the cases are used to frame a proposed classification of the pseudotumor syndrome aimed at broadening the diagnostic criteria applied currently to PTC. It is suggested that the pseudotumor syndrome has a single underlying mechanism (disturbed CSF circulation) and that recognition of this mechanism not only clarifies the pathophysiologic processes of PTC but also has important diagnostic and therapeutic implications.