Venous Sinus Pressure Research Articles

Reduction in Syrinx Size and Severity After Venous Sinus Stenting in a Patient With Pseudotumor Cerebri and Chiari Malformation: Technical Case Report.

Pseudotumor cerebri and Chiari I malformation are found to coexist in a subset of patients. Surgical cranial decompression has been the mainstay of Chiari malformation management, whereas venous sinus stenting has emerged as an effective treatment modality for pseudotumor cerebri. Gaps in our current understanding of cerebrospinal fluid (CSF) circulation and the pathophysiology behind CSF-related disorders present difficulties in the simultaneous management of these conditions. A case is presented of the successful management of both conditions with venous sinus stenting, with sustained improvement in symptoms and structural abnormalities of the Chiari malformation and associated syrinxes. An obese woman in her 20s with a history of occipital headaches who presented with progressively worsening intermittent visual obscurations was diagnosed with pseudotumor cerebri, Chiari I malformation, and associated spinal syrinxes. Magnetic resonance venography demonstrated right transverse sinus narrowing with an elevated pressure gradient. Successful endovascular intervention with venous sinus stenting achieved normalization of the venous sinus pressure gradient and symptomatic improvement. After stenting, the cervical syrinx was observed to have decreased in size, with a decrease in the extent of cerebellar tonsillar herniation and an increase in CSF signal around the cerebellar tonsils. Venous sinus stenting for treatment of concomitant pseudotumor cerebri and Chiari I malformation can be effective in patients demonstrating transverse sinus stenosis.

Intracranial pressure and venous sinus pressure gradients: what happens 3 months after stenting?

Benign Intracranial hypertension (BIH) is commonly associated with venous sinus stenosis. Increasingly, this is treated endovascularly with stent insertion. However, this treatment modality is still controversial. Clinical improvement post stent insertion has been described. Little is known about long-term control of intracranial pressure (ICP). In our unit, catheter cerebral venogram with pressure measurements is routinely performed 3 months post stent insertion in BIH patients. We aim to quantify the degree of venous pressure changes in stenosis patients treated with sinus stenting and how the changes correlate with radiographic improvements.

Cerebrospinal fluid absorption block at the vertex in chronic hydrocephalus: obstructed arachnoid granulations or elevated venous pressure?

BackgroundThe lack of absorption of CSF at the vertex in chronic hydrocephalus has been ascribed to an elevation in the arachnoid granulation outflow resistance (Rout). The CSF infusion studies measuring Rout are dependent on venous sinus pressure but little is known about the changes in pressure which occur throughout life or with the development of hydrocephalus.MethodsTwenty patients with chronic hydrocephalus underwent MR venography and MR flow quantification techniques. The venous outflow pressure was estimated from the sinus blood flow and the cross-sectional area of the transverse sinuses. Adult controls as well as a normal young cohort were selected to estimate the change in sinus pressure which occurs throughout life and following the development of hydrocephalus. Significance was tested with a Student’s t-test.ResultsThe size of the transverse sinuses was unchanged from the 1st to the 5th decade of life, indicating a stable outflow resistance. However, the blood flow was reduced by 42%, indicating a likely similar reduction in pressure gradient across the sinuses. The sinuses of hydrocephalus patients were 38% smaller than matched controls, indicating a 2.5 times increase in resistance. Despite the 24% reduction in blood flow, a significant increase in sinus pressure is suggested.ConclusionsThe size of the venous sinuses normally does not change over the age range investigated but sinus pressure is reduced proportional to an age-related blood flow reduction. Hydrocephalus is associated with much smaller sinuses than normal and an elevation in venous pressure may explain the lack of CSF absorption into the arachnoid granulations in chronic hydrocephalus.

Reply—Spontaneous Cerebrospinal Fluid Otorrhea and Rhinorrhea in Idiopathic Intracranial Hypertension Patients

Background:Spontaneous cerebrospinal fluid (CSF) leakage may occur in patients with normal or increased intracranial pressure (ICP). We describe herein spontaneous CSF leakage as a result of chronic increased ICP in 4 patients with idiopathic intracranial hypertension (IIH). Although rhinorrhea prev

Pseudotumor Cerebri Associated With Modified Fontan Anatomy

Surgical treatment of functional single-ventricle heart disease with a modified Fontan procedure results in elevated central venous pressure. The case report describes a 19-year-old boy with hypoplastic left heart syndrome and Fontan palliation that resulted in frequent debilitating headaches after transcatheter closure of systemic venous-to-pulmonary venous collaterals. Measured increased intracranial pressure and prompt relief of the headaches with lumbar puncture favored a diagnosis of pseudotumor cerebri. After implantation of a lumboperitoneal shunt, the patient's headaches improved dramatically. Headaches are frequent in patients with Fontan circulation. The current literature supports a pivotal role of elevated dural venous sinus pressure in the pathogenesis of pseudotumor cerebri. The high superior and inferior vena caval pressures characteristic of modified Fontan anatomy may account for headaches in some of these patients.

Longstanding overt ventriculomegaly in adults: pitfalls in treatment with endoscopic third ventriculostomy

The recently described condition of longstanding overt ventriculomegaly in adults (LOVA) has not been defined in terms of the need for intervention, timing of intervention, and ideal treatment. The purpose of this review was to evaluate the role of endoscopic third ventriculostomy (ETV) in the treatment of LOVA. Data collected in six patients with LOVA who had undergone ETV were reviewed retrospectively in terms of the definition of treatment success, rates of success, complications, and outcome. All six patients presented with headache disorders. In all patients, triventricular hydrocephalus had been diagnosed as aqueductal stenosis, and head circumference measurements were above the 98th percentile. All six had undergone successful ETV as documented by the free flow of cerebrospinal fluid into the basal cisterns, which remained open throughout the follow-up period. After the procedure, one patient experienced a mild degree of difficulty with short-term memory. Five patients remained symptomatic or had symptoms requiring further treatment 3 months to 3 years after ETV. Four patients received ventriculoperitoneal shunts, and one underwent venous stenting for high intracranial pressure after successful ETV. In two patients in whom aqueductal stenosis had been diagnosed, the sylvian aqueduct was patent after the procedure. In LOVA patients who present with headaches, ETV may not lead to improvement in the headaches. Despite the presence of triventricular hydrocephalus, closure of the aqueduct may be a secondary phenomenon, and flow through the aqueduct may be reestablished after ETV. If intracranial hypertension persists after successful ETV, its cause may be increased venous sinus pressure.

A Newborn Who Has Previously Undiagnosed Hydrops Fetalis

A 36-week appropriate-for-gestational age male was born with hydrops fetalis that was not diagnosed prenatally. The birth hospital had a Level II nursery. Pertinent points in the history include: Born to a 24-year-old G2P0010 (previous first-trimester spontaneous abortionwoman by emergency cesarean section due to failure to progress and decreased fetal heart rate variability. ### Prenatal Laboratory Results Preterm labor occurred 1 week prior to delivery, but was stopped successfully with tocolysis, and the mother was sent home after 6 hours of observation. Rupture of membranes occurred 6 hours prior to delivery with clear fluid. At delivery, the infant appeared grossly edematous, dusky, and floppy, with no spontaneous respiratory effort. Endotracheal intubation was difficult because of airway edema. Resuscitation consisted of positive pressure ventilation, chest compressions, and epinephrine administration via an umbilical venous catheter. ### Initial Arterial Blood Gas Results A chest radiograph showed bilateral pleural effusions. A kidney-ureter-bladder (KUB) radiograph showed ascites. Pleurocentesis released 45 mL of straw-colored fluid from the left side of the chest, but none from the right side of the chest. A total of 15 mL of straw-colored fluid was removed from the abdomen via paracentesis. ### Follow-up Arterial Blood Gas Results On physical examination, the infant exhibited gross body edema but no dysmorphic features. A II/VI systolic murmur was heard at the left sternal border. The liver was palpable 3 cm below the costal margin. There was mild glandular hypospadias with a minimal chordee, but testes were descended bilaterally. The infant developed seizures and received a loading dose of 20 …

Pseudotumor cerebri.

Pseudotumor cerebri (PTC) is a syndrome of increased intracranial pressure without hydrocephalus or mass lesion and with normal cerebrospinal fluid (CSF) composition. Although often considered to be "idiopathic," detailed investigation has revealed a high incidence of venous outflow abnormalities in PTC syndrome patients. The thought that elevated intracranial venous sinus pressure is a "universal mechanism" for PTC syndrome of varying etiologies has been called into question by a study indicating that the increased venous pressure in idiopathic PTC patients is caused by the elevated intracranial pressure and not the reverse, suggesting that "the chicken is the CSF pressure elevation and the egg is the venous sinus pressure elevation." Vitamin A toxicity may play a role in the pathogenesis of idiopathic PTC. The treatment of PTC has two major goals: the alleviation of symptoms and preservation of visual function. When medical therapy fails or when visual dysfunction deteriorates, surgical therapies for PTC should be considered. The two main procedures performed include lumboperitoneal shunt and optic nerve sheath fenestration. Because of the association of PTC with venous sinus hypertension, some authors are considering venous sinus stenting for refractory cases of PTC. It is still unclear if primary treatment of the observed venous stenosis benefits patients with idiopathic PTC. This should be no surprise, as it is not certain whether the stenoses are the cause or the result of idiopathic PTC.

VEIN OF GALEN MALFORMATIONS

Management of children with high flow arteriovenous shunts of the brain is among the most challenging areas in modern medicine. Intracranial arteriovenous shunts (AVS) in children differ considerably from those...

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.

Manometry combined with cervical puncture in idiopathic intracranial hypertension: King JO, Mitchell PJ, Thompson KR, Tress BM. Neurology 2002;58:26 -30

Idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri, is a syndrome of raised intracranial pressure, normal cerebrospinal fluid (CSF) constituents, and normal neuro-imaging findings. It typically occurs in obese young women who can present with headache, papilledema, visual obscurations, diplopia and/or pulsatile tinnitus. The cause of IIH is unknown. In a previous publication of this group of authors, cerebral venography and manometry in nine patients with typical IIH demonstrated high pressures in the superior sagittal sinus and proximal transverse sinus and a sudden drop in pressure at the level of the distal third of the transverse sinus. Venography in that study revealed tapered stenoses and filling defects in the transverse sinus, suggesting mural thrombi or arachnoidal granulations. This led the authors to hypothesize that patients with IIH have elevated venous sinus pressure and that this is a unifying cause of IIH. To investigate this hypothesis further, the authors used cerebral venography and manometry to measure cerebral venous sinus pressure before and immediately after cerebrospinal puncture between cervical spines segments one and two (C1–2) with removal of 20 to 25 mL of CSF. Lowering the intracranial pressure by lateral C1–2 puncture during manometry showed that the venous hypertension resolved immediately. The authors therefore conclude that the venous hypertension in their patients with IIH was due to compression of the transverse sinuses by raised intracranial pressure and not due to a primary obstructive process in the cerebral venous sinuses. The cause of the raised intracranial pressure in IIH remains unknown.—Nancy J. Newman

Manometry combined with cervical puncture in idiopathic intracranial hypertension

To determine by cerebral venography and manometry in patients with idiopathic intracranial hypertension the cause of the previously demonstrated venous hypertension in the superior sagittal and proximal transverse sinuses. Cerebral venous sinus pressure was measured before and immediately after C1-2 puncture with removal of 20 to 25 mL of CSF. Lowering the intracranial pressure by lateral C1-2 puncture during manometry has shown that the venous hypertension resolves immediately. These studies indicate that the venous hypertension is due to compression of the transverse sinuses by raised intracranial pressure and not due to a primary obstructive process in the cerebral venous sinuses.

Intracranial hypertension associated with unruptured cerebral arteriovenous malformations

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.

Venous Air Embolism during Neurosurgery

This study was designed to improve understanding of the pathogenesis of air embolism and thereby contribute to the development of effective preventive techniques. Dural venous sinus pressure (confluens sinuum pressure: CSP) was measured in pentobarbital-anesthetized mongrel dogs under conditions of spontaneous and controlled respiration, head elevation, neck compression, abdominal compression, drug- or bleeding-induced hypotension, extraneous fluid administration, and drug-induced hypertension. CSP was lower during controlled than during spontaneous respiration. When the head was raised, CSP decreased almost linearly, reaching -2.3±2.8 (mean±SD) mmHg at 45°. Upon neck compression, CSP increased significantly; even at a cuff pressure of only 5 mmHg, the negative pressure returned to zero. However, abdominal compression had little effect. Bleeding-induced hypotension caused a decrease in CSP, to 0.3±1.4 mmHg at a blood pressure of 90 mmHg. On the other hand, CSP increased markedly following fluid administration (except in the case of saline) and induced hypertension. These results suggest that continuous neck compression, fluid administration, avoidance of hypotension, and induced hypertension contribute to the prevention of air embolism.

Venous Air Embolism and Active Lung Inflation at High and Low CVP

To assess the safety and efficacy of the maneuver of active lung inflation (ALI) after venous air embolism, measurements were made of pulmonary artery occlusion pressure (PAOP), central venous pressure (CVP), and superior jugular bulb pressure (JbP) as an index of cerebral venous sinus pressure in eight sheep before and after a 2-ml/kg air embolus and before and in the release phase of an ALI to a pressure of 4 kPa (30 mm Hg). (PAOP-CVP) difference decreased significantly after the air embolus with a further decrease after ALI (P less than 0.01). An increase in JbP occurred with ALI only when the CVP was elevated before the injection of air. After air embolism in neurosurgery, ALI may increase the likelihood of paradoxical embolism in patients at risk and may also fail to help in identifying the site of air entry.

Parametric changes in an intracranial pressure model during plateau waves.

The intracranial pressure (ICP) is commonly monitored in patients with head trauma. A sudden rise in the ICP to an elevated level, i.e., the occurrence of a plateau wave in the ICP, often indicates the worsening of the patient's condition. Several clinical symptoms usually accompany a plateau wave, but the physiological causes for the elevated ICP are difficult to specify. In this study, a mathematical model representing the ICP dynamics is used to study possible physiological changes in the dynamics of the cerebrospinal fluid (CSF) flow, which could result in the appearance of plateau waves. The effects of changes in the CSF absorption resistance (R), in the dural venous sinus pressure (Pd), and in the mean CSF formation rate (If) on the ICP are determined by simulating the mathematical model. Simulation results indicate that plateau waves in the ICP can be produced by the aforementioned changes under certain conditions. Using a recursive parameter estimation algorithm, the mean ICP (P) and the normalized CSF absorption resistance (RO) can be tracked with time. The analysis of clinically recorded ICP data shows that the value of R0 increases during a plateau wave. Simulation results are then discussed and critically viewed.

The mechanism of shell elevation in Haliotis (Mollusca: Gastropoda) and a consideration of the evolution of the hydrostatic skeleton in Mollusca

Early in molluscan evolution, the development of a conical shell with shell or pedal retractor muscles led to the need of a mechanism for the extension of the foot or the raising of the shell. The forces generated during pedal retraction and extension have been studied in Haliotis midae, an easily obtainable and conveniently large archaeogastropod. In the mantle cavity, cephalopedal venous sinus and ventricle pressure pulses were observed during pedal retraction elicited by the shadow withdrawal reflex, but were never present during extension. However, pressure pulses were recorded in the proximal region of the columellar (or shell) muscle, both during retraction and pedal extension. Sections of this region of the muscle show a three dimensional network of muscle fibres, consisting of retractor fibres passing down to the foot and circumferential and radial fibres. Contraction of the two latter sets of fibres would bring about extension of the retractors, without the use of a discrete hydrostatic skeleton, and appears to be the principal mechanism of pedal extension. Similar muscular structures, here termed the muscular antagonistic system, have been observed in the columellar muscle of other gastropods and in the cephalopod mantle. In contrast, this system has not been observed in the proximal region of the pedal retractors of bivalves or scaphopods, for the pedal haemocoel, which allows muscular antagonism in the manner of a classical hydrostatic skeleton, has developed in association with the burrowing habit. The significance of the muscular antagonistic system in molluscan evolution is discussed.

E.E.G. MONITORING FOR THE CONTROL OF ANAESTHESIA PRODUCED BY THE INFUSION OF ALTHESIN IN PRIMATES

The continuous infusion of Althesin under electroencephalographic (e.e.g.) control provided a constant level of light anaesthesia for periods of 1--5.5 h during experimental brain hypoxia in spontaneously breathing baboons and Rhesus monkeys. Polygraphic records (respiration, heart rate, arterial pressure, cerebral venous sinus pressure, end-tidal gas concentrations) and also estimation of blood-gas tensions, pH, and concentrations of pyruvate and lactate demonstrated a steady physiological state. Various methods of e.e.g. monitoring were tested to establish an optimal assessment of depth of anaesthesia as a guide to the control of the rate of infusion of Althesin. A purpose-built modification of the Cerebral Function Monitor was found to give unequivocal recognition of changing depths of anaesthesia.

Profound hypoxia in Papio anubis and Macaca mulatta — Physiological and neuropathological effects : I. Abrupt exposure following normoxia II. Abrupt exposure following moderate hypoxia

Lightly anaesthetized and spontaneously breathing P. anubis (PA) and M. mulatta (MM) inhaled at ambient pressure 3.2% oxygen (≡ 37,500 ft or 11,430 m) from air and also after pre-exposure to 14% oxygen (≡ 10,000 ft or 3,048 m). The EEG, ECG, respiratory rate, arterial and cerebral venous sinus pressures, end-tidal pO 2 and pCO 2 and body temperature were recorded. Arterial and cerebral venous sinus blood gases, pH and pyruvate and lactate contents were estimated. Before hypoxia, MM showed a relative hyperventilation. Profound hypoxia, from air, ended with the “last breath” at 89–205 sec in PA and at 93–570 sec in MM. Brain damage was restricted to one MM (4 exposures). Profound hypoxia after exposure to 14% oxygen ended with the “last breath” at 87–210 sec in PA and at 120 sec-94 min (including 9 exposures over 5 min) in MM. Brain damage was restricted to one MM (“last breath” at 94 min). In the two MM with brain damage there was evidence of reduction in cerebral perfusion near the end of profound hypoxia. Brain damage in one animal contrasts with the frequent and often severe brain damage in MM after equivalent sub-atmospheric decompressions preceded by exposure to moderate altitude (10,000 ft).

Cyanide intoxication in Macaca mulatta: Physiological and neuropathological aspects

Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO 2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were estimated in arterial and venous sinus blood samples. There was an initial hyperventilation with tetany in all animals. A rapid rate of cyanide infusion led to apnoea. An isoelectric or near-isoelectric EEG was usually precipitated by bradycardia often with additional hypotension. Neither epileptic seizures nor their EEG concomitants were seen at any stage. Three animals died of early heart failure. Brain damage was seen in 4 animals surviving up to 98 hr. White matter was involved in all. Ischaemic neuronal alterations, restricted to the striatum of one animal, were attributed to major circulatory complications. It was concluded that under these experimental conditions there is no evidence for hypoxic neuronal damage of purely histotoxic type.