Relationship between Intracranial and Sagittal Sinus Pressure in Normal and Hydrocephalic Dogs

Olivero, William C.; Rekate, Harold L.; Chizeck, H.J.; Ko, Wen H.; McCormick, John

doi:10.1159/000120388

Cited by 43 publications

(43 citation statements)

References 10 publications

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“…The normal gradient is 2-14 cm H 2 O [17][18][19]. Flexner found the normal ratio of subarachnoid pressure to sagittal sinus pressure to be approximately 1.7:1 [6].…”

Section: Pressure Gradient From the Subarachnoid Space To The Dural Vmentioning

confidence: 99%

“…In clinical and experimental hydrocephalus, both subarachnoid and venous pressures rise, but there is a narrowing, not a widening, of the pressure gradient across the arachnoid villi [6,[18][19][20][21]. Shulman et al [19] found that the average pressure gradient of 57 mm H 2 O between the subarachnoid space and sagittal sinus in normal dogs diminished to 2 mm H 2 O in dogs made hydrocephalic by kaolin.…”

Section: Pressure Gradient From the Subarachnoid Space To The Dural Vmentioning

confidence: 99%

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A Model of Pulsations in Communicating Hydrocephalus

Egnor¹,

Zheng

Rosiello³

et al. 2002

Pediatr Neurosurg

177

115

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The traditional theory of communicating hydrocephalus has implicated the bulk flow component of CSF motion; that is, hydrocephalus is generally understood as an imbalance between CSF formation and absorption. The theory that the cause of communicating hydrocephalus is malabsorption of CSF at the arachnoid villi is not substantiated by experimental evidence or by physical reasoning. Flow-sensitive MRI has shown that nearly all CSF motion is pulsatile, and there is substantial evidence that hyperdynamic choroid plexus pulsations are necessary and sufficient for ventricular dilation in communicating hydrocephalus. We have developed a model of intracranial pulsations based on the analogy between the pulsatile motion of electrons in an electrical circuit and the pulsatile motion of blood and CSF in the cranium. Increased impedance to the flow of CSF pulsations in the subarachnoid space redistributes the flow of pulsations into the ventricular CSF and into the capillary and venous circulation. The salient features of communicating hydrocephalus, such as ventricular dilation, intracranial pressure waves, narrowing of the CSF-venous pressure gradient, diminished cerebral blood flow, elevated resistive index and malabsorption of CSF, emerge naturally from the model. We propose that communicating hydrocephalus is the result of a redistribution of CSF pulsations in the cranium.

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“…The normal gradient is 2-14 cm H 2 O [17][18][19]. Flexner found the normal ratio of subarachnoid pressure to sagittal sinus pressure to be approximately 1.7:1 [6].…”

Section: Pressure Gradient From the Subarachnoid Space To The Dural Vmentioning

confidence: 99%

Section: Pressure Gradient From the Subarachnoid Space To The Dural Vmentioning

confidence: 99%

A Model of Pulsations in Communicating Hydrocephalus

Egnor¹,

Zheng

Rosiello³

et al. 2002

Pediatr Neurosurg

177

115

View full text Add to dashboard Cite

show abstract

“…4 In cases of IIH in which there is a high suspicion of sinus thrombosis, procedures such as conventional cerebral angiography, direct retrograde cerebral venography, and manometry are performed to characterize their morphological features and venous pressures, to perform a therapeutic balloon venoplasty or endoluminal venous sinus stenting if necessary. 4,16,[30][31][32] Although most children with IIH improve with medical treatment, those who have had visual progression despite medical treatment have undergone optic nerve sheath fenestration and lumboperitoneal shunting or even ventriculoperitoneal shunting in certain cases. 38 All patients reported on in our series were of similar age and body habitus, and all had a preexisting spinal deformity.…”

Section: Discussionmentioning

confidence: 99%

Idiopathic intracranial hypertension following spinal deformity surgery in children

Kunes¹,

Thompson²,

Manjila

et al. 2011

FOC

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Idiopathic intracranial hypertension (IIH) after pediatric spinal deformity surgery has not been previously reported. The authors conducted a retrospective analysis of more than 1500 pediatric spinal surgeries performed between 1992 and 2011. From their analysis, they report on 3 adolescent patients who underwent uncomplicated segmental spinal instrumentation for pediatric spinal deformity correction and subsequently developed features of IIH. The common variables in these 3 patients were adolescent age, spinal deformity, being overweight, symptom onset within 2 weeks postoperatively, significant estimated blood loss, and intraoperative use of ε–aminocaproic acid (antifibrinolytic) injection. The authors postulate that the development of IIH could be the result of venous outflow obstruction due to derangement of the epidural venous plexus during surgery. The use of ε–aminocaproic acid could potentially have the risk of causing IIH, probably mediated through hyperfibrinogenemia, although there have not been published cases in the neurosurgical, orthopedic, cardiac, or general surgical literature. Idiopathic intracranial hypertension after spinal deformity correction is a condition that should be recognized by neurosurgeons and orthopedic surgeons, because appropriate intervention with early medical therapy can lead to a satisfactory clinical outcome.

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“…CSF absorption depends on the pressure gradient across the subarachnoid space and the sagittal sinus; therefore, any increase in the sinus pressures produced by the vascular malformation would need to be matched by the CSF pathways. Ventricular enlargement occurs as a compensatory mechanism involved in increasing CSF pressure to maintain a gradient of 5–7 mm Hg [15,16]. …”

Section: Discussionmentioning

confidence: 99%

The High Risks of Ventriculoperitoneal Shunt Procedures for Hydrocephalus Associated with Vein of Galen Malformations in Childhood: Case Report and Literature Review

et al. 2010

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Little to no pediatric or neurosurgical literature has been published about the complications of ventriculoperitoneal shunt procedures for hydrocephalus associated with vein of Galen malformations in childhood. The interventional neuroradiology literature, however, suggests that ventriculoperitoneal shunting as first-line treatment for hydrocephalus in children with vein of Galen malformations is fraught with short- and long-term dangers, including status epilepticus, intraventricular hemorrhage, subdural hematoma and hygroma, venous infarction, malignant dystrophic calcification, and worsening developmental delay. We present a single pediatric case where a ventriculoperitoneal shunt procedure for symptomatic hydrocephalus seemed to be the major contributing factor to the rapid neurological deterioration and eventual death of an infant with a vein of Galen malformation. Based on this experience and our review of the literature, we suggest the use of endovascular embolization of the vein of Galen malformation to reestablish a balance in hydrovenous dynamics as first-line treatment rather than directly addressing hydrocephalus with CSF diversion. The ventriculoperitoneal shunt procedure should be reserved for cases with symptomatic hydrocephalus in which the patient is a poor candidate for embolization, or for cases where endovascular therapy has already been maximized. The role of endoscopy in the treatment of hydrocephalus associated with vein of Galen malformations is not clear.

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Relationship between Intracranial and Sagittal Sinus Pressure in Normal and Hydrocephalic Dogs

Cited by 43 publications

References 10 publications

A Model of Pulsations in Communicating Hydrocephalus

A Model of Pulsations in Communicating Hydrocephalus

Idiopathic intracranial hypertension following spinal deformity surgery in children

The High Risks of Ventriculoperitoneal Shunt Procedures for Hydrocephalus Associated with Vein of Galen Malformations in Childhood: Case Report and Literature Review

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