J D Pickard1, Z Czosnyka, M Czosnyka, B Owler, J N Higgins. 1. Academic Neurosurgery Division, University of Cambridge, P.O. Box 167, Addenbrookes Hospital, Cambridge CB20QQ, UK. JDPsecretary@medschl.cam.ac.uk
Abstract
BACKGROUND: Narrowing of the cranial dural venous sinuses has been implicated as contributing to elevated intracranial pressure in idiopathic intracranial hypertension [IIH]. Such narrowing may be either a fixed stenosis or secondary to raised ICP. We have investigated whether narrowing of the venous sinuses may reflect direct coupling between cerebrospinal fluid pressure and sagittal sinus pressure. METHODS: Nine patients with the clinical features of IIH [8F, 1M; mean age 41 (range 22-55)] were studied as part of their standard clinical investigations by simultaneous lumbar CSF infusion study and direct retrograde cerebral venography whereby a catheter is placed within the sagittal sinus under fluoroscopic guidance. FINDINGS: In all cases, both CSF pressure (Pcsf) and sagittal sinus pressure (Pss) were elevated with Pcsf slightly exceeding Pss (27.0 +/- 2.3 mm Hg. 25.2 +/- 7.5 mm Hg; difference P = 0.026; correlation R = 0.97, P = 0.0032). There was a gradient of pressure along the sagittal and transverse sinuses. CSF infusion provoked rises in both Pcsf and Pss (R = 0.97, P < 0.0007). During drainage of CSF after the test (8 cases), Pcsf decreased to values lower than Pss (-3.26 +/- 3.9 mm Hg; P = 0.0097). There was excellent correlation between slow waves of Pcsf and Pss (mean R = 0.9) and between baseline pulse amplitudes of both pressures (R = 0.91; P = 0.03). CONCLUSIONS: In the 9 patients studied with IIH, Pcsf and Pss were coupled both statically (mean values) and dynamically (vasogenic components). During drainage, both pressures decreased until probably central venous pressure was reached and then Pcsf decreased further while Pss remained constant. This suggests that, in many cases of IIH, there is functional obstruction of venous outflow through the dural sinuses. Raised Pcsf partly obstructs venous sinus outflow, thereby increasing Pss which, in turn, leads to a further rise in Pcsf, et sequor. This vicious cycle can be interrupted by draining CSF.
BACKGROUND: Narrowing of the cranial dural venous sinuses has been implicated as contributing to elevated intracranial pressure in idiopathic intracranial hypertension [IIH]. Such narrowing may be either a fixed stenosis or secondary to raised ICP. We have investigated whether narrowing of the venous sinuses may reflect direct coupling between cerebrospinal fluid pressure and sagittal sinus pressure. METHODS: Nine patients with the clinical features of IIH [8F, 1M; mean age 41 (range 22-55)] were studied as part of their standard clinical investigations by simultaneous lumbar CSF infusion study and direct retrograde cerebral venography whereby a catheter is placed within the sagittal sinus under fluoroscopic guidance. FINDINGS: In all cases, both CSF pressure (Pcsf) and sagittal sinus pressure (Pss) were elevated with Pcsf slightly exceeding Pss (27.0 +/- 2.3 mm Hg. 25.2 +/- 7.5 mm Hg; difference P = 0.026; correlation R = 0.97, P = 0.0032). There was a gradient of pressure along the sagittal and transverse sinuses. CSF infusion provoked rises in both Pcsf and Pss (R = 0.97, P < 0.0007). During drainage of CSF after the test (8 cases), Pcsf decreased to values lower than Pss (-3.26 +/- 3.9 mm Hg; P = 0.0097). There was excellent correlation between slow waves of Pcsf and Pss (mean R = 0.9) and between baseline pulse amplitudes of both pressures (R = 0.91; P = 0.03). CONCLUSIONS: In the 9 patients studied with IIH, Pcsf and Pss were coupled both statically (mean values) and dynamically (vasogenic components). During drainage, both pressures decreased until probably central venous pressure was reached and then Pcsf decreased further while Pss remained constant. This suggests that, in many cases of IIH, there is functional obstruction of venous outflow through the dural sinuses. Raised Pcsf partly obstructs venous sinus outflow, thereby increasing Pss which, in turn, leads to a further rise in Pcsf, et sequor. This vicious cycle can be interrupted by draining CSF.
Authors: R M Ahmed; M Wilkinson; G D Parker; M J Thurtell; J Macdonald; P J McCluskey; R Allan; V Dunne; M Hanlon; B K Owler; G M Halmagyi Journal: AJNR Am J Neuroradiol Date: 2011-07-28 Impact factor: 3.825
Authors: Afroditi-Despina Lalou; James S McTaggart; Zofia H Czosnyka; Matthew R Garnett; Deepa Krishnakumar; Marek Czosnyka Journal: Childs Nerv Syst Date: 2019-07-19 Impact factor: 1.475