CSF Hydrodynamics in Superior Sagittal Sinus J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.55.4.287 on 1 April 1992

Journal of Neurology, Neurosurgery, and Psychiatry 1992;55:287-293 287

CSF hydrodynamics in superior sagittal sinus J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.287 on 1 April 1992. Downloaded from thrombosis

Bo Kristensen, Jan Malm, Peter Markgren, Jan Ekstedt

Abstract on them (17 of the investigations included only Cerebrospinal fluid hydrodynamics were resting pressure recordings). Ethical approval investigated with a constant pressure infu- and informed consent from the patients were sion method in patients with superior obtained. The remaining three other patients sagittal sinus thrombosis. Ten patients were investigated on just one occasion, and the were studied with serial examinations up results of these studies are not reported. All to 15 years after the onset ofthe disease. A patients had at least one CT scan, eight had total of 70 CSF hydrodynamic examina- two or more examinations. All patients had tions were performed. A clear increase in repeated ophthalmological examinations intracranial pressure due to raised pres- including visual fields (Goldman) and acuity. sure in the major dural sinus was seen in Fundus photographs were taken in most all patients. A striking feature was the patients. No patient died. Neuropsychological persistent intracranial pressure increase testing included the Wisconsin card sorting that declined only gradually. This had no test,6 the Halstead-Reitan neuropsychological obvious clinical impact. Change in CSF test battery,7 the Claeson-Dahl's learning and resorption facility played only a minor retention test,8 the visual retention test of role in the intracranial pressure elevation. Benton,9 and a finger tapping test for motor None of the patients developed hydro- speed.10 The first examination was performed cephalus. from nine to 60 months and the last investigation from 30 to 98 months after onset of Aseptic cerebral venous thrombosis, mainly in symptoms. the form of superior sagittal sinus thrombosis (SSST), is a fairly uncommon but important cause of raised intracranial pressure. Onset is often acute and dramatic. SSST is more CSF hydrodynamic investigation was performed common in younger adults and in women. according to the method described by There are many underlying causes but none is Ekstedt.1 After 12 hours' bed rest, two needles found in a quarter of cases. Most run a benign were inserted in the L3-L4 interspace. CSF course in the acute phase. The mortality (2 ml) was aspirated to check for free CSF

probably does not exceed 10%, and only about passage from each needle. The patient was http://jnnp.bmj.com/ 20% of survivors are left with sequelae. Little is then examined lying supine with the zero known about the long term outcome or risk of pressure reference level at the cranial sagittal recurrence.1 Recently there has been interest in centre. Drainage of CSF and infusion of unusual aspects of presentation, causes, or artificial CSF was made to and from a con- treatment of SSST.2 Simple lumbar CSF tinuously weighed bottle. The pressure in the pressure measurements have been reported bottle was regulated by means of an electronic from patients with sinus pathology3 but no control system acting on the fluid in the bottle serial investigations have been performed. CSF by means ofthe air pressure from a pump. CSF on September 28, 2021 by guest. Protected copyright. hydrodynamics have been studied by direct resting pressure (Pcl) was determined when the intrasinal and intraventricular pressure meas- resting recording had been stable for at least 10 urements in individual patients in special min, which usually required 30-60 min circumstances, such as during anaesthesia4 or recording. The conductance of the CSF out- neurosurgery,5 but fundamental pathophysio- flow pathways (G0,) was determined by apply- logical changes in CSF hydrodynamics in ing multiple pressure levels to the CSF space SSST over time have not been reported. We while recording the resulting inflow of artificial present the first long term study on CSF CSF into the patient. Thus within a few hydrodynamics in patients with SSST. minutes a stable flow at a stable pressure was Department of obtained. Usually, three different pressure/flow Neurology, University values were aimed at. The volume accounting Hospital, S-901 87 was to UmeA, Sweden method used calculate the pressure/flow B Kristensen Material and methods relation. The slope for the pressure/flow values J Malm Between 1975 and 1990, 13 patients admitted is equal to the CSF outflow conductance. The P Markgren to this department had a selective cerebral CSF formation rate (qf) was determined by J Ekstedt angiography verified diagnosis of non-septic lowering the CSF pressure to a value of about Correspondence to: Dr Kristensen SSST. Ten of the patients (seven women and O kPa for a sufficient period to produce a Received 4 March 1991 three men) were followed up over a mean of stable pressure and outflow into the bottle. and in revised form 5-8 years 2-15 and 70 CSF Finally, the pressure difference across the CSF 11 July 1991. (range years), Accepted 14 August 1991. hydrodynamic investigations were performed outflow pathways (Pdo0) and the sagittal sinus 288 Kristensen, Malm, Markgren, Ekstedt

Table 1 Normal values for CSF hydrodynamic variables Table 3 Outcome of 10 patients with superior sagittal (58 patients (for P¢,I00) and 15 to 83 years) in supine sinus thrombosis J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.287 on 1 April 1992. Downloaded from horizontal position. Reference level: cranial sagittal centre; constant pressure infusion method with artificial Time for resolution CS!? No sex or age differences noted Patient of papilloedema No Recovery (months) Sequelae 90% Confidence 1 + 12 Mean SD intervals 2 + 5 3 + 9 Lumbar resting 4 + 27 pressure (Pr,) 1-4kPa 0-2 1-2 to 1-8 5 + 84 Conductance of CSF 6 + 6 outflow pathways 7 - Discrete motor (G ) 18-0 mm3kPa-'s-' 4-0 12-0 to 26-0 dysunction, CSFI rmation (qf) 6-7 mm3s-1 1-4 4-5 to 9 5 Partial complex Pressure difference seizures across outflow 8 + 11 pathways (Pdop) 0 4 kPa 0-1 0 3 to 0-6 9 + 12 Sagittal sinus pressure 10 - Partial complex (P,,) 1-0 kPa 0-2 0 7 to 1-4 seizures

pressure (P..) were calculated according to the the four patients who had generalised epileptic formula'": seizures in the acute phase had later recurrence (patient 7). The others have stopped anti- Pdop= qf/G0p and P,, = PC - Pdop epileptic drugs. The calculated values of PS. express the mean value of the pressures in the major dural Neuroradiology Selective carotid angiography sinuses. The normal values for CSF hydro- identified seven patients with an isolated SSST dynamic variables (table 1) were obtained from (no involvement of other sinuses). The occlu- patients in whom medical history, as well as ded sinus could not be visualised in five medical and neurological investigation, indi- patients, indicating complete thrombotic cated no organic neurological or circulatory occlusion (table 4). The three patients investi- disorder. This control group included 58 gated at least one month after onset all had a patients. 3 partial, isolated thrombosis. Each patient's SI units have been used, and the following CSF hydrodynamic variables are shown in conversion factors may be useful: pressure figure 1. All patients had raised sagittal sinus (1 kPa = 102 mm H20 = 7-5 mm Hg); con- (P..) and intracranial pressure (P,.) at their first ductance (1 mm3 kPa-'sec-' = 6 x 1i3 ml investigation. The pressure difference across (cm H2Oy' = 8 x 10-3(mm Hg)-' min); and the CSF outflow pathways (PdOp) was pre- resistance (the inverse of conductance). served or slightly increased. Six patients were studied within two months after onset. The highest pressure was recorded at either the first Results or second measurement. Pressures gradually The clinical findings are summarised in table declined (P,8 and Pcl) over time in all patients 2. Six patients (patients 1, 3, 4, 5, 6, and 8) but returned to normal in only two patients

had a well defined syndrome with symptoms (case 7 and 10) after eight and 15 years, http://jnnp.bmj.com/ related to intracranial hypertension (headache, respectively. The presence of total or partial papilloedema, impaired consciousness), with thrombotic occlusion on initial angiography or without generalised epileptic seizures. The did not appear to correlate with the long term others had focal symptoms, with or without development of pressure or to clinical out- signs ofintracranial hypertension. Two patients come. Conductance was normal or slightly to were left with sequelae (table 3). Only one of moderately decreased. A more pronounced on September 28, 2021 by guest. Protected copyright. Table 2 Clinical characteristics of 10 patients with superior sagittalis sinus thrombosis. Mode of onset indicated as time interval elapsed between appearance offirst symptom and date of entry to hospital Duration CSF between Age Follow up hydrodynamic onset andfirst Patient at onset time investigations investigation Mode of Neurological No Sex (years) (months) (No) (months) presentation features Cause 1 M 20 52 4 2 Acute Somnolens, Ha, Hereditary AT III- Pe, GES deficiency 2 M 23 136 9 0-1 Subacute Partial motor Colitis ulcerosa seizures, Hp, Ha, Pe 3 F 22 70 9 1 Subacute Ha, Pe Idiopathic 4 F 36 64 6 9 Chronic Ha, Pe Idiopathic 5 F 53 184 12 24 Chronic Ha, Pe Head injury 6 F 23 25 2 5 Acute Somnolens, Ha, Post partum Pe, GES 7 F 35 99 8 2 Acute Coma, Hp, Pe, GES Post partum, hereditary dysfibrogenemi 8 F 21 122 12 1 Subacute Ha, Pe Oral contraceptives 9 M 18 60 6 2 Acute Somnolens, Hp, Idiopathic Pe, GES 10 F 40 180 2 108 Chronic Partial complex Sarcoidosis seizures, Ha GES = generalised epileptic seizures; Ha = headache; Pe = papilloedema; Hp = hemiparesis. CSF hydrodynamics in superior sagittal sinus thrombosis 289

Table 4 Angiographic findings in 10 patients with superior sagittal sinus thrombosis J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.287 on 1 April 1992. Downloaded from SSS Other sinus involvement Patient No Total Partial Yes No Cerebral veins CoUlaterals 1 + + Transcerebral 2 + LS + SS Cortical 3 + + 4 + + Cortical 5 + + Meningeal 6 + SS Cortical 7 + + + Transcerebral Cortical 8 + LS Transcerebral + extracranial 9 + + + Transcerebral + Cortical cortical 10 + + Cortical SSS = superior sagittal sinus; SS = straight sinus; LS = lateral sinus.

decrease was seen in patients with a complete Discussion sagittal sinus thrombotic occlusion. No con- The natural history of SSST has not been well sistent changes in conductance were seen documented.' We have studied CSF hydro- although in some cases an initial decreased dynamics over a mean of 5-8 years from the conductance was later normalised. The CSF acute or subacute to the chronic phase in 10 formation rate (qf), which was normal in all patients with SSST, and our patients may thus patients, did not vary over time. No optic nerve reflect the natural course of the condition. damage could be detected except for slightly None of our patients underwent shunting or enlarged blind spots three patients (1, 2, and other neurosurgical procedures, and only two 4). Hydrocephalus was not found in any of the patients were optimally treated with anti- patients on repeated CT scans (table 5). When coagulants (heparin in the acute phase) and seen, signs of cerebral oedema resolved in all some had short term medical treatment aimed cases with time. No patient had a recurrence of at reducing brain oedema in the acute phase thrombosis. (including steroids, mannitol, or diuretics). The main limitation of this study was that the Neuropsychological assessment Four patients (3, patients studied were highly selected. Most 4, 7, and 8) were evaluated at least twice in the were suspected of having intracranial hyper- chronic stage with standardised neuro- tension and were referred to our clinic, which psychological testing; one patient had four offers the facilities for CSF hydrodynamic examinations. No overt clinical symptoms monitoring. Thus neither acute cases with a related to cognitive dysfunction were found in fulminating course nor the benign forms which these four. Patient 2 had a normal test result recover rapidly and completely are likely to five years after onset. A slight decrease in fine have been referred. The clinical characteristics motor speed in the right hand and in the ability of our patients do not, however, essentially for perceptual analysis was noted in patient 4, differ from contemporary clinical materials.' http://jnnp.bmj.com/ 18 months after the onset of symptoms. In There are three intracranial components or patient 7 a discrete impairment was seen at the compartments-brain tissue, blood, and first investigation and a minor deterioration CSF-that if pathologically altered could involving inductive logistics and learning of cause intracranial hypertension. Our view of audioverbal information had occurred at final the predictable hydrodynamic consequences of testing seven years later. In patient 8 a minor a superior sagittal sinus thrombosis is illustrat- decline in tests of recent memory with in sub- ed figure 2. In our patients, the main on September 28, 2021 by guest. Protected copyright. clinical dysfunction of higher adaptive cap- hydrodynamic features were increase ofPSS and ability was detected six years after baseline PC,. Animal studies have shown a direct relation testing. between the increase in sagittal sinus pressure and CSF pressure,"4 and CSF pressure will increase by an amount equal to the increase of Table 5 Findings on CT scans in first (early) and last When sinus is (late) investigation. Time in brackets marks intervalfrom PSS.'5 sagittal pressure raised, onset of symptoms to scan engorgement of cortical veins is likely to cause an increase in total intracranial blood volume Patient consequent on the impaired venous flow into No Early Late the sagittal sinus. This excess intracranial 1 Empty delta sign (1 day) Normal (3 weeks) volume may further increase intracranial pres- 2 Diffuse oedema, slit ventricles (2 days) Normal (12 months) sure. The increase of intercerebral venous 3 Normal (1 month) Normal (23 months) blood pressure elevates hydrostatic capillary 4 Normal (9 months) 5 Normal (36 months) Normal (140 months) pressure, thereby producing an increase in net 6 Empty delta sign + central capillary filtration and the possibility of a oedema (1 week) Normal (2 months) 7 Two frontal left sided Minor left sided progressive cerebral oedema. Ventricular com- haemorraghic infarctions substance defect pression may be seen on CT scan in up to half (3 days), small ventricles (21 months) 8 Normal (1 month) Normal (46 months) of patients in the acute phase of SSST.'6 The 9 Haemorrhagic left sided Left sided hypodensity increase in brain volume may in itselflead to an frontal infarction (3 days) (15 months) 10 Normal (108 months) additional increase in Pss. Direct compression of the sinuses and lateral lacunae may follow 290 Kristensen, Malm, Markgren, Ekstedt

Figure I Course of various pressure values (PP,,P OP,,) and conductance (G ,) plotted against time. Dotted line in pressure value curves marks J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.287 on 1 April 1992. Downloaded from 90% confidence limit for Pc, upper normal value. Low conductance values are defined as values faUling within shaded area on GoP curves. 0W)12~~~~~~~~~~~~~~~~~~~~~~~~~~~~CCXit

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Figure 2 Overview of mechanisms and development of CSF hydrodynamic events after SSST; according to findings in present study. http://jnnp.bmj.com/ elimination of the parasagittal subarachnoid pletely occluded by fibrous tissue with only space, further compromising venous outflow. small sinusoidal channels present which would If further pressure elevation occurs or is not not have permitted adequate drainage of relieved, coma and death may ensue. In most venous blood from the brain.'7 In individual patients, however, the deterioration is transient patients the amount of blood flowing out and spontaneous improvement is the rule. This through collaterals or a partially patent sinus

improvement is probably more a reflection of probably varies. Collaterals were present in all on September 28, 2021 by guest. Protected copyright. the adequacy of collateral channels than to our patients who had a complete thrombosis. restoration ofblood flow through a recanalised Those patients with no collaterals on angiog- occluded sinus lumen.'7 In case 9 a first raphy would have to rely on sufficient outflow angiogram three days after onset of symptoms via the sinus (patient 3). Bousser et al reported showed a complete thrombosis but no col- that all patients with complete SSST in a group laterals, and he was in a critical phase for 10 with cerebral vein thrombosis had anastomoses days. Two weeks later a second angiogram on angiography whereas two patients with clearly showed collaterals but the thrombotic partial thrombosis did not.' In our series one occlusion was completely unchanged. The patient (patient 10) whose pressure levels persistently high PSS in our patients may well returned to normal had a repeat angiogram indicate that thrombotic occlusion is com- five years after onset which showed a more monly permanent. It should be emphasised extensive collateral system that might explain that PSS represents an indirect calculated mean the decrease in pressure levels. pressure of the major dural sinuses and is Treatment in the acute phase should aim to presumably raised in the case of obstructed induce thrombolysis and prevent further venous outflow due to thrombosis of the thrombosis. Effective thrombolysis in the early superior sagittal sinus or its bridging veins, or stage might prevent the persistent intracranial both. In patients who survived for a consider- pressure elevation that we saw in our patients. able period after SSST but were examined Several studies have reported the use of fib- postmortem the lumen of the superior sagittal rinolytic treatment with varying success."8 '" sinus has been reported to be almost com- Early heparin treatment may improve outcome 292 Kristensen, Malm, Markgren, Ekstedt

by preventing thrombus extension20 which transcerebral pressure difference between the J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.4.287 on 1 April 1992. Downloaded from further compromises the outflow of venous ventricular system and the subarachnoid cort- blood, additionally increasing intracranial ical space as a cause ofventricular enlargement pressure. Total sagittal sinus occlusion is said should not be present in those patients in to be often fatal.2' In our study, no obvious whom the freely patent CSF spaces prevent the difference in the clinical course and hydro- development of any such pressure gradients. dynamic variables was detected between cases In the event of acute intracranial pressure with partial and complete thrombosis, prob- elevation, alterations in consciousness dis- ably reflecting the limited size and selectivity of appear as cerebral oedema resolves. Survivors our material. generally recover completely. Hydrodynamic An occlusion of the superior sagittal sinus abnormalities may still be seen many years may, to some degree, obstruct resorption of after SSST but when oedema has resolved a CSF by the arachnoid villi (a lower conduct- high intracranial pressure does not seem to ance), leading to increased CSF pressure. In substantially impair cerebral function. Neuro- our patients, conductance was normal or only psychological testing, however, showed some slightly to moderately decreased (moderate patients to have discrete signs of cognitive reduction occuring in patients with a complete dysfunction. No serious visual complications thrombosis). Conductance, when failing to were found in our patients despite their persis- improve during follow up, may be a con- tently elevated intracranial pressure. The limit- sequence of a permanent disturbance of arach- ed ability to compensate for a possible addi- noid villus function. As the CSF formation rate tional increase in intracranial pressure may did not vary Pdop will be preserved or increased mean that patients with SSST who develop a when conductance is lowered according to the stroke or who receive a head injury have a classic relation Pdop = qfr/G.P. The main- higher risk. tenance of the cerebrospinal-sagittal sinus gra- Our results show that after superior sagittal dient encourages CSF resorption. Alternative sinus thrombosis, hydrodynamic abnormal- CSF pathways through venous collateral ves- ities, particularly persistently raised CSF pres- sels may also play a part in CSF drainage. sure mainly due to raised Pss, remain for many Therefore, a fairly small disturbance occurs in years. The change in conductance or CSF the CSF absorption process with only a minor resorption facility plays only a minor part in contribution to intracranial pressure elevation. the increase in intracranial pressure. Despite Under these circumstances treatment by serial the persistently raised CSF pressure hydro- lumbar punctures or various shunting proce- cephalus does not develop and the long term dures can hardly produce more than a margin- clinical course is generally benign. al pressure lowering effect. Only -a few studies have described the We thank Bjorn Haggstrom for his helpful comments concem- hydrodynamic effects of sagittal sinus obstruc- ing the neuropsychological aspects of this article. Financial tion. One of these reported a reversed or support from Karl-Oskar Hansson's foundation, The Swedish Society for the Neurologically Disabled (NHR), and Norr- nullified Pdop but conductance was normal or landsfonden is gratefully acknowledged. slightly reduced.4 Simultaneous recording of sagittal sinus pressure and intracranial pressure

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