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