Neuroradiology (1992) 35:16-24

Neuro--

radiology 9 Springer-Verlag 1992

Cerebrospinal fluid flow III. Pathological cerebrospinal fluid pulsations G. Schroth and U. Klose Department of Neuroradiology, University of T~ibingen,Federal Republic of Germany Received: 26 March 1991

Summary. Cardiac- and respiration-related movements of the cerebrospinal fluid (CSF) were investigated by MRI in 71 patients. In most patients with arteriosclerotic occlusive vascular disease CSF pulsations are normal. Decreased pulsatile flow is detectable in those with arteriovenous malformations, intracranial air and following lumbar puncture and withdrawal of CSE Increased pulsatile flow in the cerebral aqueduct was found in 2 patients with large aneurysms, idiopathic communicating syringomyelia and in most cases of normal pressure hydrocephalus (NPH). CSF flow in the cervical spinal canal is, however, reduced or normal in NPH, indicating reduction of the unfolding ability of the surface of the brain and/or inhibition of rapid CSF movements in the subarachnoid space over its convexity.

Key words: Cerebrospinal fluid (CSF) - CSF flow - Normal pressure hydrocephalus - Syringomyelia

According to the Kellie hypothesis, or the Monro-Kellie doctrine [1] 1, changes in volume of the three intracranial components - blood, brain, and cerebrospinal fluid (CSF) - are only possible with reciprocal compensation. Although diastolic blood flow in the internal carotid and vertebral arteries is relatively high, so that the diastolic/systolic flow variation is relatively small, during cardiac systole some millilitres of blood enter the cranium, whereas the veins have a relatively constant flow, almost independent of the heart's action. During its passage through

p. 102: "... it does not appear very conceivable how any portion of the circulating fluid can ever be withdrawn from within the cranium, without its place being simultaneously, occupied by some equivalent; 9 one of my oldest physiological recollections, indeed, is of this doctrine having been inculcated by my illustrious preceptor in anatomy, the second Monro . . . . standing recorded in his work on the Brain and Nervous System: 'Four', he observers, 'as the substance of the brain is nearly incompressible, the quantity of blood within the head must be the same, or very nearly the same, at all times, whether in health or disease, in life, or death...'."

the arterioles, capillaries, and venules of the brain this increased blood volume leads to an apparent overall increase in size of the brain, which causes CSF to be pushed into the cervical spinal canal as the outer surface of the brain expands. A few milliseconds later the volume increase causes pulsating flow of CSF from the third ventricle, through the fourth, into the basal subarachnoid space [2]. We investigated the effects of pathological changes in the circulatory system, the CSF drainage pathways, and the brain itself, which might lead to changes in these CSF pulsations.

Methods Over 100 investigations of CSF flow were performed on 71 patients using a 1.5 T M R I system. Cardiac-related motion of the CSF was investigated by analysis of the velocity-dependent phase of the CSF protons and flowdependent signal enhancement in magnitude images using ECG-gated F L A S H [2]. Respiration-related CSF flow was investigated by R A C E [3]. The results were compared with the flow patterns in normal volunteers, flow-phantom measurements and computer-simulated calculations [2, 3].

Results

The cerebral aqueduct In 6 of 7 patients with intra- and extracranial arteriosclerotic stenoses, but without occlusion of the arteries supplying the brain, CSF pulsation in the aqueduct was normal or, more often, increased, especially when the vascular disease was accompanied by increased blood pressure. Even in the presence of unilateral occlusion of the carotid artery, the CSF pulsation in the aqueduct may be increased. Only 1 patient with bilateral occlusion of the carotid arteries and a vertebral stenosis on one side showed a re-

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Fig. 1. a A 50-year-old patient with occlusion of both carotid arteries and stenosis of the right vertebral artery. ECG-triggered FLASH sequence reveals almost no CSF movement in the aqueduct. Only images 300450 ms after the R wave of the ECG (Store 19-21) show slight signal increase in the aqueduct (arrow) (FLASH 2D/75 ms/10 ms/90 ~ b Time-course of the value and phase of the protons in the aqueduct

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duction in the amount of CSF pulsating through the aqueduct during the cardiac cycle (Fig. 1 a). Figure 1 b shows signal intensities and phase of the CSF protons in the aqueduct during the cardiac cycle: only the positive phase peak, which registers the flow from the third to the fourth ventricle, is followed by a slight signal increase. Signal increase due to backflow of CSF from the fourth to the third ventricle could not be detected. In 12 tumours narrowing the ventricular system CSF pulsation was altered only when the mass lay close to a foramen linking the ventricles. The time-course and extent of CSF pulsations in the aqueduct were usually normal even when CT or MRI suggested impaired flow with ventr!cular enlargement. The first indication of an imbalance m CSF flow was a shortening of the expulsion period from the third to the fourth ventricle, whereby a clear but short signal peak followed the course of the phase. Furthermore, backflow from the third to the fourth ventricle occurred slowly, spread out over the remainder of the cardiac cycle.. The resulting signal peak remained small or was missing Completely (Fig. 2). There were 2 patients with space-occupying lesions at the craniocervical junction and in the upper cervical spinal

Fig.2. Time-course of the value and phase of the protons in the aqueduct of a patient with a large metastasis of the cerebellum, causing partial blockage of the caudal fourth ventricle

canal; CSF pulsation in the aqueduct was normal in one and slightly reduced in the other. CSF pulsation was normal in the aqueduct of 5 patients with cavernomas and so-called venous angiomas and of 1 with a small arteriovenous malformation. Conversely, 3 with large arteriovenous malformations showed a clear reduction of CSF f o w in the aqueduct (Fig. 3). Increased CSF pulsation was detected in 2 patients with large intracranial aneurysms. One directly abutted the lamina terminalis; presumably, the vascular pulsations were transmitted directly to the third ventricle through this thin membrane, explaining the high peak of the phase in the aqueduct, and its sawtooth-like increase (Fig. 4b). Three patients with an ectatic, high termination of the basilar artery did not show a similar pattern. Illnesses accompanied by a proven increase in the elasticity of the brain are not known. However, cerebral compliance was increased in i patient due to an intracerebral air bubble (Fig. 5 a), probably a porencephalic cyst secondarily put into connection with the ethmoid cells during mild cranial trauma a few days previously. Several preoperative examinations of this symptom-free young athlete showed CSF pulsation in the aqueduct to be reduced

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Fig.3. Arteriovenous malformation with large draining veins (SE/600 ms/22 ms). The flow-dependent signal increase in the aqueduct is very weak and only detectable 300 ms-375 ms (Store 36 and 37) after the R wave of the ECG (FLASH; 75 ms/10 ms/90 ~ Fig.& a Aneurysm of the anterior communicatingartery (SE/600 ms/22 ms) b The ECG-triggered FLASH-sequence (75 ms/10 ms/90 ~ shows the aqueduct to have high signal throughout the cardiac cycle e Time-course of value and phase of CSF protons in the aqueduct

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Fig.& a A 23-year-old patient with a large frontal, intracerebral air bubble (SE/600 ms/16 ms, gadolinium-DTPA), b Flow signals in the aqueduct are barely detectable on the ECG-triggered FLASH-sequences (75 ms/10 ms/90 ~ c Graph of CSFpulsationin the aqueduct showsa

shallow curve of phase (right) without effective signal increase due to the slowly oscillating flow (left). d MRI after replacement of the intracerebral airwith CSF shows normalpulsation in the aqueduct (e parameters as in a). f Normalphase and magnitude of the CSF protons in the aqueduct

20 (Fig. 5 c). Following closure of a tiny defect in the skull base, and replacement of the air by CSF (Fig. 5 d), MRI revealed normal CSF pulsation (Fig. 5 e, f). Seven patients with a clinical suspicion of normal pressure hydrocephalus (NPH) were studied; the diagnosis, however, remained questionable in at least 2 cases. Comparative, fractionated study of the phase and value of 1, 3, 10 and 40 voxels of CSF in the aqueduct showed that in the patients with an enlarged aqueduct the average velocity of

all voxels was approximately the same as in normal persons (Fig. 6 a). In all voxels, even those at the edge of the aqueduct (whose phase and signal intensity time-course was analysed separately, through direct input of their coordinates into the program), change of phase is followed by a rapid, extensive increase in signal. Thus, analysis of the phase and magnitude of the protons indicates large amplitude, pulsatile CSF flow through the aqueduct. Lumbar puncture and withdrawal of 50 ml CSF led to a

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Fig.6a-f. a 60-year-oldpatient with normal pressure hydrocephalus (NPH). a,b Sagittal and axial spin-echo images (600 ms/16 ms) show the enlarged aqueduct in sagittat and axial planes. ECG-triggered FLASH-sequences (75 ms/19 ms/90o) before (e) and immediately following (d) lumbar puncture and withdrawal of 50 ml CSF.

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e,f Graphs of changes in phase and magnitude of 40 CSF voxels in the aqueduct showing rapid flow characteristics, chosen by the computerized CSF-flow analysing program before (e) and after (f) lumbar puncture

21 Fig.Ta, b. A 62-year-old patient with suspected NPH

a Sagittal spin-echo image (600 ms/16 ms) shows that the aqueduct and the third ventricle are only slightly enlarged and the corpus callosum is normal b The first 16 of the 20 ECG-triggered FLASH images (75 ms/10 ms/90~ reveal reduced signal at the centre of the flow-related high signal increase in the aqueduct, indicating turbulent flow Fig.8. RACE measurements of CSF dynamics in the aqueduct of a patient with NPH over 12 s (a) and 7 s (b), retaining a constant pulsation pattern despite forced respiration (FLASH 1D/50 and 30 ms/10 ms/90 o, projection of the signals on the Y-axis of the magnetic field as shown in c)

distinct reduction of pulsation in the aqeduct (Fig.6b), which was slight or undetectable after clinically successful shunt surgery. Semiquantitative study of the CSF dynamics in N P H is more difficult when the aqueduct is not dilated or dilated to only a minor extent, because turbulent flow of CSF in the aqueduct (Fig.7), not seen in a single normal person, changes the time-cours~ of the phase and magnitude. A further characteristic of CSF pulsation in N P H is lengthening of the flow period from the third to the fourth ventricle, which often shows a two-peaked course with a second, late systolic peak. Real-time measurements of CSF dynamics by R A C E in patients with N P H showed that pulsation was very regular, without rhythmic alterations of signal intensity; in particular, the normal respirationrelated modulations were absent (Fig. 8).

The spinal canal It was interesting to see how CSF dynamics were altered by spinal blockage. Seven patients with complete (2) or almost complete (5) cervical stenosis on myelography were examined. CSF pulsation was normal cranially and re-

duced caudal to the spinal stenosis in all 7. With only slight constriction of the spinal canal, the CSF pulsation caudally was reduced, but synchronous with the pulsation cranial to the stenosis. However, in patients with obstruction of the subarachnoid space, CSF pulsation caudal to the stenosis was not synchronous with that above it. By using R A C E , it was possible to show that in these patients CSF pulsation was mainly cardiac-related above the stenosis and respiration-induced below it [4]. Gardner and his colleagues [5, 6] hypothesized that intramedullary cavity formation is due to increased CSF "water-hammer" pulsation in the aqueduct and the fourth ventricle which results in dilatation of the central canal. The CSF dynamics of 7 patients with syringomyelia were therefore examined. A definite increase of velocity and pulse volume of flow in the aqueduct could be found in only i patient (Fig. 9 a). Flow signals synchronous with the heart beat could not be found in the intramedullary cavity itself, nor in the small intramedullary track connecting the syrinx to the fourth ventricle. Insertion of a ventriculoatrial shunt led to lessing of the patient's nausea and tingling paraesthesiae in both hands the following day. Collapse of the fourth ventricle and the intramedullary cavity was shown by M R I and in the axial plane the in-

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Fig.9. a Midsagittal spin-echo image (600 ms/16 ms) shows Chiari II malformation. The dilated aqueduct and fourth ventricle communicate through a fine track with an intramedullary cavity b The first 16 of 20 ECG-triggered FLASH images (75 ms/10 ms/90 ~ reveal increased CSF pulsations in the aqueduct c, d Similar images after insertion of a ventriculoatrial shunt

tramedullary cavity changed from a round, tense shape to a transverse oval form, indicating successful decompression [7]. In addition, pulsation in the aqueduct was clearly reduced (Fig. 9 b). Pulsatile movements synchronous with the heart were not found in the intramedullary cavities in any other patient, apart from 2 whose cavities had fine calibre segments. In the first of these, the narrow segment connected large thoracic and thoracolumbar intramedullary cavities. Since flow signals were detectable with the F L A S H - 2 D technique in the narrow segment, a syringoarachnoid shunt was inserted in the lumbar enlargement, with collapse of the whole syrinx, up to the high cervical level. In the second a large cervical intramedullary cavity was connected to the fourth ventricle through a fine track. While no flow signals synchronous with the heart could be found in the cervical cavity, flow signals were detected in the fine track at the craniocervical junction [7]. Comparison of the pulsation curves in the aqueduct and fourth ventricle indicated that the pulsation in the intramedullary track occured a few milliseconds ahead of that in the aqueduct [7].

As long as the intramedullary cavity did not lead to a spinal block, the CSF movements in the spinal subarachnoid space of the patients with syringomyelia did not show obvious deviation from the normal pattern.

Discussion If CSF pulsation is caused by the diastolic/systolic fluctuation of blood volume in the brain, it would be anticipated that diseases of the brain vessels were accompanied by an alteration in CSF flow. However, our investigations revealed that even patients suffering from severe arteriosclerotic stenoses usually have normal CSF pulsation. Only in extreme cases was a reduction in CSF pulsation detectable (Fig. 1). Possible causes of the reduction in the CSF pulsation found adjacent to large arteriovenous malformations are (1) reduction of peripheral resistance through the arteriovenous shunt, leading to an increase in diastolic blood flow velocity and hence a reduction of the systolic/di-

23 astolic velocity difference; (2) replacement, through the malformation itself and especially its draining veins, of the two incompressible intracranial compartments - brain and CSF - by venous blood, which can be rapidly expressed into the extracranial space after increase of intracranial pressure; and (3) reduction in systolic/diastolic intracranial blood volume difference, because veins have arterial flow characteristics in the presence of large arteriovenous shunts; the driving force of the CSF pulsation is thereby diminished. It is not surprising that air within the cranium damps CSF pulsation; this may explain why the amplitude and velocity of CSF pulsation, determined by Du Boulay et al. [8] through the shifting of an air/CSF level, are smaller than in our work, using noninvasive MRI measurements [2]. There was no evidence of a capsule around the airfilled lesion shown in Fig. 5. It can thus be assumed that the arterial pulse is transferred directly to the air bubble, resulting in a smoothing of the CSF pulsation in the aqueduct. Since its first description by Hakim and co-workers [9, 10], the clinical syndrome of gait disturbance, mental deterioration, and urinary incontinence with ventricular enlargement despite normal CSF pressure has been referred to as NPH, but its pathophysiology is still poorly understood. In most cases the CSF pulse volume in the aqueduct is increased. As a result, the CSF flows through an enlarged aqueduct (Fig. 6) or through a channel of normal size between the third and the fourth ventricles with increased velocity and a turbulent flow (Fig. 7). Due to the limited number of patients examined, it could not be determined if this was merely a matter of degree. According to our measurements (Fig. 6b) in NPH, as in normal volunteers, the quantity of CSF moved caudally during systole is greater than the diastolic reflux from the fourth to the third ventricle. Therefore, cisternographic demonstration of reverse mixing of the CSF as far as the lateral ventricles [11] is not the result of a reversal of CSF flow; the high amplitude ventricular pulsation seems to promote this mixing. Since an increase in intracranial CSF pulsation is possible only when a corresponding enlarged compliance space is available, increased CSF flow was expected in the spinal canal. However, pulsatile CSF flow in the cervical region was not increased in 3 patients with NPH, in whom repeated flow measurements were performed in both the spinal canal and the aqueduct. On the contrary, the CSF flow signals were definitely reduced in at least 1 patient. The MRI data collected thus far are not sufficient to enable a conclusive interpretation; since regional cerebral blood flow of patients with NPH is normal [12] or even reduced [13], the increased CSF pulsation in the aqueduct cannot be the result of increased vessel pulsation. According to lumbar, intracranial-cisternal, and ventricular pressure measurements and the time-course of pressure changes in infusion and perfusion tests, intracranial compliance is likely to be reduced in these patients [14]. No information is available as to whether this can be explained by reduced compliance in the spinal canal or whether the expressible intracranial blood volume is reduced.

An attempt can, however, be made to explain the findings of increased aqueductal and decreased cervical CSF pulsation in NPH. The starting point is the consideration that due to the development of NPH, the "mobile compliance" of the intracranial subarachnoid space is initially reduced as a result of subarachnoid haemorrhage, meningitis, trauma, or any other condition which reduces the unfolding ability and mobility of the surface of the brain and/or inhibits rapid CSF movements in the subarachnoid spaces by arachnoid adhesions. Consequently, the systolic increase in volume of the brain cannot be compensated for by a rapid shift of intracranial, subarachnoid CSF into the spinal canal, following the unfolding of the brain surface. The result is increasing centripetal systolic pressure and volume load on the ventricular system, causing accelerated intraventricular CSF shift. Periventricular interstitial oedema, associated with transpendymal leakage of CSF would be explained in this model as the result of ependymal damage caused by the unphysiological pressure and volume load. A relatively steady state would be possible if sufficient CSF could be shifted caudally in the spinal canal through the enlarged aqueduct and the foramina of the fourth ventricle to compensate for the reduced compliance of the surface of the brain. On the basis of this hypothesis, NPH can be differentiated from hydrocephalus due to impaired resorption of CSE The pathological substrate of both diseases is alteration of the leptomeninges, often occurring after infection or subarachnoid haemorrhage. Fibrotic adhesions of the parietal membranes lead to disturbances in CSF resorption, resulting in a hydrocephalus. If the visceral leptomeninges are primarily affected, adhesions of the sulci lead to a reduction in expressible subarachnoid CSF which, in association with the reduced mobility of the brain surface, decreases the external compliance of the brain; NPH can then develop. According to this hypothesis, hydrocephalus due to impaired resorption and NPH are pathophysiologically distinct entities, although both have the same origin and the same morphological correlate (the leptomeninges) and often appear together in varying proportions. This may explain the confusing and often contradictory results of clinical and physiological investigations [15]. Chronic spondylotic stenoses of the cervical spinal canal can lead to intramedullary lesions, seen on axial T2-weighted MRI as bilateral "snake eye" hyperintense areas. According to our observations these lesions, detectable mainly cranial to the maximum stenosis, cannot be explained solely by the vascular anatomy of the spinal cord [4]. Since CSF pulsation is more intense cranial to the stenosis than caudal to it, it is conceivable that the CSF from the spinal subarachnoid space penetrates into the spinal cord via the enlarged Virchow-Robin spaces, as suggested by Ball and Dayan [16] in syringomyelia giving rise to the intramedullary signal change. Gardner's hypothesis as to the origin of syringomyelia suggests a malformation of the foramina of the fourth ventricle [5, 6]. In the presence with a Chiari malformation, found by Gardner in 68 of 74 patients, CSF could still drain adequately from the fourth ventricle to the basal cisterns. However, the pressure peaks evoked by arterial pul-

24 sation of the choroid plexus [6] could no longer be compensated for. Because of this, arterial CSF pulsations " h a m m e r " in the central canal of the spinal cord, which in turn dilates with time and diverticulum-like intramedull a r y cavities can arise after rupture of the primary hydromyelia. Gardner's hypothesis is supported by the results of the CSF flow m e a s u r e m e n t s in one of our patients and especially by the collapse of the intramedullary cavity following insertion of a ventriculoarterial shunt, with reduction of CSF pulsation in the aqueduct (Fig. 9). However, in the only patient in w h o m pulsations synchronous with the heart beat were detected in the fine track of a syringobulbia cavity, CSF pulsation in the cavity preceded pulsation in the aqueduct [7]. This supports the hypothesis of D u Boulay et al. [17] who assumed that the cisternal CSF pulse wave plays an important role in the development of syringomyelia. This pulse wave precedes CSF pulsation in the aqueduct by approximately 100 ms [7]. However, since no CSF pulsation synchronous with the heart beat was detected within the syrinx itself in the majority of our patients, we must assume that pressure shifts play a m o r e decisive role than volume load. However, it is possible that syringomyelia m a y in fact be caused by CSF volume shifts in connection with physical strain, coughing, sneezing, or the head-down position, as hypothesized by Williams [18]; these shifts have not yet b e e n recorded in our noninvasive M R I measurements.

References 1. Kellie G (1824) An account of the appearance observed in the dissection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were discovered in the vicinity of Leigh on the morning of the 4th November 1821, with some reflections on the pathology of the brain. Trans Med Chir Soc (Edinb) 1:84-169 2. Schroth G, Klose U (1992) Cerebrospinal fluid flow. I.Physiology of cardiac related CSF pulsations. Neuroradiology 35:1-9 3. Schroth G, Klose U (1992) Cerebrospinal fluid flow. II.Physiology of respiration - related CSF pulsations. Neuroradiology 35: 10-15 4. Faiss J, Schroth G, Grodd W, K6nig E, Will B, Thron A (1990) Central spinal cord lesions in stenosis of the cervical canal. Neuroradiology 53:11%123 5. Gardner WJ, Abdullah AF, Cormack LJ (1957) The varying expressions of embryonal atresia of the fourth ventricle in adults.

Arnold-Chiari malformation, Dandy-Walker syndrome, arachnoid cyst of the cerebellum and syringomyelia. J Neurosurg 14: 591-607 6. Gardner WJ (1965) Hydrodynamic mechanism of syringomyelia: its relationship to myelocele. J Neurol Neurosurg Psychiatry 28:247-259 7. Schroth G, Palmbach M, Steinmetz H (1989) MRI of syringomyelia: comparison with clinical symptoms and pre- and postoperative results. In: Nadjmi M (ed) XVth Congress of the European Society of Neuroradiology 1988. Springer, Berlin Heidelberg New York, pp 187-190 8. Du Boulay GH, O'Connell J, Curie J, Bostick T, Verity P (1972) Further investigations on pulsatile movements in the cerebrospinal pathways. Acta Radio113: 496-523 9. Hakim S, Adams RD (1965) The clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. Observations on cerebrospinal fluid hydrodynamics. N Neurol Sci 2:307-327 10. Adams RD, Fisher CM, Hakim S, Ojemann RG, Sweet WH (1965) Symptomatic occult hydrocephalus with "normal" cerebrospinal fluid pressure. A treatable syndrome. N Engl J Med 2: 307-327 11. Tator CH, Fleming JFR, Shepard RD, Turner VM (1968) A radioisotopic test for communicating hydrocephalus. J Neurosurg 28:327-340 12. Kushner M, Younkin D, Weinberger J, Hurtig H, Goldberg H, Reivich M (1984) Cerebral hemodynamics in the diagnosis of normal pressure hydrocephalus. Neurology 34:96-99 13. Mathew NT, Meyer JS, Hartmann A, Ott EO (1975) Anormal cerebrospinal fluid blood flow dynamics. Implications in diagnosis, treatment, and prognosis in normal pressure hydrocephalus. Arch Neuro132:657-664 14. Borgesen SE, Gjerris F (1987) Relationships between intracranial pressure, ventricular size, and resistance to CSF outflow. J Neurosurg 67:535-539 15. Vanneste J, Acker R von (1990) Normal pressure hydrocephalus: did publications alter management? J Neurol Neurosurg Psychiatry 53:564-568 16. Ball MJ, Dayan AD (1972) Pathogenesis of syringomyelia. Lancet II: 799-801 17. Du Boulay GH, Shah SH, Currie JC, Logue V (1974) The mechanism of hydromyelia in Chiari type 1 malformations. Br J Radio147: 579-587 18. Williams B (1971) Further thoughts on the valvular action of the Arnold-Chiari malformation. Dev Med Child Neurol 13 [Supp125]: 105-113 Prof. G. Schroth Department of Neuroradiology Eberhard-Karls-Universit~it Hoppe-Seyler-Strasse 3 W-7400 Ttibingen Federal Republic of Germany

Cerebrospinal fluid flow. III. Pathological cerebrospinal fluid pulsations.

Cardiac- and respiration-related movements of the cerebrospinal fluid (CSF) were investigated by MRI in 71 patients. In most patients with arterioscle...
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