Journal of Neurology, Neurosurgery, and Psychiatry, 1972, 35, 468-473

Dynamics of the cerebrospinal fluid and thespinal dura mater'

ALBERT N. MARTINS, JOHN K. WILEY, AND PAUL W. MYERS

From the Neurosurgery Service, Wilford Hall U.S.A.F. Hospital, San Antonio, Texas, U.S.A.

SUMMARY During myelography we observed the contrast material in the spinal subarachnoidspace while we changed: (1) the intracranial blood volume by CO2 inhalation, hyperventilation, andjugular vein compression; (2) the intra-abdominal and intrathoracic pressure by forced expirationwith glottis closed; and (3) the CSF volume by withdrawals and reinjections of fluid. The spinaldural sac enlarges with increases in volume of both intracranial blood and CSF. It partially collapseswith reductions in volume of both intracranial blood and CSF. With increases in intra-abdominaland intrathoracic pressure, the thoracolumbar sac partially collapses, while the cervical sac enlarges.From these observations we conclude that the spinal dural sac is a dynamic structure, readilychanging its capacity in response to prevailing pressure gradients across its walls. It acts as a reservoirfor CSF, which moves to and fro through the foramen magnum in response to changes in cerebralblood flow. By its bladder-like ability to alter its capacity, the spinal dural sac provides the 'elasticity'of the covering of the central nervous system.

By additions and withdrawals of fluid, we canquite easily change within limits the volume ofthe pool of cerebrospinal fluid (CSF) in whichare immersed the brain and spinal cord. Conse-quently, the covering of the central nervoussystem (CNS) cannot be regarded as truly rigid-that is, it possesses, for want of a better term,'elasticity'. What provides this so-called elas-ticity? Certainly not the cranial dura mater, for,with a closely applied rigid bony skull as abuttress, the cranial dura mater and the skullform together a container of unalterablecapacity. On the contrary, the spinal dura mater(together with the arachnoid mater) buttressednot by bone but by a network of veins and fat inthe epidural space seems potentially able to alterits capacity.Our current concepts of dural elasticity, how-

ever, remain influenced by the work of Weed andhis co-workers, completed almost 40 years ago(Weed, 1929; Weed and Flexner, 1933; Weed,Flexner, and Clark, 1932). Although recognizingthat the spinal dura mater has potential elas-ticity, they regarded the role of the venoussystem of the CNS as preeminent in providingfor the elasticity of the CNS covering. After aseries of animal experiments concerned with

1 Presented in part as a movie to the meeting of The AmericanAssociation of Neurological Surgeons, Houston, April 1971.

468

CSF pressure changes produced by changes inposition, Weed and his co-workers concludedthat the apparent elasticity of the dura mater isbasically provided by the changes in volume ofthe intradural venous blood (Weed et al., 1932),and that induced changes in intracranial CSFvolume were possible chiefly because the'cerebral venous bed' compensated for them(Weed and Flexner, 1933). Similarly, Ryder,Espey, Kimbell, Penka, Rosenauer, Podolsky,and Evans (1953) concluded that 'changing thevolume of the cerebrospinal fluid space inducesan immediate reciprocal change in the cranio-spinal blood volume in all men'. In 1960Bowsher discarded completely the concept of thedura mater being elastic when he wrote '. . . thedura should be regarded as a rigid container ...the elasticity of the fluid system is due mainly tothe elasticity of its contained veins'.

But to the myelographer and the surgeonalike, the spinal dural sac does not appear to berigid at all. Indeed, according to Pollock andBoshes (1936), as long ago as 1892 H. Grasheyrecognized that the spinal dural sac probablycould alter its capacity. Subsequently others alsohave implied agreement (Foldes, Keutmann,and Hunt, 1958; Kety, 1965; DuBoulay andEl Gammal, 1966; Ponssen and Van Den Bos,1971). Nevertheless, some authors continue to

Protected by copyright.

on July 7, 2020 by guest.http://jnnp.bm

j.com/

J Neurol N

eurosurg Psychiatry: first published as 10.1136/jnnp.35.4.468 on 1 A

ugust 1972. Dow

nloaded from

Dynamics of the cerebrospinal fluid and the spinal dura mater

express or imply acceptance of the concept ofdural elasticity as advocated by Weed's andRyder's groups (Von Storch, Carmichael, andBanks, 1937; Kunkle, Ray, and Wolff, 1943;Hayden, Shurtleff, and Foltz, 1970; Katzmanand Hussey, 1970; Sibayan, Begeman, King,Gurdjian, and Thomas, 1970). Therefore wefelt it would be profitable to re-examine what thespinal dural sac contributes to this elasticity. Tothis end we studied and report in this paper whathappens to a Pantopaque-filled spinal dural sacduring routine clinical myelography when onechanges: (1) the intracranial blood volume byCO2 inhalation, hyperventilation, and jugularcompression; (2) the intra-abdominal and intra-thoracic pressure by forced expiration withglottis closed (Valsalva manoeuvre); and (3) CSFvolume by withdrawals and re-injections offluid.

METHOD

Twelve informed volunteers were selected fromamong those patients who were to undergo myelo-graphy for suspected intervertebral disc disease. Thelumbar puncture was accomplished; about 12 ml.CSF was withdrawn and an equal amount ofPantopaque (iophendylate) injected intrathecally.After the diagnostic procedure was concludedroutinely, the following manoeuvres were performedwhile the changes in the column of Pantopaque wereobserved fluoroscopically and recorded both onregular radiographs and cineradiographically: withthe subjects horizontal and Pantopaque filling hiscervical canal from the rim of the foramen magnumto the fifth or sixth cervical vertebra, he was asked toperform a 'Valsalva' two or three times. Thecolumn of contrast medium was returned to thelumbosacral sac, the subject positioned horizontally,and then he was asked in turn to hyperventilate fortwo minutes, breathe 10% CO2 in oxygen for twominutes, and repeat the 'Valsalva' two or threetimes. Then both of his jugular veins were com-pressed for about 15 seconds. Finally 15 ml. CSFwas removed and then re-injected.

RESULTS

During hyperventilation the sac collapses par-tially as indicated by the Pantopaque columnnarrowing and elongating. When hyperventila-tion stops the sac gradually resumes its originalappearance within two minutes.When 1000 CO2 in oxygen is inhaled, the sac

distends as indicated by a column that widens asit moves caudally, filling the lumbosacral nerveroots. The sac regains its original appearance

within two minutes after CO2 inhalation isstopped.

In response to forced expiration with glottisclosed (Valsalva manoeuvre), the column in thelumbosacral area almost instantaneously nar-rows and elongates as the sac collapses partially.In the cervical area, with the Pantopaquecolumn positioned at the foramen magnum, thesac abruptly widens slightly during the man-oeuvre. The column does not move intra-cranially. At the end of the Valsalva manoeuvre,the column in either location returns quickly toits previous appearance and position.

In response to bilateral jugular compression,the sac again distends as indicated by the columnthat widens, moves caudally and fills the lumbo-sacral nerve root sleeves. The response reachesmaximum in five to 10 seconds. With release ofjugular compression, the column regains in afew seconds its pre-compression appearance.When CSF is withdrawn, the sac partially

collapses as indicated by the Pantopaquecolumn becoming narrower and longer; whenCSF is re-injected, the sac recovers its formerconfiguration.The changes in appearance and position of the

Pantopaque column were the same in allsubjects for each manoeuvre, although theirmagnitude did vary. The changes are somewhatdifficult to document satisfactorily with ordinaryserial radiographs, but are easy to appreciate atfluoroscopy as well as upon subsequent study ofthe cineradiographs (Figure).

DISCUSSION

In interpreting the results of these experiments,we have assumed that changes in the appearanceof the column of Pantopaque reflect changes inthe size, and hence capacity, of the visualizedsegment of the spinal dural sac. When thesilhouette of a 12 ml. column of Pantopaquebecomes longer and narrower, we have assumedthat the sac in that area has partially collapsed.When it becomes shorter and wider, we haveconversely assumed that the sac there has dis-tended and increased its capacity. If our assump-tions are valid, we may conclude from thesesimple and easily reproducible experiments thatthe spinal dural sac is a dynamic structure thatreadily changes its capacity in response to pre-vailing pressure gradients across its walls. Andsince the cranial and spinal CSF compartmentsnormally communicate freely at the foramen

469P

rotected by copyright. on July 7, 2020 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.35.4.468 on 1 August 1972. D

ownloaded from

Albert N. Martins, John K. Wiley, and Paul W. Myers

L,

,

FIG. 1. Serial radiographs of a Pantopaque-filled lumbosacral spinal dural sac from a single subject. Betweenexposures the horizontal position of the subject as well as the position of the x-ray tube and cassette holderremain unchanged. In response to changes in both intracranial blood volume andpressure within the thorax andabdomen induced by various manoeuvres, the spinal dural sac readily alters its volume and returns to the basalappearance at the end of each manoeuvre. From left to right: (a) basal appearance; (b) appearance after twominutes ofhyperventilation; (c) appearance after breathing 10% CO2 in oxygen for two minutes; (d) appearanceduring Valsalva manoeuvre; (e) appearance after bilateral jugular compression for 15 seconds. (On cin&radio-graphs the changes are more readily appreciated.)

magnum, it follows that a spinal dural sac ofvariable capacity can account for the limitedelasticity of the entire covering of the CNS.

Other data, aside from our own, conflict witha hypothesis that maintains that the apparentelasticity of the dura mater is really an attributeof its contained veins, which are presumed toexpand or collapse in response to intraduralvolume and pressure changes. Specifically, suchan hypothesis could not explain the intraduralvolume adjustments dictated by rapid changes inCNS blood volume known to accompanychanges in cerebral blood flow (Risberg, Ancri,and Ingvar, 1969). With these changes of CNSblood volume, the dural envelope must likewisechange its capacity. According to current evi-dence, neither brain parenchyma nor the CSF

compartment is able to change its own volumereciprocally and quickly enough in response tochanges in cerebral blood flow to maintainconstant the total volume enclosed within thedura mater (Mcllwain, 1966; Rubin, Henderson,Ommaya, Walker, and Rall, 1966; Davson,1967; Cutler, Page, Galicich, and Watters, 1968).Furthermore, many independent investigators,Cushing himself the first, have observed directlythat cerebral veins do not collapse significantlywhen CSF pressure is increased by intrathecalinjection of fluid (Cushing, 1902; Wolff andForbes, 1928; Fog, 1933; Wright, 1938;Hekmatpanah, 1970). Described first by Wright(1938), the 'cuff-constriction' of the bridgingveins at their junction with the dural venoussinuses, which varies in degree according to the

470P

rotected by copyright. on July 7, 2020 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.35.4.468 on 1 August 1972. D

ownloaded from

Dynamics of the cerebrospinal fluid and the spinal dura mater

CSF pressure, apparently prevents collapse ofthe veins. This phenomenon is governed by theprinciples of fluid dynamics related to flowthrough collapsible tubes that are surrounded byfluid at higher pressure than the outflow pres-sure, as elucidated by Permutt and Riley (1963).

Accordingly, the theoretical and experimentalevidence mentioned above, together with ourown observations, support an alternative view.The elasticity of the dura mater we believe canbest be explained by the collapsible nature of thespinal dural sac, which we envision as anelongated thin-walled bladder, normally notfilled to capacity, giving to or accepting fromthe intracranial spaces, via the foramen magnum,CSF according to the prevailing pressure gra-dient. In changing its capacity, true rubberballoon-like dural elasticity probably plays aninsignificant role. Rather the sac seems to fill andempty like a cloth or leather water bag. Simplyby removing and reinjecting CSF and observingthe changes in the appearance of the column ofPantopaque, one readily establishes that thespinal dural sac can change its capacity. Oneadds further evidence of a more physiologicalnature by observing the sac as the intracranialblood volume is increased either by hypercapnia-induced increases of cerebral blood flow or bythe intracranial venous congestion that followsjugular compression. The caudal sac, silhouettedby the Pantopaque column, is seen to enlargefirst and then return to its previous appearancewhen either manoeuvre is terminated, pari passuwith return of intracranial blood volume tonormal. As the intracranial blood volume fallsin response to hypocapnia induced by hyper-ventilation, the sac partially collapses as CSFleaves it to replace the volume of blood thatleft the cranial cavity. This apparent reciprocalrelationship between the intracranial blood andCSF compartments, permitted by the spinaldural sac, allows the brain both the protectionof the rigid skull and the flexibility of a vascularbed that can alter its capacity like that of any

other organ. In this generally ignored role theCSF must certainly perform one of its importantfunctions.

Because the spinal canal is rigid, we mustpostulate that with each change in the volume ofthe spinal dural sac, the volume of tissue withinthe canal, but extradural, must also change byan equal and opposite amount. Since loose fattytissue and a capacious venous plexus occupy thespinal epidural space, one or both of these

elements must be involved in the volumeadjustments. Indeed, one might argue that thechanges observed in the sac during hyperventila-tion and CO2 inhalation are initiated by changeswithin the spinal epidural compartment; butthere is little physiological evidence to supportsuch an assumption. Evidence favours the well-known alterations in cerebral blood flow, whichaccompany changes in blood CO2 tension, as thefactors that alter CSF pressure and in turn alterthe size of the sac (Lassen and Ingvar, 1963;Harper, 1965; Meyer and Gilroy, 1968).While the amount of epidural fat does seem

capable of change by sliding into and out of thespinal canal through the neural foramina, thevenous plexus seems the more likely element toplay the important role. A picture thus emergesof the spinal dural sac acting in reciprocalconcert with the epidural venous blood volumeto provide the limited but definite elasticity ofthe dura mater.

This reciprocal relationship between the CSF-filled sac and the epidural venous plexus canexplain also the exquisite sensitivity of the CSFpressure to sudden changes in intrathoracic andintra-abdominal pressure, which we observeduring the Valsalva manoeuvre, coughing,straining, and during the respiratory cycleas well. Observing a column of Pantopaqueduring lumbar myelography, we note a suddennarrowing and elongation of the column as thesac partially collapses almost immediately inresponse to a Valsalva manoeuvre, retaining thisappearance until the manoeuvre is ended. Judgingfrom the rates of change observed duringmyelography, as well as from the rapidity withwhich CSF pressure is known to rise in responseto the Valsalva manoeuvre, we conclude thatCSF pressure (and intracranial pressure as well)becomes essentially equal to the pressure withinthe thorax and abdomen in a matter of a secondor less. To account for this partial collapse of thethoracolumbar sac, filled as it is with incompress-ible tissue and CSF, we assume that with therise in pressure within the thorax and abdomen,venous blood is forced rapidly from the venacava and other large veins within the bodycavities into the thoracolumbar epidural venousplexus. Thus, through these venous channels theintrathoracic and intra-abdominal pressures aretransmitted to the collapsible dural sac to thespinal CSF, and in turn intracranially throughoutthe CSF compartment, consonant with theprinciples of hydraulics. But since the sac does

471P

rotected by copyright. on July 7, 2020 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.35.4.468 on 1 August 1972. D

ownloaded from

Albert N. Martins, John K. Wiley, and Paul W. Myers

partially collapse, some CSF must be temporarilydisplaced. Our observations of a Pantopaquecolumn in the cervical canal poised at the rim ofthe foramen magnum suggest that, in responseto the Valsalva manoeuvre, CSF flows into thecervical subarachnoid space because the columnthere widens slightly. Furthermore, since thecolumn of Pantopaque does not move intra-cranially through the foramen magnum, weassume that CSF is not forced into the rigidcranial vault by a Valsalva manoeuvre. Theseobservations lend support to the view that intra-cranial veins do not collapse in response toinduced changes in CSF pressure. For if theydid collapse, we assume that CSF would havemoved intracranially and with it the column ofPantopaque.

Since the cervical dural sac is limited in howmuch it can distend by the closely applied bonyspine, it very rapidly becomes filled to capacity.At this moment, when the pressure within thethorax and abdomen cannot reduce further thesize of the thoracolumbar sac by dislocatingfluid into the cervical canal, pressures withinthe thorax and abdomen, as well as throughoutthe entire CSF compartment, become essentiallyequal, all taking place almost instantaneously.We assume that because both the epiduralvenous plexus and the dural sac in the cervicalregion are not directly exposed to pressuresdeveloped within the body cavities, each canvary its volume independently of the thoraco-lumbar epidural venous volume.

Prolonged Valsalva manoeuvre or strainingimpedes venous return. But the contribution ofintracranial venous congestion, which attendsthis venous obstruction, is late in evolving com-pared with the dramatic and abrupt rise early inthe manoeuvre that derives from the dynamicsjust mentioned.

In applying these concepts to the clinicalsituation, we would assume for example thatthe bulge of a crying infant's fontanelle is notcaused by venous congestion but by CSF beingforced to flow from the thoracolumbar sac intothe non-rigid skull by the increased intrathoracicand intra-abdominal pressure. We may applythese concepts also to an understanding of theevents surrounding the rupture of a weakenedintracranial vessel concurrent with an episode ofcoughing or straining. There is general beliefthat the catastrophe is related in time to thesudden rapid rise in intracranial pressure. How-ever, if the dynamics are as presented here, the

intracranial vessel would be more prone torupture after the cough or strain, when the CSFpressure suddenly falls. Because initially, as theintrathoracic and intra-abdominal pressure istransmitted to the spinal CSF and thence intra-cranially, the pressure gradient from theintravascular blood to the extravascular CSFacross the blood vessel wall falls, therebyreducing the transmural pressure gradientfavouring vessel rupture. Subsequently, when theepisode is over and the intracranial CSF pressurefalls sharply, this transmural pressure gradientfavouring rupture returns to its former restinglevel, or perhaps even surpasses it. One mayspeculate that at the end of an episode of cough-ing or straining, as the intracranial pressurefalls, the autoregulatory mechanism concernedwith maintaining a normal rate of cerebralblood flow while the intracranial pressure is highwill not reverse itself with equal speed. For thisinstant, flow through the weakened vessel will begreater than normal, and the transmural pressuregradient favouring rupture will be also greaterthan normal.

CONCLUSIONS

The spinal dural sac acts as a reservoir for CSF,readily changing its capacity in response topressure gradients developed within the CSF andthe spinal epidural venous plexus. The mainimplications of this conclusion are four:

1. The elasticity of the dura mater, demon-strated when one artificially changes CSFvolume with fluid additions and withdrawals, isa function of the spinal dural sac rather than theintradural cerebrospinal venous vascular bed.

2. Because it can readily alter its capacitywithin limits, the spinal dural sac plays a primaryrole in the dynamics ofCSF pressure changes thataccompany changes in position.

3. The spinal dural sac, by acting as areservoir for CSF, permits the vascular bed ofthe brain to alter its total volume in response tochanges in cerebral blood flow.

4. The sensitivity of the CSF pressure tochanges in intrathoracic and intra-abdominalpressure depends upon the relationship of theepidural venous plexus to the spinal dural sac.

REFERENCES

Bowsher, D. (1960). Cerebrospinal Fluid Dynamics in Healthand Disease. Thomas: Springfield, Ill.

472P

rotected by copyright. on July 7, 2020 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.35.4.468 on 1 August 1972. D

ownloaded from

Dyntamics of the cerebrospinal fluid and the spinal dura mater

Cushing, H. (1902). Some experimental and clinical observa-tions concerning states of increased intracranial tension.American Journal of Medical Sciences, 124, 375-400.

Cutler, R. W. P., Page, L., Galicich, J., and Watters, G. V.(1968). Formation and absorption of cerebrospinal fluid inman. Brain, 91, 707-720.

Davson, H. (1967). Physiology of the Cerebrospinal Fluid.Churchill: London.

Du Boulay, G. H., and El Gammal, T. (1966). The classifica-tion, clinical value and mechanism of sella turcica changesin raised intracranial pressure. British Journal ofRadiology,39, 422-442.

Fog, M. (1933). Influence of intracranial hypertension uponthe cerebral circulation. Acta Psychiatrica (Kbh.), 8, 191-198.

Foldes, F. F., Keutmann, E., and Hunt, R. D. (1958). Theeffect of continuous removal of cerebrospinal fluid oncerebrospinal fluid pressure. Anaesthesist, 7, 261-265.

Harper, A. M. (1965). Physiology of cerebral bloodflow.British Journal of Anaesthia, 37, 225-235.

Hayden, P. W., Shurtleff, D. B., and Foltz, E. L. (1970).Ventricular fluid pressure recordings in hydrocephalicpatients. Archives of Neutrology, 23, 147-154.

Hekmatpanah, J. (1970). Cerebral circulation and perfusionin experimental increased intracranial pressure. Journal ofNeurosurgery, 32, 21-29.

Katzman, R., and Hussey, F. (1970). A simple constant-infusion manometric test for measurement of CSF absorp-tion I. Rationale and method. Neurology (Minneapolis),20, 534-544.

Kety, S. (1965). Remarks, in Cerebral Vascuilar Diseases.Transactions of the Fourth Conference, Princeton, N.J.,1964. Pp. 83. Edited by C. H. Millikan, R. G. Siekert, andJ. P. Whisnant. Grune and Stratton: New York.

Kunkle, E. C., Ray, B. S., and Wolff, H. G. (1943). Experi-mental studies on headache: analysis of the headacheassociated with changes in intracranial pressure. Archivesof Neurology and Psychiatry, 49, 323-358.

Lassen, N. A., and Ingvar, D. H. (1963). Regional cerebralblood flow measurement in man. Archives of Neurology,9, 615-622.

Meyer, J. S., and Gilroy, J. (1968). Regulation and adjust-ment of the cerebral circulation. Diseases of the Chest, 53,30-37.

Mcllwain, H. (1966). Biochemistry and The Central NervousSystem. 3rd edition. Pp. 412. Churchill: London.

Permutt, S., and Riley, R. L. (1963). Hemodynamics ofcollapsible vessels with tone: the vascular waterfall.Journal of Applied Physiology, 18, 924-932.

Pollock, L. J., and Boshes, B. (1936). Cerebrospinal fluidpressure. Archives of Neurology and Psychiatry, 36, 931-974.

Ponssen, H., and Van Den Bos, G. C. (1971). Influence of thecirculation on the CSF pressure wave. (Abstract.) Journalof Neurology, Neuirosurgery, and Psychiatry, 34, 108.

Risberg, J., Ancri, D., and Ingvar, D. H. (1969). Correlationbetween cerebral blood volume and cerebral blood flow inthe cat. Experimental Brain Research, 8, 321-326.

Rubin, R. C., Henderson, E. S., Ommaya, A. K., Walker,M. D., and Rall, D. P. (1966). The production of cerebro-spinal fluid in man and its modification by acetazolamide.Journal of Neurosurgery, 25, 430-436.

Ryder, H. W., Espey, F. F., Kimbell, F. D., Penka, E. J.,Rosenauer, A., Podolsky, B., and Evans, J. P. (1953). Themechanism of the change in cerebrospinal fluid pressurefollowing an induced change in the volume of the fluidspace. Journal of Laboratory and Clinical Medicine, 41,428-435.

Sibayan, R. Q., Begeman, P. C., King, A. I., Gurdjian, E. S.,and Thomas, L. M. (1970). Experimental hydrocephalus:ventricular cerebrospinal fluid pressure and waveformstudies. Archives of Neurology, 23, 165-172.

Von Storch, T. J. C., Carmichael, E. A., and Banks, T. E.(1937). Factors producing lumbar cerebrospinal fluidpressure in man in the erect posture. Archives ofNeurologyand Psychiatry, 38, 1158-1175.

Weed, L. H. (1929). Some limitations of the Monro-Kelliehypothesis. Archives of Surgery, 18, 1049-1068.

Weed, L. H., and Flexner, L. B. (1933). The relations of theintracranial pressures. American Journal of Physiology,105, 266-272.

Weed, L. H., Flexner, L. B., and Clark, J. H. (1932). Effectof dislocation of cerebrospinal fluid upon its pressure.American Journal of Physiology, 100, 246-261.

Wolff, H. G., and Forbes, H. S. (1928). The cerebral circula-tion: observations of the pial circulation during changes inintracranial pressure. Archives ofNeurology and Psychiatry,20, 1035-1047.

Wright, R. D. (1938). Experimental observations on in-creased intracranial pressure. Australian and New ZealandJournal of Surgery, 7, 215-235.

473P

rotected by copyright. on July 7, 2020 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.35.4.468 on 1 August 1972. D

ownloaded from