Acta Neurochirurgica 20, 195--209 (1969)

Neurosurgical Department of the University of Mainz, Western Germany

(Director: Prof. K. Schi~rmann, M.D.)

Cerebral Blood Flow and Cerebral Death

Preliminary Report

By
M. Brock, K. Schiirmann, and A. Hadjidimos

With r Figures

The well known clinical picture of "coma depassd" ao, ~1 which follows
lethal post-anoxic cerebral oedema (e.g. in cases of severe head trauma
or prolonged cardiac arrest with isoelectrie EEG) is sometimes accom-
panied by the angiographic phenomenon of non-filling of cerebral
v e s s e l s 4, 12-14, 21, 22, 26-29, 35, 39, 43, 44
I t is accepted--but has not been p r o v e n - - t h a t this non-filling phenom-
enon represents an arrest of cerebral circulation, supposed to be due to
an increase in intracranial pressure to levels above systolic 1, 27, 29 or
diastolic 22 blood pressure. However, "minimal residual carotid blood flow
when intracranial pressure had been elevated far above the systolic pres-
sure" has been observed 26, 27. Further, the fact that apparently no anglo-
graphic contrast has penetrated into the cranium by the carotid arteries
is no proof that there is no cerebral blood flow (CI3F) because the amount
of contrast medium able to enter the cerebral vessels may be too little to be
visualized. [Further attention will be directed to this point in the discussion.
The isoelectricity of the E E G often observed in such cases, and which
seems to precede the non-filling phenomenon 14, has been invoked by some
as a proof of cerebral (and total) death. (For an extensive discussion on
this subject see the work of Spann et a/.47). Since there are several clinical
conditions compatible with life which m a y also be associated with an
isoelectric EEG, even for long periods of time2, a, 7, ~, 82-34, 56, recovery
having been recorded even after four and five days of isoeleetrieity 51,
and since, on the other hand, in patients with isoeleetric E E G and
lethal outcome evoked potentials or central reflexes may still be ob-
tained 2, 3, 40 and others, the E E G cannot be considered a reliable criterion
of so-called cerebral death--even if the basal ganglia are also silent 25.
lYiodern resuscitative and intensive care techniques have allowed such
irreversibly comatose patients to be maintained in a state of vegetative
life for longer periods of time. However, the outcome has not been altered
196 M. Brock, K. Schfirmann, and A. Hadjidimos:

by such technical improvements. On the contrary, these improvements

have a u g m e n t e d the t r e m e n d o u s a n d u n r e w a r d i n g b u r d e n this p a r t i c u l a r
t y p e of p a t i e n t represents to the staff, t o his family, a n d to society. This
problem will persist as long as there is no reliable criterion to answer the
question of when it is correct to consider a p a t i e n t as dead a n d to dis-
c o n t i n u e t h e aids which are m a i n t a i n i n g "Life". Since medical t e a m s per-
forming organ t r a n s p l a n t a t i o n in Homo have been increasingly faced with
this delicate subject, it has received more a n d more a t t e n t i o n a n d has been
discussed with growing i n t e n s i t y .
If it is t r u e t h a t n o w a d a y s d e a t h m e a n s cerebral death, a n d if it is also
true t h a t cerebral life is impossible i n the absence of cerebral blood flow,
the demonstration of a n arrest of blood flow within the b r a i n would, then,
be a reliable criterion for the verification of death. I n such cases, ob-
viously, the u s u a l clinical m a n i f e s t a t i o n s of cerebral d e a t h will be present.
W e have r e c e n t l y been able to s t u d y the CBF of four such patients.
Since n o similar report has been f o u n d i n literature, it seems worthwhile
to p r e s e n t our findings as illustrated b y one typical ease.

Case: A. Z., a 4 ~ years-old white boy was injured in a ear accident at

2 : 30 p.m. on J u l y 12, 1968. The boy lost consciousness immediately and was
brought to a nearby hospital. Simple roentgenograms of the skull showed
no abnormalties. There was a transverse fracture of the proximal third of
the shaft of the left femur. The child remained comatose and was transferred
to our department the next morning, some 20 hours after the accident.
The pupils were moderately b u t symmetrically dilated and reacted sluggishly
to light; there was a generalized hyporeflexia. No plantar response could
be evoked. Painful stimuli elicted a barely perceptible reaction of all limbs.
Blood pressure was 120/80 m m Hg, pulse 95 per minute, temperature 37.7 ~ C
and respiratory rate 25 per minute. The echoencephalogram showed a midline
shift of 2 m m (within normal limits) from right to left. Laboratory findings
were normal.
I n the absence of focal signs it was decided to keep the child under close
observation in the intensive care unit. Chloramphenicol and Comital were
given prophylactically.
The clinical picture remained entirely unchanged until 9:00 a.m. on
J u l y 15 (about 67 hours after the accident), when the child had a sudden
eardio-respiratory arrest. Reanimation was immediately begun and the child
was intubated whilst external cardiac massage was being performed. Spon-
taneous heart activity returnd after one minute, b u t the child had to remain
connected to a Bird respirator. At this point the pupils were maximally
dilated and unresponsive. Blood pressure could not be measured by auseul-
tation. Although a control echoencephalogram still showed no pathological
midline shifting, it was decided to perform an angiographic study.
Bilateral percutaneous serial carotid angiography (puncture of the common
carotid arteries) at 10:00 a.m. revealed the non-filling phenomenon on both
sides (Fig. 1). The major part of the injected contrast medium (7 ml) circulated
through the external carotid vessels, while a fraction of it still remained
within the extraeranial internal carotid at the end of the series (about 10
seconds after injection). The "waterfall phenomenon''~s could be observed
on both sides, being more distinct on the right.
 Cerebral Blood Flow and Cerebral Death 197

A conventional E E G (16 c h a n n e l s ) w i t h surface electrodes a t t h i s t i m e was

p r a c t i c a l l y isoeleetric, c o n t a i n i n g o n l y v e r y sparse a n d slow p o t e n t i a l s con-
fined to b o t h occipital regions. B l o o d p r e s s u r e was 60/40 m m ]rig (by auscul-
t a t i o n ) . P u p i l s were fixed in m a x i m a l d i l a t a t i o n a n d n o r e s p o n s e c o u l d b e
elieted b y n o c i e e p t i v e stimuli. T h e e l e c t r o c a r d i o g r a m s h o w e d n o gross ab-
normalities.
A t 1 3 : 3 0 t h e E E G was isoeleetric.
I n o r d e r to g a i n f u r t h e r i n f o r m a t i o n c o n c e r n i n g t h e f u n c t i o n a l ( a n d vital)
s i t u a t i o n of t h e p a t i e n t ' s b r a i n i t was d e c i d e d t o p e r f o r m a C B F m e a s u r e m e n t .

Fig. 1. Bilateral percutaneous common carotid arteriogram showing ~he non-filling phenomenon on
both sides.

Measurement o] Cerebral Blood Flow. R e g i o n a l c e r e b r a l b l o o d flow (rCBF)

was m e a s u r e d a c c o r d i n g to t h e i n t r a - a r t e r i a l r a d i o a c t i v e t r a c e r i n j e c t i o n
t e c h n i q u e o r i g i n a l l y d e s c r i b e d b y t h e g r o u p s of Lassen a n d of Ingvar ~5, 19, ~0, 23
Briefly, t h e local c e r e b r a l clearance of a n i n e r t diffusible r a d i o a c t i v e t r a c e r
r a p i d l y i n j e c t e d i n t o t h e i n t e r n a l c a r o t i d a r t e r y is recorded, t h r o u g h t h e
i n t a c t skull, a t several regions of t h e b r a i n s i m u l t a n e o u s l y , b y m e a n s of
16 e x t e r n a l l y p l a c e d s c i n t i l l a t i o n d e t e c t o r s . R C B F c a n t h e n b e c a l c u l a t e d
f r o m t h e r a t e of t r a c e r clearance.
I n t h e p r e s e n t ease t h e low b l o o d p r e s s u r e did n o t allow a s a t i s f a c t o r y
p a l p a t i o n of t h e c a r o t i d vessels a t t h e neck. T h i s fact, as well as t h e neces-
s i t y of a v o i d i n g a possible r e f l u x of t h e i n j e c t e d t r a c e r i n t o t e r r i t o r i e s s u p p l i e d
b y t h e e x t e r n a l c a r o t i d a r t e r y (see discussion) led us t o expose surgically t h e
c a r o t i d b i f u r c a t i o n o n t h e left side. A p o l y e t h y l e n e c a t h e t e r was t h e n i n t r o -
d u c e d i n t o t h e i n t e r n a l c a r o t i d as is u s u a l l y d o n e for p e r e u t a n e o u s c a t h e t e r i -
zation.
R e f l u x of t h e i n j e c t e d t r a c e r was p r e v e n t e d , b y e x e r t i n g t r a c t i o n u p o n a
sling p a s s e d a r o u n d t h e i n t e r n a l c a r o t i d a r t e r y b e l o w t h e p o i n t w h e r e t h e
c a t h e t e r h a d b e e n i n t r o d u c e d , while 3 m l of ~33Xenon-in-saline s o l u t i o n
( R a d i o e h e m i c a l Centre, A m e r s h a m ) - - c o r r e s p o n d i n g t o a b o u t 3 m C - - w e r e
i n j e c t e d t h r o u g h t h e c a t h e t e r w i t h i n 1 to 2 seconds. L o c a l isotope c l e a r a n c e
Act~ Neurochirurgica, Vol. 20, :~asc. 2-3 14
198 M. Brock, K. Sehiirmann, and A. Hadjidimos: Cerebral Blood Flow

was recorded with 16 detectors placed laterally to the left hemicranium,

perpendicular to the saggital plane. The equipment employed to study rCBF
(Meditronic, Copenhagen) is essentially similar to that originally described b y
the group of Lassen and coworkers 2% I t has, however, been modified by the
addition of an automatic timing-playback unit and of an output that permits
the logarithmic playback of the clearance curves over two decades*. This
equipment was coupled to a high-speed two-channel recorder (HSfler, Ettlin-
gen) with 0.1 sec. for full scale deflection. The clearance curves stored on the
tape were transfered to paper with playback at double speed, time constant of
1 see., two decades and 50 counts per second for full scale deflection.
Three aspects of the recordings obtained (Fig. 2) seem to deserve special
attention and will be discussed further on:
1. the small amount o] activity reaching the brain,
2. the ]act that most el this radioactivity does not reach the cerebral convexity,
and
3. the virtually complete absence el isotope clearance during more than
30 minutes.
During the rCBF study arterial blood pressure was recorded continuously
through the internal carotid catheter, coupled to a system consisting of a
transducer (Statham P 23 Db), an electromanometer (lV[a88 G, Hellige,
Frankfurt) and a high-speed two-channel recorder (He 86, Hellige, Frankfurt).
During the examination blood pressure was 60/40 m m Hg.
The E E G was also recorded during the procedure. Five needle-electrodes
(Z 122/65, Schwarzer, Miinehen) were inserted into the scalp over each side of
the skull as shown in Fig. 3, their position being correlated with the location oJ
the scintillation detectors. The recordings were made with an 8-channel equip-
m e n t (Neuroscript Ee 97, Hellige) operating at a time constant of 0.1 see with
conventional (50 ~V = 7 ram) or double (50 BV = 14 ram) amplitude. Waves
of a frequency higher t h a n 30 ttz were eliminated by adequate filtration. The
obtained isoelectrie tracings contained only E K G activity. Painful stimuli did
not alter the recordings. Repeated hand clapping near to the right ear seemed
to evoke slow p o t e n t i a l s - - p r e d o m i n a n t l y in the right temporal region--only
on one occasion. These findings will be commented upon later (see Discussion).
Arterial pC0~ was determined with a micro-Astrup equipment (Radio-
meter, Copenhagen) utilizing blood withdrawn through the intcrual carotid
catheter. ApCO2 at the time of the study was 35.0 m m Hg.
The spontaneous heart activity (extremity leads) was monitored on an
oscilloscope (Visicard 7, Hugo Sachs Elektronik) during the whole procedure
and recorded (Cardiopan 531, Phillips) immediately thereafter. Cardiac
activity was ergular (52/min) b u t there was a distinct prolongation of the QT

* The automatic timing-playback unit allows the serial and automatic

playback of the 16 clearance curves, two by two, over a desired period of time,
from the 1-inch magnetic tape where they are stored during the study. WhiIe
the practical usefulness of such an improvement in the equipment is self-
evident, the present case well illnstrates the advantage of being able to
visualize regional activity over two decades (that is, from 100% down to 1~o)
additionally to one decade (from t00~o down to 10%). Since in most channels
in the present ease the registered activity remained under 10~o of full scale
deflection, it would not have been properly "seen" b y a system reproducing
the information only over one decade of decay.
100-

1 4

B
t t
lmkt
t
1

t
100.

9 10 12

10-

100 84

15 16

10.

Fig. 2. Position of the 16 channels as well as the corresponding tracings after selective injection of
l~aXe-solution into the su~'gically e x p o s e d interna! carotid artery. Notice ~he small amoun~ of traoer
r e a c h i n g the brain a n d the absence of clearance. The h i g h b a c k g r o u n d is due to a previous injection
(80 m i n u t e s before),
200 M. Brock, K. Schiirmann, and A. Hadjidimos:

1-3
@
3-13

13- 5

5-7

4-14

14-6
lO01N l ! w..
6-8

1-3

3-13 @

13-5

5-7

2-4

"14.p . . . . . .

6-8 ,~D JN [" 1 sec.

1-3

3"13
9
13-5 5 0 i N IT 1 ser

5-7
A
clapping
24 I

4-14

6-8

:Fig. 3. E E G (needle electrodes) a t the time of the CBF study. (For discussion see text.)
 Cerebral Blood Flow and Cerebral Death 201

interval to 0.63 see (the normal for this frequency being 0.38 to 0.46 see) as
commonly seen in hypothermia *.
Artificial ventilation was continued until the next morning, when cardiac
arrest ensued, some 90 hours after the accident. Body temperature at this
time was below 340 C.
Necropsy ** revealed maeroscopieal signs of increased intraeranial pressure
with marked flattening of the convolutions and signs of tentorial and cerebellar
herniation. Multiple punetate haemorrhagie feel were sparsely distributed
throughout both the grey and white matter. However there were no gross
focal lesions. Microscopic sections revealed generalized brain oedema, poor in
protein substance, with widening of the pericellular spaces and swelling of
macroglial elements. The white matter displayed a pronounced imbibition
and cribiform changes in the sense of a status lacunaris. The blood vessels to
the brain and within it were permeable.
The above findings are similar to those reported in other pathological
studies of cases of longer artificial prolongation of "life" 6, sl

Discussion

I n the following discussion of the o b t a i n e d d a t a some factors should be

borne in m i n d :
1. A n organ is to be considered dead when it has r e m a i n e d deprived
of its blood s u p p l y for a period of time t h a t surpasses its specific a b i l i t y to
survive circulatory arrest 11.
2. I n the ease of t h e central n e r v o u s system this " s u r v i v a l bime"
varies (according to several factors, e.g. site, metabolic condition, tempera-
ture, etc.) from some seconds to a few m i n u t e s 9, 10, ~6, 41, 4s
3. As clearly defined i n the " D e c l a r a t i o n of S y d n e y " of the Committee
on Medical Ethics to the 22nd General Assembly of the W o r l d MedieM
Association (Sydney, A u g u s t 5 to 11, 1968), d e a t h "is a g r a d u a l process
at the cellular level with tissues v a r y i n g i n their a b i l i t y to w i t h s t a n d depri-
v a t i o n of oxygen. B u t clinical interest lie,s not in the state el preservation el
isolated cells but in the/ate o/a person***. Here the p o i n t of d e a t h of different
cells a n d organs is n o t so i m p o r t a n t as the certainty that the process has
become irreversible *** b y w h a t e v e r techniques of ressucitation t h a t m a y be
e m p l o y e d " 51.
A l t h o u g h there are parts of the organism (e.g. limbs or paired organs)
the d e a t h of which does n o t i m p l y the d e a t h of the individual, there seems
to be general agreement t h a t h u m a n life is n o t possible i n the presence of
a dead brain, the so-called "respirator b r a i n ''zz. I n other words, death
of a h u m a n being has come to be characterized b y cerebral death.

* The authors are indebted to Dr. H. J. Just, 2nd Dept. of I n t e r n a l Medi-

cine, Univ. of Mainz, for the interpretation of the E K G findings.
** The valuable help of Prof. K. J. Hempel, Dept. of Neuropathology,
Univ. of Mainz, for p u t t i n g the necropsy data at our disposition is acknowledged
by the authors.
*** Italics have been introduced by the authors.
202 M. Brock, K. Schiirmann, and A. ttadjidimos:

The verification of cerebral death is usually founded on the absence o]

mani]estations of cerebral function over a certain period of time. However,
the absence of signs of function of an organ provides no absolute proo] of
its death. As said at the beginning of this discussion, only the demon-
stration of circulatory arrest to an organ for a period of time beyond the
limits of tolerance for this organ can prove its death. I n the ease of the
brain, circulatory arrest has not really been proven b y a n y of the criteria
usually invoked today.
1. A n isoelectric E E G cannot be t a k e n to mean an absent C B F ; it can
only be considered as the expression of an absent electrical activity. This
corresponds t o a strongly d e c r e a s e d - - b u t not necessarily irreversibly
abolished--metabolism with reduced oxygen consumption. I t does not
imply a circulatory insufficiency. I n his exhaustive review, So]cole//46
pointed out that, for instance in cases of severe barbiturate intoxication,
cerebral metabolic rate is more reduced t h a n cerebral blood flow, so t h a t
"cerebral oxygen supply is more t h a n adequate". This situation is funda-
m e n t a l l y different from w h a t happens in the post-anoxic cases here stud-
ied, although an isoelectrie E E G m a y be observed in both instances.
We have recently been able to study rCBF in a patient under severe bar-
biturate intoxication. Although the E E G showed the well known periodical
isoelectrieity characteristic of stage IV of such intoxications, CBF was well
preserved. The patient made a rapid and complete recovery 16. Bird and
Plum 7 have recently reported a similar case and stressed that "if the coma is
the result of acute drug intoxication, an isoelectrie E E G is clearly not a sign
of severe irreversible brain damage, even when accompanied by complete ar-
re]lexia, unresponsiveness, and absence el spontaneous respiration" *.

I n the case reported here the evoked potentials obtainable over both
temporal areas, m a i n l y on the right side, after clapping hands near to
the right ear are difficult to interpret. As demonstrated by Ar/el2, however,
such potentials bear no prognostic significance.
2. The lack of penetration of angiographic contrast medium into the
cranium t h r o u g h one more of its afferent arteries also does not prove
t h a t there is no brain circulation. Reversibility of the non-filling phenom-
enon (case 3 of Gros et al.la; case 11 of Pribram as) and even recovery from
it (ease 5 of Riishede and Ethelberg89; ease 6 of Pribram 3s) have been
reported. I n addition, to the objections already made to this criterion at
the beginning of this paper, we should like to add the diagnostic problem
which can be posed b y cases of t r a u m a t i c thrombosis of the internal
carotid artery. Although in such cases coma is not the ruleS, 18, 42 ann
others, it can occur 87, a2. Deep coma with unilateral non-filling m a y even
follow spontaneous carotid thrombosis (ease 2 of Horwitz and Dunsmore 21)
or a t h c r o m a t o u s occlusion (ease 8 of Pribram~S).
If, on the other hand, an inert diffusible tracer "'deposed" within the
brain is not washed out, this quite obviously means that. there is no blood

*ItMics have been introduced by the authors.

 Cerebral Blood Flow and Cerebral Death 203

flowing through this organ s . The question is: " H o w can the tracer be
deposed w i t h i n the b r a i n i n cases of non-filling ?" The m a n u a l injection
seems sufficient to " p u l l " some tracer into the c r a n i u m i n such cases,
provided re/lux /roqn the internal into the external carotid arteries is pre-
vented. This was certainly so i n the present case, as already described.

Fig. 4. Anteropostcrior scan about 10 hours after the injection of labelled (131I) albumin macro-aggregates
into the right common carotid artery of another patient of this series.

The importance of preventing reflux of tracer may be illustrated by three

reeentty observed additional eases of premortal coma with isoeleetrie E E G
and non-filling phenomenon. I n these patients the clearance studies were
performed b y percutaneou8 injection of Xe-solution. The inital part of all very
slow curves obtained had a similar, not entirely horizontal, appearance, such
as could attributed to clearance of tracer from external carotid territories
(reflux of tracer ?) a.s reported b y Ueda et M. 49 after selective injection into the
external carotid, and by H4ggendal et al. 17 after injection into the common
carotid in a patient who had undergone ligature of the internal carotid.

I n three of our cases, a n a b r u p t m e d i c a m e n t o u s increase of arterial

blood pressure (from 80/60 to 200/100, from 95/55 to 155/125 m m Hg,
204 M. Brock, K. Schtirmann, and A. Hadjidimos:

and from 105/80 to 140/85) was induced without causing any significant
change in the clearance slopes. I n one of these patients 131I-labelled
albumin macro-aggregates injected into the common carotid artery
immediately following angiography* failed to penetrate into the cranial
cavities, remaining trapped in the capillaries of the neck and the base of
the cranium (Fig. 4). I n no case was the average CBF higher than 5 ml/
100 g rain.
Although, b y preventing the reflux of tracer, it is possible to force the
indicator into the brain, its amount will not be very large (unless large
volumes are injected) since, under such circumstances, some injected
material will always remain in the extracranial portion of the internal
carotid for very long periods of time e~ and diffuse into the surrounding
tissues of the neck. In the examination of the case here reported only 3 ml
were injected. This explains (a) the very low height of the recorded plateaus
and (b) that practically only the basal brain regions have been attained
b y the tracer.
At the present stage of our researches we do not know if the demon-
stration of a practically complete unilateral flow arrest (even if undoubted)
is sufficient to demonstrate cerebral death. I t should be surprising if it
were not so, although, of course, bilateral studies will provide greater
safety. For a better understanding of the problems involved vertebral
flow studies will also have to be performed in some borderline cases.
However, it is difficult to conceive t h a t the maintainance of blood flow
to the brain s t e m - - e v e n if sufficient to allow the functioning of its centres
---is compatible with the condition of h u m a n life in the absence of blood
supply to the cerebral hemispheres.

Summary
Cerebral Blood Flow and Cerebral Death
Preliminary Report
At present the diagnosis of cerebral death is based on the absence of
manifestations of cerebral function (deep coma, wide pupils, absence of
reflexes and spontaneous respiration, isoelectric EEG, etc.) during a
variable period of time. However, the absence of vital signs of an organ,
even for prolonged periods, is no proof of its death. The death of an organ
can only be considered as proved b y the demonstration t h a t this organ
has remained completely deprived of its blood flow during a period of
time that surpasses its ability to survive circulatory arrest. I n the case
of the brain, the permanent absence of clearance of a radioactive tracer
deposed within the brain is considered to demonstrate total absence of
flow through it and, thus, to prove cerebral death. As discussed in the
text, previous attempts at angiographic "demonstration" of the arrest
of cerebral blood flow cannot be accepted uncritically.
* The authors are indebted to the Dept. of Radiology, Univ. of Mainz,
for this scan.
 Cerebral Blood Flow a~nd Cerebral Death 5)05

Th e v al u e of t h e p r e s e n t findings in d e t e r m i n i n g t h e d e a t h of ~ p a t i e n t
w i t h reference to organ t r a n s p l a n t a t i o n has been discussed.

The authors are indebted to M. Ellger, 3{.D. and to G. Busch, M.D. for their
help in the study of the cases herein reported.
We t h an k Mrs. B. MiZller for her assistance in preparing the manuscript
and Mrs. R. A d a m for the photogTaphic work.

Zusammenfassung
Hirndurchblutung und Hgrntod
Vorldiufiye Mitteilung
Zur Zeit st6tzt sich die Diagnose des zerebralen Todes auf das Fehlen yon
Zeichen zerebraler Funktion (tiefes Korea, w e r e Pupillen, Fehlen yon Reflexen
und Spontanatmung, isoelektrisches E E G usw.) w~ihrend eines versehieden
langen Zeitabschnittes. Indessen ist das Fehlen yon Lebenszeichen eines
Organes, selbst fiber ]/ingere Zeit, kein Beweis ftir dessen Ted. Der Ted eines
Organes kann nut dann als gesichert gelten, wenn nachgewiesen ist, dab dieses
Organ fiir eine Zeitspanne vollstgndig seiner Blutversorgung beraubt war, die
seine Fghigkeit iiherschreitet, einen zirkulatorischen Stitlstand zu iiberleben.
I m Falle des Gehirns wird die Ansicht vertreBen, dab ein dauerhaftes Fehlen
einer Clearance eines radioaktiven Indikators, der in das Hirn eingebraeht
worden ist, das vollst/~ndige Fehlen einer Durchblutung und damit den tIirn-
ted beweist. Wie im Text diskutiert, k6nnen frfihere Versuehe des angio-
graphiachen Beweises eines Stillstandes der Hirndurehblutung nicht0 unkritiseh
akzeptiert werden.
Die Bewertung der dargestellten Befunde bezfig]ieh der Festste]Iung des
Todes eines Patienter~ in Hinbliek auf Organtransptantationen wird diskutiert.

R6sum6
Circulation c~r~br'ale et mort du cerveau
Communication prdliminaire
Le diagnostic de mort du eerveau est bas6 jusqu' g pr6sent sur l'absence
de manifestations des fonetions cdrdbrales (coma profond, mydriase bitat6rale,
abolition des rgflexes, arr~t respiratoire, tracds E.E.G. plats ere . . . . ) pendant
un laps de temps variable. Cependant l'absence de signes fonctionnels d'un
organe, m6me pendant un laps de temps prolongd, n'est pas la preuve formelle
de sa mort. La mort d'organe ne pent ~tre prouv6e sue par la ddmonstration
que oct organe est rest6 compldtement priv6 de circulation sanguine
pendant un laps de temps qui d@asse sa eapacit6 de survie s un arr~t
eireulatoire.
Dana le eas du cerveau, l'absenee de clearance d'un produit radioactif
d6pos6 dana cet organe, est la preuve de Farr~t total de la circulation
sanguine et ainsi de la mort du cerveau. La d6monstration de l'arrgt
circulatoire par l'angiographie dans les tr a v a ux ant6rieurs, ne pent 6tre
aeeept6e sans rgserves.
La valeur des d6couverfies r6sentes pour diagnostiquer la mort d'un patient,
en cas de transplantation d'organe, a 6t6 diseut6e.
206 M. B r o c k , K . S c h t i r m a n n , a n d A. H a d j i d i m o s :

Riassunto
Circolazione cerebrale e morte cerebrale
t~apporto preliminare
A1 m o m e n t o a t t u a l e la d i a g n o s i di m o r t e c e r e b r a l e si b a s a s u l l ' a s s e n z a di
m a n i f e s t a z i o n i della f u n z i o n e c e r e b r a l e ( c o m a p r o f o n d o , d i l a t a z i o n e p u p i l l a r e ,
a s s e n z a di riflessi e di r e s p i r a z i o n e s p o n t a n e a , E E G isolelettrico ecc.) d u r a n t e
u n p e r i o d o di t e m p o v a r i a b i l e . T u t t a v i a l ' a s s e n z a di segni v i t a l i d a u n o r g a n o
a n c h e p e r u n p r o l u n g a t o periodo, n o n e' p r o v a della s u a m o r t e .
L a m o r t e di u n o r g a n o p u o ' essere c o n s i d e r a t a c o m e p r o v a t a solo c o n la
d i m o s t r a z i o n e che q u e s t o o r g a n o e' r i m a s t o p r i v a t o della s u a cireolazione p e r
u n p e r i o d o t e m p o che s o r p a s s a la s u a e a p a c i t a ' di s o p r a v v i v e r e a d u n a r r e s t o
circolatorio.
Nel caso del cervello la a s s e n z a p e r m a n e n t e della c l e a r a n c e di u n m a r c a n t e
r a d i o a t t i v o d e p o s i t a t o d e n t r o il cervello e' c o n s i d e r a t a c o m e d i m o s t r a z i o n e
d e l l ' a s s e n z a t o t a l e della circolazione i n esso e q u i n d i c o m e p r o v a di m o r t e
cerebrale.
Come discusso n e l t e s t o , p r e c e d e n t i t e n t a t i v i di u n a ~(d i m o s t r a z i o n e ~)angio-
g r a f i c a d e l l ' a r r e s t o della eireolazione c e r e b r a l e n o n p u o ' essere a e e e t t a t a s e n z a
eritiche.
I1 significato delle p r e s e n t i r i c e r c h e p e r la d e t e r m i n a z i o n e d e l l a m o r t e di u n
p a z i e n t e e' discusso a n c h e i n r a p p o r t o ai t r a p i a n t i di o r g a n o .

Resumen
Circulacidn cerebral y muerte cerebral
Communicacidn provisional
Actualmente el diagndstico de muerte cerebral se funda en la falta de
sefiales de funcidn cerebral (coma profundo, pupilas dilatadas, falta de
reflejos y respiraci6n espontdnea, EEG isoel~ctrico, etc.) durante un espa-
cio de tiempo de distinta duraci6n. La falta de signos de vida de un 6r-
gano, afin durante largo tiempo, no es una prueba de su muerte. La mu-
erte de un 6rgano solo puede asegurarse cuando se ha demostrado que
para ese 6rgano su irrigaci6n de sangre fu~ suprimida totalmente durante
u n espacio de t i e m p o , el eual s o b r e p a s a s u c a p a c i d a d de s o b r e v i v i r u n
p a r e circulatorio. E n case del c e r e b r o se d e f i e n d e ]a o p i n i d n , de que l a
f a l t a d u r a d e r a de a c l a r a m i e n t o (Clearance) de u n i n d i e a d o r r a d i o a c t i v e ,
t r a n s p o r t a d o al eerebro, d e m u e s t r a la f a l t a c o m p l e t a de c i r c u l a c i 6 n y c o n
ello la m u e r t e c e r e b r a l . C o m e se d i s c u t e e n el t e x t o , n o loueden ser acep-
f a d e s sin crltica, p r u e b a s a n t e r i o r e s de la d e m o s t r a c i d n a n g i o g r s de u n
p a r e de la c i r c u l a c i d n cerebral.
Se d i s c u t e la v a l o r a c i 6 n de los h a l l a z g o s e n r e l a e i d n a la d e m o s t r a c i 6 n
de m u e r t e de u n p a c i e n t e , e n v i s t a de u n a t r a n s p l a n t a c i 6 n de 6rganos.

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Authors' address: Dr. reed. M. Brock, Prof. Dr. reed. K. Sehi~rmann,

Dr. reed. A. Hadjidimos, Nem'ochirm'gisehe Universit/ttsklinik, D-65 B'Iainz,
LangenbeekstraBe 1.