The formulae for the arterial contributions
are more complex and will not be illustrated.

In the above treatment, both shunts are as-
sumed to arise on the right and appear on the
left. Anatomically, these shunts can arise on
either side or not exist at all; thus, there are nine
separate cases which require individual treat-
ment. Further, two sets of criteria must be de-
rived to indicate which of the nine cases must
be used in the analysis of a particular rheoen-
cephalogram.

Since the current field of a pair of electrodes
permeates the entire head, it is reasonable to
expect that contralateral circulatory events con-
tribute to the resistance changes. The problem
lies not in the existence of these contributions
but in whether they must be considered at the
level of accuracy required of tracing analysis.
The above method was thoroughly tested for
several years in the routine analysis of clinical
tracings. The extracranial cross-registry frac-
tion was found to average 0.07% while the aver-
age ipselateral change was 0.014 ohm. The re-
sulting 0.001 ohm tracing contribution falls
within the inaccuracy of the method and can be
ignored safely. Analysis of the intracranial
cross-registry fraction is more difficult. In 58
patients with intracranial vascular disease, it
averaged 0.38 with a range of 0.00-0.93; for 29
normal subjects it averaged 0.65 with a range of
0.22-1.00. Of the total subjects, 22 (25%) fell
below 0.35. Four values (5%) were zero. One
normal subject is included in the above 25%;
other findings suggest cerebrovascular disease in
this man.

The derivation of the cross-registry fraction
assumes all contralateral tracing changes arise
from cross-registration of ipselateral changes
and denies any possibility of blood distribution
around a patent circle of Willis. Unilateral
carotid compression can be expected to cause
bilateral circulatory reductions if the circle is
patent; the contralateral reduction should be
smaller than the ipselateral reduction. Since
this contralateral effect would be added to the
true cross-registry effect, the calculated cross-
registry fraction would be larger by a possibly
significant amount. The high cross-registry frac-
tion seen in the normal subject group supports
this conclusion as does the lower cross-registry
fraction observed in the group of patients with
cerebrovascular disease. Six (10%) of this lat-

13

ter group gave fractions of. 0.12 or less (average
0.02) ; their average ipselateral change was 0.038
ohm (0.009 ohm-0.068 ohm). Of particular
note is one patient who gave the large change
of 0.068 ohm with zero contralateral change. It
would appear the intracranial cross-registry
fraction is small and possibly negligible within
the limits of the present methodology. This
question is under further investigation.

3. Model Without Temporal Arterial Com-
pressions: The first model can be simplified by
omitting the compressions of the scalp arteries.
While the following treatment is no longer used
by the author, much of the clinical material to
be presented was obtained before the extracranial
contribution to the tracing was recognized. As
the data deficiencies cannot be repaired, this
method must be presented.

Notation:
The previous notation will be used plus: .
m-=ipselateral tracing component contributed
by the left common carotid artery
n=ibid, right common carotid artery
Si=contralateral tracing component contrib-
uted by the left common carotid artery
Sz=ibid, right common carotid artery
Equations similar to those in the first model
can be written :
(48)
(49)
(50)
(51)
(52)
(53)
(54)
(55)
The solutions are:
(56) RCC=Right common carotid
=R.—R;+Li-Ls
eft common carotid
=R,—-R,+Li—Le
(58) NS=Net shunt=|S,—S;| and is directed:
right to left if Sp>S, or
left to right if Su>Sr
(59) PAg=Right vertebral-basilar shunt=f
(60) PAy=Left vertebral-basilar shunt=e

IV. Conclusions:

It should be emphasized that the above gen-
eral approach to rheoencephalographic analysis
has been derived from theory alone and is based
on a number of explicitly stated or implied as-

Ri=n+S.+f
Li=m+Sat+e

(87) LCC



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or STE



male has been analysed and the following ar-
terial component values determined :
RT=.032 ohm LT=.036 ohm
RIC=.067 ohm
PAg=.010 ohm
RP=.068 ohm LP=.080 ohm
RCC=.099 ohm LCC=.092 ohm
NECS=.004 ohm left-to-right
NICS =.009 ohm left-to-right
Their ratios are:
RT RT RT
1 yp 789% RIG 18% RG = 82%
LT _ LT _
ric 8% = Taq=89%
RCC _ RIC _,, RP _
2. LCG =108% Tic 120% Tp =85%
PAn _ RIC-NICS _
3. RP =15% —RP =85%
PAx _ LIC _ NICS _
TP =19% LP =10% Lp =11%

The arterial component values are first ex-
amined for abnormality; all appear normal al-
though perhaps somewhat high for the patient’s
age.

The ratios are next examined for abnormality.
The temporal ratios appear normal; therefore,
if disease is present, it has either spared the ex-
ternal carotid circulation or is entirely intra-
cranial.

The second set of ratios is next examined.
The common carotids are almost equal, which
supports extracranial sparing; the left internal
carotid is somewhat decreased (or the right in-
creased) but the ratio is not significantly ab-
normal. Both carotid ratios agree within 12%
and are self-consistent; the carotids are reason-
ably symmetrical. If disease is present, it does
not affect the carotids. Therefore, the disease
must be not only intracranial but also may lie
above the circle of Willis. The perfusion ratio
is now examined and is found significantly re-
duced in opposite symmetry to the carotid ratio.
Right hemispheric disease may be present.

The third set of ratios is now examined. The
posterior ratios are equivalent and normal. The
internal carotid ratios are relatively normal al-
though the right internal carotid not only sup-

30

plies most of the circulation to the right hemi-
sphere, despite the apparent perfusion decrease,
but also supplies a portion of the left hemisphere.

The salient features of this patient’s circula-
tory pattern are now established. The carotid
systems and circle of Willis are normally and
adequately patent if not slightly increased; the
right cerebral perfusion is decreased; and the
right internal carotid supplies an appreciable
part of the left perfusion. The interpreter now
must decide if this pattern suggests a possible
diagnosis.

The decreased right perfusion first suggests
ischemic or occlusive disease. If true, the right
internal and common carotid should be reduced,
the left internal carotid should be increased and
supply collateral ¢o the right perfusion, and the
posterior components should be increased. There-
fore, primary ischemic vascular disease is un-
likely. The interpreter must look to other
etiologies for an explanation of the pattern.

The reversed NICS is the important clue.
While the intracranial circulation monitored by
the right electrode pair is decreased, the intra-
cranial circulation monitored by the left electrode
pair has increased. Each electrode pair monitors
a relatively constant geometric volume irrespec-
tive of its contents; the right decrease and left
increase suggest a partial displacement of the
brain and its circulation to the left. The diag-
nosis of relatively avascular, space-occupying
lesion on the right is now clear; the slightly in-
creased amplitudes suggest an increase in intra-
cranial pressure.

Unfortunately, patients frequently have a
combination of diseases and present difficult pat-
terns to diagnose. In such cases, the interpreter
should try various combinations of diseases and
anomalies consistent with the pattern. Fre-
quently, a definite diagnosis cannot be reached
and a series of probabilities must be listed; oc-
casionally, only lateralization can be determined
(which is usually all that is necessary clinically) ;
rarely, no conclusion at all can be reached. In
these latter cases, significant information can
often be obtained from analysis of the waveform
and its timing. We routinely use both ap-
proaches and interpret waveform changes in
terms of the possibilities suggested by the mathe-
matical patterns.

B. Waveform Analysis; In our experience, both
the reference and bitemporal arterial occlusion


TABLE V.

Continued

Rhecencephalographic Findings in Patiente with Subsequently Known Definitive Disgnoses

Waveforms
veak ining
inputs Inflow Delayed Runoff Delayed
ee ean w.
(ret | neforence | ttenporer | neforence | nttespora: | neterence | sttemporet
ide)
siie [9 [ sue fet a Pa fe fe |e fe fa fe
58L R 0.2 + oO oO oO a
ou ° + + + + Bedeide tracing using portable single- 2,
‘chanel 2K
a oo 0 0 Ps
98R R Ow + + oO oO Possibly unsatisfactory tracing ae
m 4% om o + oo 5.
om ° or) oo 6
TM = Roa om .
0 + + +o 8.
eb L 0.13, + + + + oe
om + + o oO 10.
100 + 4 + + a.
ena + + 4 1.
an 4 * + b.
mTM oR ao 4 ua
an 0 om oo w.
ean ° o + oo 16.
a re) + + 4 wn
oon ° om oo a.
oa ° om + 4 ».
ou 0 a 20.
on Lb om 4b om 0 + 0 0 0 + 0 0 aL
oe ket 2.
oe, 0 o 0 © 0 0 0 96 © 06 23.
Se a a i a.
TM 0 a 2.
oa 0 o + Fe HO Ol 2.
eet 0 Ce zn.
on LOM 2.
et = RnR em ps.

39



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89+



are not surprising and indicate the potential
value of rheoencephalography as a screening
procedure,

B. Criteria for Diagnosis of Carotid Occlusive
Disease: Since this series contains 18 cases with
proved and 45 cases with presumptively signifi-
cant carotid occlusive disease (carotid ratios of
65% or less), a discussion of diagnostic criteria
is worthwhile,

Jenkner’ considers peak timing delays of 0.01
second and longer and differences of amplitude
greater than 10% to be significant. While not
offering specific criteria, he indicates internal
carotid artery occlusions are usually associated
with decreased amplitudes and timing delays of
0.10 second or longer on the affected side. Perez-
Borja and Meyer" and McHenry" find no such
correlation and note that such criteria frequently
give false lateralization to the unaffected side.

1. Timing Delay: In this series, 88 tracings
showed timing delays of 0.04 seconds or longer
on either the reference or bitemporal compres-
sion tracings. Five tracings showed no delay
during bitemporal compression, while three trac-
ings showed delay only on the latter (see Tables).

The side delayed on the reference tracing was
compared with various tracing factor asymme-
tries, no matter how slight. Random correlation
was found with asymmetries in the reference
amplitudes, cerebral perfusions, and common
carotid, internal carotid, and temporal arterial
components. Similarly, xo correlation was found
with delays on the bitemporal compression trac-
ings. Timing delays are, therefore, equally likely
to appear on either side and are not reliable in-
dicators of lateralization. Further, at least 47
tracings showed no delay despite significant dis-
ease; the absence of a delay does not reliably
indicate an absence of disease. Finally, as might
be expected, timing delays correlate well (84%)
with abnormal waveforms showing delayed in-
flow.

Timing delays, either on the reference or bi-
temporal compression tracings have zo lateraliz-
ing significance and non-specifically indicate the
presence of disease.

2. Reference Amplitude Asymmetry: Refer-
ence amplitude asymmetries of 90% or less were
compared to asymmetries in various factors.
Agreement with cerebral perfusion asymmetry
was excellent in 20 (91%) of 22 tracings. Agree-

49

ment with temporal artery asymmetries was less
satisfactory and was found in 17 (77%) of 22
tracings. Agreement with common carotid asym-
metries was poor and was found in 29 (60%)
of 48 tracings while agreement with internal
carotid asymmetries was equally random in 11
(55%) of 20 tracings.

Reference amplitude asymmetry is an excel-
lent indicator of cerebral perfusion asymmetry,
is less reliable in assessing the temporal arteries,
and is unreliable in carotid artery asymmetry.
There is a similar lack of reliable correlation
between cerebral perfusion asymmetries of 95%
or less and carotid asymmetries.

3. Reference Amplitude Asymmetry Plus Tim-
ing Delay: Fifteen tracings combined the two
criteria; all tracings showed significant abnor-
mality. Both findings were consistent with
lateralization in five tracings (33%); the delay
was consistent with lateralization in four trac-
ings (27%); the amplitude asymmetry was con-
sistent in three tracings (20%); and both find-
ings were self-consistent in three tracings (20%)
but greater vascular abnormality existed on the
opposite side (false lateralization). The two
criteria are reliable indicators of disease but not
of lateralization.

4, Cerebral Perfusion Asymmetry Plus Timing
Delay: Thirteen tracings combined the two cri-
teria; all showed significant abnormality. Both
findings were consistent with lateralization in
four tracings (31%); the delay was consistent
with lateralization in three tracings (23%) ;
the amplitude asymmetry was consistent in four
tracings (81%); and both criteria were falsely
lateralizing in two tracings (15%). The two
criteria are reliable indicators of the presence
of disease but not of lateralization.

5. Combination of Criteria: There is no single
criterion or set of criteria which will collect all
of the significantly abnormal tracings in this
series. A combination of one or more of the
following criteria—timing delays in either the
reference or bitemporal compression tracings,
reference ratios of 90% or less, and cerebral
perfusion ratios of 95% or less—loses 16 tracings
showing significant disease. Twelve of the latter
tracings lack bitemporal compressions and might
possibly have been included in the abnormal
group. If inflow retardation, either in the refer-
ence or bitemporal compression tracings, is added
to the above criteria, only the arteriovenous



TABLE VITT.--Continued
caleulated Riecencephlographie Factors in Patients without Definitive Studies

Tracing Component Ratios (Fereent)--contimuea |
erence
Cerebral Perfusion ‘apie
Carotia | Cere- Components rude Rheoencephalographic Clinical Diagnosis
fitice’ | Ee wee | HES Dlagnoois (Gt how) Romar
i | totemar or
Anterior i
fuston| carotids | shunt | larger
HRatios| Shunts side)
Con-|_tn-
‘on terme ete a]
a a a BIL Moderate bilateral carotid Generalized cerebrovascular 2%,
‘Gisease greater on right, disease and diabetes
8 excelent posterior col-
eral
BL UL 9 0 6h 8 ot 96R Right internal carotid steno- Bastlar insufficiency Probably unsatisfactory 35.
‘fs at or above bifurcation tracing
6 marke peotertor collat=
92R @R 95R XS Go 98% vasomotor instabiitty, Hypoglycenic episodes Fasting tracing 36.
Otherwise noraal
eR eR PR 8 mm 92h Nornal stable tracing, Hypoglycemic episodes 30 ain. post-prandial 37,
{proved tron Tasting trace
ToL TOL ML 3 375763) B7L_—_RANE common carotta ‘Chronic brain synd. & aleo- 38
decreased slightly compared holisn
to left, possibly signif~
foant
47 3OR L372 63393 BOL_ Signi ffcant Lett common Weft carotid ese palpable + 2.

‘carotid occlusive disease
at or below the bifurcation

©OL 2%L 89R 2722-27-78 AER BOR_—Right internal carotid steno- Generalized ASCVD ” 40.
sis of clinical signifi-

92L 95L OR 0 1 92 99 BR -9BL_—No significant carotid occlu a
‘sive disease; FO verte
bral-basilar dlgeace

@OR WR 72 16 36 8 56 BL 87L_—«-Y/O Thght space-cccupying Headaches of unknown oticl- 42.
leston ony

aL 25L gen 48

é

21 60K SAR Significant right common 43.
carotid insufficiency

99R 75R 9R 52 46 48 44 © -LOL_«««99L- Normal tracing with large Diabetes with hypoglycenic bh,
posterior contributions; episodes
‘excellent collateral
tential,

OL %L OL 16 6 75 La /o right space-occupying 4.
Lesion

SL ML L472 53 ML SL BBL Bilateral carotid occlusive Generalized ASCVD 46.
‘disease more marked on
right

68L 72L GL 55 «47-4553 THL Lateral carotid occlusive an.

‘disease, probably clini~
cally significant on the

right
BL GIL 100 23-3155 69 ARR TE right carotid compreaaién Possible abdominal A-V 48.
valuea are correct. the fistula; R. carotid bruit
right internal carotid te
‘significantly stenosed
SAL 65L 87L 67 «75S BR OLL CB Lmteval common carotid 49.
occlusive disease nore
marked on the right

au 79L Decreased right cerebral 2 Intracranial otastatic dis- 50.

‘perfusion ease

67L AbL 89 102056 BOHR OR Stgnificant right carotid a
stenosis

TOL 89L Decreased right comon Right carotid bruit Normal subject ++ 52.
carotid

oL BL Above confirmed Right carotid bruit 5 D interval ++

BBL 75 98L 353457] BTL. Improved right carotid Bruit still present 24M interval ++
‘etroulation

47



Schwarz and Mitchell and Gurdjian et al.*
We have not as yet analyzed our data considering
the known incidence of anomalies of the circle of
Willis****, Such anomalies may in part explain
the incidence of apparently significant carotid
stenosis in our normal series, as previously dis-
cussed (page 48).

D. Mean Tracing Amplitudes: The entire Schu-
fried tracing series was reviewed eliminating un-
satisfactory or incomplete tracings, cases with
proved or suspected disease and cases with com-
mon or internal carotid ratios of 75% or less,
leaving a remainder of 36 rheoencephalograph-
ically normal tracings; similar review of the
Schufried tracings in the previously discussed
groups leaves 20 tracings of unilateral right caro-
tid disease, nine tracings of unilateral left carotid
disease, 19 tracings of bilateral carotid disease
more marked on the right, and 12 tracings of
bilateral carotid disease more marked on the left.
The average amplitudes for each group and the
combined group are presented in Table IX. As
a variable number of tracings in each group lack
the complete series of arterial compressions, the
averages are not strictly intercomparable.

‘Taste X. Ratios of Average ‘Tracing Components

Ratios (Percent of Right or Left Side)
Carotid Disease
racing Unilateral Bilateral
Components | Normat Greater | Greater
Right | Left
Involve- | Involve-
Right | Left | ment | ment
Temporal
Arteries 86%R | 144%L | 188%R | 10%L | 169%R
Internal
Carotid
Arteries 959R | 38%L | 88%R | T1%L | 52%R
Common
Carotid
Arteries 94%R | 50%L | 50%R | 69%L | 88%R
Cerebral
Perfusions| 105%R | 103%L | 115%R | 94%L | 93%R
Posterior-
Anterior
Shunts 1259%R | 88%L | 89%R | 9%L | 105%R

Eight tracings (28%) in the unilateral carotid
disease group (five right, three left) give ampli-
tudes considerably higher than any encountered
in the normal group and raise the group averages

53

and standard deviations; the group reference
amplitudes otherwise fall within the normal
range and support the previous conclusions re-
garding the difficulty of diagnosing carotid dis-
ease from the reference tracing alone. We have
no explanation for the increased amplitudes
which do not correlate with youth.

Reference tracing amplitudes in bilateral ca-
rotid occlusive disease generally fall well below
the normal range and may often be diagnostic;
they do not reliably indicate the side of major
involvement.

Arterial component ratios calculated from the
group averages are presented in Table X.

E. Temporal Arterial Inversion as an Obscuring
Factor in Internal Carotid Occlusive Disease:
The temporal arterial component ratios in uni-
lateral internal carotid occlusive disease suggest
that there is a strong tendency for the ipselateral
temporal artery (and probably the external ca-
rotid artery) to be larger than the temporal
artery on the uninvolved side (Table X). In-
version is also seen in the bilateral disease group
having greater left carotid involvement.

The individual tracings were reviewed; 33
tracings include temporal arterial compressions
and could be evaluated for temporal arterial in-
version. The common carotid is the presumed
or actual site of disease in 17 tracings; all 17
tracings show a marked decrease in the ipse-
lateral temporal artery. The internal carotid is
the presumed or actual site of disease in 16
tracings; 15 of the ipselateral temporal arteries
show marked increases compared to their con-
tralateral arteries, while both arteries are equal
in one tracing. Fifteen tracings with bilateral
disease greater on the right include temporal
arterial compressions; 12 tracings indicate right
common rather than internal carotid disease.
This group (Table X) is strongly biased by com-
mon carotid disease and shows consistent tem-
poral, internal, and common carotid ratios.

This marked tendency for the temporal artery
to increase in internal carotid occlusive disease
probably is part of the well-established external
carotid response;*° it may also reflect the
Horner’s syndrome occasionally associated with
this disease.“* This unilaterally increased extra-
cranial circulation may partially explain the
difficulty of diagnosing carotid disease from the
reference tracings alone. The increased temporal



ABLE VIII.~-Continued

Calculated Rheoencephalographic Factors in Patients without Definitive Studies

‘Tracing Component Ratios (Percent) --Continued

ete
Cerebral Pertusion erence
carotid | core- jomponente 4zpli- | pheoencephalographic cLinteal Diagnosis Remarks Wo.
Ratios | bral - wer | tHe Diagnosis
Per- [Posterior- | tneemat Ratios
fusion] Anterior | BML | shunt | (Foe
ftatios| | Shunts larger
Goa | In ide)
non | ternal eye {Rye
oot 46R Right carotid Insutficfeney Generalized cerebrovascular L
inauftictency
vat GOR Right carotid insufficiency Generalized cerebrovascular 2 M anticoagulation 2.
3 isprovenent, ‘nouffiotency
oat 92 Moderate cerebrovascular Occipital dechomta + 3
disease
on 79R Left carotid insufticieney Seizure, undetermined etfology + 4
41 S58 Right carotid insufficiency : 3.
sak 53 Noma tracing : e
36 80L ‘Right carota: inourtSeiency n
aan aOR —_=Bilatorml carotid inouffi- 4M anticoagulation a
‘oleney
an ‘UR weft carotid SneuffScfeney Transient cerebral insuffi- + °.
lene
aR 842 Moderate corebrovasculér _Baoilar insufficiency 10.
icease nore marked on the
deft
2b SOL Right carotid insufficiency Sane ne
TPR 89L —Wommal tracing Myocardial infarction 1963. + 2
aan 73H Slight left carotéa ineurfi- Migraine + cen
‘ciency
on UR Significant Iefe carotid Generalized severe ASCVD + ue.
Snsurttetency
oon 92k Normal tracing Migraine + 1s.
62 942 Significant right carotid Generelized severe ASCWD, ie.
fneuttictency Ventricular fibriiiation
oon wo Stgnificant rignt carotid Selure, undetermined etiology + yw
‘noutfielency
en &1R Moderate cerebrovascular Parkinson's disease uw.
‘ice
7R 100 Sight left earotid insufei~ Normal subject with less pul- ++ as.
‘slenoy with excellent com>" atile left carotid
pensation
uR yeu bilateral carotid insuffi- Baoilar insufticieney 2.
‘leney, nore marked on Letts 9/0
sieht space-occupying Lesion
een sol Slight lett carotid’ intutfi= a.
cheney; moderate general~
zed cerebral ASCWD
0b aot Normal tracing Fainting + 2.
100 93 Nomal tracing with vaso- Migraine 3
notor instability
co 951 Marked generalized cerebral Right carotid ees palpable; + oa
ASCVD; right carotid Serebral insufficienty
slightly tapaired
eet SL Slight Bilateral carotid Basler inoufricieney + 2B.
impairment
een 59R Generalized cerebral ASCYD; Generalized cerebral ASCYD + 2%.
bilateral catotid iepaiz~
ent gore marked on the
Tere
on SOL Geelunive disease above Right middle cerevral insuftt- 2.
circle of Hillis on right" elensy
eab 89 —Shgnificant right carotid Generalized cerevral tschenta 2.
inouffieiency
SOR Resolving left insufficiency Left internal carotid or 2.
provess ‘middle cerebral, throaboeis
eat 87R Bilateral carotid insuffi- Generalised cerebral iechenia x.
‘tency, sore marked on
right
768 100 Generalized moderate Generalized cerebral ischemia ae
rebrovescular disease
Slight left carotid in-
paiment
olL 32, 97k 252M TL~S3AR_ BAL Sgmtdcant right internal 32.
Sarotid stenosis at oF
hove the bitureation
92k 55k SOL 63 6837-23. 7OL_—Bnveral marked carotid Generalized cerebrovascular 23.

stenosis, significantly ‘disease
greater on left

45



3, Electrode Contact Material.

a. Criteria for choice: We chose to use
commercial electrode pastes rather than the
saline-soaked sponges used by Jenkner Such
pastes offer the advantages of considerably
higher conductivity, more easily reproducible
thickness of the layer between electrode and skin,
better continuity over the entire electrode area,
greater dimensional stability after application,
and slower drying rate.

Measurements (1963) using Radiometer con-
ductivity equipment* on a variety of such pastes
at room temperature disclosed that one prepara-
tiont had a conductivity half that of saturated
saline solution and 12 times that of the next
highest paste. This paste was therefore chosen
as standard. Of the other preparations, the
creams in particular were considerably less con-
ductive and often contained substances which
absorbed firmly on the platinized electrode
surfaces rendering them hydrophobic. These sub-

‘Radiometer Type CDM 2d Conductivity Meter and appro-
priate cells. The London Company, Westlake, Ohio.

*Telectrode” electrode jelly, Telemedics, Inc., Southampton,
Pennsylvania.

Fievre 11,

17

stances could not be removed by repeated wash-
ing with water and a variety of organic solvents.
b, Method of Application: Electrode paste
is applied in sufficient quantity to wet thoroughly
the skin and hair beneath the retracted electrodes
and is rubbed in well. The electrodes are low-
ered into the paste and moved about slightly to
seat them and equalize band tension. More paste
is added as necessary to achieve a thoroughly
wet, stable, contact area which should not extend
more than 0.5 cm. beyond the electrode edges.
The small excess forced from under the elec-
trodes is permitted to remain; marked excess is
removed. Electrode placement and symmetry is
again checked and final adjustments are made.
If properly performed, the above procedure re-
sults in an electrode-patient contact which adds
negligible resistance to the circuit, remains stable
throughout an hour or more of tracing, and gives
a minimum value for the patient resistance.
4, Instrumentation.
The Schufried instrument* has been described
by Jenkner,* While not without its peculiari-

*Available from Schick X-Ray Company, 444 North Lake
Shore Drive, Chicago, Hlinois.

Electrode placement for rheoencephalography.



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35



Table of Contents—Continued

II. Tracing Interpretation --.
A. Mathematical Analysis
1. Tracing Measurement

c. Reference Tracing ---
d. Occlusion Tracings --
e. Error Analysis and Data Selection ---

2. Calculation of Arterial Components -_-----------------------
3. Provisional Diagnosis

a. The Normal Circulatory Pattern _
b. Abnormal Circulatory Patterns __-
(1) Common Carotid Arterial Occlusions -.
(2) Internal Carotid Arterial Occlusions _
(8) Bilateral Carotid Arterial Occlusive Disease -.

ce. General Approach -

B. Waveform Analysis -__
1. Basic Waveform __

III. Results -------_----------_-----------------------------------

A. Population
1. Normal Subjects
2. Patients

B. Tracing Values

1, Normal Subjects __.
Table I. Rheoencephalographic Findings in Normal!
Subjects __.__----_----2_---------------------------------
Table II. Calculated Rheoencephalographic Factors in
Normal Male Subjects --_---------------------------------
2. Patients
a. Patients with Known Disease
Table III. Rheoencephalographic Findings in Male
Patients with Known Disease ---------------------------
Table IV. Calculated Rheoencephalographic Factors in
Male Patients with Known Disease ___
b. Patients with Subsequently Known Definitive Diagnoses
Table V. Rheoencephalographic Findings in Patients with
Subsequently Known Definitive Diagnoses ----------------
Table VI. Calculated Rheoencephalographic Factors in
Patients with Subsequently Known Definitive Diagnoses —--
c. Patients Without Definitive Studies ____..._--_---------_--
Table VII. Rheoencephalographic Findings in Patients
Without Definitive Studies -_----------------_---_-------
Table VIII. Calculated Rheoencephalographic Factors in
Patients without Definitive Studies --.---------_-________

vi


easier to obtain a second tracing at another
time when the subject is more relaxed, better
rested, or has eaten.

Finally, as we have attempted to indicate
throughout the above discussions, our concepts
of tracing analysis are based on two points:
First, values should be obtained from the tracing
which are as representative of the tracing as
possible. Second, only those methods of analysis
should be used which can reasonably be derived
from the data itself. While our initial diagnos-
tic successes suggested our approach was valid,
the remarkable self-consistency of our method
was not suspected. When we dared attempt
bilateral carotid occlusions, it was immediately
manifest and, in turn, dictated further refine-
ments in analysis.

2. Calculation of Arterial Components: Once
obtained, the average values are tabulated ac-
cording to the notation on page 11 and used
in the formulae on page 12 to calculate
arterial contributions. The calculations are
simple and require no discussion. Negative
values may be encountered on rare occasions;
such values are, of course, impossible. If the
data is adequately simultaneous, negative values
usually fall within the experimental simul-
taneity error and may be considered zero.
Negative values larger than experimental error
were encountered in the initial portion of this
study when the possibility of checking simul-
taneity was unsuspected. Carotid occlusion
tracings were brief; the small samples were
skewed by the initial low amplitudes.

‘We next tabulate the arterial contribution
values and calculate various percentage ratios
to assist diagnosis. We have found the following
sets of ratios (or their inverses) valuable:

LRT RT RT LT Lr.
LT’ RIG’ RCC’ Lid’ Loc’
2.RP RIC RCC.
TP’ Lic’ cc}

3, a. If the NICS is supplied by the right
internal carotid artery to the left hemisphere:

PAn
RP’

PA,
LP’

RIC-NICS NICS LIC,
RP” =LP LP’

or:

28

b. If the NICS is supplied by the left in-
ternal carotid to the right hemisphere:

PA,
RP’

PA,

, RIC NICS, LIC-NICS
LP

RP’ “LP LP

Other appropriate ratios can be used to dem-
onstrate particular interrelations.

Reference to the assumptions on which the
above method of analysis is based, page 10, in-
dicates that there is some theoretical inaccuracy
in directly comparing the temporal with the in-
ternal carotid values since their factors for con-
version to blood volumes may be different. Simi-
larly, the common carotid values are not strictly
analogous to blood volumes but are also useful
approximations if this inaccuracy is recognized.

3. Provisional Diagnosis: A clinically valid
method should yield reliable and objective in-
formation about the patient without prior refer-
ence to the clinical findings. To be maximally
useful, such information should clearly indicate
the presence of disease and offer criteria for its
diagnosis without clinical reference. Failing
this, the information should indicate the diag-
nosis or permit selection between alternate diag-
noses when correlated with the clinical findings.
Equivocable or misleading information should
be minimal and easily recognized. If reliable
and objective information cannot be obtained,
the method offers little of value to the clinical
situation. We have attempted to derive diag-
nostic patterns from the tracing itself based on
our concept of cranial circulatory physiology
and its relation to the tracing; it should par-
ticularly be noted that such analysis does not
require prior knowledge of the clinical history
and findings. In our view, clinical information
unnecessarily prejudices the interpreter’s judg-
ment and may lead to conclusions which, while
perhaps correct, are unwarranted from the data.

Detailed analysis of the patient’s cranial cir-
culation is now possible. We will discuss the
normal pattern, present illustrative patterns we
have found associated with various types of vas-
cular disease in this case series, and finally de-
scribe our general approach. As stated on pages
6 and 14, disease may or may not alter the
cranial circulation sufficiently to alter the trac-
ing. Rheoencephalography, in common with all
diagnostic methods, has inherent limitations;


sumptions. Several of these assumptions, while
reasonable in the ideal normal case, perhaps are
oversimplifications, are overly rigid and may not
hold within experimental error in certain patients
or during particular tracing periods. The ana-
lytic approach can be expected to give equivo-
cable or even misleading results when applied to
such tracings; further, various dissimilar diseases
can be expected to cause either similar alterations
in those portions of the cranial circulation moni-
tored by REG or to be indistinguishable in the
analysis. Thus, if the above approach is to have
any practical clinical usefulness, the validity of
its predictions must be clinically substantiated
and its limits of reliability and requirements for
further modification must be clinically deter-
mined.

The above analytic method suggests a further,
more general method which could greatly extend
the value of REG. The derivation of the above
equations uses the average peak amplitude of a
series of pulse waveforms to represent various
circulatory situations. Such an amplitude is, at
best, an approximation to its average pulse wave-
form; a better representation can be obtained by
averaging the pulses on a suitable computer as
Lifshitz has done for the reference tracing®**.
The average waveforms can then be computer-
processed further according to the above equa-
tions to give waveforms representative of each
arterial component. This approach is under
investigation.

Certain predictions can be made at this point.
After REG has been thoroughly tested and es-
tablished, it should be possible to:

1. Detect, lateralize, and diagnose carotid
occlusive disease, localize the major site above
or below the carotid bifurcation, estimate the
degree of impairment, and estimate the extent
of collateral compensation ;

2. Detect, lateralize, and diagnose other forms
of intracranial disease and estimate their degree
of development; and

3. Use rheoencephalography reliably in any
of the myriad situations in which a knowledge
of the cranial physiological events which it moni-
tors would be valuable.

Hopefully, since the above methodology is
time consuming, clinical experience may develop
objective criteria for the diagnosis of disease
reliably by eye alone similar to present practice
in electroencephalography.

14

Clinical Studies
J. H. Seipel, Ph.D., M.D. and
A. R. Kessler, M.D.*

The controversy regarding the clinical value
of REG is. illustrated by the marked dichotomy
between the reports of Jenkner’, in whose hands
it has been extraordinarily successful, and those
of Perez-Borja and Meyer’? and McHenry who
found it not only of little diagnostic value but
also frequently misleading. Thus, the first ques-
tion any clinical study of REG must answer is
the basic one that all potential additions to the
clinical armamentarium must answer—can the
method detect and diagnose disease with suffi-
cient reliability to warrant its clinical use?

The rheoencephalographic studies in the
author’s laboratory have followed two major
interlocking plans simultaneously: first, to col-
lect a sufficiently large series of clinical cases to
determine if the method has clinical value and,
if so, to determine its range of applicability;
and second, to elucidate as much of the biophysi-
cal basis of the method as possible. The clinical
studies will be discussed; the biophysical studies
will be presented in later papers.

I. Methodology:

A. Standardization: Rheoencephalography has
not escaped the methodologic diversity which
frequently arises following the introduction of
a new research or clinical tool. It was recognized
at the inception of this study that rheoencepha-
lography might be markedly influenced by ap-
parently minor variations in methodology and
that much of the diversity of opinion probably
arose from such sources. Therefore, a rigidly
standardized method was necessary for intercom-
parability within the projected clinical series and
for comparison with results obtained by other
investigators. A standard method might also
permit the isolation and study of individual
factors in the procedure.

Preliminary analysis suggested particular
sensitivity to variations in a number of factors
for which standardization would be important.
These were:

A. Patient factors:

1. Body position

2, Head position
~“*Medieal Officer, Laboratory of Neurology, Georgetown
Clinical Research Institute, Federal Aviation Administration,

and Clinical Instructor in Neurosurgery, Department of Sur-
gery, Georgetown University Hospital.


amplitudes are measured. If not 10 mm. on the
REG channels, the Rheograph output dials are
adjusted towards this value and the procedure
is repeated. Several readjustments may be nec-
essary until the channels are reasonably equalized
close to the above value; exact equalization at
10 mm. is difficult to attain and is not necessary.
Minor variations affect visual waveform com-
parisons only slightly and the quantitative meas-
urements not at all. If the tracing amplitude
is less than 6 mm. at 0.10 ohm per 10 mm., the
0,05 ohm (50 mohms) setting can be used with
the tracing amplified to 0.05 ohm per 10 mm.

Once satisfactory equalization has been at-
tained, the patient is requested to relax and re-
frain from moving, blinking, coughing, and
swallowing. The recorder is again started and
at least 80 adequate calibration pulses are placed
on the record. These pulses should occur not
more frequently than every second pulse, should
appear on the falling phase after the dichrotic
notch, and should be contained within the linear
pen excursion range. The calibration pulse am-
plitude and waveform will depend slightly on
the calibration button action. Firm, rapid,
deliberate pressure is recommended. A certain
amount of practice is usually required before
properly timed, identical calibration pulses are
routinely attained. Since these pulses are, in
theory, square waves, the pulse appearing on the
tracing should be as close to a square wave super-
imposed on the REG activity as the recorder
frequency response will permit (Figure 13).
Trains of calibrations are also entered at various
stages of the tracing and at its end. These serve
as a stability check during the run and help
compensate for unsuspected changes which may
have occurred.

A certain amount of variation in calibration
pulse amplitude and shape must be accepted as
peculiar to the instrumentation and tracing pro-
cedure. Under ideal conditions, the amplitude
will not vary more than 0.4 mm. throughout a
series but may vary as much as 2.0 mm. with
some recorders. Irregular calibration pulses
usually indicate dirty contacts within the button
assembly; these should be cleaned as indicated.
Occasionally, careful calibrations will be irregu-
Jar, too small, or otherwise appear aberrant on a
seemingly clinically adequate tracing. This is
one of the innate perversities of inanimate ob-
jects for which we have no explanation; it may

20

be inherent in the Rheograph circuitry. The
best solution we have found is to shut off the
equipment and try again later.

A word of warning is necessary. Should it
be necessary to readjust, repaste, or otherwise
disturb the electrodes at any time during the
tracing, or if it is suspected that the electrodes
have slipped or otherwise changed position, the
bridges must be rebalanced and the tracing must
be recalibrated. This is necessary since any
such disturbance changes the balance point and,
therefore, the tracing calibration amplitude. Fur-
ther, since the bridges cannot be rebalanced
closer than to within several ohms of the same
point, recalibration must always be performed
after balance checks or changes during a trac-
ing. Balance values should always be recorded
on the tracing.

It should be noted that the use of the standard
resistance setting on the Rheograph has not been
mentioned as part of our procedure nor has its
possible use in calibration been presented. This
Rheograph setting is intended for use in the pre-
liminary adjustment of the recorder gains as
suggested in the Rheograph instruction manual.
Since we equalize channels using calibration
pulses on the patient tracing, we have found this
setting of little use except when trouble-shooting.
Further, one investigator? has advocated cali-
bration on this setting alone and has indicated
not only that further calibration on the patient
tracing is unnecessary but also that calibration
on subsequent patients throughout the day is
unnecessary. This usage is contrary to that pre-
sented in the Rheograph instruction manual and
to that of Jenkner’, many of whose illustrations
clearly show calibration pulses on the tracing.
We have investigated this point and find that
neither the calibration pulse amplitudes nor their
ratios transfer from balance on the standard
setting to balance on the patient setting. Al-
though inconvenient and somewhat wasteful of
time, it is absolutely necessary to calibrate each
time the bridge has been balanced whether on a
new patient or during a tracing run.

Our pretracing procedure has been detailed
at length for several reasons: first, to facilitate
its repetition by others; second, to propose it as
a standard method for rheoencephalography ;
third, to indicate possible sources of error in-
herent in rheoencephalography; and fourth, to
present our reasoning and approaches. This


The procedure is described to the patient who
is encouraged to relax, breathe evenly, re-
main still and quiet, and sleep if possible. Be-
tween recording periods, the patient is permitted
to readjust position slightly, speak, sneeze, swal-
low, and otherwise perform those small actions
employed by the human to relieve boredom or
tension. He is informed such actions cause arti-
fact during recording periods and prolong his
stay—a most effective way of insuring coopera-
tion! Pads or eye shields are used if eye move-
ment and blink artifact are excessive. Conversa-
tion is kept to a minimum during the tracing
period. Room lighting is subdued and glare is
avoided. Adequate walkway space is preserved
about the bed to permit easy access from all
sides without patient distraction or movement.

2. Electrode Preparation and Placement.

a, Electrodes; The 7.5 cm.’ aluminum block
electrodes supplied with the Schufried instru-
ment were originally employed without modifi-
cation. While satisfactory when relatively new,
internal corrosion from the salts in the electrode
paste rapidly rendered them unreliable. Heavy
(0.020’’) platinum sheets of the same dimensions
with welded 0.020’ platinum leads were next
tried. These afforded excellent tracings but their
rigidity caused excessive movement artifact.
New Rheograph aluminum electrodes vacuum-
impregnated with clear epoxy resin proved rea-
sonably corrosion-resistant and were used for
most of the study. Eventually, these also cor-
roded despite careful cleaning and were dis-
carded.

Standard 9.4 mm.? German silver EKG disc
electrodes were next tested and have proved
satisfactory. As supplied, the centerpost is
somewhat large and occasions difficulty in lateral
electrode placement using standard perforated
rubber electrode straps. These posts were re-
moved and replaced by solder nubbins. Enlarge-
ment of the binding-post holes may be necessary
to accept the Rheograph electrode leads. Elec-
trode faces are cleaned with fine emery cloth as
necessary to remove surface film and oxidation.
The slightly roughened metal surface so obtained
is considered advantageous.

b. Skin preparation; Electrode placement
sites are carefully cleaned with acetone or alcohol
before placing and pasting the electrodes. Fe-

16

male patients are requested to shampoo their
hair before reporting.

c. Electrode placement: Electrodes were
originally placed as suggested by Jenkner* and
illustrated in our previous paper.*? They are
secured firmly in place by a not uncomfortably
snug, perforated rubber electrode strap encirc-
ling the head. The anterior electrodes are placed
as close together as the band perforations permit
without touching and are centered on the sagittal
midline of the forehead. The lower electrode
edges are slightly above the frontal eminences.
Further consideration of possible current flow
paths in the Jenkner placement suggested that
the electrodes should be positioned both to mini-
mize paths through bone and extracranial tissue
and to maximize paths through the intracranial
volume supplied by the carotids. The frontal
“indifferent” electrodes were already positioned
slightly above the cranial floor. The lateral
“active” electrodes were shifted to a similar level
between the ears and the skull and centered on
the bi-auricular line. The anterior electrode
edges do not extend beyond the anterior ear line
(Figure 11). This change shortened the inter-
electrode distance slightly with no apparent
effect on the tracing. After preliminary place-
ment, the interelectrode distances are measured
and the lateral electrode positions are adjusted
to agree within 0.5 cm., keeping the interelectrode
distance as long as possible. After paste appli-
cation, the placements and distances are again
adjusted as necessary and the distances are re-
corded. Distances are rechecked at the end of
the tracing.

The importance of careful electrode placement
cannot be overemphasized, as Jenkner’ indicates.
The previous theoretical discussion indicates the
electrode pairs must be placed in close anatomic
symmetry. Interelectrode distances should not
only be closely equal but also should be as long
as possible to avoid near-field overlap. Inter-
electrode distance can be expected to vary
slightly from patient to patient. However,
standard anatomic electrode placement and bi-
laterally equal interelectrode distances insure
that the fraction of the cranial volume moni-
tored by each lateral pair remains reasonably
constant throughout the patient series. A  pos-
sible source of methodologic error is thereby
minimized and intercomparability is strength-
ened.


some alterations may fall within the patterns
of normal variation; some may be borderline or
suspicious; some may be definitive; and some
may be uninterpretable or actually misleading.

a. The normal circulatory pattern: In
theory the ideal normal head should show com-
plete lateral anatomic symmetry in all of its
structures; the ideal normal cranial circulation
should equally show the same complete lateral
symmetry in all of its components. Therefore,
the ideal rheoencephalogram should show the
same lateral symmetry, within the limits of ex-
perimental error, if the calculated arterial com-
ponents are valid analogs of the contributions
of their arteries to the cranial circulation. The
ideal normal pattern is obvious and, in terms of
the previous ratios, is:

R
L,

RT _ RIC _ RCC _ RP
LT LIC LCC LP

NECS=NICS=0

In practice, a completely symmetrical tracing is
rarely obtained; as might be expected, tracings
obtained from a series of apparently normal
subjects give different ranges of values for each
of the component amplitudes and their ratios.

= 100%

b. Abnormal circulatory patterns: The suc-
cessful interpretation of abnormal patterns de-
pends greatly on the interpreter’s familiarity
with the pathophysiology of the cranial circula-
tion associated with various diseases and his
previous experience in this type of analysis and
its limitations, Certain patterns are immediately
and obviously pathognomonic; others may be
obscured by individual variations. Patients
with several concurrent diseases may give trac-
ings that can tax the interpreter’s ingenuity.

(1). Common carotid arterial occlusions:
If a common carotid artery is completely oc-
cluded at or below the carotid bifurcation and
collateral has become established, the pattern is
easily recognized. The ipselateral temporal, in-
ternal carotid, and common carotid values are
zero; the corresponding contralateral values are
markedly increased; both transmidline shunts
are markedly increased, arise from the contra-
lateral circulation, and supply the ipselateral
circulation; one or both posterior values are in-
creased; and the ipselateral perfusion may be

29

slightly smaller, the same, or larger than the
contralateral perfusion depending on the effec-
tiveness of collateral compensation.

(2). Internal carotid arterial occlusions:
If an internal carotid artery is completely oc-
cluded at or above the bifurcation, the external
carotid artery is not impaired, and adequate
collateral is established, the pattern is again
clear. It follows the first case except for ap-
preciable temporal values and for the ipselateral
common carotid value which is equal to or some-
what larger than its temporal value.

(3). Bilateral carotid arterial occlusive dis-
ease: This case is more difficult to diagnose.
Lesions may be incomplete and may occur above
or below the bifurcations; many patterns are
possible with or without adequate collateral
from the posterior circulation. In general, the
posterior values will be markedly increased and
reflect the carotid decreases; the carotid values
will be decreased significantly below normal
while their ratios will indicate the artery with
greater involvement; and the shunts will arise
from the less involved artery to supply the more
ischemic side. If both carotid circulations are
relatively equal, their ratios may fall within the
normal range; the only clues may be normal or
increased posterior values in a set of otherwise
uniformly low values.

ce. General Approach: The first three ex-
amples presented above illustrate how analysis
patterns are associated with cranial circulatory
disease and can be used diagnostically. Unfor-
tunately, the interpreter is frequently faced with
an unfamiliar pattern for which he must devise
a diagnosis. In such circumstances, we have
found a strong sense of logic to be most useful,
particularly when coupled with a knowledge of
cranial pathophysiology. Further, it is impor-
tant for the interpreter to be aware that the
current field of each electrode pair monitors a
relatively constant geometrical volume irrespec-
tive of its contents (page 10). Finally, the in-
terpreter should have some familiarity with the
normal range of values for each arterial com-
ponent and ratio.

We will use a hypothetical case to illustrate
our reasoning. A tracing from a 56 year old



RIGHT

Ficure 9. Model for the analysis of the rheoence-
phalogram.
Notation:
1. Representative tracing amplitudes:
R,=—AR,=Average peak-to-peak pulse
amplitude on the right without arterial
manipulation (reference or “baseline”
amplitude)
—AR,=Average peak-to-peak pulse
amplitude on the right during occlusion
of the right superficial temporal artery
R,=ibid, left superficial temporal artery
R,=ibid, both superficial temporal arteries
R;=ibid, right common carotid artery
Re=ibid, left common carotid artery
R,=ibid, both common carotid arteries
eL, L, Ls, Ls, Ls, Le, L,=corresponding
— AR values on the left
2. Representative vascular component ampli-
tudes :
a=Ipselateral tracing component contributed
by the left superficial temporal artery
ibid, right superficial temporal artery
id, left internal carotid artery
bid, right internal carotid artery
id, left. vertebral-basilar system
f=ibid, right vertebral-basilar system
gu=contralateral tracing component con-
tributed by the left superficial temporal
artery
ge=ibid, right superficial temporal artery
hy=ibid, left internal carotid artery
hg=ibid, right internal carotid artery

R=

b

11

NECS=net transmidline extracranial com-
ponent (collateral shunt from the opposite super-
ficial temporal artery)

NICS=net transmidline intracranial com-
ponent (collateral shunt from the opposite in-
ternal carotid artery)

The following equations can be written for
each tracing period:

1. Baseline:
(8) Ri=bt+gutd+ft+h,
(9) Li=at+getoteths
2. Right superficial temporal arterial com-
pression :
(10) R,=grtd+f+hy
(11) L,=a+c+e+thr
8. Left superficial temporal arterial compres-
sion:

(12) R,=b+d+f+hz
(18) L,=grtet+ethr
4, Bilateral superficial temporal arterial com-
pression :
(14) R=d+f+h,
(15) Ly=ctetha
5. Right common carotid arterial compression:
(16) Ro=g.tfth
(17) L,;=atcte
6. Left common carotid arterial compression:
(18) R,=b+dt+f
(19) Le=geteth

7. Bilateral common carotid arterial compres-
sion:
(20) R=f
(21) Li=e
If the initial assumptions are valid within the
error of the recording procedures, the above equa-
tions are simultaneous and can be solved for the
values of the various arterial tracing components.
‘A check on the simultaneity of the values is
possible if bilateral compressions have been per-
formed. Values for the bilateral compression
amplitudes can be calculated:

(22) Ri=R. +R. Ri
(23) Lyo= Ly +Ls—Ly
(24) Rio=Rs+Re—R,
(25) Lr=L;+Le-lh

The differences between the observed and calcu-
lated values are a measure of the simultaneity
of the equations,



REFERENCES

1. Jenxner, F, L., “Rheoencephalography,” C. C Tho-

mas, Springfield, Illinois, 1962.

Nyzozr, J., “Electrical Impedance Plethysmography,”

C. C Thomas, Springfield, [inois, 1959.

. Keprov, A. A, and Naumenko, A. I, “Problems in
the Physiology of Intracranial Blood Circulation
and Their Clinical Implications,” NASA Technical
Translation #¥F-156.

. MoskatenKo, Y. Y, and Navmenxo, A. L., On the

Theory of Electroplethysmography, NASA Technical

Translation #F-157.

Lirsuirz, K., Rheoencephalography: I, Review of

The Technique, J. Nerv. Ment. Dis., 136, 388-398
(1963).

. Larsuirz, K., Rheoencephalography: II. Survey of

Clinical Applications, ibid, 137, 285-296 (1963).

Geppes, L, A. and Horr, H. E., The Measurement

of Physiologic Events by Electrical Impedance, Am.

J. Med. Elect., 3, 16-27 (1964).

Geppes, L, A., and Horr, H. E., The Measurement

of Physiological Events by Impedance Change, Proc.

San Diego Symp. Biomed. Eng., 115-122 (1968).

Geppes, L, A., et al, Card. Res. Center Bull, II,

112-122 (1964).

Perez-Borsa, C. and Meyer, J. S., A Critical Bvalua-

tion of Rheoencephalography in Control Subjects

and in Proven Cases of Cerebrovascular Disease,

J. Neurol. Neurosurg, Psychiat., 27, 66-72 (1964).

McHenry, L. D., Jn, Rheoencephalography:

Clinical Appraisal, Neurology, 15, 507-517 (1965).

Nazor, G .L,, and Seren, J. H., The Selective Locali-

zation of Alkaloids in Pancreatic Tissue, Surgical

Forum, VII, 381-885 (1965).

Serer, J. H., and Morrow, R. D., The Magnetic

Field Accompanying Neuronal Activity, J. Wash.

Acad, Sci., 1-4 (Fall 1960).

Guasstong, S., “An Introduction to Electrochem-

istry,” D. Van Nostrand Co., New York, N.Y., 1942.

. Ropinson, R, A., and Sroxes, R. H., “Hlectrolyte

Solutions,” Butterworths, London, 1959,

Scuwan, H. P. Determination of Biological Im-

pedances, “Physical Techniques in Biological Re-

search,” Volume V, Academic Press, New York, N.Y.,

1961.

Hopeman, ©. D., “Handbook of Chemistry and

Physics,” Chemical Rubber Publishing Co., Cleveland,

Ohio, 44th edition, 2690-91, (1962-63).

Sieman, E., et al, Effect of Motion on the Electrical

Conductivity of the Blood, Am. J. Physiol, 118, 708—

719 (1987).

VeuicK, S., and Gortn, M., The Electrical Conduct-

ance of Suspensions of Ellipsoids and its Relation-

oy

7.

10.

i. A

12,

13.

14,

16.

1.

18.

19,

55

23

P

22,

24,

26.

27.

28,

29.

30.

31,

82.

34,

ship to the study of Avian Erythrocytes, J. Gen.
Physiol., 23, 753-771 (1939-40).

Courrer, N. A,, and Pappennermer, J, R., Develop-
ment of Turbulence in Flowing Blood, Am. J, Phy-
siol. 159, 401-408 (1949).

Motner, G. W., Nysogr, Jan, and Levine, R. L,
“The Effect of Temperature and Flow on the Spe-
cific Resistance of Human Venous Blood,” Report
#127, Army Medical Research Laboratory, 1953.
Mosxatenxo, Y. E., and Naumenxo, A. I., Move-
ment of the Blood and Changes in its Blectrical
Conductivity, Bull. Exper. Biol. Med. 47, 211-215
(1959) ‘Translation by Consultants’ Bureau, Ine.,
New York, N.Y.

Sueano, H., and Opa, M., A New Method for Blood
Flow Measurement, Jap. J. Pharmacol., 10, 80-37 (1960).
LiepMan, F, M., et al, The Electrical Conductance
Properties of Blood in Motion, Physics Med. Biol.,
7, 177-194 (1963).

LresMan, F, M., and Cosenza, F., Study of Blood
Flow in the Dental Pulp by an Electrical Impedance
Technique, ibid, 7, 167-176 (1962-63).

Gottan, F., and NaMon, R., Hxperimental Analysis
of the Rheoencephalogram (REG), Proc. Soc. Hxper.
Biol. Med. 118, 809-811 (1965).

Srezy, O., Zur Theorie der Hlektrolytischem Dop-
pelschict, Z. Elektrochem., 80, 508-516 (1924).
Verwey, E. J. W., The Hlectrical Double Layer and
the Stability of Lyophobic Colloids, Chem. Rev., 16,
368-415 (1985).

CraxrorD, S. R., On the Electrochemistry of Simple
Interphases, with Special Reference to That between
Mercury and Solutions of Electrolytes, Trans. Far.
Soc., $6, 85-101 (1940).

Krvuyt, H .R., and Overseex, J. Th. G., Part IT—
Theoretical Treatment of the Double Layer and its
Implications, Introductory Paper. ibid, 36, 110-116
(1940).

Brxerman, J. J., Electrokinetic Equations and Sur-
face Conductance. A Survey of the Diffuse Double
Layer Theory of Colloidal Solutions, ibid, 36, 154-160
(1940).

Lanpav, L .D., and Lirsmirz, E. M, “Electrody-
namics of Continuous Media,” Pergamon Press, New
York, N.Y., 1960.

. ScHwaN, H. P,, Table #279, “Handbook of Biologi-

cal Data,” W. S. Spector, editor, W. B, Saunders
Co., Philadelphia, Penna., (1956).

Ortte, F. W., Hosaer, H, R. and Rowranp, A. F.,
The Electrical Conductivity of Animal Tissues Under
Normal and Pathological Conditions, Am. J. Physiol.,
60 59-106 (1922),



ducting species per unit volume increases, The
resistivity also varies with temperature’ (Figure
2) and falls as the ionic mobilities rise with
temperature. . In effect, the resistance of a
biological material at constant temperature is a
quantitative measure of the total number of con-
ducting species in the current field.*

Within a living tissue the cellular and inter-
stitial constituents probably change very little
over moderate time periods; the major changes
in conducting species would be due to blood con-
tent. The total resistance of a tissue thus con-
sists of an almost constant resistance and a
variable resistance due to its blood content; both
resistances usually have unknown magnitudes.
Since more conducting species appear between
the electrodes with systole, the total tissue re-
istance will decrease in an amount quantitatively
related to the net increase in blood volume.

The above discussion indicates there should be

a quantitative relation between changes in tissue
resistance and blood volume. A second mech-
anism is also considered to contribute to the ob-
served tissue resistance changes. The resistivity
of flowing blood is less than that of static blood
and decreases with increases in flow rate.!*
Therefore, the observed systolic tissue resistance
decrease is partly due to the lowered resistivity
of the rapidly inflowing blood; the diastolic re-
sistance increase is also partly dependent on the
resistivity increase of the slowing blood. Such
tissue resistance changes are undecipherable mix-
tures of changes due to volume and flow.°?*
This mechanism has been cited sufficiently fre-
quently against the use of impedance methods
as a reliable means of studying cranial hemo-
dynamics that detailed consideration is war-
ranted.

Present understanding of electrode mechanisms,
particularly those involving electrokinetic phe-

900,

RESISTIVITY

200-—-

0.1N POTASSIUM CHLORIDE SOLUTION

15°

TEMPERATURE

Fieure 2. Variation of solution resistivity with temperature.

3



frequently close to the average of the remaining,
more uniform pulses. Measurement should
start after the trace has stabilized if the first
several pulses cannot be used. Multiple respira-
tory cycles should be measured if detectable.

Average occlusion amplitudes will always be
less than the corresponding average reference
amplitudes when occlusions of a significantly
functioning artery are performed properly and
are complete; the only exception to the above
rule occurs when the patient’s circulation has
altered from the reference state during the trac-
ing. Such higher amplitudes are occasionally
encountered in temporal arterial occlusion trac-
ings, particularly in young normal subjects; we
have never encountered increased amplitudes
during correctly performed carotid occlusions.
This will be discussed under error analysis. Oc-
clusion values occasionally may be several mil-
liohms greater than their corresponding refer-
ence values. We use the reference values as
more representative since the values are probably
identical within experimental error.

The above discussions apply quite generally
to all tracing measurements. There are several
classes of patients on whose tracings such meas-
urements are more than routinely difficult :

First, patients with cardiac arythmias whose
stroke output is randomly variable. Such trac-
ings reflect. the abnormality as variable pulse
amplitudes; representative carotid occlusion am-
plitudes are, therefore, difficult to obtain, par-
ticularly since prolonged occlusion usually cannot
be tolerated. The interpreter must devise his
own criteria; we have traced one such patient
and can make no recommendations.

Second, patients with markedly irregular and
deep respiration which cannot be controlled.
Again, we have traced but one such patient (the
same one mentioned above) and can make no
recommendations.

Third, patients with frequent extrasystoles.
We consider such pulses to be artifacts and ob-
tain sufficient tracing to ensure artifact-free
averages.

Fourth, patients on whom bilateral carotid
occlusion results in an almost flat, almost feature-
less curve. The interpreter frequently has a
decided problem in locating the systolic inflow
points defining each pulse and in placing his
penciled baselines. Here, the EKG tracing offers

26

the best clue and affords intervals which are
transferable to the REG channels. Systolic
amplitude rise can occur at quite long and often
variable intervals after the EKG wave and may
be almost unrecognizable. No firm rules can be
suggested; each tracing must be individualized
from the interpreter’s experience.

Bilateral carotid occlusions are difficult to per-
form, usually cannot be prolonged sufficiently
to obtain reliable averages, and may give quite
variable amplitudes and waveforms. We select
comparison values from either single or average
amplitudes.

e. Error analysis and data selection: The
interpreter obtains average pulse amplitudes for
the various temporal and carotid arterial occlu-
sion tracings according to the above general
procedure. These and the reference amplitude
values are tabulated according to the notation
on page 11. The occlusion values are inspected
and, if all are less than or equal to the reference
values, simultaneity is checked.

Values for the bitemporal compressions are
calculated from Equations (22) and (23) and
are compared to the corresponding observed
values, R, and L,. Initial agreement within 2-3
milliohms is not unusual; the series is acceptable.
If disagreement between observed and calculated
values exceeds three milliohms, the tracing meas-
urements are re-examined for possible error
sources,

Since different interpreters may employ dif-
ferent approaches to error analysis and have
different concepts of data selection, no attempt
will be made to discuss all possibilities. We will
detail those procedures we have found most use-
ful; the interpreter may devise others as neces-
sary. If one or both observed bitemporal occlu-
sion values are larger than their calculated values,
the major error is probably in the former; there-
fore, the bitemporal occlusion tracings are ex-
amined first.

A number of possible sources of error in a
particular average occlusion amplitude should
be considered. First, the measured occlusion
may have been incomplete unbeknownst to the
operator; measurement of a second, more repre-
sentative occlusion tracing may be necessary.
Second, the sample measured may have been too
short; one or more additional respiratory cycles
may give a more representative average. Third,
particularly in young normals, there may be a


attention. Thus, we usually report “Good” if
the operator believes the compression is complete
or “Poor” if incomplete or artifactual.

Calibrations may be entered as desired and
are routinely entered after the temporal and
carotid occlusions but before the final reference
waveform run,

Occlusions should be performed firmly, quickly,
and completely, without hesitancy, fumbling,
slippage, or movement artifact. Sufficient pres-
sure should be applied over sufficient vessel
length to obliterate the flow and insure complete
occlusion. The area surrounding the vessel and
included in the compression is kept to a minimum
to avoid interference with venous return. Sig-
nificant venous occlusion is quickly recognized
by an increase in pulse amplitude rather than
the expected decrease and is probably the basis
for the amplitude increases observed by Perez-
Borja and Meyer’ during carotid compressions.
In our experience, one finger is sufficient for
smaller arteries, such as the superficial temporals,
while two or more may be required for the caro-
tids. If the operator is properly positioned and
his fingers are properly placed, only the latter
need to be moved in effecting an occlusion. Com-
pression techniques will vary according to the
operator’s previous training and personal profer-
ences. The important criteria are completeness,
non-interference with venous return, rapidity,
and minimum motion and circulatory artifact.
Practice is usually required before reliable trac-
ings are obtained routinely, no matter how ex-
perienced the operator may be.

b. Superficial Temporal Arterial Occlusions :
These arteries are easily accessible and are easily
occluded completely. They contribute most of
the extracranial tracing component and can be
considered to represent their related external
carotid arteries as will be demonstrated later.
We have found that positioning the hands for
bilateral simultaneous compression is of value
prior to starting the temporal occlusions; during
single artery occlusions, the contralateral hand
braces the head without touching the contra-
lateral artery. With both hands in place,
the operator can rapidly compress one artery,
the opposite artery, and then both, with a mini-
mum of artifact. As previously noted, sufficient
time should be allowed for the tracing to stabilize
between compressions.

ce. Common Carotid Arterial Occlusions:
We have had only brief, transient, reversible
reactions to this manipulation throughout our
experience. We have had no fatalities, no pro-
longed or irreversible sequellae, and few reac-
tions lasting more than 1-2 minutes. We ascribe
our experience to good fortune, caution, and the
carefully safeguarded techniques we employ.
We are well aware of the possible dangers of
carotid manipulation,** would much prefer to
eliminate it from our procedure and will do so
when a substitute which is equally effective in
diagnosis is developed. In the interim, we will
continue to include common carotid arterial oc-
clusions in our rheoencephalographic armamen-
tarium since we consider that its diagnostic value
far outweighs its possible dangers to the patient.
Since we have placed ourselves in the hopefully
temporary position of advocating the use of
common carotid occlusions during diagnostic
rheoencephalography, we will present our method
at length to illustrate the safeguards employed
and our methods of avoiding potentially dan-
gerous reactions.

Operator; A physician is always present
throughout the procedure and performs all com-
pressions. He is responsible for patient evalua-
tion and controls the tracing situation.

Patient Selection: We do not routinely per-
form carotid occlusions on patients who show
cardiac irregularities, who are in extremis, ob-
viously seriously ill, or markedly debilitated; who
have calcific, rigid, inelastic, or possibly friable
arteries; or who are so restless, irritable, or un-
cooperative that an interpretable tracing prob-
ably cannot be obtained. We have performed
carotid occlusions on such patients when the
possible diagnostic value of the manipulations
outweighed the patient risk.

We also have one final category. We do not
perform occlusions on patients whom our medical
intuition suggests may be poor risks.

Patient Position: This has been discussed.
Proper initial patient position reduces the total
amount of carotid manipulation and the need
for multiple repetitions. It is particularly im-
portant with obese or thick-necked patients in
whom carotid access is difficult.

Occlusion Site: Particular care is taken to
compress the common carotids at a site as
distant as possible from the carotid sinus and



10.

il.

SUMMARY

. The electrochemical and biophysical basis of rheoencephalography

(REG) and its clinical applications are discussed.

. The effect of flow on blood resistivity is reviewed and is shown to be

probably negligible in REG.

. Theoretical analysis suggests REG is a quantitative method which

reliably reproduces changes in tlie cranial blood volume.

. The presence of significant and valuable extracranial circulatory

components in the REG tracing is confirmed; these components use-
fully represent the external carotid arteries.

. A simple, standardized, reproducible tracing procedure and various

methods of analysis are described in detail. Sources of error are
discussed and methods of compensation and avoidance are presented.

. Individual extracranial and intracranial arterial contributions to the

tracing are demonstrated and measured for the first time. These
measurements afford a quantitative evaluation of the patient’s cranial
circulation,

. Analyses of 136 normal and pathological tracings are presented; a

95% diagnostic accuracy is demonstrated clinically.

. Difficulties in REG diagnosis using previously reported criteria are

presented and elucidated.

. Incidences and patterns of arterial involvement and collateral com-

pensation are presented and discussed.

The potential value of REG screening of normal populations for
cerebrovascular anomalies and early disease is demonstrated.

Several previously unreported REG syndromes are described.

viii


Table of Contents—Continued

IV. Discussion _--------------------------------------------------
A. Diagnostic Accuracy

B. Criteria for Diagnosis of Carotid Occlusive Disease -
. Timing Delay -----------------
. Reference Amplitude Asymmetry
. Reference Amplitude Asymmetry Plus Timing Delay
. Cerebral Perfusion Asymmetry Plus Timing Delay --
. Combination of Criteria
. General
C. Sources and Patterns of Collateral in Carotid Insufficiency
D. Mean Tracing Amplitudes

Table IX. Mean Tracing Amplitudes

Table X. Ratios of Average Tracing Components

E. Temporal Arterial Inversion as an Obscuring Factor in
Internal Carotid Occlusive Disease

Ct Cm

vii



Solution of the simultaneous equations gives
the following formulae for the various vascular
components :

(26) a=L,—L,
(27) b=R,—-R,
(28) c=L;—Le
(29) d=R:—Rs

(30) o=Le +L, —Ly=Ly
(31) f=R;+R,—R,=R,
(32) gr>

(38)

(34)

(35)

The contributions arising from the various
arteries can be calculated from the above com-
ponents:

(36) RT=Right temporal artery=b+gn
(37) LT=Left temporal artery=at+gy
(38) NECS=Net extracranial shunt=|gz—gz|
and is directed:
right to left if gx>g. or
left to right if g.>gr
(39) RIC=Right internal carotid artery
=d+hp
(40) LIC=Left internal carotid artery=c+h,
(41) NICS=Net intracranial shunt =|hr—h,|
and is directed:
right to left if hy>hz or
left to right if hu>hr
(42) RCC=Right common carotid artery
=b+gatdthe
(48) LCC=Left common carotid artery
=atgitcth,
(44) RP=Right cerebral perfusion=d+f£+h,
(45) LP=Left cerebral perfusion=c+e+hp
(46) PAn=Right vertebral-basilar shunt=f
(47) PA,=Left vertebral-basilar shunt=e

The above vertebral-basilar components are
worthy of brief discussion. The scalp is essen-
tially completely supplied by the external carotid
arteries while the majority of the structures
within the anterior compartment of the skull is
supplied by the internal carotid arteries. If
REG monitors only these structures, as is highly
probable, the conclusion is inescapable that any
remainder seen during bilateral common carotid
compression arises from the vertebral-basilar
system. These values, therefore, represent to
some degree the blood volume supplied to the
anterior compartment by the vertebral-basilar
system.

This simple model and its treatment is the
basis for our method of rheoencephalographic
analysis. This approach to plethysmography is
probably general and can be used to identify
and determine the circulatory contribution of
any artery if measurements can be made during
appropriate occlusions.

The above model is presented because of its
simplicity of calculation and its circulatory rele-
vance. There is an alternate, somewhat similar
model which will be briefty presented.

2. Model Assuming Partial Contralateral
Monitoring: In this model, assumption No. 3,
page 10, is modified by assuming that the current
field from an electrode pair may be sufficiently
diffused throughout the entire cranial volume
that the pair monitors an appreciable fraction
of the contralateral circulatory events, as Berta
et al indicate?

The previous notation will be used plus:
a=extracranial cross-registry fraction
f8=intracranial cross-registry fraction

Assuming that the intracranial and extra-
cranial collateral shunts (gz and hg) arise on the
right and appear on the left, equations can be
written such as the following for the reference
amplitude:

Ri=b+a(a+ge) +d+f+B(c+e-+ha)
L=a+gatab+c+e+he+R(d+f)
The remaining equations for the set will not be
illustrated.

The solutions are somewhat more complex than

in the previous model :

_R-R _ RR,
a as re B= T=E
a Bic Bime (a= Le)
_ rs
c=L,—-Le an ee eh)
ga LetLe— a= f (Ret Re—R)
ee
t= Rs+Re—R.—f8 (lst+Ls—L,)
1-,?
_L,-L,—a (RRs)
Sr a
_L,-Le—B (Be—Bs)
ha=———q =r


mersed electrodes, the resistance and capacitance
measured between the electrodes are described
by simple equations :

— el
(3) R=
(4) C=ee0y-

where p is the resistivity of the solution, e is the
relative dielectric constant of the solution, eo is
the dielectric constant of free space, “1” is the dis-
tance between the electrodes, and “a” is their
area.* The above equations apply to any solution
or material so long as all factors except ] and a
are held constant and the applied measuring cur-
rent is sufficiently low; changes in 1 and a
affect both the resistance and capacitance and,
therefore, the impedance.

If one solves for the impedance of a biological
material in terms of the geometrical factors 1
and a, one obtains (5) and (6):

*These equations hold only in the special case where | is
small compared to the electrode dimensions and edge effects
can be neglected.

1

wea

1 4% 1 1
= 2 —=k—
(6) 2 ( ee =) a k a

Equation (6) indicates that geometrical altera-
tions in a material which alter its resistance
will also alter its capacitance. Further, such
reactance and resistance changes affect the im-
pedance change in a similar manner. For sim-
plicity the following discussions will be restricted
to the resistive component; analogous reasoning
is applicable to the reactance and impedance. It
should be noted that the resistivity and dielectric
constant of a biological material may vary mark-
edly with the frequency of the measuring cur-
rent..* The frequency therefore must be kept
constant for intercomparability of measurements.

Reference to a standard handbook" indicates
the resistivity of a solution varies inversely as
the electrolyte concentration in a nonlinear man-
ner (Figure 1) and falls as the number of con-

(5)

SODIUM CHLORIDE SOLUTIONS
°

15}— 18°C
yf
5
a
@

Co

1 i it
0 5 10 15 20 25
CONCENTRATION

Ficure 1. Variation of solution resistance with concentration.

2


ties, we have found it more reliable than other
instruments we have tested and have used it al-
most exclusively in our series without modifica-
tion. Since this section is devoted to a descrip-
tion of our tracing procedure, the instrument’s
characteristics will not be presented in detail
except where required to support specific pro-
cedures,

a. Line Current Stability: The Doppel-
Rheograph is quite sensitive to sudden line cur-
rent variations and will reproduce such artifacts
on the tracing. Elevator artifacts were particu-
larly annoying but even lights switched on or off
on the same line could be detected. After un-
successfully testing several methods, a 2000 VA
constant voltage transformer} was installed to
power the entire instrumentation train. It elimi-
nated line transients almost completely.

b. Preparation of Rheograph for tracing:
The Rheograph should be placed on a firm sur-
face without tension on the leads to the recorder
or to the patient. The patient leads should be
fixed to the bed to prevent motion artifacts. The
Rheograph and amplifier-recorder are turned on
and allowed to stabilize for at least 15 minutes
before starting a tracing. The electrodes are
connected to the Rheograph and the bridges are
carefully balanced on the patient setting. Sev-
eral balance checks are usually performed. Re-
sistance values are read from the dials, converted
to true values from previously determined cali-
brations, and compared. If the procedure has
been carried out properly, the values usually
agree to within the balancing error of the instru-
ment, about 5 ohms. If the values differ by
more than 10 ohms, insufficient paste is usually
indicated on the higher side but electrode place-
ment, interelectrode distances, and amount of
paste are rechecked. The bridges are rebalanced
and the new values are compared; these will
usually agree within 10 ohms. If not, a small
amount of paste may be added to the higher
side and the balance rechecked. Any lack of
agreement at this point is probably valid ana-
tomic variation. Balance and . interelectrode
distance values are recorded on the tracing. If
unfamiliar with the instrument, the operator
should practice balancing various known stand-
ard resistors in the patient circuit. Balance
points can be repeated to within 5 ohms with

Sola Harmonic Neutralized Constant Voltage Transformer,
Sola Electric Company, Elk Grove Village, Illinois.

18

practice. Balancing is most easily performed
with the room darkened or the electronic indi-
cator well shaded. The capacitance should be
balanced first.

c. Recording instruments: A variety of strip
chart recorders can be used; we have obtained
useful clinical tracings from a single-channel
bedside EKG machine, Grass Models III and
VI and Offner Type T EEG’s, and Grass, Offner,
and Sanborn polygraphs. In emergency bed-
side situations, an interpretable tracing can be
obtained using an EKG machine to record the
right and left tracings in succession. However,
this is far from satisfactory as tracings should
be obtained simultaneously. We presently fol-
low Jenkner’s practice: and trace the EKG,
right and left REG’s, and their derivatives. The
derivatives were not recorded during the earlier
portion of our series.

Our earliest. several recordings were taken on
an Offner Type T EEG machine.* This instru-
ment gave excellent, linear, full-scale deflec-
tions; a simultaneous EKG could not be obtained.
The difficulty was later traced to interaction of
the high-frequency Rheograph patient current
with the preamplifier choppers. We next em-
ployed a Grass Model IIID EEG machinet
which permitted simultaneous EKG and REG
tracing. This instrument is reasonably linear
throughout the center 20 mm. of its pen deflec-
tions; signals extending beyond this range are
attenuated in amplitude with some loss of ac-
curacy. A D.C. coupled Sanborn Model 850
polygraph’ was used for a short period; its
tracings were linear but were unsatisfactory
because of the wide baseline swings with respira-
tion and movement.

Our present recording instrument is an Offner
Type R polygraph modified by installing low-
pass filters on the EKG inputs. This instrument
has a linear amplitude response throughout most
of its pen range.

We have also had excellent results using a
Grass Model VI EEG and Grass Model V and
VII polygraphs.

d. Preparation of Recorder for Tracing
Amplification: The EKG tracing should be of
reasonable amplitude according to customary

*Offner Electronics, Inc., Chicago, Illinois.

Grass Instrument Co., Quincy, Massachusetts.

§Sanborn Company, Waltham, Massachusetts.


AM 67-11

CHE BIOPHYSICAL BASIS AND CLINICAL APPLICATIONS
OF RHEOENCEPHALOGRAPHY

John H. Seipel, Ph.D., M.D.

Released by

}

wo

P. V. Srecen, M.D.
Ferperat Arr SurGEON

May 1967

FEDERAL AVIATION ADMINISTRATION
Office of Aviation Medicine



TABLE VI.~-Contimed

Galevlated Rhecencephalographic Factors in Patients with Subsequently Known Definitive Diagnoses

‘Tracing Component, Ratios (Percent)

Refer
Cerebral Perfusion once
fatioe | Geree Gonporents ae Rheoencenhalographi
28 tide encenhalographic ve Diagnosis -
tral [Rotarians ante, Devens Definitive Diagnost Resarks to.
Pert intermi | net | (Gor
Te [ston | mtertor | Garocids | mont | (FOS,
Gom | vera [Ratios siae)
ab afelele
28, Partial right curotta High right intermm carotid — Artertogrenty L
‘ceclusion Scelusion
69L Right extravascular space- Right subdural & eubarachnold Crantotoay 2
eeuying Lesion Renorzhage
on 92 Lett common carotid and eft comon carotid occlusion Thoracotony 3
vertebral occlusions & left subclavian "steel"
73L 988 Slight right comon carotid Slight loft common cerotié _Arterdogrephy 4
restriction; right cerebral Insufficlency
insufficiency
on 87 Lett comon carotid ant Left comon carotid ocolu _Arterfography >
vertebral insufficiency sion; left vertebral steno-
sis; night carotid stenosis
oa 98 No signif. intracranial Slight right cerebral atrophy Pnousoencephalogrephy 6
pathology; poderete right
Sarotid stenoste
on 77, Tovar occlusion of right Total oceluston of right yr. postrentarterectom 7.
common carotid ‘common carotid Thromosed, pulseless
right curouia
eR 90L Wo significant disease below Saue (at exploration of left Aortography showed prob- 8
circle of Willis bifurcation) able occlusive disease
at left biturcation
oa 851 Bilateral cerotid tnpatrment, Bllateral carotid tayetraent, Aortography 8
warked on rights met. more marked on right;
impairment of bestler tortuous vertebrais
etreulation
een 9M Norma tracing Same 2 Mon entteoaguietion & 10.
vasodiiators
om 100 lateral carctid occlusive _BLlateral internal carotid —_Aortography a
disease oeelusive disease
aan 83 Bilateral carotid occlusive Sane Aortograpty BR
disease
ma 98R Left carotid hss increases Sane 3 weeks on vasodtiators 3.
tarkedly fd anticoagulation
vw ‘DL Right compon cerotid occluded Same Aortograpty ue
oR 91R Left comon carotid occluded Sane Aortogrephy B.
40R B8R eft carotid occlusion; im- Sane Pulseless left carotid ak 16.
proved right carotid elrou- fatter right carotid end
ation arterectony. See #5 above
ean 75 Bilateral carotid occlusive Sane portogrenhy v.
tsenge, nore marked on the
94 90h liaterad carotid occlusive Sane) plus ocoluded right sortopresty ws.
‘disease; feir vertebral- vertebral
tebiler collatersl
aon 92 Moderate biteterel cerotid Diffuse cerebrovascular sortogranty ».
‘oeelusive disease, more disease with acute lett
narked on the left internat carotid throxbosts
Dyes da
geR UR OL Bw 6 37 10 65% Left internal carotid occluded Left internal carotid 90% Surgery 2
‘at of above the bifurestion  stenosed at origin, ex-
ternal carotid spared
4m 30R 9B 50L Left Internat carotid oceiuded Sane artertography a.
fat o above the bifureation
78L GOL ML 30-25-56 75-—«R_«96R_— ght internal carotid steno See # 11-13 above 2
Sis st or above bifurcation,
Sone general Inprovenent
93L 97, 98RD FBR 9B, Normal tractng & high anpli- Left A-V fistula artertogranty 2.
‘tudes for age
OL OL 88, 68-57-43 58R_— BSL Total occlusion of right Sane Right common & internal 24.
common carotid earotids surgically
occluded
STR 8 TL 33 37647 Monmah curotice, 21 spaces Normal carotide, sight carotid arteriography 25.
occupying lesion in poste- slightly 2a
sior eireulstory fela
TR TAR 98,26 7~—7H_~—«D_~—«AL_~—«9GR_—Lett common carotid stenosis Left comon carotid partially Endarterectomy 2.
at or below bifurcation; 77 occluded et bifurcation
AV evomaly
94a 05k 89-9897 «AOL GL lateras common carotia Sane autopsy a
‘oeclusive disease
ob el oom 70 68 © 2OR_—-99R_—Shgnifcant right comon Sane sortogrenhy (1966) 28.
serotid disease
TL TL R22 68 88 «Re, hove confirmed Sane

41



In the static case, the layers of altered concen-
tration should have a somewhat higher electrical
cesistance than would be expected for the same
volume of unaltered solution and should increase
she steady-state resistance measured between the
slectrodes. Since solution movement constantly
orings more ions into this region, different levels
of constant flow should establish different steady-
state electrode layers which would become thin-
ner with more rapid flow. Therefore, the steady-
state resistance falls as flow increases. Fur-
sher, the effect should be non-linear, lessening
with higher flow levels until a minimum resist-
ance is reached which is independent of further
ow increase. Since the measured resistance de-
zermines the resistivity of the solution, the latter
should also apparently decrease with flow. The
reported blood studies**** were carefully reviewed
for evidence of the above electrode effect; the
nvestigators used conductivity cells which were
lirectly or indirectly subject to the above elec-
srode effect in most of the measurements.

However, Sigman et al?* describe experiments
which unambiguously demonstrate a true de-
swrease in blood specific resistance with flow.
First, they modified the conductivity cell designs
ised for their initial studies by placing the elec-
‘rodes in sidearms where there was no disturb-
ince due to the moving blood and found identical
esistivity changes with flow. Second, they
studied a series of solutions and suspensions in
che unmodified apparatus and observed a measur-
ible flow effect only with blood. Finally, the
nagnitude of this effect was directly related to
the concentration of erythrocytes in the moving
dlood. Somewhat similar results are found by
sthers.*5> Different authors postulate various
nechanisms to explain the effect but all agree it
s associated with the presence of erythrocytes
n the flowing blood.

Therefore, while it is uncertain to what degree
slectrode effects contribute to the observed de-
srease in blood resistivity with flow, they are
orobably negligible in comparison with the total
low effect. Thus, the contribution of this flow
fect to tissue resistance changes must be evalu-
uted in reference to rheoencephalography.

Liebman et al** measure a maximum decrease
n blood impedance of 8% at a steady 20 cm./sec.
jow in a 3.5 mm LD. tube; the change with
pulsatile flow is considerably smaller (1.4%

estimated from graph). Velick and Gorin’
find 8.2% at an unspecified flow rate which gave
complete erythrocyte orientation. Coulter and
Pappenheimer® measure maximum effects (esti-
mated from graphs) of 18% at 63% hematocrit,
9% at 58% hematocrit, 11% at 44% hematocrit,
and 9% at 40% hematocrit. At 12 cm./sec.
Moskalenko and Naumenko*? measure a 2.7%
change. Sigman et al*® measure a maximum
effect of 5.3% at comparable steady flows but
observe average changes of 2.2% (3.4%-1.0%)
at 60% hematocrit, 1.3% (3.1%-0.0%) at 40%
hematocrit and 0.17% (+1.0% to —1.0%) at 20%
hematocrit. Of the above, only the studies by
Moskalenko and Naumenko” and Liebman et al**
were performed on human blood.

The contribution of the flow effect to the
rheoencephalogram may be difficult to estimate
accurately from the above range of values. How-
ever, the maximum blood resistivity change that
might occur at high flows and normal human
hematocrits would be about 10%. At steady
flows equivalent to maximum levels likely to be
encountered in the bulk of tissue circulation, the
effect should be smaller, probably about 24%.
If the further pulsatile flow reduction observed
by Liebman et al** is valid, the final flow resis-
tivity change may be less than 0.4-0.8%, a neg-
ligible error. Thus, tissue resistance (impedance)
variations associated with blood circulation al-
most certainly arise solely from blood volume
variations and contain little or no “flow con-
tamination.” Tracings of these variations are
plethysmograms and are analogous to volumet-
rically obtained tracings.

The total magnitude of the resistance is not
plotted in impedance plethysmography; instead,
variations about a particular constant resistance
value are recorded. Such tracings are analogs
of the total resistance from which a constant
resistance has been subtracted to accentuate
variations, exactly as volume plethysmographic
tracings reproduce variations about a constant
volume. Therefore, impedance plethysmograms
should be capable of yielding information en-
tirely equivalent to that obtained by any other
plethysmographio method provided due allow-
ance is made for the various inherent methodolo-
gic differences. The great advantages of the
impedance method lie in its safety, its simplicity,
and its essentially instantaneous accurate response



nomena, is based on the double layer model**?*-**
of the region about an electrode (Figure 3).
According to this theory the distribution of posi-
tive and negative charges about an electrode is
nonuniform. The electrode attracts a firmly ad-
herent layer of oppositely charged ions, possibly
covered by a second layer of similarly charged
ions. Surrounding this thin inner layer is a
second diffuse layer in which the electrode electro-
static field attracts oppositely charged ions and
repels similarly charged ions until equilibrium
charge and ionic concentration gradients have
been attained. This latter layer extends a con-

CONCENTRATION

siderable distance until it becomes indistinguish
able from the solution. These layers exist abou
any electrode immersed in a solution, whethe:
or not externally charged, since the electron clouc
within the metal itself can attract ions from thi
solution. Movement of the solution past th
electrode disturbs the equilibrium concentratior
gradient and its electrode potential producing
streaming potentials. Movement of the electrod
with respect to the solution produces the familia
“movement artifacts” frequently seen in biologi
cal studies,

SOLUTION

ADHERANT
No LAYER

INTERFACE

DIFFUSE LAYER

DISTANCE FROM ELECTRODE

HOMOGENEOUS REGION

Ficure 3. The double layer model of the region about an electrode.

4


artery usually supplies appreciable blood to the
opposite side; the overall effect is to obscure the
evidence of internal carotid disease even though
common carotid arterial compressions may have
been performed. Fortunately, the inversion ef-
fect has not been large enough to hide a signifi-
cantly diseased carotid completely or to falsely
lateralize a diagnosis in our series. Both are pos-
sible and may be seen in various tracings. For
example, Tracing #39, Tables I and II, gives a
relatively normal 84% common carotid ratio
which would miss the more significant 63% in-
ternal carotid ratio if temporal arterial compres-
sions had not been performed; Tracing #23 in
the same tables gives equal and normal common
and internal carotid ratios but with a complete
laterality reversal between them. Case +20,
Tables V and VI, in whom the ipselateral angu-
lar and posterior auricular arteries were mark-
edly increased, will be reported separately.

Common carotid arterial compressions are
probably sufficient to indicate laterality for
further clinical studies in cases of symptomatic
cerebrovascular disease or suspected carotid im-
pairment. The complete arterial compression
series is recommended for screening purposes, for
continued observation of developing disease, or
for localization of disease above or below the
carotid bifurcation.

F. Final Remarks: In conclusion, we again wish

54

to emphasize that our tracing procedures and
analytical methods are based on a number of
assumptions which may be oversimplifications or
which may not be generally applicable. We re-
gard the results reported in this paper as some-
what fortuitous since the referring physicians
and the authors were sensitized to and
looking for carotid occlusive disease which occurs,
of course, in a high percentage of patients with
cerebrovascular disease? The significance of
these results, in our view, lies less in the success-
ful detection of carotid disease in a preselected
high incidence group than it does in other, less
obvious demonstrations. Thus, the extracranial
and intracranial circulations can be separated
and studied rheoencephalographically; both are
important in clinical diagnosis. Contributions
from individual arteries, whether manually ac-
cessible or not, can be determined and are diag-
nostically useful. Modifications which improve
the clinical usefulness of rheoencephalography
can be predicted from theory or empirically de-
termined; within its own inherent limitations, the
method is flexible and can be tailored for specific
applications. Finally and most importantly, we
have demonstrated that rheoencephalography can,
at least in this one disease, accurately Jateralize
carotid occlusive disease and indicate the major
involvement site in reference to the bifurcation.
This much maligned technique is worthy of
further intensive investigation.


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Priore 450T
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Teaqayten 4geT eBrey ‘AyderZo
“Heqae fq opjouars ¥o9 pryotso uomioo wusTY = sTTO.UST og wm ¢ oo - 8 -- ST BZ BLE GOTT 6
Pr}oreo Teureyxe
Buyreds uoysntooo pryoueo TeuToquT WUBTY = Tseé GL o ge 0 - 8 - 9 ust 96 6 S68T 8
suezSoyz0y22 TeULON
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suezZ0yI9,.18 TeutON
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squoucduog uofsnyzeq TeyuEIQ

SPUNYS TOTIoqUy-ToyIEys0g

spryoreg wommog

(quoszed) soprey quouodueg Buyoesy,

(SMUCFITIN) squsuodmog Butoerz, peyeTnoTeg

asbOSTd UMOUY UITA sqUETIed STEN UT sLojoRd oTUdesZoTeyTeouscoy peYeTNOTeD
AI SIaVL

37



I. Tracing Interpretation:

Our initial evaluation of the diagnostic possi-
bilities of the rheoencephalographic tracing sug-
gested it offered two types of information which
were important. Obviously, “abnormal” pulse
waveforms should be significant; particular
waveforms might be diagnostic of particular
diseases as is common in electrocardiography.
Further, since rheoencephalography was a po-
tentially quantitative method, tracing amplitudes
should be significant; mathematical analysis
might give a description of the intracranial cir-
culation in sufficient detail to be diagnostic. We
routinely employ both approaches in tracing
interpretation. Mathematical analysis has af-
forded more consistently correct predictions
throughout our study and will be presented first.

A. Mathematical Analysis:
dure involves three steps:

1. The determination in ohms of tracing am-
plitudes which represent the right and left sides
of the cranial circulation in the unmanipulated
state and during arterial occlusions;

2. The calculation of various arterial contri-
butions to the cranial circulation and their com-
parison; and

3. The formulation of a tentative diagnosis.

1. Tracing Measurement:

a. Equipment: The equipment required is
that customarily used for tracing measurement.
In our experience, amplitudes can be scaled off
the tracing to 0.1 mm. without difficulty; a milli-
meter scale readable to this tolerance is advis-
able.* Since the width of inked lines varies and
is appreciable, we measure all calibration and
pulse amplitudes from lower edge to lower edge
rather than from lower edge to upper edge.

b. Calibration: The tracing is rapidly
scanned to determine the sequence, location, and
interpretability of the various portions and the
last set of calibrations before the tracing proper
is identified. Sufficient of the final, adequate
calibration pulses are measured on each REG
channel to give reliable average values and the
channel calibration factors in ohms per mm. are
calculated. These’ factors usually remain con-
stant unless the electrodes or bridge balances are
disturbed. A few calibration pulses should be
measured wherever encountered through the

Briefly, the proce-

*Paragon Triangular Scale #56-3662,

Company, Hoboken, New Jersey.

Keuffel & Esser

25

tracing to check for reasonable constancy. If
any marked change is noted, new calibration fac-
tors should be determined.

c. Reference Tracing: The unmanipulated
tracing is inspected and a representative artifact-
free portion comprising at least ten pulses and
two or more complete respiratory cycles is se-
lected for measurement. Pulse amplitudes often
vary considerably throughout the respiratory
cycle but are reasonably consistent when com-
pared at specific times within ‘successive cycles.
Thus, the interpreter may start at any place
within a respiratory cycle but must measure in
cycle multiples to obtain representative average
values. We draw fine, narrow, straight lines
from pulse to pulse, tangent to the tracing lower
edge at the points at which systolic inflow ap-
parently begins. In an occasional patient, the
trace may dip below the pencil line; this is dis-
regarded. Maximum pulse amplitudes are then
measured from the pencil line, averaged, and
converted to ohms, using the previously deter-
mined calibration factors. These values are the
reference or baseline pulse amplitudes.

d. Occlusion Tracings: All similar occlu-
sions throughout the tracing are inspected and
one which appears representative of the group
is selected for measurement. Our selection cri-
teria are minimum average amplitude, freedom
from artifact, consistency of waveform with
other tracings in the occlusion series, and equiva-
lency of the pre-occlusion waveforms with the
reference waveform. A typical ipselateral oc-
clusion tracing channel usually shows a brief
occlusion artifact for one or two pulses, a series
of low-amplitude pulses followed by several of
higher amplitude, and finally, throughout the
remainder of the occlusion, relatively stable, in-
termediate amplitude pulses showing only respi-
ratory variations. In young normal patients a
trend towards slight amplitude increase may be
seen in prolonged occlusions. Prolonged occlu-
sion artifact may obscure some of the above
variations. Lesser but analogous changes are
seen in the contralateral tracing.

Ideally, measurement should begin with the
first pulse after complete occlusion and include
sufficient succeeding pulses to give a representa-
tive average. We prefer to measure as many
pulses per occlusion as were measured for the
reference tracing. Interestingly enough, the
average of the initial low and high values is



‘TABLE VII.
Rhecencephalographic Findings in Patients without Definitive Studies

Average Arterial Compression Amplitudes (i11Liohss)

Resistance Average
oo Sicaaetoiiaan reeset’ Righ lett | Binaterat
Iapedance (af) [amplitudes | aiene tect | Bitateral t tere
Patient Year (tition) smporel | Teapor comson | comson | common
Wo. Je str. eRpor “al
wo. | S°* | AB | aracea | TY (otme) Temporal | Tenporal | 7 Cerotia | Cerotia | cerotia

nignt | vert | Régnt | vert] mi} tr | Re | te | ms | ts | Re] te] Rs | ts | we | te | wm |

L305" MSL 196 Sch, NOt Recorded UO & 8 53 BFS
ee ” 65 Not Rec. 5146. BB 2» n

3. 87m Mm PLT, 400 36D we 203208 13 ve us 3

4 mM 27 2650 TD 96 ln Me Le

5. 499M "Sch, «425365 Not. Rec. Bh 156 6 14 8B

6 "eM " " wo 750 ak Cr a ee)

1% 1206 M55 " wo 0 7] BB he % 5 36

8 a " 25-5 00 00 02 BL 7% 92

% 365 Mae " uo wo 7m 0 A oF 42045 OW

wo ws oF mf " wo MO 5030 43% 8 55
uaF ae . ws 0 OL 40 87 5830

mB um Mw 45 " oO] Bw 38 42
Bm ” wo 160] 26 45 5h

we mM ” wo Ms = 100 Ok 2 40 7% 30

we nse Mk " Te a i 3604548,

i. 1898 " 1g 170100 399 © 45 0
CC oe " Ce a a 39 62 Ls
a a . wo 15 8S 393948

» 6% Mow " oS 0 08 0 © % 42

ce a a ” ws 2s 10 1m OO ae eS)

2. oO F 4 ” " 15S] ka 43 68 73 BL
Pe a a ” 5 5 100 0 86 35 655338

3 wl uM 3 # ” 230 «O10 43°97 50 50

2% ee ML " 230 «So. 7 nm 39

25. RMB Ce a a a} 39 65 52h DLS
2. «136 MB ” 5 51008 3647 53S
m7 woe Fw . Sr a a a 1 46

2.0 De FOB ” yuo yom 7m wm 2 52 B50

2. 1903 Fe ” uo BO 10 Oo - -

3. ule " ws 5250250 7 Rn ow

Be 9h " ys us 7% OT 40 508

32. 05 MS . 20 wo 250-80 aes S_s92_ HAs 7950.

33, 1906 FO ” 20 0100 OHH n mM 5. 8 8 67

a a ae ” D5 S059. Sl 58 39624607

33. 07 FO 86s uo M5 7% «773166 ua us 19 we 19 97

36. 69H . us 0 7 n6 98 93 («33H
a . ce a, a i? Bo 9 Om 8 OS
38. «8 Ft . Ca a i a a, a a a a i CD
3. wo M55 . yO 150 Not Ree. «8393577 SR SBT STH

4 87 MO . uo 10 5071 BDZ 5B AB 50 SB THe
a. 7 M8 “ ws 25 «0 OB HH] OBL HHH

42, 08 F268 . Us 5055 BBS BSCS
3. ee M7 " 105° 005K BL 5 HCH DLs sw
re ee a . ao 02502507 HOB: HD 37
45. OL FG * us us 5007 Dsl sw Hs
46. woo MH " m0 D250 250 Ts CSCZD sD HCHO 9B

47 wee Me " 15 120-250 250 5h eC 5 SLL BK
48. Wl F538 " wo 0202s sw. 9s 8B

49. 8s FR * wo 120-250-250 100-110 %* BH BS HCH

3. 18566 . wo 165 250 7957 HCCC SC HCW UP fore

pL ges Fe " BS 135-50 2506S FD BCS

52. 73h ME wo YO 50 48 655945
oD " 120 12000100 ww 46075-5837
ae up 02502502 HC HTS 46 KB 2a

Starred tracings were improperly calibrated; values may be erroneous.


bifurcation. Attention to this one point has com-
pletely eliminated carotid sinus reactions and
has probably avoided the sequellae arising from
manipulation of diseased bifurcations.

Patient Warning: As with other portions of
our procedure, the manipulation is described to
the patient and he is warned to expect some local
neck discomfort. Possible neurological symp-
toms such as faintness, dizziness, weakness,
numbness, and other unusual or peculiar feelings
are described and he is cautioned to report them
and any other odd sensations immediately so the
compression can be discontinued. He is also
cautioned of their possible significance and brav-
ery is discouraged.

If the patient makes any report, reacts, or at-
tempts to do so, the occlusion is immediately
discontinued; the reported symptoms are entered
on the tracing. The occlusion may or may not
be repeated after the tracing has stabilized, de-
pending on the adequacy of the immediate and
previous similar occlusion tracings which may
have been obtained.

Visual Monitoring: We have one important
safety factor in our favor; we can visually moni-
tor the cranial circulation via the REG tracings.
With experience, the operator soon recognizes
abriormally low pulse amplitudes and can dis-
continue occlusions after 5-10 representative
pulses have been recorded but before symptoms
develop or are reported.

Duration of Occlusion: If not discontinued
for other reasons, the occlusion is held until 15-20
reasonably similar, presumably representative
pulse waves have been recorded. Bilateral com-
mon carotid occlusions are performed only on
those patients in whom both carotids are easily
accessible and easy to occlude. Such occlusions
are held very briefly, only long enough to obtain
3-5 interpretable pulse waves. Longer single
and bilateral occlusions have been performed but
only for research purposes in normal subjects
who were able to tolerate the procedure without
symptoms and who were adequately warned.

8. Post-Occlusion Tracing: After satisfactory
completion of the occlusions and return of cir-
culatory stability, the tracing is recalibrated and
an adequate final sample of reference tracing is
obtained. The procedure is usually terminated
at this point although other additions may be
made at the investigator’s option. When in-

cluded, Queckenstedt and Valsalva maneuvers
should be performed after the occlusions since
these maneuvers significantly alter circulatory
dynamics for an appreciable time.

D. Post-Tracing Procedure: Bridge balances
and interelectrode distances are rechecked and
the values recorded. AI electrodes are removed
from the patient, who receives appropriate
cleanup. The electrodes and head-band are care-
fully washed to remove all traces of paste and
dried prior to reuse. All meaningless pages used
in the pretracing procedure are removed and
discarded after transferring any useful informa-
tion therein to the remainder. The record is
identified with the patient’s number, name, ad-
dress, age, referring physician, and so on. The
plethysmographic instrument used, electrodes,
interelectrode distances, balance values, and so
on, are recorded. Arterial occlusions are listed
as are any appropriate remarks or observations.
The channels are checked and identified as is
the calibration pulse amplitude. The record is
finally scanned and the occlusions are identified
and clearly marked with any remarks or obser-
vations.

E. Final Comments; On first reading, the above
detailed procedure may seem lengthy and time-
consuming; in practice it is neither. The basic
procedure is quite simple, easily learned,
and rapidly becomes automatic for technician
and operator. A complete rheoencephalogram
can be obtained in the time required for a rou-
tine electroencephalogram, or less if the patient is
stable and cooperative. Instrumentation prob-
lems most frequently cause delays. They cannot
be anticipated, and usually are transient. We
have completed tracings in 30 minutes or less
although our usual time is about 45 minutes; we
schedule an hour per patient.

As is true for any new or unfamiliar procedure,
a certain amount of practical experience is re-
quired before adequate tracings can be obtained
routinely. The technique is tolerant of varia-
tions and qualitatively useful tracings may be
obtained almost immediately; for example, the
tracing diagnosis in our second case‘ is obvious
without detailed mathematical analysis. How-
ever, if there is to be any hope of determining
firm diagnostic criteria from rheoencephalo-
grams, the investigator must accept the require-
ment of a rigidly standardized technique.


THE BIOPHYSICAL BASIS AND CLINICAL APPLICATIONS
OF RHEOENCEPHALOGRAPHY*

Joun H. Serer, Pu.D., M.D.

‘ntroduction

Many reviews of cranial impedance plethysmo-
waphy, or rheoencephalography (REG), a
aethod of studying the cranial circulation, have
een published2+ While it is agreed that
hheoencephalograms are at least partially plethys-
aograms, the above references and their bibliog-
aphies indicate considerable controversy con-
erning the exact relationship of the rheoen-
ephalogram to the intracranial circulation.
This controversy has engendered disagreement
ver the value of REG in both clinical diagnosis
nd physiological research.

Much of this controversy arises from factors
nherent in the use of novel or unfamiliar meth-
ids. Such factors include comparisons based on
lifferent methodologies and concepts of tracing
aterpretation, unfamiliarity with vascular hy-
traulics in general and intracranial hydraulics
a particular, unfamiliarity with the scope, ap-
slications, and inherent limitations of the method,
ack of experience with its use, and predetermined
avorable or unfavorable but enthusiastic preju-
lice.

The author’s attention was first drawn to
heoencephalography by his continuing search
‘or methods which could be used to study living
ystems without perturbation or injury.?* It
vas immediately apparent that the method was
votentially quantitative, that the cerebral circu-
ation could be monitored, and that individual
arotid arterial contributions might be deter-
ained by tracing during brief manual carotid
eclusions. It also appeared likely that the
nethod had the great potential for disease de-
ection and diagnosis claimed by Jenkner.t. These

*A contribution from the Neurology Laboratory, Georgetown
‘linical Research Institute, Office of Aviation Medicine, Federal
wiation Administration and the Department of Neurology,
feorgetown University Hospital, Washington, D.C.

intuitive considerations have sustained the au-
thor’s studies throughout the above controversy.

This paper is intended as a summary of more
than five years research into the biophysics of
REG and experience with its clinical use. Some
theoretical considerations will first be presented
followed by a more practical demonstration of
the possible value of REG in clinical diagnosis.

Theory
I, Electrochemical

Plethysmography.

A detailed discussion of the many factors in-
fluencing conduction of an electric current
by solutions of electrolytes is beyond the scope
of this paper.*** There are, however, a num-
ber of concepts which should be presented to
assist the understanding of biological impedances.
The discussion will be deliberately superficial
and is intended only to indicate present reason-
ing and conclusions. The occasionally difficult
underlying mathematics have been omitted and
will be presented in future publications.

An inherent property of matter is its exhibi-
tion of an impedance (Z) to the passage of an
electrical current; such impedances are composed
of a real component, resistance (R) and an “imag-
inary” component, reactance (X) where:

(1) Z= (R?+X?)%

Reactance can be a variable combination of
capacitance (C) and inductance (Li):

1

(2) X=oL— rel
where o is the angular frequency of the applied
current. Inductance is a negligible component
of the reactance of biological materials, if present
at all, and will not be considered further.

For a given electrolyte solution, for example,
aqueous sodium chloride, containing two im-

Basis of Impedance



8. Skin preparation
4, State of relaxation

B. Electrode factors:

. Anatomic placement
. Lateral symmetry

. Fixation

Area

. Contact medium

. Material

PoP wpe

C. Instrumentation factors:
1. Lead resistance
2, Calibration
3. Rheoencephalograph characteristics
4, Recorder characteristics

The above factors will be discussed during the
description of our tracing procedure.

B. Pretracing Procedure: Since the senior au-
thor was aware of Jenkner’s extensive studies

and had obtained a “Doppel-Rheograph” from
Dr. Schufried, he arbitrarily selected as standard
a tracing procedure similar to that reported by
Jenkner.* While experience has suggested slight
modifications, our present procedure is almost
identical with that originally employed.

1. Patient Position

Constant patient position relative to gravity
is absolutely necessary for tracing intercompara-
bility.» Our patients lie comfortably recumbent
in slight semi-Fowler’s position with a head ele-
vation of 7° relative to horizontal. The shoul-
ders, neck, and occiput are supported and par-
tially immobilized by a thin pillow; the head is
slightly extended; and the neck is exposed to
permit access to the carotid arteries. The wrists,
with attached EKG electrodes, lie naturally,
slightly away from the sides (Figure 10). Shoes
are usually removed.

Ficure 10. Patient position for rheoencephalography.

15



TABLE IX.
Mean Tracing Amplitudes

Mean Tracing Amplitudes and Standard Deviations (Milliohms)

Carotid Disease

Unilateral Bilateral
Combined
Normal Greater Greater Grou
Right left Right left Pp
Involvement Involvement
Ry 88417 98 +31 6+ 58419 58413 81 + 29
lh 90 +19 103 +31 101 + 33 62 + 23 60 + 18 85 + 29
Re +13 83 +23 78 + 30 51 +17 49 + 16 65 + 22
L 90+16 95+ 27 101+ 33 63 + 22 56 +17 78 + 26
Rg 88 +14 97+ 22 90+13 57 + 18 52418 75 + 25
Lg 78418 88 +24 83416 53 + 20 44 414 67 + 2%
Ry T1+13 86+30 72+ 48 + 20 47 +18 64 + 23
ly 73413 88 +31 84+ 20 4D + 23 48 + 20 66 + 24
Rs 38+ 11 60424 354+ 9 35 + 16 30 + 12 41 +18
Ls 62414 89428 54419 52 + 20 46 + 16 63 + 24
Re 62413 59+2% 80417 42417 47413 57 + 20
Le 43413 36417 63419 30 +17 34 415 40 + 18
Ry 19+ 9 194+ 9 20 16+ 7 15+ 9 z+ 8
ly 20+ 9 W+ 8 20 17+ 8 16+ 9 18+ 8
Average 45 54 47 47 51 48
age
Number of 36 20 9 19 12 96
tracings

52


Figure 14, Normal and abnormal REG waveforms. (a.) Normal (b.) Delayed inflow (c.) Delayed runoff (d.)
Delayed inflow and runoff.

82


2. Patients: The patient group is heterogen-
ous and includes subjects from many sources:

a. Subjects from the Institute’s ageing study
who showed sufficient cardiovascular or neurolo-
gical abnormality, by history or examination, to
warrant tracing. Most of these subjects were
entirely normal except for a slightly less palp-
able carotid ;

b. Subjects referred to the Institute in con-
sultation for evaluation of cardiovascular or
neurological disease. Most of these subjects had
previously received extensive studies; their diag-
noses were known to the tracing interpreter; and

c. Patients referred to the author by local
physicians who either wished tracings to assist
in their diagnosis or who already had obtained
definitive studies and wished to test the inter-
preter’s accuracy. These physicians were aware
of the interpreter’s interest in developing diag-
nostic criteria from the tracings alone and there-
fore carefully withheld clinical information.
They were, however, aware of the interpreter’s
interest in cerebrovascular disease.

Almost all patients were ambulatory and were
usually traced as out-patients; neurological dis-
ease was not readily apparent on observation.
Their tracings were reported without biasing
knowledge of the patient’s clinical status. Sev-
eral patients from the interpreter’s personal
practice were traced prior to definitive diagnostic
studies and are included in the series.

B. Tracing Values:

1. Normal Subjects: Values obtained by
measurement of the tracings from 40 normal
male subjects are presented in Table I. As our
procedure has changed slightly, the data is pre-
sented in yearly groupings; the column of refer-
ence amplitude ratios is included to simplify
later discussion.

Table II presents the results of mathematical
analysis of the values from Table I.

2. Patients: The patient series is presented
in two groups: patients with proved disease
whose diagnosis was known by the inter-
preter prior to the tracing, and patients whose
diagnosis was unknown prior to tracing. The
latter group is further subdivided into patients
who have-subsequently come to definitive diag-
nosis and patients who have received no further
studies or on whom no further information is
available.

33

a. Patients with known disease: Values
obtained by measurement of the tracings from
18 patients who had undergone arteriography
prior to referral are presented in Table III; the
interpreter was aware of these patients’ diag-
noses. The tracings from the first two patients
were obtained during our initial investigations
and were improperly calibrated; the values in
ohms are unreliable.

Table IV presents the results of mathematical
analysis of the values from Table III.

b. Patients with subsequently known defini-
tive diagnoses; We include in this group those
patients whose defitiitive diagnosis was unknown
to the interpreter until after the interpretation.
In almost all cases the final diagnoses were de-
termined after rheoencephalography.

Table V presents the raw tracing data and
Table VI the analytic data.

ce. Patients without definitive studies: We
include in this group all other patients on whom
a diagnostic rheoencephalogram was obtained
but who have had no further definitive studies
or who have been lost to follow-up. Table VII
presents the raw tracing data and Table VIII
the analytic data.

IV. Discussion:

A. Diagnostic Accuracy: Tf rheoencephalog-
raphy has any clinical value, diagnostic conclu-
sions derived from its tracings should be in
agreement with the disease actually present.
Comparison of the data in Table IV with the
diagnoses proved in these patients indicates
clearly that excellent agreement was attained;
even the improperly calibrated tracings gave
clear indications of the proved diagnoses. The
potential value of rheoencephalography was ap-
parent; an extensive clinical study was therefore
undertaken.

As previously stated, patients were referred
without clinical information. Very early in the
study (1962) we set this criterion both to avoid
biasing tracing interpretations in favor of ob-
vious clinical diagnoses and to force development
of analytic methodology. Since the referring
physicians were aware of our belief that rheoen-
cephalography monitored the cerebral circulation,
almost all of the patients traced had originally
sought medical attention for cerebrovascular in-
sufficiency symptoms and were frequently diag-
nostic problems. No attempt was made to obtain



other types of disease since the author primarily
wished to determine if rheoencephalography was
clinically useful in at least one disease and so
to stimulate further investigations.

The results of this study are presented in
Tables V-VIII. The patients listed in Tables
V and VI are, to the best of the author’s knowl-
edge, ail of the patients in this series who have
come to definitive diagnosis. The patients in
Tables VII and VIII are the remainder who
have had no further studies. Some were lost to
follow-up, had single certification examinations
or consultations, died without autopsy, or are
under continuing observation or treatment.

The predictive accuracy of our rheoencephalo-
graphic method is clearly demonstrated in Table
VI; the 27 (93%) correctly diagnosed tracings
require no further comment.

Patient #4 was possibly unsatisfactorily
traced; his recording was again analyzed for this
report. Re-analysis by our present method gave
equivocable findings as before and did not change
the final diagnosis. This patient received uni-
lateral left. carotid angiography at Georgetown
and was later bilaterally studied at a different
medical center; to the best of his attending phy-
sician’s knowledge, he remains a diagnostic
problem.

Patient #23 gave suspiciously high amplitudes
for his age but clues to the lateralization and
diagnosis of his disease could not be obtained.
This is the only arteriovenous fistula we have
traced and represents a failure of our method.

Tracings #:9 and #10 deserve comment. This
patient had moderately reduced carotids bilat-
erally with less filling on the right (as best as
can be determined from the rather poor films) ;
there was, however, no evidence of focal occlu-
sive disease. She improved markedly on anti-
coagulation and vasodilators; anticoagulation
was discontinued after four months and all medi-
cation after one year without recurrence of
symptoms.

Patient #8 is particularly significant when
considering the reliability of rheoencephalo-
graphic diagnosis. His arteriographic findings
suggested marked occlusive disease at the left
carotid bifurcation (Figure 15) which was ex-
plored.

We quote from the operative note: “A small
arteriotomy [at the bifurcation] was carried out
which failed to reveal stenotic lesions within the

lumen of the vessel. The lumen was adequate.”
In retrospect, the bifurcation was partially oc-
cluded by surrounding tissue when the head was
rotated for the lateral films.

The results presented in Table VIII are al-
most as significant; the diagnostic predictions
are quite compatible with the clinical diagnoses
given by the attending physicians and consult-
ants. Three otherwise normal subjects who had
palpably unequal carotids are included.

The normal subject group presented in Tables
I and II may now be reviewed in the light of
the above diagnostic accuracy. Six (15%) of
these supposed normal males have common or
internal carotid arterial contributions which are
65% or less of the corresponding contralateral
value; two (5%) have ratios of 51% or less,
Asymptomatic at present, these men either have
anomalies of the circle of Willis, early disease,
or both. They are potential candidates for in-

Figure 15. Misleading aortography in Patient #8,
‘Tables V and VI.

sufficiency problems if other major arteries later
become impaired. Considering the known vari-
ability of the cranial vasculature, such findings


Ficure 13. Page from a normal REG illustrating channel sequence and calibrations.

21



The high incidence of right carotid involve-
ment is noteworthy and is probably significant
(0.02>p>0.01). The right carotid is involved
unilaterally twice as often (67%) as the left
carotid (33%); in bilateral disease, the right
carotid is more frequently the site of greater in-
volvement (59%) than the left carotid (41%).
As previously noted, our normal series contains
10 men selected at random from our panel of
examinees, and 30 men having similar occupa-
tions; our patient series includes other Institute
normal and consultation examinees and referrals
from 14 local physicians. While cerebrovascular
insufficiency was frequently suspected, it is diffi-
cult to postulate a mechanism capable of biasing
so many patient sources toward right carotid
disease.

The above data suggest that, as might be antic-
ipated, occlusive disease of the major arteries
supplying the circle of Willis is likely to occur
simultaneously in all four arteries but progres-
sion is usually unequal. The higher incidence of
contralateral posterior-anterior collateral increase
(rather than the expected ipselateral increase)
in single carotid disease may indicate a tendency
toward diffuse unilateral progression rather than
completely random arterial involvement, at least
before generalized involvement becomes severe.
Further, the temporal compressions indicate the
preferential site of right involvement is below
the bifurcation in bilateral carotid disease with
major right involvement. On the other hand,
when major involvement occurs on the left in bi-
lateral carotid occlusive disease, the preferential
site is usually above the bifurcation.

A search of 37 appropriately titled references
listed in a recent report on cerebrovascular dis-
ease” disclosed many papers presenting extensive
studies of the incidence of cervicocephalic sten-
otic and occlusive disease. None of these refer-
ences report an overall incidence of preferential
right carotid involvement as high as in our series.
Gurdjian et al°* find twice as many occlusions at
the right bifurcation as at the left but no lateral
preference in their total series of carotid studies.
Poser et al® find the right carotid involved 23%
more frequently in their patient series and a ratio
similar to ours in their normal series. Their com-
bined series shows 33% more right carotids ab-
normal than left carotids. Other series show no
laterality preference or favor left involvement.
For example, Weiner et al®° find a higher inci-

b1

dence (68%) of complete left carotid occlusion
in their 61 cases with complete occlusion of one
or both carotids.

As in our series, when one carotid is involved
the opposite carotid frequently shows significant
disease. Schwartz and Mitchell® indicate that,
if one carotid is severely affected, 81% of the
opposite carotids also will be affected; Gurdjian
et al®* give a 29% incidence of bilateral disease;
and Hutchinson and Yates*? find a 45% in-
cidence of bilateral disease in their overall series
and a considerably higher incidence (68%) in
their cerebral infarct series.

The incidence of posterior circulatory disease
has also been studied. Schwarz and Mitchell*
find 43% more stenoses in the right vertebral
system than in the left, a 23% higher incidence
of right rather than left vertebral involvement in
right carotid stenosis, and a higher tendency
(30%) for right vertebral involvement in left
carotid stenosis. In their cases with severe ste-
nosis, there is no preferential vertebral involve-
ment in severe right carotid stenosis but the left
vertebral is more frequently involved (64%) than
the right in severe left carotid stenosis. Gurdjian
et al®® find equal vertebral arteries in 51% of
their vertebral-basilar studies while the right
vertebral is larger in 20% and the left is larger
in 29%. Poser et al*® find a slightly in-
creased incidence (15%) of left vertebral in-
volvement in their patient series and a markedly
higher incidence (91%) of right involvement in
their normal series. Their overall incidence in-
dicates no lateral preference. Hutchinson and
Yates* and Baker and Iannone® also find no
lateral preference. In a study of circles of Willis
from 350 normal brains, Alpers et al find 52.8%
follow the normal or classical pattern while the
remainder show anomalies. Stringlike vessels
were frequent (27.4%) but 92% of the circles
were uninterrupted and potentially patent. In
our series, one or both posterior-anterior shunts
are increased in 59 patients with no lateral pre-
ference (85% on the right, 86% on the left);
single posterior-anterior shunts are increased with
no lateral preference (14% on the right, 15%
on the left); but there is a distinct preference
for greater left increase when both posterior-
anterior shunts are increased (26% right > left,
26% equal, and 48% left> right). If a lesser
or absent increase is an indication of stenosis
or occlusion, our findings agree with those of



TABLE OF CONTENTS

Theory
I. Electrochemical Basis of Impedance Plethysmography
II. Biophysical Basis of Rheoencephalography ~--------------------
III. Individual Arterial Contributions to the Rheoencephalogram -

A. Basic, Assumptions
B. Anatomic Models for Rheoencephalography -.
1. Basic Circulatory Model ---------------.
2. Model Assuming Partial Contralateral Monitoring
3. Model Without Temporal Arterial Compressions -

IV. Conclusions --------------------------------------------------
Clinical Studies -..-------.---------------------------------------

I. Methodology
A. Standardization —-—_.
B. Pretracing Procedure

1. Patient Position -.
2, Electrode Preparation and Placement
a. Electrodes
b. Skin Preparation
¢. Electrode Placement
8. Electrode Contact Material
a. Criteria for Choice ------
b. Method of Application
4, Instrumentation ---------
a. Line Current Stability --.
b. Preparation of Rheograph for Tracing
¢. Recording Instruments ~------------
d. Preparation of Recorder for Tracing
e. Calibration ~-------------
C. Diagnostic Tracing Procedure
1. Reference Tracing -------
2. Arterial Occlusions
a. General _
b. Superficial Temporal Arterial Occlusions
c. Common Carotid Arterial Occlusions
8. Post-occlusion Tracing -
D. Post-tracing Procedure
E. Final Comments



TABLE VI
Caleulated Rheoencephalograrhic Factors in Patients with Subsequently Known Definitive Diagnoses

cuicuinsd Tne Soopomate (aT) Tete fant vic
calares |—_ __
Teajor Rte
Tolerant a cerebnat Pestuson
peut | teyorte | Rah ee, (| roses anerin
No. | Passe shunts Onn om
Net Net ‘Net larger ‘Internal Common
she ate ath [Tae [ee] me [ew | ee | SES | See
R L to Rg L ‘to Rg L ‘to @ a poral
otis ste stan [emer | on, [oan [ots [ae [oe [ome [abe Ee
wai »
sater
au 0 wh °
«ta oom om on 2
5 Te wom 7
6 maw Ba me oa
1 wer a ee
bees om & www 2»
oes oe ma
oo eon a 22
ae 7% om won oe
Bo oe m 6 9 8 8
Boe ee ee
ue ie a
wo a
aren we a 0 oe
se oo me x
ue ao 8 maw wx
ws ee 1 ew
Dene pw wom om 6 ‘ ee ee ae
A we 8 Pare a ae ne mo
we Ook ww wm ww
2. owe aa akan www
Mmm 2 we 0 8 Mo mk ot me om 0 oo me ew
Bm % A om on % 2 OH 0 vw Bo BM © Hm mM Aw
wae OR Mew wat
nome 8 wom we Me me Be Om A me
we 6 om Rh MB ww
Bo ee @ we mM oom we ue 7 eo oe em ow

sStezred, tracings wore improperiy calibrated; values any be erroneous,
4Diagnosis further confirmed at Surg

40


ecencephatogrehie Fintings in Fattente with Suboequntly Show DeeSnttive Diagnoses
Tvorage Arterial Goapression Anplitutes (1114ch)
average
Com) ana snplivutes ‘Right Left a Right Left Bilateral,
westont Lage | Xone, | saute, CHES) oR | ool, | S4sseT | ccmon, | comon, | Comoe”
Right | Left] Rignt | Left] Ri ta | Re | be | Rs | bs | Re | be | Rs | Ls | Re | be | Ry | ty
Lams Se ~» 2
2 sero Not Recorded m2 178
ra a re so 195 0 10s
de HS, Recorded 1m) 1B no
ee eC ee eC Cae 2 em a
ee ee ee ee eo am
wer 85 Dw n 2 @ 2
8 wee 51050) ALP yo km
as o 8 6 w
ee ee om wm &
or a Ce 2» wm a mM
0505 mak pon was 6
i ee re
ee ee a @ 2B
oe 2 2 mB %
eka wou @ o
ee a 6 @ 8
wows a ee ess
pos Not Recoraead 2 7 Pee
mw Dama? mw @ 8 8 B
A. 199 5H Dw nw» em
ee ee ee 2 6 2 © 5% 2 we 10
a. mss DOMES ea HO He
re ee
ee es
ee ee re ee re ee ee a
mom 3 8 ww wt
nv ee
Bo wm on we Be wR

starred tracings wore improperly calibrated; values may be erroneous.

38


electrode size, Lifshitz’ reaches a similar con-
clusion.

Qualitative predictions about the influence of
interelectrode distance can be made from the
model. Initially, surface electrodes will estab-
lish separate, relatively “independent” near-field
volumes as the interelectrode distance shortens
from diametrical placement; such volumes will
have extracranial/intracranial tissue ratios ap-
proximately equivalent to those at diametrical
placement (assuming reasonably constant anat-

Ficure 5. Multishelled spherical model of the head.

omy). This situation will remain relatively un-
changed with shorter interelectrode distances
until the near-field volumes begin to overlap.
Here the electrodes register less “independent,”
partially coalesced, near-field volumes whose sub-
cutaneous tissue content is increased. As co-
alescence becomes pronounced. with shorter dis-
tance, the subcutaneous weighting will rise rap-
idly. At sufficiently close electrode placements,
practically all of the current may shunt extra-
cranially. Thus, at long interelectrode distances
the majority of the current necessarily traverses
small volumes of subcutaneous tissue and bone,
despite their high resistance, to reach a large
low-resistance volume of intracranial contents;
this path offers lower overall resistance than
paths traversing only the subcutaneous layer.
At short interelectrode distances the inverse is
true; the direct subcutaneous paths offer less re-
sistance than the more oblique paths through

large volumes of bone and a small volume oi
intracranial contents. Similar reasoning can be
applied to the total resistance. Initially, the
latter should remain relatively constant with de-
creasing interelectrode distance and then shoulc
fall, at first gradually but later rapidly, as the
interelectrode distance shortens beyond a par-
ticular value. Such curves of total resistance
versus interelectrode distance have been presented
by Grey Walter.®®

The preceding discussion indicates an appreci-
able volume of subcutaneous tissue will always be
monitored despite wide electrode separation
Thus, the total impedance plethysmogram car

Pom ELECTRODE

Ficure 6. Geometrically approximated electrode “near-
field” volume for the multishelled cranial model.

be expected to arise in part from the extracranial
circulation. Further, since the current density
is greatest in the tissues closest to the electrodes,
blood volume variations in the near-field region
will have a greater influence on the tracing than
equivalent variations occurring at a distance, for
example, intracranially. The magnitude of this
extracranial “artifact” depends on the magnitude
of the extracranial blood volume variations oc-
curring primarily in the near-field volumes. The
contribution from blood variations occurring
more remotely from the electrodes in the fraction
of the current shunting wholly extracranially is
probably slight. The above conclusions have
been anticipated in part by Lifshitz.*

On the other hand, since most of the current
eventually traverses the intracranial region but
is only partially concentrated in the intracranial
portion of the near-field volume, almost the re-
verse situation would exist for intracranial blood
volume variations. Both tracing components
may be appreciable; their ratio will depend both
on the current distribution throughout the head
and on the ratio of the extracranial to intra-
cranial circulatory changes. In some subjects,
the extracranial “artifact” may comprise a large
fraction of the total tracing despite widely sepa-
rated electrodes and the known favorable ratio
of scalp circulation to cerebral circulation.


fistula patient is lost. Waveform retardation
alone is as unsatisfactory as are the other single
criteria. A combination of all of the above cri-
teria gives information only on the possible
presence of disease and gives neither reliable
lateralization nor diagnosis. Thus, present in-
formation indicates there is no simple and re-
liable approach to rheoencephalographic diag-
nosis short of the full method we have presented.
The authors must indicate, however, that we have
not as yet attempted to correlate specific wave-
forms with specific diseases, Consideration of
the various tables indicates that very few com-
pletely normal waveforms are found in the pres-
ence of significant disease; such correlation may
be possible.

6. General: The lack of specific, easily meas-
urable criteria is not unexpected if one remem-
bers that the cerebral circulation is supplied by
four relatively independent carotid and vertebral
arteries. Significant: impairment may be com-
pensated by increases in one or more of the
others, often in unexpected patterns and at the
expense of other regions. Thus, in Tracing #39,
Table II, the right internal carotid is signifi-
cantly decreased, the left internal carotid is un-
changed but supplies the deficit on the opposite
side, the left posterior-anterior contribution has
increased to compensate for the left perfusion
deficit, while the right posterior-anterior contri-
bution has remained essentially normal. In ef-
fect, the right cerebral perfusion is supplied at
the expense of the left vertebral-basilar system.
One is tempted to label this another “steal”
syndrome.*

Such phenomena may explain our high inci-
dence of carotid impairment in patients with
clinically diagnosed vertebrobasilar insufficiency ;
such findings strongly suggest that these cases
should be screened routinely for carotid occlusive
disease since the latter is often amenable to
surgery.

C. Sources and Patterns of Collateral in Carotid
Insufficiency: The tracings showing carotid oc-
clusive disease afford information regarding
possible sources of collateral circulation. Sixty-
five tracings showing significant insufficiency of
one (51%) or both (49%) carotids were reviewed.

*We are reminded of a correlation from the evening paper
which daily informs us that aims accomplished easily by the
wealthy through generosity are accomplished with difficulty

by the poor and often through crime, for example theft . . .
Of course, here the age correlations are usually reversed!

50

Sixty tracings (92%) indicated the contralateral
carotid had increased and supplied the insuffi-
cient side to some degree. In five tracings (8%),
the contralateral carotid was not significantly
increased; all collateral was supplied at the ex-
pense of the posterior circulation.

Of the 60 tracings showing contralateral caro-
tid increase, six (10%) showed collateral sup-
plied only by that carotid, eight (13%) showed
collateral additionally supplied only by the ipse-
lateral posterior-anterior shunt, and nine (15%)
showed collateral additionally supplied only by
the contralateral posterior-anterior shunt. Thirty-
seven tracings (62%) showed collateral addi-
tionally supplied by both posterior-anterior
shunts; in nine tracings (24%), both collateral
channels ‘had increased equally; in 18 tracings
(49%), the contralateral posterior-anterior shunt
had increased more than the ipselateral shunt,
while the reverse was true in ten tracings (27%).

Of the five tracings showing only posterior-
anterior collateral increases, both channels were
equally increased in two cases and both channels
were increased with the ipselateral response
greater in three cases. Wo patients were traced
in whom collateral compensation had not oc-
curred to some degree.

From the above data, the following conclusions
can be drawn regarding possible sources and
patterns of collateral circulation in unilateral and
bilateral carotid insufficiencies. These conclu-
sions are valid to the extent that the tracing
analyses reflect the actual circulatory status of
the patients and to the extent that this group
represents an adequate sampling of the disease.

1. The less involved carotid is an important
collateral source in almost all cases (92%), but
is the sole source in few (9%) ;

2. The carotid collateral is assisted by either
one of the posterior-anterior shunts on an essen-
tially random basis (12% and 149%) ;

3. All three less involved sources are increased
in the remaining majority (57%). The posterior-
anterior shunt contralateral to the lesser carotid
is larger twice as often (28%) as when both
shunts are increased equally (14%) or the ipse-
lateral shunt is the larger (15%) ;

4, In very few cases (8%), the less involved
carotid is not increased; the sole collateral source
is the posterior circulation.


35,

36.

387.

38.

39.

40.

41.

42,

44,

47.

Zremnowicz, S. A. R. McWituaMs, J. C., and
Kucuarski, W. E., Conductivity versus Frequency
in Human and Feline Cerebrospinal Fluid, Proc.
17th Annual Conf. Eng. Med. Biol., 108 (1964).
Freyeana, W. H., and Lanpavu, W. M., Some Rela-
tions Between Resistivity and Electrical Activity in
the Cerebral Cortex of the cat, J. Cell. Compar.
Physiol., 45, 877-892 (1955).

Weexs, A. W., and Atexanper, L., The Distribution
of Electrical Current in the Animal Body: An
Experimental Investigation of 60 cycle Alternating
Current, J. Indust. Hyg. Toxicol., 21, 517-525 (1989).
Grey Watrer, W., in “Electroencephalography”
edited by Hill, D. and Parr, G., Macmillan Co., New
York, N.Y., 1963, page 65.

vaN Harrevetp, A., and Scape, J. P., On the Dis-
tribution and Movements of Water and Electrolytes
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of the Cerebral Cortex,” Tower, D. B. and Schade,
J. P. editors, Elsevier, 1960.

Simonson, E., in “Cerebral Ischemia,” edited by
Simonson, E., and McGavack, T. H., C. C Thomas,
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Donras, A. S., and Simonson, E., Carotid Pulses
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454 (1961).

Zmmnowicz, 8, A. R., Techniques of Regional Rheo-
gtaphy for Monitoring the Circulation of the Brain
and in the Eye, Proc. 16th Annual Conf. Eng. Med.
Biol., Baltimore, Md., 96-97 (1963).

Zmmnowicz, S, A. R. McWirtrams, J. C, and
Kucarsxi, W. E., Proc. 17th Annual Conf. Eng.
Med. Biol., 29 (1964).

. ZreMNowicz, S, A. R., The Present Status of Stand-

ard and Regional Rheoencephalography (REG), in
“Cerebral Vascular Diseases” edited by Siekert, R.
G., and Whisnant, J. P., Grune & Stratton, New
York, 74-80 (1965).

Zemnowicz, S, A. R., Rheographic Regional Method
for Evaluation of Cerebral and Ocular Circulation
in Cardiac and Cerebrovascular Disease, J. Am.
Geriatrics Soc, XIII, 35-43 (1965).

Berra, H., et al, Zur Deutung des Schadelrheo-
grammes, Z. Neurochir., 15, 257-266 (1957).
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56

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. Jenkner, F. L., Rheography, Confin, Neurol. 19,

1-20 (1959).

. Srronson, E., Personal Communication.
. ZIEMNowicz, S, A. R., Personal Communication.
. JenKner, F. L., Personal Communication.

Van Busxirx, C., Intracerebral Vascular Disease,
in “Clinical Neurology,” edited by Baker, A. B.,
Hoeber-Harper, New York, N.Y., 589 and 597
(1962).

. SerPet, J. H., Unpublished Data.
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Williams and Wilkins Company,
196 (1960).

Survey Report, Joint Council Subcommittee on Cere-
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Institute, edited by J. L. O'Leary, July 1, 1965.
Gurpsian, E. S., Harpy, W. G., Lanpyer, D. W., and
Tuomas, L. M., Four-vessel Angiography: Experi-
ence With Three-Hundred Consecutive Cases, Clin.
Neurosurg., 10, 251-274 (1963).

Poser, C. M., Zosa, A. J., Gomez, A. J., and Hanrprn,
H. A,, Cervicocephalie Angiography for Cerebrovas-
cular Insufficiency, Acta Neurol. Scand., 40, 321-886
(1964).

Werner, L. M., Berry, R. G., and Kunorn, J., Intra-
cranial Circulation in Carotid Occlusion, Arch.
Neurol., 11, 554-561 (1964).

Scuwartz, ©. J. and Mircnett, J. R. A. Atheroma
of the Carotid and Vertebral Arterial Systems, Brit.
Med. J., 2, 1057-1063 (1961).

Baltimore, Md.,

. Hurcuinson, E. ©., and Yates, P. 0., Carotico-

vertebral Stenosis, Lancet, I, 2-8 (1957).

A. B., and Iannone, A., Cerebrovascular
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Willis, Neurology, 9, 321-332 (1959).

. Atpers, B, J., Bargy, R. G. and Pappison, R. M.,

Anatomical Studies of the Circle of Willis in Normal
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21760


though an appreciable fraction continues to
permeate the contralateral volume; the fraction
of the total current flowing ipselaterally is
greater than half of the total current, while the
contralateral fraction has fallen in the same
amount. The resulting plethysmogram, while
still composite, no longer contains equal contri-
butions from each side. The intracranial tracing
component is weighted in favor of the ipselateral
side in approximately the ratio of the intracranial
current fractions. The extracranial component
is much more heavily weighted in favor of the
ipselateral side since the extracranial current
path is much shorter along the are directly be-
tween the electrodes. than around the remaining
portion of the circumference. As the interelec-
trode distance lessens, the contralateral extra-
cranial contribution to the plethysmogram van-
ishes relatively quickly and more rapidly than
the contralateral intracranial portion of the
plethysmogram.

In summary, the cranial impedance plethysmo-
gram, or rheoencephalogram, is a complex quan-
titative analog of changes in cranial blood vol-
ume and is composed of component “sub-plethys-
mograms” from the ipselateral and contralateral
extracranial and intracranial regions. The
weighting of these components in large part de-
pends on electrode size and placement, normal
and pathological anatomic and circulatory asym-
metries, and normal and pathological passive
electrical properties of the various component
biological materials. At present, most of the
above factors can only be estimated; conversion
of the various component impedance plethysmo-
grams to blood volume values and extrapolation
of these values to values representative of the
total blood volume variations in each tissue region
are qualitative at best.

III. Individual Arterial Contributions to the
Rheoencephalogram.

A. Basic Assumptions: The previous discus-
sions indicate that the following assumptions
may be reasonably applied to rheoencephalog-
raphy:

1. Cranial resistance changes are quantitatively
associated with changes in blood volume.

2. With bilaterally symmetrical placement,
each electrode pair monitors similar extracranial

10

and intracranial tissue volumes and their con-
tained blood.

3, Each electrode pair monitors a major frac-
tion of its ipselateral tissue volume. Monitoring
of the contralateral tissue volume is negligible.

4, Appreciable fractions of the tracing may
arise from both the extracranial and intracranial
circulations.

5. Additive contributions from each artery to
the total blood volume change are reproduced
as additive changes in the tracings.

6. Extracranial changes are intercomparable
and intracranial changes are intercomparable;
but extracranial changes are not intercomparable
with intracranial changes unless their relative
weighting is known.

The following additional assumptions will be
made:

1. Each electrode pair monitors its current
field independently; i.e, no interaction exists
between channels.

2. Barring catastrophic circulatory occurrences,
cranial hydrodynamics remain constant through-
out the tracing interval and are not perturbed
significantly by the tracing procedure,

8. Brief, deliberate, complete arterial occlu-
sion removes only the appropriate components
from the tracing. Collateral compensation oc-
curs slowly, if at all, during the compression
interval unless the latter is unduly prolonged.

B. Anatomie Models for Rheoencephalography:

1. Basie Circulatory Model: A relatively
small number of arteries may be expected to
contribute most of the circulation monitored by
rheoencephalography in the normal subject. For
the scalp, skull, and meninges, these are the
angular, superficial temporal, posterior auricular,
and meningeal branches of the external carotid
arteries and the supraorbital branches of the
internal carotid arteries. For the brain, these
are the internal carotid and vertebral arteries.
The meningeal, internal carotid, and vertebral
arteries are not easily accessible for manual oc-
clusion while the angular, posterior auricular,
and occipital arteries are small and probably
add negligible contributions to the rheoencephalo-
gram. The following model was chosen as a!
first-order approximation of the cranial circula-
tion for use in analysis of the rheoencephalogram
(Figure 9).


Dr. John H. Seipel, Chief, Neurology Laboratory, Georgetown Clinical
Research Institute, was awarded the S. Weir Mitchell Award on April 29,
1966, by the American Academy of Neurology during their annual meeting
in Philadelphia, Pennsylvania.

Dr. Silas Weir Mitchell, 1829-1914, was a pioneer physician and neurolo-
gist who lived and practiced in Philadelphia. His interests ranged widely;
in addition to his many medical papers and books he became equally well
known as a poet and novelist publishing over 180 novels and books of poetry.
Several of the medical syndromes, signs, and treatments he devised still are
in use and carry his name.

The S. Weir Mitchell Award, consisting of a bronze medallion, a hon-
orarium, and the opportunity of presenting the research at the Academy
meeting, is given annually to encourage research by young physicians and
scientists in the general field of neurology.

Dr. Seipel was honored for his Georgetown Clinical Research Institute
studies in rheoencephalography, a simple, rapid, innocuous method of study-
ing the brain circulation which had previously received little favorable in-
terest in the United States. In his paper, “The Biophysical Basis and
Clinical Applications of Rheoencephalography,” Dr. Seipel has demonstrated
the high level of accuracy inherent in the method in diagnosing various forms
of brain disease, developed a reliable procedure for its use, demonstrated its
value in screening normal subjects for early, asymptomatic disease and dem-
onstrated various hitherto unknown syndromes.

This research was undertaken to develop rheoencephalography into a
simple office procedure, comparable to electrocardiography, which could be
used for certification and screening purposes to detect brain problems likely
to cause sudden incapacity, such as stroke, prior to their occurrance and in
sufficient time to begin adequate treatment.

Dr. Seipel’s receipt of the award in Philadelphia was particularly ap-
propriate since he received part of his medical training at Pennsylvania
Hospital; Dr. Mitchell was a member of that hospital’s Board of Managers
and probably also practiced there.

iv


pulse waveforms are significant; the latter oc-
casionally show changes which are obscured by
the extracranial circulation. In analyzing wave-
forms, we consider three factors: basic wave-
form, superimposed notching, and timing. The
following discussion will assume no cardiac ab-
normalities are present since these can signifi-
cantly alter the waveform in an otherwise normal
patient.

One or more representative or typical waves
are usually studied.

1. Basie Waveform: Various REG wave-
forms are shown in Figure 14.

Theoretical analysis of the plethysmogramTM
indicates arterial inflow and venous outflow are
equal at waveform maxima and minima. Ar-
terial inflow exceeds venous outflow during ris-
ing portions of the curve; the reverse is true
during falling portions of the curve. We assume
that the initial portion of the normal curve,
Figure 14(a), from end-diastole (1) to peak
amplitude (2) primarily reproduces arterial in-
flow and filling of the vascular bed, while the
final portion from (2) to end-diastole (1) pri-
marily reproduces vascular emptying and venous
outflow. We designate these phases as “inflow”
and “runoff.” In the normal case, Figure 14(a),
inflow and runoff are rapid.

Deviations from the normal may give some
estimate of the underlying disease if the inter-
preter considers how such deviations can arise
by alteration of normal circulatory mechanisms.
Thus, the abnormal waveform, Figure 14(b),
shows delayed or retarded inflow which may be
due to flow restriction in the major arteries or
to a more generalized inability of the vascular
bed to fill normally, The abnormal waveform,
Figure 14(c), shows rapid inflow but delayed
runoff and may be due to continued filling, in-
ability of the vascular bed to empty readily, or
to venous outflow restriction. These may be
combined in generalized or multiple diseases,
Figure 14(d). Presystolic waves are often seen
and are probably normal.

2. Notching: The presence or absence of su-
perimposed notching and its location in the
waveform is important. Thus, a well-marked
dichrotie notch (3), Figure 14(a), suggests that
the cranial arteries are normally elastic and re-
sponsive to pressure changes, while flattening of
the notch or its absence suggests increased vas-
cular wall rigidity. A well-marked anachrotic

31

notch was seen in a case having markedly in-
creased intracranial pressure‘®; the waveforms
were similar to those later presented by Mc-
Henry" and may be pathognomonic.

3. Timing: Jenkner* discusses this factor ex-
tensively. A marked peak timing delay, when
present, is usually significant. Its significance
must, however, be determined in combination
with the remaining tracing information since
delays can arise from asymmetries in the extra-
cranial circulation. A delay on the bitemporal
arterial occlusion tracing is almost always sig-
nificant.

The interpreter can usually reach a diagnosis
from synthesis of all the information available
from the tracing. Rarely, disease may be missed
despite the above analysis. Failure occurred
with an arteriovenous fistula suggesting either
that further analytic criteria must be developed
or that the method or our procedure is insensi-
tive to this disease. .

It should be noted that the above analysis is
based on the assumption that the patient’s circle
of Willis originally was widely patent and had
the normal or classical pattern; anomalies in an
otherwise normal patient may mimic occlusive
disease. If both anterior cerebral arteries are
solely supplied by the right carotid, both cerebral
perfusions will be equal; the net intracranial
shunt will be appreciable, flow from right to
left, and arise from the right carotid; and the
right carotid will be appreciably larger than the
left carotid. The left carotid will appear in the
analysis as though it were appreciably stenosed
although such is not actually the case.

UI. Results:

149 tracings have been obtained from 126 pa-
tients and normal subjects. Twelve tracings
were technically unsatisfactory and could not be
salvaged. All tracings were analyzed by the
author.

A. Population:

1. Normal Subjects: A normal subject is de-
fined as a subject examined at our Institute who
showed no evidence of significant disease, either
by history or on examination, and who was
eligible for routine aviation medical certification.
Included in this category is a group of male
pilots who were studied as part of a special re-
search project.



practice; it need not be calibrated. The REG
and differential tracing channels should be set
and equalized preliminary to the start of the
tracing and should afford sufficient amplification
for final tracing equalization using the output
gain controls on the Rheograph. Once deter-
mined, these settings rarely require future change.

Frequency Response: The importance of the
low frequency cutoff must be emphasized. The
normal heart rate varies from 60-100 per minute
while respiration rate varies from 10-20 per
minute. The normal rheoencephalographic wave-
form thus contains significant and important
low-frequency components which must be repro-
duced by the recorder. Our early experience
quickly indicated that the low-frequency cutoff
at the usual EEG setting was too high and that
much of the waveform was not reproduced
(Figure 12). Figure 12 illustrates how the
waveform differs with low-frequency cutoff level
and may mislead the investigator; here the
higher cutoff level gives an almost normal ap-
pearing tracing.

A D.C. response was thought ideal. In prac-
tice, the wide baseline swings with movement
and deep respiration required reduced amplifi-
cation which obscured the waveforms and made
tracing interpretation difficult. We therefore
chose a low-frequency cutoff level of 0.2 Hz (one

1.0 SECOND

0.04 SECOND

Figure 12.

second time constant) for our routine trac-
ings. This response setting offers an excellent
compromise between maximum pulse wave am-
plitude and respiratory excursion.

The high frequency response is usually lim-
ited by the mechanical system of the recorder
and is not changed. 60 Hz and muscle filters
are not routinely used. Appreciable 60 Hz arti-
fact usually indicates poor electrode contact or
tube failure in the Rheograph.

Paper Speed: Standard EEG paper and cor-
responding paper speeds (25-30 mm. per second)
are used. We have found the 100 mm. per sec-
ond speed used by Jenkner? of little advantage.

e. Calibration: Adequate and reliable trac-
ing calibration is perhaps the most important
single factor in rheoencephalography. Simon-
son® has indicated that a standard tracing am-
plitude should be adopted for rheoencephalog-
raphy and has suggested a value of 0.10 ohm
per 10 mm. This value affords tracings of ade-
quate amplitude and good visual quality; it is
used routinely in our tracings.

The Rheograph calibration dial is set to the
0.10 ohm (100 mohms) calibration setting and
the recorder is started. Several calibration
pulses are applied to the tracing during the
smoothly falling, diastolic portion of the pulse;
the recorder is stopped; and the calibration pulse

Influence of time constant on the tracing.



ACKNOWLEDGEMENTS

The author is indebted to Dr. Arthur E. Wentz, Jr., director, George-
town Clinical Research Institute, and Dr. Desmond S. O’Doherty, professor
and chairman, Department of Neurology, Georgetown University Hospital,
for their patient support and encouragement, and to Dr. Ralph S. Hender-
son, professor of physics, Georgetown University and Mr. Maurice B. Whit-
lock, Georgetown Clinical Research Institute, for their invaluable assistance.

The portion of this research performed at the Georgetown University
Hospital was partly supported by NASA Grant NsG-388.

Qualified requesters may obtain Aviation Medical Reports from Defense Documentation
Center. The general public may purchase from Clearinghouse for Federal Scientific
and Technical Information, U.S. Dept. of Commerce, Springfield, Va. 22151

iii



TABLE VIZ.~-Continued
Rheoencephalographic Findings in Patients without Definitive Studies

Peak Tintrg weveforme
feterence
orion Reference | Bitemporal ‘Inflow Delayed Runoff Delayed
% of ‘Remarks Now
larger Reference Bitemporal Reference ‘Bitemporal
0) | seas | Bar| sce |

rione | vere | atent | rere | nian] sort | mtane | sore
wen ° so + oe h
oon 0 oo a) Ditterent tise constant 2
oz 0 oo too x
a ° oo ers a
on 0 oo oo Protabie inctrunent fatture x
_ ° oo oo soe ‘@
ou ° pan oo 2
aon ° oo oo at snterven 2
a 0 oo 0 0 °.
a ° toe oo w.
wn ° fot foe a
oo 0 a oe 2.
RRO + 0 0 0 ».
nua ° to oo a
cn kOe oe oo B.
sun 0 soe + .
mo Ro? Po to v.
or kee + 3G 1s.
00 ° ° en) ».
ru RO sos oo ~.
son ° : oo 2.
en ° 38 oo z.
oo ° so oo B
osu ° nom a) ms
oun ° 0 0 2° 0 zB
oon ° ae toe 2.
wo 0 foe 08 zn
ek 0. toe +o 2.
soa ° oo 6 2.
om 0 0 0 oo x.
0 ° + oe oo a
oa ° a 2
o er ee a 3.
ou ° oe ee eG ”
pa a a %.
oan 0 0 OO gt tery unstabte retorence x.
son 0 0 0 0 0 8 8 a
a ° a a a 3.
ox a ».
soa ° Fa a “.
ost 0 ee a a
oh kok ma : 2
oun ° ee ee e.
oo ° Se “
mt 0.6 oe ra e
set 0 ot rr rr rs ‘e
mu 0 RoR ome Gt a
om ° oom mt a.
ou ° nr a a °
ro ° a a wo.
oon ° a a
oo ° tot 38 x.
os ° coe 00 3.
om ° re ee er er os

43



trend towards increasing amplitude as the occlu-
sion continues; measurement of only enough ini-
tial post-occlusion pulses to give a representative
average may be necessary. Fourth, aberrantly
formed pulses may be present which can be dis-
carded. Finally, one or more pulses may have
waveforms similar to the remainder but have
amplitudes considerably lower or higher than
the remainder (usually higher). Such pulses
can be discarded unless they recur at regular
intervals and must be considered valid observa-
tions. A thorough analysis of the data as above
will usually result in excellent simultaneity. If
not, the interpreter has one further recourse
which we have found useful.

The above analysis assumes arterial contribu-
tions to the tracing remain constant throughout
the tracing period. It is possible that a transient
variation may have occurred before a particular
occlusion but with later reversion to the refer-
ence state; likewise, a permanent change may
have occurred after one or more occlusions.
These changes can be unilateral or bilateral ; they
are usually the explanation for the previously
mentioned compression values larger than the
reference values; and they are easily recognized
by associated changes in the pre-occlusion refer-
ence pulse waveform and its amplitude. In our
experience, the most reliable occlusion tracing
before the carotid occlusions is that during bi-
temporal arterial occlusion.

If any of the unilateral temporal arterial oc-
clusion values are significantly larger than their
reference values, or if adequate simultaneity has
not been obtained after the above error analysis,
we first check intra-tracing calibrations for in-
strumentation stability. If calibration changes
are not a factor, we select the occlusion tracing
which appears most likely erroneous and aver-
age the immediately preceding reference wave-
forms on each channel. In practically all such
cases, these amplitudes are significantly larger
than the initial reference amplitudes. The ratios
of the initial reference amplitudes to the pre-
occlusion reference amplitudes are used as factors
to “normalize” the high occlusion amplitudes to
the initial reference state. The resulting simul-
taneity is usually excellent. These normalization
factors frequently agree within several percent
between channels and suggest equivalent bilateral
changes; the change may also be unilateral. A
number of occlusion tracing amplitudes may

27

appear high and have prior reference values
agreeing closely for each channel but differing
significantly from the initial reference values.
Rather than normalize a large number of values
to the initial ‘reference amplitudes, we use the
later reference values, particularly if they agree
with the reference values appearing at the end
of the tracing. If the above methods are un-
successful, the remaining error must be accepted.
It has not exceeded six milliohms in our temporal
occlusion series,

Error analysis based on observed bilateral
carotid arterial occlusion values is considerably
more difficult since this maneuver is neither
easily performed nor measured. Equations (24)
and (25) are used to calculate values which are
compared with R, and L, as with the temporal
occlusions, Occasionally, the measured pulse
amplitudes are too high; the bilateral occlu-
sions were presumably incomplete and are worth-
less.. Frequently, one pulse or a few pulses from
each channel may agree within five milliohms,
the others being too high; these lower observed
values are accepted. Occasionally, all goes well
and a stable, relatively long, low-amplitude
tracing is obtained, its averaged values usually
agreeing closely with the calculated values. If
the observed values are significantly lower than
the calculated values, an infrequent occurrance,
the unilateral occlusion values are analysed as
described for the temporal occlusions. Excellent
agreement is usually easily attained. Occasion-
ally, agreement may be within 1-2 milliohms on
one channel but less close on the other. We can
offer no explanation.

In general, if the tracing has been properly
obtained from a stable patient, the initial aver-
ages often give excellent simultaneity. The
majority of the remaining tracings requires only
rejection of aberrant values, enlargement of one
or more samples, or inclusion of pulses occurring
earlier in the occlusion tracing to achieve simul-
taneity. The full battery is rarely required and
normalization almost never. The latter has been
used three times to salvage tracings obtained
from young normals who were not available for
retracing. Fortunately for its use as a diagnostic
tool, older patients with cerebrovascular disease
usually give stable and self-consistent tracings;
young normal subjects with labile extracranial
circulations present the most difficult tracings to
analyse. In the latter cases, it is sometimes



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36


pretracing procedure is followed on all human
tracings performed in our laboratory, whether
diagnostic or research studies, and has been very
successful in affording interpretable tracings; it
can also be used for animal studies with appro-
priate modifications. Our diagnostic tracing
procedure will be similarly detailed.

C. Diagnostic Tracing Procedure:

1. Reference Tracing: After an adequately
equalized and calibrated tracing has been ob-
tained, the recorder is permitted to run for a
sufficient period of time to give an artifact-free
train of at least 30 pulses and/or five respiratory
cycles. This portion of the tracing will later
be used as the reference, comparison, or baseline
tracing; it is important that sufficient artifact-
free tracing be obtained to represent the patient
reliably throughout subsequent analyses. If the
patient is tense or movement-prone, the recorder
is stopped and he is again cautioned that move-
ment delays the procedure. If the patient is
restless and unable to coperate, a long artifact-
free sequence may be difficult to obtain. In such
cases, sufficient tracing should be obtained to as-
sure that enough representative pulses are avail-
able for analysis. Movement artifact may be
lessened by a not uncomfortably tight electrode
strap. Various manipulations or maneuvers may
next be performed depending on the purpose of
the tracing.

2. Arterial Occlusions: The importance of
rheoencephalographic monitoring during delib-
erate arterial occlusions has been apparent from
the onset of our studies. Such occlusions have
been employed as part of all clinical diagnostic
studies in our series*® except where clinically
contraindicated or prevented by circumstances.
Partial or complete deliberate carotid occlusion
is not new to rheoencephalography* but appar-
ently has not been employed routinely. We now
routinely occlude the superficial temporal ar-
teries unilaterally and bilaterally. Other acces-
sible arteries may be occluded as part of the
study as desired.

a. General: We usually wear insulating
plastic or rubber gloves when performing oc-
clusions, as suggested by Jenkner® in questioning
the validity of our results. We have investigated
this question in a series of patients by perform-
ing each occlusion alternately with and without
rubber gloves; no difference between the pro-

22

cedures could be detected and identical results
were obtained.

The procedures are always described to the
patient and he is warned to expect a small
amount of localized discomfort, especially dur-
ing carotid manipulation. He is also again
warned that movement of any sort may disturb
the tracing and make repetitions necessary.

The operator may stand behind the patient’s
head or on either side as desired. He should be
in a position which is as comfortable as possible
and which he can sustain throughout the ma-
nipulation without transmitting movements or
tremors to the patient. The operator should not
contact the bed frame during the tracing period.

The recorder is always positioned so the opera-
tor can monitor the tracing visually. This fac-
tor is important in obtaining adequate tracings
safely. Artifacts and variations in technique
are immediately apparent to the operator and
permit immediate correction; the completeness
of the occlusion can be estimated; and the need
for further repetition quickly determined. Fur-
ther, if a carotid unsuspectedly supplies a ma-
jority of the total cranial circulation, this will
also be immediately apparent and the procedure
can be terminated quickly.

The artery to be occluded is found manually
with one hand, using the other for assistance or
for head bracing, and is lightly held beneath
one or two fingers. The artery should not be
occluded during these preliminary maneuvers.
When ready, the operator requests that the re-
corder be started and observes the tracing. When
the waveform has stabilized and appears similar
to the reference waveform, about a page of trac-
ing is obtained. The artery is then compressed
as the operator simultaneously signals his as-
sistant who marks the tracing. The occlusion
is held until the tracing stabilizes and a sufii-
ciently long, representative sample has been ob-
tained. The artery is then quickly released
with a simultaneous signal to the assistant who
again marks the tracing. The procedure is re-
peated after the tracing has returned to stability.
At least two apparently identical occlusion trac-
ings should be obtained, preferably three. More
may be necessary if difficulty is encountered.
The operator should hold his position until the
run is completed. Comments may be made to
the assistant for immediate chart entry where
indicated but should not attract the patient’s


capabilities and its applicability to tissue volumes
which would be difficult or impossible to study
by other methods.

It should be emphasized that any plethysmo-
gram is a volumetric measurement which depends
on the time integral of the difference between
two unknown dynamic quantities, arterial inflow
and venous outflow. Plethysmography by any
method cannot give either arterial or venous flows
or total tissue blood volumes without modifica-
tion. Conversion of an impedance plethysmo-
gram to its corresponding volumetric changes is
particularly difficult and cannot be successful
without detailed knowledge of current fields
throughout the monitored volume.

It is apparent that any disease which suf-
ficiently alters the normal circulation of blood
anywhere in its course to, through, or from
the monitored tissue volume or which sufficiently
alters the normal conductivity characteristics of
the tissue can alter the tracing. Thus, the clini-
cal use of impedance plethysmography can be
established on a purely empirical basis; such use
need not be postponed awaiting elucidation of
the biophysical basis of the method.

II Biophysical Basis of Rheoencephalography.

The simplest head analog is a homogeneous,
isotropic, conducting sphere. Measurement of
surface voltages between two current-carrying
point electrodes diametrically placed on the sur-
face of such a sphere gives a non-linear voltage
curve (Figure 4).

This surface voltage variation is described by
equation (7) :*?

-Jf4a_ a
7) o= ole RT +]
where:

atrcosé
r sing

Rio = (at+ry2arcos6)*

wa sinh! an

yo aL — sinh?

The non-linearity arises from the concentration
of the current field in the volume near the elec-
trodes and its dispersion as the volume increases
with distance. In the illustrated case, the
tion-linear “near-field” region extends to 5 cm.
from the electrodes; the voltage curve is approxi-
mately linear in the intervening region. This
concept of an electrode “near-field” volume is

introduced for discussion purposes, recognizing
that the properties of a conducting volume are
continuous and that such division is artificial.

A better head approximation is a multishelled
sphere having homogeneous isotropic layers cor-
responding to the scalp, skull, and cerebrospinal
fluid surrounding a central spherical volume
corresponding to the brain. Each region is as-
signed “lumped” passive electrical properties
and average dimensions corresponding to the
appropriate tissue. Few human cranial tissue
resistivities have been measured under living
conditions at any frequency. The values for
blood, 150 ohm cm.,** and cerebrospinal fluid,
60 ohm cm.,***> are perhaps the most reliable.
Intact living cat brain measures 225 ohm cm.**
Values for the remaining tissues may be esti-
mated from measurements on somewhat anal-;
ogous tissues° Skin and subcutaneous tissue
are assumed comparable to muscle at 700 ohm cm.
(30 kHz). Bone, having a dense matrix which
should constrain ion movements despite its blood
and electrolyte content, is assigned 3000 ohm cm. ;
the true value may be much smaller.*3* The’
model is illustrated in Figure 5. In this
model the “intracranial” region has a much lower!
resistance than the remaining layers; the cere-
brospinal fluid and the brain with its high blood
content® offer a marked shunt path beneath the
meninges and bone. The cranial near-field
volume for such a model must be highly dis-
torted. It probably has a relatively constant
radius in the subcutaneous tissue, a considerably’
shortened radius within the bony layer, a longer
radius in the cerebrospinal fluid, and a somewhat
shorter radius in the brain for diametrically
placed electrodes. The deepest penetration would
coincide with the interelectrode axis. Since the
intracranial contents offer paths of lesser resist-
ance, the majority of the current should traverse
the intracranial cavity; the highest current dens-
ity most probably lies along the interelectrode
axis (Figure 6).

Since the major portion of the total resistance
lies in these near-field volumes which contain
large fractions of subcutaneous tissue and bone,
the total resistance is heavily weighted by these
tissues. Therefore, extracranial blood volume
variations will give rise to larger resistance
changes than equivalent intracranial blood vol-
ume variations. Reasoning from the effects of


TABLE VIII.

Calculated Rhecencephalographic Factors in Patients without Definitive Studies

Calculated Tracing Components (Iéi1Liohes)

‘Tracing Component.

Ratios (Percent)

Arteries
al Pert ‘Tenporal, Ratios
Patient ‘Temporals Interna Carotids | Coston carotids | Posterior-anterior | Cerebral Perfusion
No. | Nos ‘Shunts Om
Ove
Net Net. Net Larger | 0% | comon
‘Shunt Shunt Shunt at ‘Teas | Internal | Coretta
afi fm bat. fom] oa da fom Righ Lett Right sare | Tem | arotta
side side side [caic.] obs.[care. ors. cate. ons. Rie jede
1. 305m 66 102 4aR a2 4
a on a 97 OR °
3. a7 160 173 WR 5 53
4 10wo 79 10 ORB 6
5. 4998 00 206 56R 28 6
6 7 03 lig Roh 0
T1206 eo 1 mR 20
a . 55 48 oR AL 433836
o 365 mM 4 LB ws
wo. aas 9 70 ROB 30
a. ase 65 10% RO we
Bw nv 67 53 ML 1
BL lose 54 OR ue
le 194 89 54 OL 2 3
us. usa 395 Bb
Yer 1838 39063 RD 23
vw ws 490% oR 15 @ 12 20
18. us 45 530 aR 6
1. 6 96 76 (BLO 4
20, 1899 037 »
al. 1900 we 92 La 6
2. 1285 % 9 2 3
2. 1901 oO 6 oo 6 ea
2%. 322 6 87 DR 2 as
25. 1366 599 67 0 Oks
2%. 1336 3% IR mh mh oD
27. 1902 % 19 wR 2 °
28. 1385 3585 kR aL 30
29. 1903
3. ae 32039 R “
BL. 1908 mR 5 WL 8 2
32, 19054729 SL 33 RAR DSLR 25 96 92 99 102 aR 2 BC's
33. ea a ee ed ba a 2 pL 9 8 8 45



‘TABLE VIII.--Continued
Calculated Rhecencephalographic Factors in Patients without Definitive Studies

Calculated Tracing Components (MMil1ichns)

‘Tracing

‘Component
Ratios (Pereent)

iateries
Cerebral Pesfusion Temporal Ration
Patient Temporals | internal carotide | comon carotide | Posteriorcintertor
wo. | he Om Om
> Net Net tet targer | internat | —comon
shunt Shunt ott, | met | ere mgmt | tere | fem | Carotia | Carotia
R L to Rg L to R L ‘to
site side sh, [me]. [one tl Lele
eee en ee 2% a 4 Rw % 33h
2%. wer 2 8 42 109 3k 6 us us OR 20 mk OD
% DD ne 100 Ww HOD 98 2 m= » ow wD
mo “um or a a ee oy eR SB
38. we RT HCMC MLD OTH COL HHO HB
3. moda LHL ae 552 568 RH 5
oo OLS R52 DRS noo8 5 58 4 48 SIR mr om 3
A. ow 8 OL mH ORR a 6% 8 2 WM Uu Bw B
2 woe Ra wa LC ww
2. ee ROR TOUR Ow HMO 8
HORCHOW
a (wo. oR OL: Ls sw HOH HL Mw
6. 00885 ML we 1% 7 % L198 ake 3855
Pe ae ae a
as. was aR HR_ DAM 2s mo ww 1 9 0 6 BL
a. 8s ROR RRO p eu 7 TL kw
0. aR 50 50 62 OL
sl. 1865S SR HTH AR HRC “ 6 8 1 mM sR wm 1 & 6
52. a 8
2. " 9% UR 2 ms mw B
a "om we kh OOO THR KOSH

sStarred tracings were improperly calibrated; values may be erroneous.

4P.A.A. certification consultation case

44FVA.A. normal examinees.

46


With close electrode placement, significant
near-field volume overlap can be expected to oc-
sur; the tracing will then contain a larger frac-
sion of extracranial “artifact”. At sufficiently
slose placement it is reasonable to expect that
ulmost no intracranial changes are likely to be
jetected. Nyboer? illustrates frontal electrode
placement without comment. Simonson‘? pre-
sents evidence for a high level of extracranial
‘contamination” in tracings obtained from nor-
nal subjects using various electrode positions
which include close (34’’) frontal placement.
The pulse waveforms he obtains from electrode
dairs positioned on the forehead and occiput,
aowever, show definite contour dissimilarities
which are probably not significant considering
she different interelectrode distances and the dis-
similarity between his right and left forehead-
reciput tracings. Simonson** and Dontas and
3imonson* describe studies using forehead elec-
srode placement and consider that such tracings
represent essentially extracranial circulation. It
's difficult to accept recent uncritical claims that
echniques using relatively close electrode place-
nent register localized or “regional” cerebral
sireulation and monitor blood volume variations
n the circulatory fields of individual cerebral
urteries without extreme extracranial contami-
aation.**4¢

The current field extends throughout the en-
sire head despite the location of the major por-
sion of the total resistance in the near-field
volumes of tissue about the electrodes. Varia-
dions in blood volume anywhere in the head will
uffect the total resistance but will be detectable
mly to the degree they modify a sufficiently
arge fraction of the total current. This sug-
zests that impedance plethysmography may de-
sect changes in blood volume anywhere in the
head although weighted to detect changes in the
aear-field volumes (see also Lifshitz*).

With electrodes placed at opposite ends of a
diameter of the head, for example, forehead and
seciput, the current field is symmetrically dis-
sributed throughout the entire intracranial and
oxtracranial volume. If the intracranial and
axtracranial structures and circulation are per-
fectly symmetrical about the midline, half of the
surrent will flow through the right and half
shrough the left side of the head (Figure 7).
The resultant plethysmogram will be a composite

of identical contributions from each side where
each side contributes half of the total amplitude.

LEFT RIGHT

Ficure 7. Estimated current distribution with antero-
posterior electrode placement.

With placement of the posterior electrode
closer to the anterior electrode on the same
ideally symmetrical head, the current field still
permeates the entire volume, but the previous

Fieure 8, Estimated current distribution with antero-
lateral electrode placement.

symmetrical distribution is lost (Figure 8). The
current field now concentrates ipselaterally al-