T H E H A E M O D Y N A M I C E F F E C T O F A N I N T R A C R A N I A L

A R T E R I O V E N O U S A N O M A L Y

A DOPPLER-HAEMATOTACHOGRAPHIC STUDY

J. M. M. Nies*

SUMMARY

Determination of the mean blood flow velocity by means of Doppler haematotachography is suggested as an aid in evaluating the haemodynamic changes associated with an intracranial arteriovenous anomaly. A Doppler haematotachogram (HTG) was obtained in 13 patients with a radiologically diagnosed arteriovenous anomaly, with marked interindividual variations in dimensions and blood supply; in 6 of these patients the Doppler HTG was obtained before and after total neurosurgical extirpation.

The large majority of the patients showed a significant increase in diastolic, and to a lesser degree in systolic flow velocity at the level of the common carotid artery. In most cases the flow velocity curve of the ophthalmic artery showed a decrease in amplitude. These are the most useful parameters in evaluating the baemodynamic effect of an intracranial arteriovenous anomaly. After the surgical removed of the anomaly, the carotid flow velocity decreased significantly.

In the internal and external jugular veins, Doppler-haematotachographic pulse waves were registered for the first time. These may have been conducted from the internal carotid artery to the jugular veins via the arteriovenous anomaly. The usefulness of this parameter is re- duced because of the cumbersome calculations required to determine the time within which an arterial pulse wave conducted via the arteriovenous anomaly reaches the jugular vein. Registration of this unusual pulse wave is solely of theoretical value.

INTRODUCTION

An ar ter iovenous anomaly , whether in t racrania l or elsewhere in the body, can have

impor tan t haemodynamic consequences (BESSE, CARIOU, CHOUSSAT and BRICAUD, 1970; PROSENZ, HEISS, KVICALA and TSCHABITSCHER, 1971; MARTIN, SCHRIER and

SMITH, Jr., 1972). Cardiomegaly and cardiac decompensat ion, however, are rarely

due to an ar ter iovenous anomaly in adults (BERNSMEIER and SlEMONS, 1952; GOLD,

RANSOHOFF and CARTER, 1964; WALLACE, NASHOLD and SLEWKA, 1965; PAYNE, SODER-

BLOM, LOBSTEIN, HULL and MULLINS, 1972; LINDSTEDT, 1972). According to BERNS-

MEIER and SIEMONS (1952), the effect of an ar ter iovenous anomaly on heart and

circulat ion depends on the diameter of the ar ter iovenous anastomosis and the dura t ion

of the anomaly. Cardiac decompensa t ion has been described frequently in children

* From the Departments of Neurology and Clinical Neurophysiology, St. Elisabeth Hospital, Tilburg, The Netherlands.

Clin. Neurol. Neurosurg., Vol. 79-1

30

and especially in neonates with an arteriovenous anomaly which opens up into the great cerebral vein (SILVERMAN, BRECKX, CRAIG and NADAS, 1955; POLLOCK and LASLETT, 1958; HOOK, WERK6 and 6HRBERG, 1958; GLATT and ROWE, 1960; and many others). The steal of the arteriovenous anomaly reduces the circulatory pressure at the site of the carotid sinus and the baroreceptors of the aortic arch, and the result is a compensatory chronotropic (tachycardia) and inotropic (increased cardiac output) effect on the heart muscle (GOMEZ, WHITTEN, NOLKE, BERNSTEIN and MEYER, 1963; CRUVEILLER, HARPEY and LAFOURCADE, 1967; LAVOIE, GILBERT, and LAFONTAINE,

1972; and others). The increased cardiac output and the increase in total blood volume due to renal retention finally lead to the terminal stage of high output failure (BERNSMEIER and SIEMONS, 1953; LEVINE, JAMESON, NELLHAUS and GOLD, 1962). GLATT

and ROWE (1960) maintained that cardiac decompensation is observed more frequently in neonates because in these patients the output of each ventricle is increased to three times the prenatal value. This explains why the neonatal heart decompensates at the slightest overstrain (in this case as result of an intracranial arteriovenous anomaly).

At the site of the arteriovenous anomaly, an abrupt transition develops between the arterial high pressure system and the venous low pressure system, and this results in a significant decrease in vascular resistance and an increased blood supply (ARSEN1 and NASH, 1963; ROSENTHALL, 1968; SILL, TILSNER and BAUDITZ, 1969; SOLTI, SOLT~SZ and BODOR, 1972). The increased blood supply is partly caused by an increased diameter of afferent arteries, which show dilatation probably due to a nervous reflex (MORE, 1954; GEYER, 1968; RAZl, BELLER, GHIDONI, L1NHART, TALLEY and URBAN, 1970), and partly results from an increased mean flow velocity (fi) of the blood. Applying the law of Poiseuille (a basic law in flow theory but only applicable to the blood stream in a rigid tube), we find that:

r a Q = Ap x (1)

8 ~L

in which Q = flow (output); A p = pressure gradient between two points along the length of the tube; ~q ---- coefficient of viscosity; r = radius of the tube; L ---- length of the tube.

The output equals the mean flow velocity multiplied by the surface area, i.e.

Q = fi X ~r 2 (2)

Inserting (2) into (1) we find that:

r 2 fi = AP × (3)

8 ~ L

In other words: the mean flow velocity fi at the site of the arteriovenous anomaly is directly proportional to the length of the arteriovenous anomaly. At a larger distance

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from the arteriovenous anomaly the mean flow velocity is lower than that at the site itself; this is due to a negative influence of blood vessels which do not supply blood to the arteriovenous anomaly and therefore alter the rheological situation.

Doppler haematotachography can be used as a reliable method for approximately quantitative determination of the mean blood flow velocity 0 (MOL, 1973) (fig. I):

A F x c O------ (4)

2F x cos

in which fi ---- mean flow velocity; A F = mean difference between transmitted and received ultrasonic frequency (so-called frequency shift); c = velocity of the sound in the blood = 15 x l0 s m/sec; F = transmitted ultrasonic frequency; ~ = the angle between the ultrasound beam and the direction of blood flow.

_ A F . e u- ~ . - ~ ~

contact medium/skin ~ . c/vessel

/ / / / / / / / / / / / / //, 0!~.. . . o. ..... :. ~ . . ~ . . " ..~ : ~. . : : . : . " . . . " . . . ' - " : - :. . ' . . ' 0 ////////////////////////////////////// Fig. 1. Diagram of the Doppler principle.

In other words: if factors F and c are known and factor 8 is approximately known, then the mean flow velocity is directly proportional to frequency shift AF. Because angle 8 is only approximately known, this determination is only 'approximately quantitative'.

The intention of this Doppler study of the afferent and efferent vessels of an arteriovenous anomaly is to demonstrate that calculation of a partial feature (i.e. mean flow velocity fi) can be of diagnostic importance in the evaluation of a possible haemodynamic effect.

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PATIENTS, METHOD, CRITERIA

1. Patients

The patients examined were 9 males and 4 females ranging in age from 12 to 59 (average 33). Of these 13 patients, 6 were examined both before and after total neurosurgical extirpation of the arteriovenous anomaly. One of the 13 patients died, and a postmortem investigation was performed.

2. Doppler Haematotachography

For Doppler haematotachography we used the directional (direction-sensitive) apparatus of Parks Electronics, model 806 with a transmission frequency of 5.26 MHz. The haematotachogram was obtained via an EEG apparatus (type Elema- Sch6nander) by the method which MOL described in his thesis (1973).

3. Criteria. Explanation of the &dices

In each case the Doppler HTG was studied in combination with pertinent clinical findings, chest X-rays, cranial X-rays and an angiogram.

A. Clinical criteria Complaints of fatigue, exertional dyspnoea, malleolar oedema. At examination: venous congestion of jugular or temporal veins, determination of central venous pressure, blood pressure and pulse rate. Determination of presence or absence of a hyperdynamic circulation in the cervical region.

B. Radiological criteria 1 Chest X-ray (cardiomegaly?) and cranial X-ray (erosive bone lesions?) (AGEE and

GREER, 1967; FOtJRNmR, LMNE, C¢OLE, COUSIN, SOM1N and DUTILLEUX, 1970). 2 Serial angiography: position and dimensions of the arteriovenous anomaly;

afferent arteries, draining veins and their calibre; presence of early venous filling.

C. Doppler-haematotachographic criteria As a yardstick for normal values, we used the tables of maximum and minimum normal values according to age (pooled standard deviation) as described by MOL in his thesis (MOL, 1973).

1. Common carotid artery: Sc: systole; DIc: beginning of diastole; DIIc: end of Sc DIc

diastole; Dlc : systolic-diastolic index; DI-Ic : index related to diastolic velocity

ScR DIcR gradient; Sc-L : left-right comparison of systoles expressed in ~ ; DIcL : left-right

comparison of diastoles expressed in ~ .

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2. Ophthalmic artery: Velocity, direction of blood flow measured at the level of the supraorbital and/or supratrochlear branch of the ophthalmic artery. Verification by compression tests of the superficial temporal artery and, if necessary, of the facial artery. Left-right comparison (only approximately quantitative due to unknown angle ~). Qualitative aspects.

3. Vertebral artery: Rate, direction of blood flow and left-right comparison (only approximately quantitative; cf. ophthalmic artery).

4. Brachial artery: Flow velocity, left-right comparison and possible qualitative aspects.

Sc 5. - - : The ratio between the mean flow velocity in the common carotid artery and

Sb the one in the brachial artery.

6. Internal and external jugular veins: Evaluation of pulsations, if present, and the time relationship to the classical A-C-V-H curve of the jugular vein (HARTMAN, 1960) and to the R-peak of the ECG (Peak-to-Pulse-Foot Interval), taking into account the possibility of an arterial pulse wave conducted via the arteriovenous anomaly. For calculation of the margin within which a virtual pulse wave conducted via the arteriovenous anomaly should occur, the distance carotid artery - arteriovenous anomaly - jugular vein was calculated, and the margin was based on a possible pulse wave velocity variation of 3-8 m/sec.

RESULTS

I. The Doppler HTG in patients with an (operable or inoperable) arteriovenous anomaly (table I)

A preoperative Doppler HTG was obtained in 6 of the 13 patients examined.

A. Systolic HTG ampfitude of the common carotid artery (Sc) In 3 patients reliable registration of the systole was impossible, probably due to a technical flaw and to the hyperdynamic character of the carotid artery pulsations. In only 2 of the remaining 10 patients (nos. 8 and 9) the Sc values on the side of the anomaly had increased significant. Significant left-right differences were observed in only 3 of the 13 patients (nos. 4, 9 and 11).

B. Diastolic HTG amplitude of the common carotid artery (DIc) The number of patients with a pathologically increased DIc value was highly signifi- cant. With the exception of patient 11 (intracerebral haematoma), 8 of the remaining

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TABLE 1 Radiological versus Dopp le rhaemato tachograph ica l da ta in patients with an intracranial arterio- venous mal format ion . + = deceased: patient 7. P T P F I = Peak - To - Pulse - Foot - Interval. C = C - wave in the venous tracing. A = A - wave in the venous tracing. V = V - wave in the venous tracing. X = Pulse wave, possibly caused by the anomaly .

Pat ient Posi t ion o f the A-V Size Main arterial Main venous dra in Early Con Sex / age a n o m a l y supply away venous Right

filling

1. BA 8' Pa ramed ian part r ight Right Internal Superior 44 yr. f rontal lobe 12 × 9 x 10 cm Carot id Artery Sagittal Sinus ÷ ÷ ScR

D I c R

2. BE 3' Pa ramed ian part left 2.5 x 2 x 3 cm Right and left Transverse Sinus 59 yr. f rontal lobe Anter ior Cerebral Grea t Anas tomo t i c ScR

Artery Vein o f Tro lard ÷ D I c R

3. BR ~ On the base o f skull Very small Right and left U n k n o w n 39 yr. Internal Carot id - - ScR

Artery. DIcR

4. E ~ Left tempora l lobe 5 x 2 x 3 cm Left Middle U n k n o w n 54 yr. (basal du ra mater) Meningeal Ar tery ScR

D I c R

5. H A ~ Pa ramed ian part r ight Right and left Grea t Vein o f 16 yr. parietal and occipital 5 x 4.5 x 3 cm Ant . Cerebral Galen ScR

lobe Artery. Right Superior Sagit. ÷ Post. Cerebr. A. Sinus D I c R

6. H E 8' Mesencephal ic Right Int. Car. Grea t Vein o f 17 yr. in the midline 7.5 x 6 x 5.5 cm Artery Galen ScR

Vertebral A. + D I c R

7. H E Y c~ Tha lamomesence - Right and left Great Vein o f 18 yr. phalic above the 6.5 x 5.5 x 4 cm Int. Carot id A. Galen ScR

+ ten tor ium cerebelli Vertebral A. Transverse Sinus + ÷ D I c R

8. H O ~' Right occipital lobe Right Post. Superior 27 yr. 2.5 x 2 x 2 cm Cerebral Artery Sagittal ScR

Sinus + D I c R

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I Carotid Artery Left/right Ratio Ophthal PTPFl-range Pulse-Waves Left mic jugular veins Int. Jug. vein Ext. Jug. Vein

artery Right Left Right Left

ScR - R r / 228-332 C C C - ScL Sc-L milliseconds

DIcR DIcL /~/zt DlcL 7 70 li > r e L f f X - - -

ScR 770 re>l i R N 156-250 ScL N ScL milliseconds

DIcR DIcL ,7",7' DIcL 5 70 r e> li L N

C C C C

X - X

ScR 670 re>l i R f f 137-200 ScL N ScL milliseconds

DIcR DIcL N li = re L

DIcL

C C

ScR 4470 l i> re R ~/" 183-266 ScL N Sc--L milliseconds

DIcR DIcL -"~-'~' DIcL 7370 l i> re L f f

C C A A

ScR ScL N

ScL DIcR

DIcL N DIcL

2070 l i> re R f f R 162-266 ms. C

197o l i> re L ~/ L 178-272 ms. X

C

ScR ScL N

ScL D I c R

DIcL ,S DIcL

6701i>re R N 156-250 milliseconds

570 re>l i L N

A CA

ScR ScL

ScL DIcR

DIcL N DIcL

R f f 156-250 milliseconds

670 l i> re L N

CA CA CA

ScR ScL N

ScL DIcR

DIcL N DIcL

7% re>l i R N R 172-266 ms. ACV -

3270 re>l i L N L 156-250 ms. - -

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Patient Position of the A-V Size Sex / age anomaly

Main arterial supply

Main venous drain Early Co~ away venous Right

filling

9. K ~ Right frontal lobe 3 >'. 2.5 x 2.5 cm 33 yr.

Right Anterior Superior Cerebral Artery Sagittal

Sinus + ÷ ScR

DIcR

10. L 3 Paramedian part of 12 yr. the left parietal lobe 6.5 × 4.5 x 2.5 cm

Left Anterior Superior Cerebral Artery Sagittal

Sinus + + + ScR

DIcR

11. M c~ Left temporal lobe 41 yr. ( + intracerebral 4 x 3 × 2 cm

hematoma!)

Left Middle Superior Cerebral Artery Sagittal

Sinus + +

ScR

DIcR

12. V ~' Left frontal and 43 yr. parietal lobe 3.5 x 3 × 2 cm

(convexity)

Left Middle Superior Cerebral Artery Sagittal

Sinus

ScR +

DIcR

13. VER ~ Paramedian part left 30 yr. temporal and parietal Unknown

lobe (medium size)

Left and right Superior Sagit. Internal Carotid Sinus (megalocarotis R) Great Vein of Galen

? ScR

DIcR

12 pat ients showed a significantly increased dias tol ic flow veloci ty curve, which

was b i la tera l in 6 and uni la tera l on the side of the a n o m a l y in 2 pat ients (nos. 4 and 9).

In 3 pat ients (nos. 4, 8 and 9), a left-r ight difference o f over 30 % co r re sponded with

the local iza t ion of the a r te r iovenous anomaly . The remain ing lef t-r ight differences

were no t significant.

C. Ophthalmic artery Al though the D o p p l e r H T G of the branches o f the oph tha lmic ar te ry canno t be

regarded as s t ra igh t forward quant i ta t ive , the H T G showed a significant b i la te ra l

decrease in 7 o f the 13 pat ients and an uni la tera l decrease in 3 o f the 13 pat ients

(cor responding with the side of the anoma ly in 2). In view of the increased flow

veloci ty in the caro t id ar tery, this low veloci ty of flow can be regarded as a s t r iking

finding.

D. Vertebral artery and brachial artery N o s ignif icant ly deviant results were obta ined .

E. Internal and external jugular vein The D o p p l e r H T G of the in ternal and external j ugu l a r vein showed marked inter-

individual var ia t ions . Of the classical A-C-V-H pat te rn as expression of pressure

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m Carotid Artery Left/right Ratio Ophthal PTPFI-range Pulse-Waves left m ic jugular veins Int. Jug. vein Ext. Jug. Vein

artery Right Left Right Left

ScR 4 4 ~ re> l i R ~/" 162-266 C - - - ScL N ScL milliseconds

DIcR /~ DIcL N 4570 re> l i L ~/ - X - -

DIcL

ScR 970 re> l i R ~/ 162-266 - - - ScL N ScL milliseconds

DIcR /~ DIcL /~'Tt DIcL 5 70 l i> re L / / XX XX XX

ScR 4570 re> l i R ~/ 178-282 ScL V / ScL milliseconds

DIcR DIcL ~/" DIcL 2270 re> l i L z /

C C - C

ScR SfL N Sc~ 3701i>re R N R 145-249 ms. - - - -

DIcR DIcL S / n ' DIcL re = li L ~/ L 162-266 ms. - X - X

ScR SoL - - R - 156-250 ms. - - - -

ScL DIcR

DIcL / r S DIcL 1070 re> l i L ~-/ X X - X

v a r i a t i o n s in the r igh t a t r i u m a n d pu l s a t i ons o f the n e a r b y ca ro t id ar tery , on ly the

C - w a v e was as a rule read i ly r ecogn i sab le , a l t h o u g h s o m e cases a l so s h o w e d a d i s t inc t

A - w a v e . C - w a v e s were o b s e r v e d in 10 o f the 13 pa t i en t s e x a m i n e d . W i t h i n the

i nd iv idua l ly ca l cu l a t ed m a r g i n o f t ime in wh ich a c a ro t i d pulse w a v e re tu rns to the

j u g u l a r ve in v ia the a r t e r i o v e n o u s a n o m a l y , 7 o f the 13 pa t i en t s s h o w e d in a t leas t

o n e j u g u l a r ve in pu l se waves wh ich were n o t i m m e d i a t e l y i n t e rp r e t ab l e as e i the r

C - w a v e o r V-wave . W e r ega rd these waves ( ind ica ted by X in t ab le 1) as poss ib le

a r te r i a l pu lse waves c o n d u c t e d v ia the a r t e r i o v e n o u s a n o m a l y .

2. The Doppler HTG before and after operation in patients with an arteriovenous anomaly ( table 2, f igure 2)

I n pa t i en t 5 ( table 2), all p r e o p e r a t i v e f low ve loc i ty va lues s h o w e d an u n e x p e c t e d

s igni f icant decrease . D u r i n g the o p e r a t i o n , a la rge i n t r ace r eb ra l h a e m a t o m a o f the

left h e m i s p h e r e was ex t i rpa t ed in a d d i t i o n to the a r t e r i o v e n o u s a n o m a l y . A f t e r the

Sc o p e r a t i o n all f low ve loc i ty va lues were n o r m a l i z e d . T h e - - r a t io s h o w e d an u n m i s t a k -

Sb

able increase.

A p a r t f r o m the a b o v e - m e n t i o n e d pa t ien t , the r e m a i n i n g 5 pa t i en t s all s h o w e d a

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TABLE 2. Comparative Doppler mean velocity values before and after operation.

Patient Main arterial Common carotid artery Sex/age supply Right Left

Before After Before After Comments

1. BE ~' Right and left ScR 29 24 ScL 29 20 59 yr. Anterior

Cerebr. DIcR 18.5 12.5 DIcL 19 8.5

Artery Dlc Dlc DII~ R 1.54 1.13 ~ L 1.26 i.30

Sc Sc ~--R 0.9 0.77 sb-L 0.9 0.62

C-waves and anomalywaves disappeared

2. HA ~ Right and left ScR 35 41 ScL 43 32.5 ' 6 yr. Anterior

Cerebral A. DIcR 16 15 DIcL 19.5 13

Right Post. Dlc DIc Cerebr. A. - - R 1.23 1.57 - - L 1.21 1.18

Dllc Dl lc

Sc Sc ~ - R 1.34 1.05 ~b-L 1.34 0.72

Disappeared anomab pulse- wave Right Int. Jug. Vein

3. K ~' Right ScR 41 21 ScL 26 23 33 yr. Anterior

Cerebral DIcR 19 12 DIcL 12 10

Artery Dlc Dlc - - R !.46 1.2 - - - L 1.2 1.25 DIIc Dl lc

Sc Sc g-~-R 1.02 0.67 ~ - L 0.61 0.76

Disappeared anomalypulse- wave Left Int. Jug. Vein

4. L ~' Left ScR 44 33 ScL 40 36 12 yr. Anterior

Cerebral DIcR 20 17 DIcL 21 15

Artery Dlc Dlc DI I~R 1, I 1 1.30 D--~--c L 1.90 1.30

Sc Sc ~ - R 1.18 1.13 ~ - L 1.02 1.16

Disappeared anomaly pulsewaves C-waves present

5, M c~ Left ScR 17.5 33 ScL I1 25 41 yr. Middle

Cerebral DIcR 10 16 DIcL 8 12

Artery Dlc Dlc (Intracerebral D~-~-c R I. 17 1.18 D~cc L 1.23 1.2 Hematoma !)

Sc Sc ~ - R 0.40 0.83 g-b-L 0.29 0.80

C-waves present

6. V ~' Left ScR 31 21 ScL 32 21 43 yr. Middle

Cerebral DIcR 18 11 DIcL 18 11

Artery Dlc DIc - - R 1.12 1.22 - - L 1.28 1.37 Dlic Dl lc

Sc Sc ~ - R 1.34 1.05 ~ - L 1.39 1.10

Disappeared anomaly pulsewaves C-waves present

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Angiogram of a patient (pt. L., nr ~4, table 2) with a left-sided A-V malformation.

fig. 2

postoperative diastolic flow velocity (DIc) which was significantly decreased on both sides as compared with preoperative findings. In 3 of the 5 patients (nos. 1, 3 and 4), the greatest difference between preoperative and postoperative diastolic flow was found on the side of the anomaly. In patient 2, the greatest difference between pre- operative and postoperative DIc was found on the contralateral side (dual supply by both anterior cerebral arteries). In patient 6, finally, the difference between pre-

40

R i g h t Common Carotid A r t e r y

B e f o r e

B - c h a n n e l

4 4 2O

A f t e r

i

33 17

L e f t Common C a r o t i d A r t e r y

B e f o P e

i • I

4 0 21

After

I

i

r;Z_ 36 15

Fig. 2b Common carotid artery haematotachographic pattern in the same patient, before and after e~tirpation. Note the diastolic elevated mean velocity value of the left carotid artery before operation.

operative and postoperative DIc, although significant, was the same on the left as on the right.

In 4 of the 5 patients the systolic flow velocity (Sc) was decreased on both sides after the operation. In 1 patient (no. 2) the Sc value was decreased on one side and increased on the other.

DIc The study of the index - - before and after operation yielded no relevant results.

DIIc Sc

The i n d e x - as expression of the ratio between the flow velocity in the common Sb

carotid artery and that in the brachial artery showed a bilateral decrease in 3 and a unilateral decrease in 2 patients (due to the reduced flow velocity in the carotid artery after extirpation of the arteriovenous anomaly).

The abnormal pulse waves in the jugular vein described before operation in 5 patients as deviant from the classical A-C-V-H pattern, disappeared after operation in each of these patients.

LITERATURE

Doppler haematotachography in intracranial as well as extracranial arteriovenous anomalies

Doppler haematotachography was initially used to localize afferent vessels of arterio- venous anomalies in the extremities (BINGHAM and LICHTI, 1970; STEPHENSON and LICHTI, 1971; LICHTI and ERICKSON, 1974) and peroperatively in a case of temporal extracranial arteriovenous anomaly (KEITZER and LICHTI, 1971). Others (BARSOTTI

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POURCELOT, GRECO, PLANIOL, KINIFFO and CASTELLANI, 1972) described the Doppler curve in an arteriovenous anomaly of the femoral artery. In arteriovenous anomalies of the legs, one author (PARTSCH 1974) registered Doppler-haematotachographic pulsations in the femoral vein; he assumed that the venous pulsations could originate

from the anomaly as well as from the nearby femoral artery.

PLANIOL (1972) mentioned one patient with an intracranial arteriovenous anomaly in whom the systolic and diastolic flow in the carotid artery had increased, while in the homolateral ophthalmic artery, it had decreased. In his thesis on the Doppler H T G in cerebral circulatory disorders, MOL (1973) mentioned 3 patients with an intracranial arteriovenous anomaly, which in one case was combined with occlusion of the homolateral internal carotid artery and in two cases with a pathological vascular convolution in the area of the ophthalmic artery.

DISCUSSION

The diastolic H T G amplitudes in particular are most consistent with the notion that - on the basis of the law of Poiseuille - the mean flow velocity fl should increase in arteriovenous anomalies. This confirms the theory of POURCELOT (1975) that the exceptionally high diastolic flow in the internal carotid artery (as compared with other arteries) must be ascribed to a low tissue pressure in the brain, with consequently low vascular resistance. The fact that the systolic and diastolic flow velocity is often bilaterally increased in the presence of an arteriovenous anomaly localized in one hemisphere, can only be an expression of a wellfunctioning circle of Willis or of a dual blood supply to the anomaly, chiefly by the anterior cerebral arteries. In one patient (no. 11, table 1) the cerebral resistance evidently exceeded the 'suction force' of the arteriovenous communications, as a result of a complicating space-occupying process. In this patient a classical arteriovenous anomaly was combined with an extensive homolateral intracerebral haematoma. After drainage of this haematoma the H T G

values returned to normal. Although a quantitative evaluation of the H T G amplitudes of the ophthalmic

arteries seems hardly justifiable, the very low mean flow velocity can be an expression of a relative steal in favour of the arteriovenous anomaly at the site of the carotid

siphon. The pulsations of unknown origin described in the internal and external jugular

veins fell within the calculated margin of time in which a hypothetical arterial pulse wave returns to the jugular vein via the arteriovenous anomaly. In the case of an arteriovenous end-to-end anastomosis with dilatated afferent and efferent vessels, the wave resistance Rw can be significantly reduced due to an increase in the dia- meter of the vessel at the level of the arteriovenous shunt (BORGHGRAEF 1968). As a result, the decrease in amplitude of a pulse wave, which increases with an increasing distance from the heart, can be so small that a few arterial pulsations of low amplitude can still enter the draining veins (HARDUNG 1962). Pulsations in the jugular veins in

42

patients with an intracranial A-V anomaly are described before (POTTER, 1955; SCHWARZ, KUCZERA and TENNSTEDT, 1969; T1NGAUD, VIDEAU, MASSE, MAGENDIE,

BOISSIERAS and MAYEUX, 1970). Complex factors such as the flow rate at the level of the anomaly and wave rebound are the cause of the marked individual variations in the shape of this pulse wave. These factors, together with the diameter of the arteriovenous anastomosis, determine whether or not an arterial pulse wave appears in the jugular veins. Conduction of an arterial pulse wave via the arteriovenous anomaly seems theoretically possible, and the pulsations registered (X in table 1) should be considered in this light. It was therefore all the more surprising that these pulsations could no longer be registered once patients had undergone an operation. Another striking finding was the dilatation of the temporal veins in patients with pulsations in the external jugular vein (POULIAS, COSTEAS and KOUR|AS, 1969; TAKAHASHI and OHTA, 1970).

CONCLUSION

In patients with an intracranial arteriovenous anomaly, a combined Doppler haema- totachogram of the common carotid, ophthalmic, vertebral and brachial arteries and the internal and external jugular veins is a convenient and useful means to evaluate the haemodynamic effect of the arteriovenous shunt on the basis of the mean flow velocity curves. The most useful parameters are, in the order of their importance: the significant increase in absolute protodiastolic (DIc)and systolic (Sc)flow velocity in the common carotic artery, the decreased flow velocity in the ophthalmic artery (semi-quantitative) and, secondarily, the ratio between the flow velocity in the carotid (sc) and that in the brachialartery S~ and possibly also the diastolic flow velocity

profile \ ~ c J '

Abnormal pulsations in the jugular veins - if they occur within the time theoretically required for an arterial pulse wave to return to the jugular vein - can give a supple- mentary impression of the size of the arteriovenous anastomosis. However, we have no certainty about the authenticity of these abnormal pulsations in the jugular veins.

Of course Doppler haematotachography - as a physiological method of investiga- tion - does not enable us to establish the morphological diagnosis ~intracranial arterio- venous anomaly'. However, in cases in which abnormally high flow velocity ampli- tudes are an incidental finding, the Doppler HTG can give an indication of the possible presence of an arteriovenous anomaly.

ACKNOWLEDGEMENTS

I wish to thank Dr. B. P. M. Schulte, for his advice and the neurologists J. H. van Luijk, A. C. M. Leyten, C. W. G. M. Frenken and the neurosurgeons Dr. M. P. A. M. de Grood, K. T. A. Lie, D. Wijnalda, Dr. H. F. H. G. Defesche for their kindness in allowing me to investigate subjects in their care.

43

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