Decrease in Pulsatile Flow in the Anterior Cerebral Arteries in Infantile Hydrocephalus

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Decrease

in Pulsatile

Flow

in the Anterior

Cerebral

Arteries

in Infantile

Hydrocephalus

Alan

Hill, MD,

PhD,

and Joseph

J. Volpe,

MD

From the Departments of Pediatrics, Neurology, and Biological Chemistry, Washington University School of Medicine, St Louis

ABSTRACT.

The effect ofventriculomegaly with or

with-out elevated intracranial pressure (ICP) on pulsatile flow

in the anterior cerebral artery has been studied by a

noninvasive Doppler technique in 11 infants with

hydro-cephalus. The cause of hydrocephalus was

intraventric-ulax hemorrhage in nine infants, Arnold-Chiari

malfor-mation in one, and bacterial meningitis in one. The

pul-satility index (P1) (inversely related to pulsatile flow) was calculated from the systolic and diastolic amplitudes of

flow in the anterior cerebral artery. All 11 patients with elevated P1 had marked ventriculomegaly, and all but

two had raised ICP. Four patients with massive ventri-culomegaly and elevated ICP had maximal P1 (ie, 1.00).

The finding of elevated P1 with ventriculomegaly and

normal ICP, observed in two patients, suggested that

ventriculomegaly is a more critical factor than ICP in the

pathogenesis of the impaired flow. Treatment of

ventri-culomegaly in seven patients resulted in a decrease in P1.

Of the four untreated patients, three died and one was not available for further study. Compromised flow in the anterior cerebral artery may be a sensitive barometer of

impending ischemic injury with evolving ventriculome-galy, particularly following intraventricular hemorrhage.

The P1 may be a valuable parameter for the study of the mechanism of brain injury and for determination of

op-timal timing of corrective intervention. Pediatrics 69:4-7, 1982; hydrocephalus, cerebral blood flow, pulsatility in. dex.

Hydrocephalus in early infancy is caused by a variety of pathologic processes which include: intra-ventricular hemorrhage (IVH) in the premature

infant, neonatal bacterial meningitis, and

develop-mental disturbances, of which mernngomyelocele

with an Arnold-Chiari malformation is the most common. Following IVH, the incidence of hydro-cephalus is related to the severity of hemorrhage and approaches 100% in severe lesions.’

Received for publication March 19, 1981; accepted April 24, 1981. Reprint requests to (J.J.V.) Washington University School of

Medicine, P0 Box 14871, St Louis, MO 63178.

PEDIATRICS (ISSN 0031 4005). Copyright © 1982 by the

American Academy of Pediatrics.

Although brain injury is related in part to the underlying disorder responsible for the

hydroceph-alus, ventricular dilation per se may cause cerebral

injury. Such injury may be due to direct compres-sion2 or to vascular compromise.5

The noninvasive measurement of pulsatile flow in the anterior cerebral artery (ACA) is possible

with a transcutaneous Doppler technique in infants

who have an open anterior fontanel.6 The measure-ment may be performed at the bedside without

disturbing the infant. This report assesses the effect of ventriculomegaly with or without increased in-tracranial pressure (ICP) on pulsatile flow in the ACA of young infants and addresses the issue of the mechanism of brain injury in hydrocephalus.

MATERIALS

AND

METHODS

Pulsatile flow was measured with a bidirectional Medasomcs Versatone D-9 Doppler flowmeter with a two-channel R2 recorder. A 5-MHz transducer (P94) was placed over the anterior fontanel and

directed toward each ACA independently. Strong

signals of advancing arterial pulsations were re-corded and the mean systolic and diastolic ampli-tudes of flow were measured relative to an internal

1 KHz standard. A pulsatility index (P1) was

cal-culated for each ACA from the formula (S

-

D)/S,

as adapted from Pourcelot’s index of resistance7 by Bada et al,6 where S is the mean systolic amplitude of flow, and

D,

the mean diastolic amplitude of flow.

This index, rather than absolute values of blood flow velocity, was used to minimize errors due to probe placement. The P1 measurements of each

ACA were in close agreement (<5% difference), and

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S Each P1 value is mean of at least two separate

mea-surements that varied by less than 5%.

Figure. Computed tomography scans show marked

ventricular dilation with maximal pulsatility index in patients 1 (left) and 2 (right).

ARTICLES

5

47 patients without IVH who ranged in gestational age from 32 to 40 weeks.

IcP was measured with the Ladd ICP monitor

and a fiberoptic sensor applied to the skin over the anterior fontanel.’#{176} This noninvasive technique provides excellent correlation with concomitant measurements of ICP obtained at simultaneous lumbar puncture or ventricular tap, when the in-strument is applied to the anterior fontanel accord-ing to a specific technique.”

Eleven infants with ventriculomegaly and in-creased P1 were studied; hydrocephalus was caused by intraventricular hemorrhage in nine patients,

Arnold-Chiari malformation in one patient, and

bacterial meningitis in one. Six

patients

with post-hemorrhagic hydrocephalus were followed from

birth with serial measurements of ICP and

ventric-ular size. In two of the six patients, P1 measure-ments were made at least weekly from birth (pa-tients 5 and 6), and in the other four (patients 8, 9, 10, and 11), P1 was measured for the first time after marked ventriculomegaly had developed. The

re-maining three patients with posthemorrhagic hy-drocephalus, as well as the patients with postmen-ingitic hydrocephalus and Arnold-Chiari malfor-mation had marked ventriculomegaly at the time of referral. At the time of all measurements of P1, the blood pressure was stable and within the normal range.

RESULTS

The mean values for P1 and ICP and the age at time of study in the 11 patients are shown in Table 1. The range of P1 in untreated hydrocephalus was

0.84 to 1.00 and the range of ICP was 11 to 30 cm!

H2O (normal sli cm/H2O).

The maximal P1 of 1.00 in four patients indicates an absence of advancing blood flow in the ACA

during diastole (ie, when D =

0

in the equation [S

-

D]/S). In each of these four patients the ICP was elevated significantly, and there was massive yen-tricular dilation, the most severe of any of the patients studied. The computed tomography (CT)

scans of two of these patients are shown in the Figure. By using the Student’s t test, the P1 (mean

± SEM, 0.91 ± 0.02) of patients with ventriculo-megaly was significantly greater than the P1 in normal infants (0.66 ± 0.01)

(P

< .001).

The evolution of ventriculomegaly, P1, and ICP

is exemplified by patients 5 and 6. In patient 5, the P1 increased from 0.60 before ventricular dilation to

0.84 after ventricular dilation and the ICP increased from 8 to 15 cm H2O. In patient 6, the P1 increased from 0.60 to 0.87 and the ICP from 11 to 18. In each case, there was a decrease in both P1 and ICP after

ventricular drainage (Table 2).

Elevated P1 with ventriculomegaly was also ob-served

in

the absence of elevated ICP. This

state

of normal pressure hydrocephalus’2 is exemplified by patients 10 and 11 in Table 1.

Effective treatment of ventriculomegaly resulted uniformly in a decrease in P1 (Table 2). Table 2 shows the mean values for P1 and ICP and the age at time of study in the seven patients with posthe-morrhagic hydrocephalus in whom ventricular drainage was performed by ventriculostomy or by ventriculoperitoneal shunt. For each case this de-crease was statistically significant, based on the Student’s t test for paired data

(P

< .001).

Of

the four patients in whom ventricular drainage was not

performed,

three died and one was not available for

further study.

DISCUSSION

The data presented in this report demonstrate an inverse relationship between marked ventriculo-megaly and pulsatile flow in the ACA. Thus, all of the patients with marked ventriculomegaly had

el-TABLE

I. Pulsatility Ind

(ICP), and Age at Time o

Untreated Hydrocephalus

ex (P1), Intracr f Study in 11

anial Pressure Patients with

Patient No. P1 ICP (cm HO) Age (days)

1 1.00 2 1.00 3 1.00 4 1.00 5 0.84 6 0.87 7 0.88 8 0.87 9 0.85 10 0.90 11 0.85 16 15 18 30 15 18 15 16 19 11 11 25 160 180 44 19 54 130 36 44 13 39

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TABLE 2. Pulsatility Index, Intracranial Pressure, and

Age at Time of Study in Seven Patients with

Hydroceph-alus Before and After Treatment

Patient No. P1 ICP (cm H2O) Age (days)

3 1.00 0.72 18 8 180 185 4 1.00 0.70 30 9 44 90 5 0.84 0.70 15 8 19 33 6 0.87 0.75 18 8 54 150 8 0.87 0.75 16 7 36 47 9 0.85 0.65 19 7 44 65 10 0.90 0.60 11 7 13 26

CEach P1 value is mean of at least two

surements that varied by less than 5%.

separate

mea-evated P1. This elevation in P1 occurred because of a sharp decrease or, in four patients, a total cessa-tion of blood flow in the ACA during diastole. Because the cerebral circulation, unlike the periph-eral circulation, has an important diastolic compo-nent to blood flow, our data indicate that this

important component is compromised with ventri-culomegaly. (In the absence of data relating direct

measurements of cerebral blood flow to P1, this

effect of ventriculomegaly cannot be quantified more precisely.) In addition, our observation that lesser degrees of ventricular dilation, not uncom-mon after IVH, are not associated with abnormal P1 (unpublished data) suggests that there is a cnt-ical ventricular size beyond which there may be compromise of flow in the ACA. More data are needed to define this size in a more quantitative

fashion.

The relative importance of ventriculomegaly vs increased ICP in the genesis of the elevated P1 is

difficult to define precisely. Most of our patients exhibited elevated ICP as well as marked

ventri-culomegaly. Several facts suggest that ventriculo-megaly is the more critical factor: (1) two of our patients with elevated P1 had normal ICP; (2) the four patients with the most marked

ventriculome-galy had the most markedly elevated P1; and (3) studies of normal pressure hydrocephalus in adult

patients demonstrate diminished flow in the ACA and improvement in flow after a decrease in yen-tricular size was effected by shunting.’3

The mechanism by which ventriculomegaly

might lead to diminished blood flow in the ACA

most probably is related to a compromise of these arteries by stretching or compression by enlarged ventricles. The aforementioned data from the study of adults with normal pressure hydrocephalus

sup-port this notion. Experimental studies also demon-strate an adverse effect of ventriculomegaly on cere-bral blood flow, apparently via displacement, defor-mation, stretching and a decrease in caliber of cere-bral arteries, and a dilation of cerebral vessels after ventricular drainage.5

The finding of compromised blood flow in the ACA may have implications for the genesis of brain

injury in infants with hydrocephalus and may be of value in determining the necessity for surgical in-tervention in such patients. Specifically, the clinical findings of lower limb spasticity in infants with hydrocephalus may be related in part to the effects

of ischemia in the distribution of the ACA, in ad-dition to the well recognized effect of compression by dilated ventricles of the nerve fiber tracts which subserve lower limb function. If cerebral blood flow

to other areas of the brain is similarly compromised, it is possible that prolonged partial ischemia may contribute to other abnormal neurologic findings in infantile hydrocephalus.

Comprised flow in the ACA may prove to be a sensitive barometer of impending ischemic injury

with evolving ventriculomegaly after IVH. Thus, determination of P1 may prove valuable in defining one mechanism for the genesis of brain injury with infantile hydrocephalus and for determining opti-mal timing for corrective intervention.

ACKNOWLEDGMENT

Dr Hill is supported by a Fellowship from The Hospital for Sick Children Foundation, Toronto, Canada.

REFERENCES

1. Volpe JJ: Neurology of the Newborn Philadelphia, WB

Saunders Co, 1981

2. Weller RO, Schulman K: Infantile hydrocephalus: Clinical, histological and ultrastructural study of brain damage J

Neurosurg 36:255, 1972

3. Rubin RC, Hochwald GM, Teill M, et al: Hydrocephalus. I.

Histological and ultrastructural changes in the pre-shunted cortical mantle. Surg Neurol 5:109, 1976

4. Fishman RA, Greer M: Experimental obstructive hydro. cephalus: Changes in the cerebrum Arch Neurol 8:156, 1963 5. Wozniak M, McLane DG, Raimondi AJ: Micro- and

macro-vascular changes as the direct cause of congenital murine

hydrocephalus. J Neurosurg 43:535, 1975

6. Bada HS, Hajjar W, Chua C, et al: Noninvasive diagnosis of neonatal asphyxia and intraventricular hemorrhage by

Dop-pier ultrasound. J Pediat 95:775, 1979

7. Pourcelot L: Applications cliniques de l’examen Doppler

transcutane, in P#{233}ronneau P (ed): V#{233}locinietre ultrasonone

Doppler, Paris, Institut National de la Sante et de la

Re-cherche M#{233}dicale1975, p 213

8. Vidyasagar P, Raju TNK: A simple noninvasive technique

of measuring intracranial pressure in the newborn. Pediat-rics 59:957, 1977

9. Vidyasagar D, Raju TNK, Chiang J: Clinical significance of monitoring anterior fontanelle pressure (AFP) in sick

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10. Philip AGS: Noninvasive monitoring of intracranial pres- newborn. Pediatrics 68:623, 1981

sure. A new approach for neonatal clinical pharmacology. 13. Mathew NT, Hartmann A, Meyer JS, et al: The importance

Clin Perinatol 6:123, 1979 of “CSF pressure-regional cerebral blood flow

dysautoregu-11. Hill A, Volpe JJ: Measurement ofintracranial pressure using lation” in the pathogenesis of normal pressure

hydrocepha-the Ladd intracranial pressure monitor. J Pediatr 98:974, ins, in Lundberg N, Ponten V, Brock M (eds): Intracranial

1981 Pressure Two: Proceedings. New York, Springer-Verlag,

12. Hill A, Volpe JJ: Normal pressure hydrocephaius in the 1975, pp 145-149

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OF PEDIATRICS

RESIDENCY

FELLOWSHIPS

STIPULATIONS

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1982;69;4

Pediatrics

Alan Hill and Joseph J. Volpe

Hydrocephalus