Pediatric Cranial Doppler Sonography in
Children: Non-Sickle Cell Applications
Amy M. Soetaert, DO,a,d Lisa H. Lowe, MD,b,d and Christopher Formen, MDc
This article presents an overview of transcranial Doppler,
well known for its use as a screening tool in children with
sickle cell disease. However, there are many other pediatric
applications in which cranial Doppler ultrasound can sup-
ply otherwise unavailable information regarding neurovas-
cular flow dynamics. Images illustrate examples of normal
anatomy and pathologic conditions that can be evaluated
with cranial Doppler ultrasound. Characteristic imaging
features of various pediatric applications of cranial Doppler
ultrasound are discussed and illustrated. This image pre-
sentation discusses cranial Doppler ultrasound technique
and normal findings and illustrates various pediatric disor-
ders including benign enlargement of the subarachnoid
space versus subdural hematomas, vasospasm, vasculitis,
venous sinus thrombosis, vein of Galen varix, hydroceph-
alus, hypoxic ischemic injury, traumatic brain injury, and
brain death.
In 1982, Aaslid and coworkers introduced transcranial
Doppler to evaluate cerebral blood flow.1 During the
examination, sonographers listened and viewed Dopp-
ler spectral tracings via the transtemporal fontanel at
particular depths from the transducer to identify and
interrogate major intracranial vessels. Nonimaging
transcranial Doppler was not popular with radiologists
and sonographers due to the lack of images, the lack of
training, and the lack of availability of nonimaging
machines at most imaging centers. Today, imaging
cranial Doppler ultrasound (through the anterior fon-
tanel or transcranially) is widely available using an 8-
From the aDepartment of Radiology, St. Luke’s Hospital, Kansas City,
MO; bDepartment of Radiology, Children’s Mercy Hospitals and Clinics,
Kansas City, MO; cDepartment of Radiology, North Kansas City Hospital,
Kansas City, MO; and dDepartment of Radiology, The University of
Missouri-Kansas City, Kansas City, MO.
Reprint requests: Lisa H. Lowe, MD, Department of Radiology, Children’s
Mercy Hospitals and Clinics, 2401 Gillham Road, Kansas City, MO 64152.
E-mail: lhlowe@cmh.edu.
Curr Probl Diagn Radiol 2009;38:218-227.
© 2009 Mosby, Inc. All rights reserved.
0363-0188/2009/$36.00 ⫹ 0
doi:10.1067/j.cpradiol.2008.05.004
218
to 5-MHz curved array transducer that allows simul-
taneous color and spectral Doppler interrogation of
vessels with direct visualization. The advantages of
neurovascular Doppler ultrasound include portability,
ease of repeating studies, low cost, and lack of need
for sedation or ionizing radiation. Doppler ultrasound
is well-known for its value in screening children with
sickle cell disease; however, there are many other
pediatric disorders where it is useful, which are dis-
cussed in this image presentation.2
Imaging Doppler Technique
Neurovascular structures can be evaluated transcrani-
ally (any age) or through open fontanels (infants only).
Calculations collected during the sonogram include
peak systolic velocity (PSV), end diastolic velocity,
resistive index (RI), time average mean velocity
(TAP), and pulsatility index. Ultrasound machine
manufacturers have used various abbreviations to
indicate time average maximum mean velocity; thus,
interchangeable abbreviations have appeared in the
literature including TAP, TAM, TAMX, and
TAMMX.3,4
When performing transcranial Doppler sonography,
angle correction is avoided because it may falsely
elevate velocity measurements by up to 20%.3,5,6
Further, normative data are widely available and well
established without angle correction. It is important to
note that TAP velocities tend to be 5 to 10% lower
with imaging versus nonimaging cranial Doppler.3,5
Normal Neurovascular Color and
Spectral Doppler Ultrasound
The vessels of the Circle of Willis can be routinely
evaluated with color and spectral Doppler ultrasound
(Fig 1). Other vessels that may be interrogated include
the distal internal carotid, basilar, vertebral, and oph-
Curr Probl Diagn Radiol, September/October 2009

FIG 1. Normal Circle of Willis in a male neonate with posthemor-
rhagic hydrocephalus. (A) Color Doppler cranial sonogram via the
left temporal approach demonstrates a normal patent circle of
Willis. MCA, middle cerebral artery; PCA, posterior cerebral
artery; ACA, anterior cerebral artery. (B) A normal arterial spectrum
from the left middle cerebral artery shows the quick systolic upstroke
(arrow), followed by a gradual decrease in cranial flow during
diastole (arrowhead). Calipers are in place for calculation of the
resistive index (RI).
thalmic arteries as well as the major venous sinuses
(Fig 2).
Resistive Index and Pulsatility Index
The usefulness of the RI and pulsatility indexes are
that they both minimize the affect of angulation. The
Curr Probl Diagn Radiol, September/October 2009
FIG 2. Normal sagittal Doppler ultrasound via the anterior fontanel in
a 2-month-old girl. (A) Doppler spectrum of the Vein of Galen (VOG)
illustrates the normal venous pattern of continuous flow with gentle
undulations (arrow). Small pulsations above baseline are from minimal
adjacent arterial flow. (B) Sagittal color Doppler image reveals the
normal color flow in the vein of Galen (arrowhead).
RI is defined as PSV ⫺ end diastolic velocity/PSV.
The normal RI value is age dependent, being highest
in the premature infant (0.77) and gradually decreas-
ing for a term infant (range: 0.65-0.75) to a normal
adult value by age 2 years (range: 0.43-0.58).7,8
Changes in the RI indicate alterations in intracranial
neurovascular flow dynamics, which may include
variations in blood volume, flow velocity, and vascular
resistance. An elevated RI is usually due to less
diastolic flow, which may or may not be due to
intracranial processes (Fig 3). Left to right cardiac,
liver, or brain shunts can cause elevation in intracra-
nial RI that will not correlate with intracranial pres-
219
FIG 3. Six-day-old infant with a patent ductus arteriosus. Cranial
Doppler spectrum of the middle cerebral artery obtained via the right
transtemporal fontanel shows brisk antegrade flow during systole
followed by rapid reversal of diastolic flow (arrow) related to runoff
through the patent ductus (left to right shunting). Before a neurovascular
cause for elevated RI can be presumed, it is essential to exclude a left
to right cardiac shunt. (Color version of figure is available online.)

sure. Without a left to right shunt, a RI greater than 1.0

indicates reversed diastolic flow. A low RI is due to
vasodilatation with a resultant relative increase in
diastolic flow, which may occur with loss of autoreg-
ulation or compensatory response to decreased perfu-
sion or hypoxia. In general, a low RI can be considered
a warning that the brain is at risk for injury.

Benign Enlargement of the

Subarachnoid Spaces versus
Subdural Hematoma
Developmentally normal children often have inciden-
tal macrocephaly between 6 months and 2 years of
age, termed benign enlarged subarachnoid spaces,
benign macrocrania, or external hydrocephalus. This
condition is thought to be due to transient hydroceph-
alus that may be related to immaturity of the arachnoid
granulations and/or a developmental mismatch of
relatively rapid calvarial growth compared with brain
growth.4 Infants are often imaged due to primary care
physicians’ concerns for clinically significant macro-
cephaly as a result of hydrocephalus or an intracranial
mass. Due to stretching of bridging veins that traverse
the abnormally broad subarachnoid spaces, children
with benign macrocrania are at a slight increased risk
FIG 4. Three-month-old male victim of nonaccidental head trauma with
subdural hematoma. (A) Coronal color Doppler sonogram demon-
strates bilateral arachnoid membranes (arrow) separating the superfi-
cial subdural space (which only contains rare crossing vessels) from the
deeper subarachnoid space (which contains numerous vessels). Note
crossing vessels in the subarachnoid space (arrowhead). (B) CT
confirms a small amount of hyperdense subdural hematoma anterior to
the right frontal lobe (arrow) that extends along the falx cerebri. Left
subdural hematoma seen on CT is not shown.
for subdural hemorrhage (Fig 4). While the mere
presence of subdural hemorrhage is nonspecific, it is
most common in the setting of nonaccidental trauma
and thus an abuse investigation is prudent.

220 Curr Probl Diagn Radiol, September/October 2009

Vasospasm
Vasospasm appears most often in the first 2 days post
subarachnoid hemorrhage. It typically peaks at around
2 weeks, followed by progressive resolution over the
subsequent 2 to 4 weeks. Before clinical symptoms of
ischemia, an abnormal increase in velocity predicts
vasospasm with a high level of sensitivity and is useful to
guide interventional and/or surgical therapy.2,9 Vaso-
spasm is significant, requiring therapy, if the velocity
increases by more than 50 cm/s per day or if the middle
cerebral artery velocity is more than 200 cm/s.10,11 It is
important that Doppler ultrasound findings be interpreted
in the context of clinical and laboratory data, such as
elevated intracranial pressure, reduced blood volume,
and peripheral vasoconstriction (Fig 5).9

Cerebral Vasculitis
Pediatric cerebral vasculitis is rare but should be sus-
pected in children presenting with symptoms of acute
stroke. Numerous causes (postinfectious, autoimmune,
idiopathic) of cerebral small-vessel vasculopathy have
been reported in children.12,13 Aggressive treatment is
aimed at preventing further progression of stroke or
additional stroke. Treatment may include aspirin, pred-
nisone, and/or cyclophosphamide. Unfortunately, the
only determinant of failed therapy is worsening of stroke
symptoms or recurrent stroke, which is why these chil-
dren must be monitored closely. While magnetic reso-
nance (MR) and catheter angiography are the imaging
gold standards, frequent reevaluation can be accomplished
most easily with cranial Doppler ultrasound (Fig 6).2,12

Venous Sinus Thrombosis

Venous sinus thrombosis (VST) is often the result of
dehydration, coagulopathy, and infection. Although
neonatal cranial Doppler ultrasound can detect loss of
flow in major venous structures, MR venography is the
imaging study of choice. Progression from VST to
venous infarct may be complicated by hemorrhage in FIG 5. Sixteen-year-old boy status post subarachnoid hemorrhage
25% of cases.14 The specific site of venous thrombosis with vasospasm. (A) Cranial Doppler ultrasound shows elevated peak
systolic velocity (PSV) in the left MCA of 289 cm/s (abnormal over 200
can be determined by the characteristic distribution. cm/s). (B) Axial CT image of the head reveals hyperattenuated
Specifically, thromboses of the sagittal sinus, internal material in the suprasellar and perimesencephalic cisterns (arrow),
cerebral veins/vein of Galen/straight sinus, and vein of indicating subarachnoid hemorrhage. (Color version of figure is
Labbe occur within the parasagittal, thalamic, and available online.)

temporal lobe, respectively2 (Fig 7). Treatment in-

cludes anticoagulation in older children and severe
thromboses, but is mostly supportive in infants.

Curr Probl Diagn Radiol, September/October 2009 221


FIG 6. Fifteen-year-old girl with acute stroke due to cerebral vasculitis.
(A) Left MCA Doppler spectrum via the right temporal approach shows
markedly elevated peak systolic velocity of 385 cm/s and turbulent
flow seen as increased echoes in the area under the curve. RI is
normal. (B) MR angiogram reveals decreased caliber of the irregular,
beaded left MCA (arrow). (Color version of figure is available online.)
Vein of Galen Malformation or Varix
Intracranial vascular lesions in infants can be interro-
gated with Doppler ultrasound and in some cases
establish a particular diagnosis. The clinical presenta-
tions of Vein of Galen varix in infants include hydro-
cephalus, high-output congestive heart failure, and/or
seizures. Much less often, older children may present
with venous hypertension and hemorrhage (Fig 8).
These malformations are usually treated with neuroint-
erventional embolization in the early infantile period.
Postprocedural evaluation of the varix, residual drain-
222
ing veins, and feeding vessels can also be accom-
plished with cranial Doppler ultrasound.15
Hydrocephalus
With ventricular enlargement due to rapidly progres-
sive hydrocephalus, an increase in RI may occur due
to decreased of diastolic flow secondary to elevated
intracranial pressure. In infants and children, an RI
exceeding 0.8 and 0.65 is abnormal, respectively.16,17
Baseline measurements are useful to distinguish be-
tween an overlap in normal and abnormal values.
Treated hydrocephalus may be assessed with serial
follow-up of the RI as needed (Fig 9). Another useful
technique in infants includes a significant change in RI
and TAP before and after fontanel compression in
children with altered cranial compliance due to hydro-
cephalus.18 A caveat is that the RI may be falsely
normal with cerebrospinal fluid leak, as in myelome-
ningocele.2
Hypoxic Ischemic Brain Injury
Loss of autoregulation (peripheral neurovascular va-
sodilatation) with resultant decreased RI can occur in
the setting of hypoxic ischemic brain injury (Fig 10).
A very low RI (⬍0.5) in the first 48 hours of neonatal
life has been strongly associated with a poor neuro-
logic outcome.19-21 After 48 hours, the RI generally
normalizes, indicating recovery of normal brain per-
fusion (Fig 11). However, if cerebral edema develops,
the RI may become elevated.
Traumatic Brain Injury
Cerebral blood flow dynamics are altered by traumatic
brain injury in several ways. First, after subarachnoid
hemorrhage, vasospasm may cause elevated cerebral
blood flow. Second, if severe injury leads to cerebral
edema, the elevated RI reflects increased intracranial
pressure.22 If the intracranial pressure exceeds mean
arterial pressure (RI ⬎ 1.0), then reversed diastolic
flow may be identified (Fig 12). Following a traumatic
brain injury, cranial Doppler sonography can be ap-
plied to determine the impact of therapy, includ-
ing hyperventilation.23 Normally, CO2 administra-
tion causes vasodilatation.24,25 With severe brain
injury, there is a lack of response to CO2, which is
associated with major morbidity and death.
Curr Probl Diagn Radiol, September/October 2009
FIG 7. Two-week-old male with seizures and hemorrhagic venous infarct secondary to venous sinus thrombosis. (A) Coronal sonogram
demonstrates bilateral thalamic hyperechogenicity (arrows), suggesting ischemia, infarct, and/or hemorrhage. (B) Sagittal color Doppler
sonogram shows lack of flow in the internal cerebral veins (arrowheads). (C) CT confirms abnormal hyperattenuated thalami due to venous
hemorrhage (arrows). (D) Sagittal T1-weighted MR image shows hyperintense blood occluding the internal cerebral veins, vein of Galen, and
sagittal sinus (arrows).

Brain Death inexpensive, and convenient method for evaluating the

Brain perfusion scintigraphy has been used to deter- presence of supratentorial cerebral perfusion, which
mine brain death but usually requires the unstable has been used to predict brain death with a high level
patient to be removed from the intensive care unit. of accuracy.26 Doppler ultrasound can be used to
Bedside cranial Doppler ultrasound adds a simple, prescreen brain perfusion and plan the appropriate

Curr Probl Diagn Radiol, September/October 2009 223

FIG 8. Newborn male with high-output congestive heart failure due to a Vein of Galen varix. (A) Coronal gray scale and (B) sagittal cranial
Doppler ultrasound images via the anterior fontanel demonstrate an anechoic structure in the midline at the tentorial incisura (arrows) with a venous
spectrum on Doppler interrogation. Ultrasound may also be used to assess for variable thrombus and feeding vessels, which were not present in
this case.

FIG 9. Four-week-old premature female with a full fontanel due to posthemorrhagic hydrocephalus. (A) Coronal grayscale image shows
ventriculomegaly with extensive retracting clot in left lateral ventricle (arrow). (B) Doppler ultrasound via the right transtemporal approach
demonstrates elevated RI of 0.92, consistent increased intracranial pressure. (C) Doppler spectrum after ventricular shunt placement demonstrates
a normal RI of 0.78. (Color version of figure is available online.)

time to perform brain scintigraphy. Patterns on Dopp- Conclusion

ler ultrasound most specific for brain death include
near total absence of forward flow or complete ab-
sence of flow and TAP of less than 10 cm/s over 30
minutes (Fig 13).2,16,26 A caveat is that Doppler
ultrasound should not be used in young infants to
determine brain death since it has not been 100%
reliable.16
In addition to screening sickle cell patients, cranial
Doppler ultrasound is an excellent adjunct study to
evaluate many pediatric conditions. Although com-
puted tomography and MR imaging are often the gold
standard, cranial Doppler ultrasound can provide valu-
able information in the appropriate clinical setting.

224 Curr Probl Diagn Radiol, September/October 2009

FIG 10. One-day-old term infant with profound hypoxic ischemic brain injury. (A) Coronal Doppler ultrasound via the anterior fontanel, including
a spectrum obtained from the left MCA demonstrates increased diastolic flow with a low RI of 0.61. (B) Axial CT image of the head obtained on
the following day reveals foci of hypoattenuation within the thalami (arrows) and diffuse loss of gray–white differentiation, indicating diffuse
cerebral edema compatible with profound hypoxic ischemic injury. (Color version of figure is available online.)

FIG 11. Three-day-old infant with prolonged labor and perinatal depression. (A) Coronal grayscale sonogram demonstrates focal hyperecho-
genicity in the left temporal lobe (arrows), consistent with an area of focal ischemia infarct and/or hematoma. (B) Doppler spectrum of the left MCA
obtained on the same day demonstrates a low RI of 0.57, indicating increased diastolic flow related to loss of autoregulation. (C) Doppler spectrum
obtained 4 days later shows normalization of the RI, which corresponded with the infant’s significant clinical improvement. (Color version of figure
is available online.)

Bedside cranial Doppler ultrasound can prove useful
when the patient is too unstable to be transported to the
radiology department or if contraindications prevent
computed tomographic contrast administration or MR
imaging. Specific conditions in which cranial Doppler
ultrasound can be applied include benign enlargement
of the subarachnoid space versus subdural hematoma,
vasospasm, vasculitis, venous sinus thrombosis, vein
of Galen varix, hydrocephalus, hypoxic ischemic in-
jury, traumatic brain injury, and brain death.

Curr Probl Diagn Radiol, September/October 2009 225

FIG 12. Fifteen-year-old male motor vehicle crash passenger with traumatic brain injury. (A) Left MCA Doppler spectrum via the right transtemporal
approach demonstrates dampened, rapid systolic upstroke and reversal of flow throughout diastole (arrow). (B) CT shows an occipital bone
fracture (arrowhead) and effacement of the basilar cisterns due to impending herniation and severe cerebral edema (white arrows). There is also
a subdural hematoma along the anterior falx (black arrow). (Color version of figure is available online.)

FIG 13. Brain death in a 7-year-old girl with fixed, dilated pupils after near drowning. (A) The Doppler ultrasound appearance of brain death
follows a predictable pattern beginning with a gradual progression from elevated RI (less diastolic flow or reversed diastolic flow and cerebral
edema) to gradual decline in systolic flow, until finally only small early systolic spikes are seen. This lack of effective brain flow throughout the
cardiac cycle indicates brain death. (B) Lateral static image from nuclear perfusion scan shows absent parenchymal brain activity, indicating
absence of brain perfusion.

226 Curr Probl Diagn Radiol, September/October 2009

 REFERENCES
1. Aaslid R, Markwalder TM, Nornes H. Noninvasive transcra-
nial Doppler ultrasound recording of flow velocity in basal
cerebral arteries. J Neurosurg 1982;57:769-74.
2. Bulas DI. Transcranial Doppler: Applications in pediatrics.
Appl Radiol 1999;28:7-15.
3. Bulas DI, Jones A, Seibert JJ, et al. Transcranial Doppler
(TCD) screening for stroke prevention in sickle cell anemia:
Pitfalls in technique variation. Pediatr Radiol 2000;30:733-8.
4. Lowe LH, Bulas DI. Transcranial Doppler imaging in
children: Sickle cell screening and beyond. Pediatr Radiol
2005;35:54-65.
5. Bulas D. Screening children for sickle cell vasculopathy:
Guidelines for transcranial Doppler evaluation. Pediatr Radiol
2005;35:235-41.
6. Krejza J, Mariak Z, Babikian VL. Importance of angle
correction in the measurement of blood flow velocity with
transcranial Doppler sonography. AJNR Am J Neuroradiol
2001;22:1743-7.
7. Allison JW, Faddis LA, Kinder DL, et al. Intracranial resistive
index (RI) values in normal term infants during the first day of
life. Pediatr Radiol 2000;30:618-20.
8. Yazici B, Erdogmus B, Tugay A. Cerebral blood flow mea-
surements of the extracranial carotid and vertebral arteries
with Doppler ultrasonography in healthy adults. Diagn Interv
Radiol 2005;11:195-8.
9. Hurst RW, Schnee C, Raps EC, et al. Role of transcranial
Doppler in neuroradiological treatment of intracranial vaso-
spasm. Stroke 1993;24:299-303.
10. Frontera JA, Claassen J, Schmidt JM, et al. Prediction of
symptomatic vasospasm after subarachnoid hemorrhage: The
modified fisher scale. Neurosurgery 2006;59:21-7; discussion
21-7.
11. Vora YY, Suarez-Almazor M, Steinke DE, et al. Role of
transcranial Doppler monitoring in the diagnosis of cerebral
vasospasm after subarachnoid hemorrhage. Neurosurgery
1999;44:1237-47; discussion 1247-8.
12. Lowe LH, Morello FP, Jackson MA, et al. Application of
transcranial Doppler sonography in children with acute neu-
rologic events due to primary cerebral and West Nile vascu-
litis. AJNR Am J Neuroradiol 2005;26:1698-701.
13. Razumovsky AY, Wityk RJ, Geocadin RG, et al. Cerebral
vasculitis: Diagnosis and follow-up with transcranial Doppler
ultrasonography. J Neuroimaging 2001;11:333-5.
Curr Probl Diagn Radiol, September/October 2009
14. Leach JL, Fortuna RB, Jones BV, et al. Imaging of cerebral
venous thrombosis: Current techniques, spectrum of findings,
and diagnostic pitfalls. Radiographics 2006;26(suppl 1):S19-
41; discussion S42-3.
15. Jones BV, Ball WS, Tomsick TA, et al. Vein of Galen
aneurysmal malformation: Diagnosis and treatment of 13
children with extended clinical follow-up. AJNR Am J Neu-
roradiol 2002;23:1717-24.
16. Chiu NC, Shen EY, Lee BS. Reversal of diastolic cerebral
blood flow in infants without brain death. Pediatr Neurol
1994;11:337-40.
17. Goh D, Minns RA. Intracranial pressure and cerebral arterial
flow velocity indices in childhood hydrocephalus: Current
review. Childs Nerv Syst 1995;11:392-6.
18. Taylor GA, Madsen JR. Neonatal hydrocephalus: hemody-
namic response to fontanelle compression—Correlation with
intracranial pressure and need for shunt placement. Radiology
1996;201:685-9.
19. Archer LN, Levene MI, Evans DH. Cerebral artery Doppler
ultrasonography for prediction of outcome after perinatal
asphyxia. Lancet 1986;2:1116-8.
20. Bada HS, Hajjar W, Chua C, et al. Noninvasive diagnosis of
neonatal asphyxia and intraventricular hemorrhage by Doppler
ultrasound. J Pediatr 1979;95:775-9.
21. Stark JE, Seibert JJ. Cerebral artery Doppler ultrasonography
for prediction of outcome after perinatal asphyxia. J Ultra-
sound Med 1994;13:595-600.
22. Byrd SE, Seibert JJ. Transcranial Doppler imaging in pediatric
abnormalities in older children. Neuroimaging Clin North Am
1999;9:17-40.
23. Saliba EM, Laugier J. Doppler assessment of the cerebral
circulation in pediatric intensive care. Crit Care Clin 1992;8:
79-92.
24. Adelson PD, Clyde B, Kochanek PM, et al. Cerebrovascular
response in infants and young children following severe
traumatic brain injury: A preliminary report. Pediatr Neuro-
surg 1997;26:200-7.
25. Lee JH, Kelly DF, Oertel M, et al. Carbon dioxide reactivity,
pressure autoregulation, and metabolic suppression reactivity
after head injury: A transcranial Doppler study. J Neurosurg
2001;95:222-32.
26. Ducrocq X, Hassler W, Moritake K, et al. Consensus opinion
on diagnosis of cerebral circulatory arrest using Doppler-
sonography: Task Force Group on cerebral death of the
Neurosonology Research Group of the World Federation of
Neurology. J Neurol Sci 1998;159:145-50.
227