Am J Electroneurodiagnostic Technol

49:342-360. 2009
© ASET. t^issouri

Transcranial Doppler Series Part IV: Case Studies

Heather A Nicoletto, BS, RVT and

Marilyn H. Burkman, BS, RDCS, RVT

Neurodiagnostic Laboratory
Duke University Hospital
Durham, North Carolina

ABSTRACT, Traiiscraniai Doppler (TCD¡ is considered (me of

the mo.st difficult ultra.sound studies to pe/form. Knowledge of cerebral
hemodynamics is essential to the interpretation of the TCD study. The
most common uses for TCD are the evaluation for va.sospasm after sub-
arachnoid hemorrhage and for sickle cell vosculopathy. Other uses are
the detection of vessel narrowing or occlusion, collateral flow secondary
to internal carotid artery occlusion, arteriovenous malformations, and
to confirm cerebral circulatory arrest. Case studies are presented to
demonstrate the hemodynamic parameters thai are used to interpret the
TCD study.

KEYWORDS. Cerebral circulatory arre.st, collateral flow, sickle

cell, .subarachnoid hemorrhage, transcranial Doppler. va.sospasm,
vertebrobasilar insufficiency.

INTRODUCTION
This is the final paper in the Transcranial Doppler (TCD) series. In Part I of the
series we discussed neurovascular anatomy and ihe vessels that are insonaled with
TCD(Nicoieltoand Burkman 2008), Part II was an overview of the TCD equipment
and how to perform a TCD exatn {Nicoletto and Burkman 20()9a). In Part HI we
discussed the mosl comtnon uses of TCD and which cerebral hemodynamics iire
used to make an interpretation (Nicoletto and Burkman 2009b), In this paper we
present case studies from the various disease processes ihal TCD is used to evaluate.
Within each case study are the patient history, the patient's TCD wavefonns.
and explanations regarding which hemodynamic parameters were used to make the
interpretation.

: September 25. 2(H)*). Accepted for publication: October 8. 2()(19.

342
 TCD CASE STUDIES 343

CASE STUDIES
Normal
You must fully understand wha( normal velocities, pulsatility indices, systolic
upstroke, and direction of flow are in order to recognize when they are abnormal.
A 58-year-oid female with a history of migraines and hypcrlipidemia presented
after having a severe headache which lasted 48 hours. She also complained of
dizziness, blurred vision, and decreased balance that lasted several days. A brain
magnetic resonance imaging (MR!) scan showed multiple hyperdensities that were
strongly suggestive of demyelinating plaques. A work-up for multiple sclerosis was
negative. A carotid ultrasound was negative for hemodynamicaliy significant
narrowing. She was diagnosed with possible small vessel disease and TCD was
ordered to evaluate the basal cerebral arteries.
The bilateral transtemporal windows were insonated and the middle cerebral
arteries (MCA) were followed throughout tbeir course with samples taken every
5 mm (Figure lA). The anterior cerebral arteries (ACA) (Figure IB) and posterior
cerebral arteries (PCA) were also insonated. The carotid siphons and ophthalmic
arteries (OA) (Figure IC) were insonated through the transorbital window. The
basilar artery (BA) (Figure ID) and bilateral vertebral arteries (VA) were insonated

D«»tk! ( I

FIG, 1A. Transcranial Doppler of a middle cerebral artery (MCA) with normal flow
velocity, normal pulsatility indices (PI), and sharp systolic upstroke.
FIG. IB. Transcranial Doppler of an anterior cerebral artery (ACA) with normal flow
velocity, normal pulsatility indices (Pi), and sharp systolic upstroke.
FIG. IC, Transcranial Doppler of an ophthalmic artery (OA) with a normal resistive
waveform morphology (very little diastolic flow} and flow toward the probe.
FIG. ID. Transcranial Doppler of a basilar artery (BA) with normal flow velocity, normal
pulsatility indices (PI), and sharp systolic upstroke.
344 TCD CASE STUDIES

Table 1. Thc uverage mean finw velocities for an adiill in the vesst'l.s insonaled
hy inmscranial Dopplcr.

Direction
Arlcrv Wi ndo\* DL-pth Mean Velocity ol' Flow Resisiance

ECICA Retroniandibular •15-50 mm 30 +/- 9 cm/scc Away Low

MCA Tränst eni pora I M)-(^f' mm 55 +/- 12 cm/sec Toward Low

ACA Transtemporal 611-75 mm 50 +/- 11 cm/sec Away Low

PCA-Pl Transtemponii 60-70 mm 39+/- 10 cm/sec Toward Low
PCA-P2 TranslcmpoKil 60-70 mm 40+/- 10 cm/sec Away Lx)w
OA Tiansorbitiii 45-55 mm 21 +/-5 cm/sec Toward High
Supi'uclinoid Tninsorbiuil 65-80 mm 41 +/- 11 cm/scc Away Low
[CA
Parasellar ICA Transorhilal 65-80 mm 47 +/- 14 cm/sec Toward Low
VA Tran sforami nal 60-75 mm 38+/- 10 cm/sec Away Low
BA Transforaminal 80-120 mm 41 +/- 10 cm/scc Away Low

ECICA - exirücranial internal carotid artery; MCA - middle CL-rcbra! arlcry: ACA - anterior
cerebral artery; PCA - posterior cerebral ariery. OA - ophthalmic artery; ICA - internal carotid
artery; VA - vertebral artery; BA - basilar arter)'

using the transforamenal window. The BA wa.s followed throughout it course with
satnples taken every 5 uuii (Nicoletto and Burkman 2009a).
Flow velocities in all basal cerebral aileries were within normal limits. The
systolic upstrokes were sharp and the hlood flow in each vessel is flowing in its
normal direction (Table 1 ). The ophihalmic arteries were antegrade (flowing toward
the probe) and demonstrated a high resistance waveform (little to no diastolic flow).
The Lindegaard ratio was below 3.00. The BA/extracranial vertebral artery (ECVA)
ratio was below 2.5. All pulsatility indices (PI) were above 0.5 and below 1.2
demonstrating normal low resistance wavefomis (Nicoletto and Burkman 2009b).
The final interpretation was: 'TCD flow velocities are within normal limits in al!
investigated vessels at this time."
Because her vascular work-up was negative she was declared at small risk for
stroke. She continues to take simvastatin (Zocor^") to manager her hyperlipidemia
and has started taking an 81 milligram aspirin. She will follow-up with her primary
care physician if any symptoms recur.

Vasospasm
Vasospasm secondary to subarachnoid hemorrhage (SAH) is one of the most
common uses of TCD. The critical period for vasospasm after SAH is post bleed day
3 through 14. although it can persist beyond that time frame (Sloan 1993).
A 51-year-old Caucasian woman with a history of hypertension presented with a
progressively worsening headache over the course of three days. Head computed
tomography (CT) showed a moderate sized subarachnoid hemorrhage. Angiogram
 TOD CASE STUDIES 345

revealed multiple aneurysms. The left supraclinoid internal carotid artery (ICA)
aneurysm wa.s coiled and stented. Serial TCDs began on post bleed day 4.
The left MCA velocity was 153 cm/sec with a PI of 0.60. The Lindegaard ratio
was 4.94. There was disturbed flow along the baseline and an audible bruit that
is consistent with a narrowed vessel (Figure 2A). An MCA velocity between 150 to
199 cm/sec along with a ratio of 3.0 or greater is consistent with moderate vasospasm
{Aaslidetal. 1984).
The left anterior cerebral artery ( ACA) velocity was 137 cm/sec with a PI of 0.47
(Figure 2B). An ACA velocity of 130 cm/sec or greater is consistent with vasospasm
(Aaslid et al. 1984). However, in the setting of moderate left MCA vasospasm this
elevated velocity could represent collateral flow. The PI of 0.47 suggests that the
distal arterioles are dilated.
The right MCA velocity was 132 cm/sec with a PI of 0.69 (Figure 2C). The
Lindegaard ratio was 4.26. An MCA velocity between 120 to 149 cm/sec along with
a ratio of 3.0 or greater is consistent with mild vasospasm {Aaslid et al. 1984). The
right ACA velocity was 144 cm/sec wilh a PI of 0.53 (Figure 2D). This is consistent
with vasospasm (Aaslid et al. 1984).
The BA velocity was 99 cm/sec with a PI of 0.74. The BA/ECVA ratio was 3.70.
There was disturbed flow along the baseline and an audible bruit consistent with a
narrowed vessel (Figure 2E). A BA velocity of 85 cm/sec or greater with a ratio
of 2..5 or greater is consistent with vasospasm (Svid et al. 2006). Al! other vessels
demonstrated normal velocities and Pis.
The final interpretation was: 'TCD flow velocities are consistent with the
following:
1. moderate left middle cerebral artery vasospa.sm
2. left anterior cerebral artery vasospasm vs. collateral flow
3. mild light middle cerebral artery vasospasm
4. right anterior cerebral artery vasospasm
5. basilar artery vasospasm
6. low pulsatility indices in the left anterior cerebral artery are suggestive of distal
vasodilation.
All other investigated vessels are within normal limits at this time."
The patient was treated with hypervolemic-hypertensive-hemodilution (HHH)
therapy throughout her admission (Nicolctio and Burkman 2009b). However, her
neurological exam worsened and on post bleed day 10 she lost brainstem function.
A cerebral perfusion scan showed no cerebral perfusion and she was declared brain
dead on post bleed day 11.

Sickle Cell
The irregular shape of their red blood cells puts children with sickle cell disease at
risk for vessel narrowing and subsequently, stroke. By Ihe age of two years, children
346 TCD CASE STUDIES

FIG. 2A. Transcranial Doppler of the left middle cerebral artery (MCA) in a patient with
subarachnoid bemorrbage (SAH). The flow velocity is 150 to 199 cm/sec with disturbed
flow at tbe baseline consistent with moderate vasospasm.
FIG. 2B. Transcranial Doppler of the left anterior cerebral artery (ACA) in a patient with
subaracbnoid bemorrbage (SAH). The flow velocity is greater than 130 cm/sec in tbe set-
ting of moderate left middle cerebral artery (MCA) vasospasm consistent witb vasospasm
versus collateral flow.
FIG, 2C. Transcranial Doppler of the right middle cerebral artery (MCA) in a patient witb
subarachnoid bemorrbage (SAH). The flow velocity is 130 to 149 cm/sec consistent witb
mild vasospasm.
FIG. 2D. Transcranial Doppler of the right anterior cerebral artery (ACA) in a patient with
subarachnoid hemorrhage (SAH). The flow velocity is greater than 130 cm/sec consistent
witb vasospasm.
FIG. 2E. Transcranial Doppler of the basilar artery (BA) in a patient with subarachnoid
bemorrbage (SAN). Tbe flow velocity is greater than 85 cm/sec with disturbed flow at the
baseline consistent witb vasospasm.

should hegin having TCDs at least yearly to evaluate for elevated velocities that are
consistent with sickle cell vasculopathy.
At the age of three motiths, an African American male was referred to the hematol-
ogy oncology clinic after sickle cell anemiii was found on his newborn screen. TCD
 TCD CASE STUDIES 347

studies were begun at age 34 months. At four years of age he began to have velocity
increa.ses on his TCD.
At age five years, his right MCA velocity was 171 cm/sec with a PI of 0.50
(Figure 3A). The right ACA velocity was 174 cm/sec with a PI of 0.57 (Figure 3B).
Velocities of 170 cm/sec to 199 cm/.sec are consistent with conditional sickle cell
vasculopathy (Adams et al. 1998).

B
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D«e 8/7/200912:18:50 PM Fillet 200 Dale flm2009 12:20:03 PM Fitter 200

Probe 2PW Max 214B8 'robe 2PW Max 15S223
Sampte Voluntefmml 8 Mean 171/24 Sample Volugrelmm] 8 Mean iia'174
Gaio(%J 6 Min 129A) G»n(%] 6 Mm 86/125
ISPTA 420 PI 0.50/1.60 SPTA 420 PI 0.56(037
Doplhjmm] 45 >epthjinfii) 57
Scals(Hz| 9009 Sca\^Hz\ 11111
Label MCA R Labet ACA R

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Date 8/7/2009 12:26:17 PM FIKer 200 Dale 8/7/200912:35:41PM F«w 200

Probe 2PW Max 256/68 Pmbe 2PW Max 38/280
Sample V(Ajme|fnm| 8 Mean 197/46 Sample Voh«ne|mni| 8 Mean 23/204
GBin[%| 31 Mm 152/27 Gain{%l 38 MM 7Í146
ISPTA 460 PI 0.53/0.90 ISPTA 430 =»l 1.35/0,65
Dep^lmml 55 Deplti[(Tim] 65
Sc3le[h1z| 10526 Scale{Hz| 10000
LatMl MCA L LatMf SUPRA L

FIG. 3A. Transcranial Doppler of the right middle cerebral artery (MCA) in a patient
with sickle cell disease. The flow velocity is 170 to 199 cm/sec consistent with conditional
sickle cell vasculopathy.
FIG. 3B. Transcranial Doppler of the right anterior cerebral artery (ACA) in a patient with
sickle cell disease. The flow velocity is 170 to 199 cm/sec consistent with a conditional
sickle cell vasculopathy.
FIG. 3C. Transcranial Doppler of the left middle cerebral artery (MCA) in a patient with
sickie cell disease. The flow velocity is 197 cm/sec consistent with conditional sickle cell
vasculopathy versus sickle cell vasculopathy,
FIG. 3D. Transcranial Doppler of the left supracllnoid internal carotid artery (ICA) in a
patient with sickle cell disease. The flow velocity in greater than 200 cm/sec consistent
with sickle cell vasculopathy.
348 TCD CASE STUDIES

The left MCA velocity was 197 cm/sec with a PI of 0.53 (Figure 3C). This
velocity is consistent with conditional sickle cell vasculopathy. However, since the
velocity is nearly 200 cm/sec the interpretation of sickle cell vasculopathy could be
made.
The left carotid siphon velocity was 204 cm/sec with u PI of 0.65 (Figure 3D).
A velocity of 200 cm/sec or greater is consistent with sickle cell vasculopathy
(Adams et al. 1998). All other vessels had normal velocities and Pis for his age.
The final interpretation was: "TCD flow velocities are consistent with the
following:
1. sickle cell vasculopathy in the left carotid siphon
2. conditional sickle cell vasculopalhy in the bilateral middle cerebral arteries,
right greater than left. However, the left middle cerebral artery is likely in
sickle cell vasculopathy since its velocity is nearly 200 cm/sec.
3. conditional sickle cell vasculopathy in the right anterior cerebral artery
All other investigated vessels are within normal limits al this time."
Sickle cell vasculopatby was detected on two consecutive TCDs. Because of this,
he was started on chronic blood transfusions. His velocities continue to be high,
however, he continues to be free of stroke symptoms.

Intracranial Vessel Narrowing

Intracraniai vessel narrowing can cause transient ischémie attack (TIA) and stroke.
TCD is a reliable study for detecting narrowing in the basal cerebral arteries.
A 52-year-old diabetic female left work sick on a Tuesday and she was not heard
from for two days. Her family went to check on her and found her at home, unrespon-
sive, with fever. In the emergency department (ED) she was non-verbal but moving
all extremities. A lumbar puncture showed bacterial infection consistent with
meningitis. She was treated with antibiotics: however, there was no improvement
in neurological exam. A head CT was positive for cerebritis and areas of cerebellar
infarction. A TCD was ordered to look for intracranial vessel narrowing.
The right MCA velocities were 58 to 71 cni/sec with normal Pis. The left MCA
velocities ranged from 68 to 76 cm/sec at depths of 35 to 50 tnm and were 137 to 140
cm/sec at depths of 55 to 60 mm. The Pis were normal (Figure 4A). A focal velocity
increase in the proximal left MCA with a side to side difference of more than
30 cm/sec is consistent with a mild vessel narrowing (Brass et al. 1989).
The left carotid siphon velocity was 136 cm/sec with a normal PI. There was dis-
turbed flow seen al the baseline with an audible bruit (Figure 4B). The right carotid
siphon velocity was 48 cm/sec wilh a normal PI. A side to side difference in the
carotid siphon velocities along with a left carotid siphon velocity between 85 to
149 cm/sec is consistent with a mild vessel narrowinjj.
 TCD CASE STUDIES 349

cwtt

a LMCA
s M( * • ; 144

a PI O.Tt

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FIG. 4A. Transcranial Doppler of the left middle cerebral artery (MCA) with a focal flow
velocity of 85 to 149 cm/sec consistent with mild vessel narrowing.
FIG. 4B. Transcranial Doppler of the left supraclinoid internal carotid artery (tCA) with a
flow velocity of 85 to 149 cm/sec consistent with a mild vessel narrowing.
FIG. 4C. Transcranial Doppler of the basilar artery (BA) with a flow velocity greater than
85 cm/sec and disturbed flow at the baseline consistent with vessel narrowing.
FIG, 4D. Transcranial Doppler of the right posterior cerebral artery (PCA) demonstrating
a slowed systolic upstroke consistent with a proximal vessel narrowing (the basilar artery
IBA] vessel narrowing).

The proximal BA velocities were 21 to 28 cm/sec. At a depth of 100 mm the BA

velocity was 122 cm/sec. Pis throughout the BA were normal (Figure 4C). The focal
velocity increase, with a velocity of 85 ctn/sec or greater in the distal BA is consistent
with vessel narrowing. The bilateral PCAs had slowed systolic upstrokes with
normal velocities and Pis (Figure 4D). The slowed systolic upstroke in the PCAs is
consistent with the downstream effect of the BA vessel narrowing. All other vessels
had normal flow velocities and Pis.
The final interpretation was: "TCD flow velocities are consistent with the
following:
1. mild vessel narrowing in the left middle cerebral artery
2. mild vessel narrowing in the left carotid siphon
3. vessel narrowing in the basilar artery
All other itivestigated vessels are within normal limits at this time."
Because of the narrowing in her cerebral vessels her blood pressure was kept high
to help with perfusion. Upon discharge to a skilled nursing facility, the patient was
350 TCD CASE STUDIES

opening her eyes but not following commands or moving her extremities. She
was readmitted to the hospital ten days later for drainage of a brain abscess. She was
discharged four days later to a specialty rehabilitation facility. Upon discharge she
was alert, following commands, and talking in single words,

Vessel Occlusion
Vessel occlusion often causes permanent neurological deficits. TCD is useful in
detecting intracranial vessel occlusion once adequate acoustic windows have been
established.
A 55-year-old male with a history of hyperlipidemia presented to the ED with
right arm dyscoordination, generalized weakness, and slurred speech which pro-
gressed to right sided paralysis and aphasia. A head CT showed left temporal
lobe and basal ganglia infarcts. Computed tomography angiography (CTA) showed
an inlracranial left ICA dissection with ibronibus in the left MCA. A TCD was done
to evaluate for vessel occlusion.
The right MCA velocity was 44 cm/sec with a PI of 1.09 (Figure 3A). The proxi-
mal (depths of 60 to 65 mm) left MCA waveform had no diastolic flow (known as a
pre-occlusive thump) (Figure 5B). The mid to distal (depths of 45 to 55 mm) left
MCA could not be identified. The presence of a pre-occlusive thump in the proximal
left MCA without identification of the mid to distal MCA is consistent with vessel
occlusion. The right extracranial internal carotid artery (ECICA) velocity was
63 cm/sec with a PI of 1.18. The left ECICA velocity was 35 cm/sec with a PI of 1.91
(Figure 5C). A PI greater than 1.2 in the left ECICA is suggestive of a distal vessel
(îcclusion. A significant difference in side to side flow velocities in the ECICAs is
also suggestive of a distal occlusion ( Kaps et al. i 990).
The left ACA wa.s not identified. This is suggestive of vessel occlusion considering
all other vessels through ihe temporal windows were easily identified. The right ACA
velocity was 137 cm/sec with a PI of 0.80 (Figure 5D). This elevated velocity,
compared to the contralateral MCA velocities, is consistent with collateral flow to
the left ACA-A2 segment. All other vessels had normal flow velocities and Pis.
The final interpretation was: 'TCD How velocities are consistent with the
following:
1. left middle cerebral artery occlusion
2. lel'l anterior cerebral artery occlusion
3. right to left crossover collateral to the left anterior cerebral artery-A2 segment
via the anterior communicating artery
4. All other investigated vessels are within normal limits at this time."
The patient was put on heparin. He began to demonstrate minimal movement of
his righl extremity and his speech and comprehension improved. He was discharged
to a rehabilitation facility and now walks with a cane.
 TCD CASE STUDIES 351

FIG. 5A, Transcranial Doppler of the right middle cerebral artery (MCA) with normal flow
velocity, normal pulsatility indices (PI), and a sbarp systolic upstroke.
FIG. 5B. Transcranial Doppler of tbe left middle cerebral artery (MCA) demonstrating
a pre-occlusive thump (forward flow with no diastolic flow) consistent with distal vessel
occlusion.
FIG. 5C. Transcranial Doppler of the bilateral retromandibular internal carotid arteries
(extracranial internal carotid arteries [EClCAs]). Notice tbe elevated pulsatility indices (PI)
and lower flow velocity in the left ECICA compared to the right ECICA consistent witb a
distal vessel occlusion.
FIG. 5D. Transcranial Doppler of tbe rigbt anterior cerebral artery (ACA) with an elevated
velocity in tbe setting of a left ACA occlusion. This is consistent with collateral flow through
the anterior communicating artery (AcoA) to the left ACA-A2 segment.

Collateral Flow

Collateral flow in the circle of Willis develops secondary to a hemodynamically

significant narrowing or occlusion of the ICA. TCD can detect changes in How
directi()n and veliicity that occur when a vessel functions as collateral.
A 61-year-old male with a history of smoking and hypertension was found lying
on the floor with right facial droop, right sided paralysis, and aphasia. He had a large
hematoma on the left forehead. A head CT showed a left basal ganglia and subinsular
352 TCD CASE STUDIES

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2PW Max 132/61 =robe 2PW Max 50f20
Sampte Volume(ninil 8 Mean 70/23 Sampte Volumelnan] 8 Me«n 30/1
Gaui{%| 31 Min 34/0 3ain[%| 25
ISPTA 720 PI 1.4/2.6 SPTA 720 PI 1.1O5
[Jeplhlmm] 45 DIS 3eptftlmm| 46 D/S
Sc8le(Hzl 9009 Scale[Hz| 4525
Label MCA R Labal MCA L

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tobe 2PW Max 71M93 Probe 2PW Max 254/73
Sampte Voluma(nim) 8 Mean î/106 Sample Volume mm| B Mean 154/34
3aln[%| 36 Min 1163 Galn(%| 44 Min 91/0
SPTA 720 PI Í.4/1.2 ISPTA 720 PI 1.1/Zl
70 D/S Depthlmm] 68 D/S
ScalefUi 9009 ScalefHzj 900S
Label ACA R Label ACA_L

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Date 6/2/2006 10:17:24/VM MeanAp Date 6/2/2006 10:22:13 AM MealAp

Piobe 2PW Max 134/24 »robe 2PW Mai 60/51
Sample Vohjmelmml 8 Mean 55M SarqjteViAnefrrwnl 6 Mean 32/24
Ganntl 31 Min 53« GainrMil 44 Mm 6/0
ISPTA 720 PI 1-(V5-9 ISPTA 560 PI 1.7/Z1
Depttilmml 63 D/S 3epth|mm 1 51 D/S
Scale(Hz! 7519 Scale(Hz! 9524
Label PCAIL Label OA L

FIG. 6A. Transcranial Doppler of the right nniddle cerebral artery (MCA) with normal flow
velocity, normal pulsatility indices (PI}, and a sharp systolic upstroke.
FIG. 6B. Transcranial Doppler of the left middle cerebral artery (MCA) with low flow
velocity and a slowed systolic upstroke consistent with a proximal hemodynamically
significant narrowing versus occlusion.
 TCD CASE STUDIES 353

region infarct. A CTA showed occlusion of his left ICA. A TCD was done to evaluate
for collateral flow.
The right MCA velocity was 70 cm/sec with a PI of 1.4 (Figure 6A). The left MCA
velocity was 30 cm/sec with a PI of 1.1. The waveform demonstrated a slowed
systolic upstroke, which is a downstream effect of a hemodynamicaliy significant
narrowing or occlusion (Figure 6B). Low flow velocities and Pis in the left MCA,
compared to the right MCA. along with the slowed systolic upstroke, are consistent
with the known proximal ICA occlusion (Rosenkranz et a!, 1991).
The right ACA velocity was 106 cm/sec with a PI of 1.2 (Figure 6C). The left ACA
is reversed with a velocity of 154 cm/sec and a PI of 1.1 (Figure 6D). The reversal
of the left ACA along with elevated velocities in both ACAs is consistent with
collateral flow from the right ACA to the left ACA and MCA via the anterior
communicating artery (AcoA) (Rosenkranz et al. 199J).
The right PCA-Pl segment velocity was 31 cm/sec with a PI of 1.4. The left
PCA-Pl segment velocity was 85 cm/sec with a PI of I.O (Figure 6E). The velocity
in the left PCA-Pl segment is more than 125% greater than the left MCA velocity
(Rosenkranz et al. 1991) and the PI is low, compared to the right PCA-PI segment.
This is consistent with collateral t1ow from the posterior circulation to the anterior
circulation via the posterior communicating artery (PcoA).
The right OA demonstrated a normal, high resistance waveform. The left OA
demonstrated a hesitant waveform that is consistent with partial collateral flow from
the external circulation to the internal circulation (Figure 6F).
All other vessels had normal velocities. Pis throughout all normal vessels were
above 1.2. which is often seen with elevated intracranial pressure (ICP) or may be
due to cardiac function (Nicoletlo and Burkman 2()09b).
The final interpretation was: "TCD flow velocities are consistent with the
secondary hemodynamic effects associated with a known left internal carotid artery
occlusion with the following:

FIG. 6C. Transcranial Doppler of the right anterior cerebral artery (ACA) with elevated
flow velocity consistent with crossover collateral to the left middle cerebral artery (MCA)
via the anterior communicating artery (AcoA).
FIG. 6D. Transcranial Doppler of the left anterior cerebral artery (ACA) with elevated flow
velocity and reversed direction of flow consistent with right to left crossover collateral via
the anterior communicating artery (AcoA).
FIG. 6E. Transcranial Doppler of the left posterior cerebral artery (PCA) PCA-Pl segment
with a flow velocity greater than 125% ofthe left middle cerebral artery (MCA) consistent
with posterior to anterior collateral via the left posterior communicating artery (PcoA).
FIG. 6F. Transcranial Doppler of the left ophthalmic artery (OA) demonstrating a hesitant
waveform morphology. Notice the partial reversal of flow during systole consistent with
a latent external to internal collateral.
354 TCD CASE STUDIES

R-VA 66 -M 2
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Mean
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FIG. 7A. Transcranial Doppler of the right vertebral artery (VAl with normal velocity and
flow direction away from the probe.
F1G.7B. Transcranial Doppter of the left vertebral artery (VA) with alternating flow
(reversal of flow in systole and forward flow In diastole) consistent with a latent
subclavian steal.
 TCD CASE STUDIES 355

1. right to left crossover collateral via the anterior communicating LU

2. posterior to anterior collateral via the left posterior communicating artery
3. latent external to internal collateral via the left ophthalmic artery
All other investigated vessels are within normal limits at this time. Globally elevated
pulsatility indices may be due to intracranial hypertension/cardiac function."
The patient's occluded artery was treated with heparin. Three days after admission
his neurological status declined. A repeat head CT .showed hemorrhagic conversion
of ihe left MCA infarct. At the time of discharged he was alert and fully oriented.
He now goes to physical therapy and has improved range oí motion of his righl side.
He has residual aphasia but is able to follow commands if given enough time to
proces.s the request.

Vertebrobasilar InsufUciency
People with vertebrobasilar insufficiency often experience episodes of dizziness or
syncope. Subclavian steal is one possible cause of vertebrobasilar insufficiency.
An alternating or hesitant waveform in the VA can be due u> a hypoplastic VA, a
proximal VA naiTowing. or subclavian narrowing resulting in subclavian steal. To
differentiate subclavian steal from the other two possibilities, a TCD with reactive
hyperemia may be performed. The VA is continuously monitored wilh TCD while a
blood pressure cuff placed on ihe ipsilateral arm is inflated to 30 mmHg above the
systolic pressure. The cuff remains inflated for three minutes and is then quickly
released causing the blood to rush to the hand. If the alternating or hesitant waveform
is due lo sLibclavian steal, the blood tlow in the VA will reverse upon reiease ofthe
blood pressure cuff (Klingelhoferet al. 1988).
A 6fi-year-old female pre.sented after an episode of severe dizziness, nausea,
bilateral lower extremity weaknes.s, and buzzing in her right ear. These symptoms
occurred while she was standing and shuffling papers at work. She has a prior
medical history of hyperlipidemia. A TCD was performed to evaluate for narrowing
in the vertebral and basilar aileries and subclavian steal.
The right VA velocity was 39 cm/sec with a PI of 1.44 (Figure 7A). The left VA
demonstrated alternating waveform morphology (Figure 7B) and the BA (Figure 7C)
and bilateral PCAs demonstrated hesitant flow. Hesitant and alternating flow is

FIG. 7C. Transcranial Doppler of the basilar artery (BA) with hesitant flow (partial
reversal of flow during systole) consistent with a latent sutaclavian steal.
FIG. 7D. Transcranial Doppier of the left vertebral artery (VAI pre and post reactive
hyperemia testing. Notice complete reversal of flow as the blood pressure cuff is released
consistent with subclavian steal.
356 TCD CASE STUDIES

suggestive of proximal narrowing versus subclavian steal. A reactive hyperemia

study was performed. Upon release of the blood pressure cuff flow in the left VA
completely reversed consistent with subclavian steal (Figure 7D). All other vessels
had normal flow velocities and Pis.
The final interpretation was: 'TCD flow velocities in the left vertebral artery,
basilar artery and bilateral posterior cerebral arteries along with complete reversal of
flow in the left veitebral artery during reactive hyperemia testing are consistent with
left stibclavian steal. Al! other investigated vessels are within normal limits at this
time."
The patient was discharged on simvastatin (Zocor'^"). aspirin, and clopidogrel
bisulfate (Plavix^"). At her six-month follow-up appointment she did not complain of
further symptoms. She will continue medical therapy for one year at which time her
subclavian steal will be re-evaluated by CTA.

Arteriovenous Malformation
Arteriovenous malformations (AVM) may be asymptomatic or may lead to
seizures, neurological symptoms, or hemorrhage (Giller 1993). TCD can be useful to
determine which vessels are feeding the AVM.
The patient is a 38-year-old female who initially had a cerebellar hemorrhage
due to AVM in 1997. Her AVM was treated with gamma knife radiosurgery in 1999.
She continued to have balance and dysmetria problems but otherwise did well until
2006 when she presented with a severe headache, nausea and vomiting, photophobia,
phonophobia. and feeling off balance. An MRI showed a left cerebellar AVM and
u head CT showed a hemorrhage. A TCD was performed to evaluate the feeding
vessels of the AVM.
The right PCA-P2 segment velocity was 44 cm/sec with a PI of 0.84 (Figure 8A).
The left PCA-P2 .segment velocity was 136 cm/scc with a PI of 0.49 (Figure 8B). The
elevated velocity in the left PCA-P2 segment, compared to the right PCA-P2
segment, along with a PI below 0.5 is consistent with a feeding vessel to the AVM
(Giller 1993). All other vessels had normal flow velocities and Pis.
The final interpretation was: "TCD flow velocities are consistent with the left
posterior cerebral anery-P2 segment acting as a feeding vessel to the arteriovenous
malformation. All other investigated vessels are within normal limits at this time.""
Five months after her admission, Ihe patient underwent stereotactic gamma
knife radiosurgery of her AVM. Follow-up MRI showed decreased flow to the AVM.
She remains asymptomatic.

Cerebral Circulatory Arrest

As cerebral perfusion pressure decreases and intracranial pressure (ICP)
increases, diastolic flow decreases and is eventually absent (Ducrocq et al. 1998).
 TCD CASE STUDIES 357

A
250
R PCA P2
I Mean: 44

PI: 0.84

Depth: 61
8

50

cnVs

L PCA P2

Mean: 13S

PI: 0.49

Depth: 17

FIG.8A. Transcranial Doppler of the right posterior cerebral artery (PCA) PCA-P2
segment with normal velocity and normal pulsatility indices (PI).
FIG. 8B. Transcranial Doppler ofthe left posterior cerebral artery (PCA) PCA-P2 segment
with an elevated flow velocity and low putsatility indices (PI) consistent with a feeding
vessel to an arteriovenous malformation (AVM).

This progression into cerebral circulatory arrest can easily and reliably be detected
on TCD.
Two days prior to admission, a 32-year-old female had been in a motor vehicle
accident in which she briefly lost consciousness, but did not require medical atten-
tion. On the day of admission she was found unrespon.sive at her home. A head CT
showed cerebral edema and multiple small hemorrhages consistent with anoxic brain
injury. On admission day eight she had a coughing .spell that increased her ICP.
A neurological exam showed blown pupils suggestive of herniation. A repeat head
CT showed increased cerebral edema with obliteration of the basilar cisterns.
There was no return of brain function. A TCD was performed to evaluate for cerebral
circulatory arrest.
358 TCD CASE STUDIES

I r f

If r

RMCA

i i I i I Depth: 4C

BASILAR

Depth: 100

FIG. 9A. Transcranial Doppler of the bilateral extracranial internal carotid arteries
(ECICAs) demonstrating resistive waveform morphology (very little diastolic flow).
FIG. 9B. Transcraniat Doppler of the right middle cerebral artery (MCA) demonstrating a
systolic spike consistent with cerebral circulatory arrest.
FIG.9C. Transcranial Doppler ofthe basilar artery (BA) demonstrating a systolic spike
consistent with cerebral circulatory arrest.
 TCD CASE STUDIES 359

Flow in the bilateral ECICAs demonstrated a high resistance wavefonn

(Figure 9A). Flovy in the bilateral MCAs, carotid siphons, and BA demonstrated
systolic spikes (Figures 9B and 9C). A repeat study a half hour later also demon-
strated high resistance signals in the bilateral ECICAs and systolic spikes in the
bilateral MCAs. carotid siphons, and BA. Decreased diastolic ttow in the ECICAs
and loss of diastolic flow in all other vessels is consistent with cerebral circulatory
arrest (Ducrocq et al. 1998).
The final interpretation was: "TCD flow velocities are consistent with cerebral
circulatory arrest.""
The patient was taken off all sedatives and was pronounced clinically brain dead
24 hours later.

CONCLUSION
TCD is an ultrasound study that is most commonly used to look lor vasospasm
secondary to subarachnoid hemorrhage and sickle cell vasculopathy. It can also be
reliable when looking for ves.sel narrowing, occlusion, or collateral flow in the circle
of Willis, feeding vessels to AVMs. and cerebral circulatory arrest. Knowledge of
cerebral hemodynamics, such as velocity, pulsatility indices, systolic upstroke, and
bruits helps you make an accurate interpretation of the TCD study.

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