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- •Foreword
- •Acknowledgments
- •Contents
- •Contributors
- •1.2 How Is Critical Care Humanized?
- •References
- •2.1 Introduction
- •1.2.2 Communication
- •1.2.5 Post-ICU Syndrome
- •1.2.6 Humanized Infrastructure
- •1.2.7 End-of-Life Care
- •2.2 Which Patients Should Undergo ICP Monitoring?
- •2.5.2.3 CSF Drainage
- •2.5.2.4 Osmotherapy
- •2.5.2.5 Ventilation
- •2.5.2.6 CPP Augmentation
- •2.5.2.7 Metabolic Suppression
- •2.5.2.8 Pharmacologic Suppression
- •2.5.2.9 Temperature Modulation
- •2.5.2.10 Decompressive Craniectomy
- •2.7.1.1 Pressure Reactivity Index (PRx)
- •2.7.1.2 Multimodality Monitoring
- •2.8 Conclusion
- •Algorithm
- •References
- •3.1 Introduction
- •3.2 Intracerebral Hemorrhage (ICH)
- •3.3 ICH: Presenting Symptoms
- •3.5.1 Blood Hypertension
- •3.5.2 Other Risk Factors
- •3.6 ICH: Pathophysiology
- •3.7 ICH: Initial Management
- •3.7.1 Airway: Intubation
- •3.7.3 ICH: Imaging
- •3.7.4 ICH: Grading Scales
- •3.7.5 Fluid Management
- •3.7.6 Follow-Up Imaging
- •3.7.7 Blood Pressure Management
- •3.7.9 ICP Monitoring
- •3.7.10 Surgical Considerations
- •3.7.13 ICH: Venous Thromboembolism Prophylaxis
- •3.7.14 ICH: Seizure Management
- •3.8 ICH: Medical Complications
- •3.8.1 Glycemic Management
- •3.8.3 Disposition
- •3.9 Conclusion
- •Algorithm
- •Appendix: Direct Oral Anticoagulant Reversal
- •Reversal Strategies
- •References
- •4.1 Introduction
- •4.2.1 Hemodynamic Management
- •4.2.2 Hormonal Replacement Therapy
- •4.2.3 Respiratory Management
- •4.3 Cardiopulmonary Resuscitation (CPR)
- •4.4 Conclusion
- •Algorithm
- •References
- •5.1 Introduction
- •5.2.1 Vasoactive Agents
- •5.2.1.1 Vasodilators (Table 5.1)
- •Calcium Channel Blockers
- •Nimodipine
- •Nicardipine
- •Other Vasodilators
- •Magnesium
- •3-Hydroxy-3-Methyl-Glutaryl-CoA (HMG-CoA) Reductase Inhibitors (Statins)
- •Nitroprusside
- •Endothelin-1 Antagonists
- •Hydralazine
- •Phosphodiesterase Inhibitors
- •Papaverine
- •Norepinephrine
- •Epinephrine
- •Dopamine (DA)
- •Phenylephrine
- •Vasopressin
- •Neuromonitoring
- •5.2.2.1 Benzodiazepines
- •5.2.2.2 Barbiturates
- •5.2.2.3 Opioids
- •5.2.2.4 Anticonvulsant Medications
- •5.2.2.5 Other Sedatives/Anesthetics
- •5.2.3 Hemodynamic Agents
- •5.4 Conclusion
- •Algorithm
- •References
- •6.1 Introduction
- •6.2.3 Ultrasound Behaviour at Acoustic Boundaries
- •6.3 Pulse-Echo Principles (B-Mode Techniques)
- •6.4 Transducers
- •6.5 Artefacts
- •6.6 Doppler Principles
- •6.6.1 Pulsed Wave Doppler
- •6.6.2 Duplex Scanning
- •6.6.3 Colour Flow Imaging (CFI)
- •6.7.2 Flow Changes
- •6.7.3 Cerebrovascular Resistance
- •6.8 Transcranial Colour-Coded Duplex Sonography (TCCS)
- •6.9 Ultrasound Safety
- •6.10 Conclusion
- •References
- •7.1 Introduction
- •Mesencephalic Plane
- •7.2.1.2 Diencephalic Plane (Thalamic Plane)
- •6.6.4 Power Doppler Imaging (PDI)
- •6.7 Transcranial Doppler Ultrasound (TCD)
- •6.7.1 Velocity Measurement
- •7.2.1.3 Ventricular Plane (Cella Media)
- •7.2.1.4 Upper Pons Plane
- •7.2.1.5 Lower Pons Plane
- •7.2.2 Transforaminal Window
- •7.3.1.2 Anterior Circulation
- •Carotid System
- •Anterior Cerebral Artery
- •Anterior Communicating Antery
- •7.3.1.3 Posterior Circulation
- •Vertebrobasilar System
- •Posterior Communicating Artery
- •Posterior Cerebral Arteries
- •7.5 Cerebral Circulation: Anatomical Variations
- •7.5.1.1 Anterior Circulation
- •Most Common Variations [28]
- •7.5.1.2 Posterior Circulation
- •Most Common Variants [28]
- •7.6.1.1 Deep Middle Cerebral Vein (DMCV)
- •7.6.1.2 Basal Vein (of Rosenthal)
- •7.6.1.3 Great Cerebral Vein (of Galen)
- •7.6.2.1 Sphenoparietal Sinus
- •7.6.2.2 Superior Petrosal Sinus
- •7.6.2.3 Inferior Petrosal Sinus
- •7.6.2.4 Cavernous Sinus
- •7.6.2.5 Transverse Sinus
- •7.6.2.6 Straight Sinus
- •7.7 Conclusion
- •Algorithm
- •References
- •8.1 Introduction
- •8.2 Cerebral Blood Flow Measures
- •8.3 Transcranial Doppler (TCD/TCCS)
- •8.4.1 Cerebral Autoregulation (CA)
- •8.4.2 CO2 Vasoreactivity
- •8.6.2 TCD/TCCS: Use After Traumatic Brain Injury (TBI)
- •8.7 Conclusion
- •References
- •9.1 Introduction
- •9.3 TCD Hemodynamic Parameters: Variations by Sex
- •9.4 TCD Hemodynamic Parameters: Variations by Age
- •9.5 TCD Hemodynamic Parameters: Variations by Laterally
- •9.7 TCD Normal Values: Latin American Population Sample
- •9.8 TCD Hemodynamic Parameters: Altitude
- •9.10 Conclusion
- •References
- •10.1 Introduction
- •10.2 TCD/TCCS: Acoustic Windows
- •10.2.1.1 Technique
- •10.2.2.1 Technique
- •10.2.3.1 Technique
- •10.2.4.1 Technique
- •10.2.5.1 Technique
- •10.4.1 Decompressive Craniectomy
- •10.4.2 Patient’s Position
- •10.5 TCD/TCCS: Contrast-Enhanced
- •10.6 Conclusion
- •Algorithm
- •References
- •11.1 Introduction
- •11.2 Basic Methods
- •11.2.1 Flow Velocities
- •11.2.2 Pulsatility Index (PI)
- •11.3 Advanced Methods
- •11.3.2 TAU (Cerebrovascular Time Constant)
- •11.3.4 Autoregulation
- •11.4.1 Traumatic Brain Injury
- •11.4.2 Aneurysmal Subarachnoid Hemorrhage
- •11.4.3 Stroke
- •11.4.4 Other Clinical Scenarios
- •11.5 Conclusion
- •Algorithm
- •References
- •12.1 Introduction
- •12.2 TCD: Spectral Wave
- •12.4 TCD: Clinical Utility
- •12.6 TCD: Technique
- •12.6.2 Transtemporal Acoustic Window
- •12.6.2.1 Anterior Circulation
- •Middle Cerebral Artery (MCA)
- •12.6.2.2 Posterior Circulation
- •Posterior Cerebral Artery (PCA)
- •12.6.3 Submandibular Acoustic Window
- •12.6.3.1 Internal Carotid Artery (ICA—Extracranial Portion)
- •12.6.4 Transoccipital Acoustic Window
- •12.6.4.1 Posterior Circulation
- •12.6.5 Transorbital Acoustic Window
- •12.6.6.2 Pulsatility Index
- •12.7.1 High-Velocity Pattern
- •12.7.2 Low-Velocity Pattern
- •12.7.3 High Resistance Pattern
- •12.7.4 Cerebral Circulatory Arrest Pattern
- •12.8 TCD: Other Clinical Uses
- •12.8.1.1 Cerebral Vascular Reactivity
- •12.9 TCD: Limitations
- •12.10 Conclusion
- •Algorithm
- •References
- •13.1 Introduction
- •13.2 Acoustic Windows
- •13.3 2D-Guided TCD Monitoring
- •13.6 Conclusion
- •Algorithm
- •References
- •14.1 Introduction
- •14.2 TCCS: Anatomical Aspects
- •14.3.1 Anterior Circulation
- •14.3.1.1 Carotid System
- •14.3.2 Posterior Circulation
- •14.3.2.1 Vertebro-Basilar System
- •14.5 TCCS: Examiner Considerations
- •14.6 TCCS: Acoustic Windows
- •14.7 TCCS: Examination Protocol
- •14.7.1.1 Considerations
- •Doppler: (Convention)
- •14.7.2 Transtemporal Acoustic Window Examination (Coronal Planes)
- •14.7.3 Transoccipital (Transnuchal/Transforaminal) Acoustic Window Examination
- •14.7.4 Submandibular Acoustic Window Examination
- •14.7.5 Transorbital Acoustic Window Examination
- •14.7.6 Frontal Bone Window Examination
- •14.8 TCCS Protocol: Clinical Applications
- •14.9 TCCS Protocol: Hemodynamic Parameters
- •14.10 TCCS Protocol: Limitations
- •14.10.1 Limitations
- •14.10.1.1 Acoustic Windows
- •Transtemporal Acoustic Window
- •Suboccipital Acoustic Window
- •14.10.1.2 Middle-Line Shift Measurement
- •14.11 Conclusion
- •Algorithm
- •References
- •15.1 Introduction
- •15.2 Clinical Applications
- •15.2.1 Intracranial Stenosis
- •15.2.2 Cerebral Vasospasm
- •15.2.3 Cerebral Veins
- •15.3 Conclusion
- •References
- •16.1 Introduction
- •16.3.1 Autoregulation Index (ARI)
- •16.3.2 Mean Flow Velocity Index (Mx)
- •16.5 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Cerebrovascular Resistance (CVR)
- •17.2.2 Cerebral Autoregulation
- •17.2.4 Carbon Dioxide Reactivity
- •17.3.2 Collateral Flow
- •17.3.3 Elastic Reservoir (“Windkessel Effect”)
- •17.4 TCD: Waveform Interpretation
- •17.4.1 TCD Waveforms
- •17.5.1 Aneurysmal Subarachnoid Hemorrhage
- •17.5.2 Increased ICP
- •17.6 Conclusion
- •References
- •18.1 Introduction
- •18.3.1 Subarachnoid Hemorrhage (SAH)
- •18.3.1.1 Cerebral Autoregulation (CA)
- •18.3.1.2 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.1.3 Cerebral Blood Flow
- •18.3.1.4 Electrophysiology
- •Seizure Detection
- •18.3.1.5 Cerebral Metabolism
- •18.3.2 Intracerebral Hemorrhage (ICH)
- •18.3.2.1 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.2.3 Electrophysiology
- •18.3.3 Traumatic Brain Injury (TBI)
- •18.3.3.2 Cerebral Autoregulation
- •18.3.3.3 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.3.4 Cerebral Blood Flow
- •18.3.3.5 Electrophysiology
- •18.3.3.6 Cerebral Metabolism
- •18.3.4 Acute Ischemic Stroke (AIS)
- •18.3.4.1 Cerebral Blood Flow
- •18.3.4.2 Electrophysiology
- •18.3.5.1 Cerebral Blood Flow
- •18.4 Conclusion
- •References
- •19.1 Introduction
- •19.2 Cerebral Blood Haemodynamic Measurements
- •19.3 Cerebral Blood Flow (CBF): Physiology Principles
- •19.4 Vasoreactivity Determining: Methods
- •19.6 Technical Tips
- •19.7 Vasoreactivity: Clinical Importance
- •19.8 Conclusion
- •References
- •20.1 Introduction
- •20.5.4.1 Experimental Endotoxemia
- •20.6 Conclusion
- •Appendix
- •Methods
- •Group 1: Graphic Methods
- •“Beat-by-Beat Method”
- •Method Described by Aaslid
- •Group 2: Multiparameter or Impedance Methods [14]
- •References
- •21.1 Introduction
- •21.2.1 Brain Compliance
- •21.2.2 TCD/TCCS: Cerebral Hemodynamics
- •21.4 Pulsatility Index (PI): Intracranial Pressure (ICP)
- •21.5.1 Cardiovascular Factors
- •21.5.2 Cerebrovascular Factors
- •21.5.3 Cardiopulmonary Factors
- •21.5.4 Metabolism Factors
- •21.5.5 Vascular Factors
- •21.5.6 Other Factors
- •21.6 Conclusion
- •Algorithm
- •References
- •22.1 Introduction
- •22.2 Aneurysmal Subarachnoid Hemorrhage (aSAH)
- •22.3 Cerebral Vasospasm After aSAH
- •22.5.1 TCD/TCCS: Examination Protocol
- •22.5.1.1 Transtemporal Window
- •22.5.1.2 Orbital Window
- •22.5.1.3 Suboccipital/Transforaminal Window
- •22.5.1.4 Submandibular Window
- •22.7 Conclusion
- •Algorithm
- •References
- •23.1 Introduction
- •23.3.1 Premise
- •23.3.3 Limitations
- •23.4.1 Technical Requirements
- •23.4.3 Limitations
- •23.6 Future Directions
- •23.7 Conclusion
- •Algorithm
- •References
- •24.1 Introduction
- •24.2.1 Vasospasm
- •24.2.2 Vasospasm Diagnostic Criteria
- •24.3 TCD/TCCS: Cerebral Vasoreactivity
- •24.4 TCD/TCCS: Intraoperative Monitoring
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 CAD: Diagnosis
- •25.6 Pupil: Ultrasound Examination
- •25.11 Conclusion
- •Algorithm
- •References
- •26.1 Introduction
- •26.2 Optimal Settings
- •26.2.1 Probe Types
- •26.2.2 Frequencies
- •26.2.3 Focus
- •26.2.4 Depth
- •26.2.5 Pulse Repetition Frequency (PRF)
- •26.2.6 Frame Rate
- •26.2.8 Freeze
- •26.2.9 Cine Loop
- •26.2.10 Smoothing (Interpolation), Interlacing, Correlation
- •26.2.11 Postprocessing
- •26.2.12 Resolution
- •26.2.13 Doppler-Technique
- •26.2.14 PW-Doppler (Pulsed-Wave Doppler)
- •26.2.15 Color Duplex
- •26.3 Indications
- •26.4.1.2 Morphological Differences
- •26.4.1.3 Flow Differences
- •26.4.1.4 Compression
- •26.5 B-Mode Examination
- •26.5.1 Dilation
- •26.5.2 Intima-Media Thickness (IMT)
- •26.5.3 Plaque Analysis
- •26.5.3.1 Location
- •26.5.3.3 Maximal Thickness
- •26.5.3.4 Surface
- •26.5.3.5 Echogenicity
- •26.5.4 B-Flow Imaging
- •26.6.1 Color Doppler Imaging (CDI)
- •26.6.2 Power Doppler Imaging (PDI)
- •26.7.1 Stenosis Measurement
- •26.7.1.1 Diameter Stenosis
- •26.7.1.2 Area Stenosis
- •26.7.1.3 Residual Luminal Diameter
- •26.7.2 Occlusion
- •26.7.3 Subtotal Stenosis: (>95% Stenosis)
- •26.7.4 Long Segment Stenosis
- •26.8 Doppler Spectrum
- •26.10 Contrast Enhanced Ultrasound (CEU)
- •26.11.1 Common Carotid Artery
- •26.11.2 Internal Carotid Artery
- •26.11.2.1 Stenosis
- •26.11.2.2 Dissection
- •26.11.2.3 Occlusion
- •26.11.2.4 Subtotal Occlusion: (95–99% Stenosis)
- •26.11.2.5 Multiple (Tandem) Stenosis
- •26.11.2.6 Long Segment Stenosis
- •26.11.3 External Carotid Artery (ECA)
- •26.11.3.1 Occlusion
- •26.13 Negative Report
- •26.14 Conclusion
- •Algorithm
- •References
- •27.1 Introduction
- •27.2 Anatomy: Vertebrobasilar System
- •27.3 Vertebrobasilar Circulation: Ultrasound Examination
- •27.4 TCD: Aneurysmal Subarachnoid Hemorrhage
- •27.4.1 Delayed Cerebral Ischemia
- •27.4.2 Vasospasm
- •27.5 TCD: Vertebrobasilar Dissection
- •27.6 TCD: Intracranial Stenosis
- •27.7 TCD: Microembolus Detection
- •27.9 Subclavian Steal Syndrome
- •27.10 TCD: Multimodal Monitoring
- •27.11 TCD: Traumatic Brain Injury
- •27.12 TCD: Brain Death Determination
- •27.13 Conclusion
- •References
- •28.1 Introduction
- •28.2 Cerebral Venous System: Anatomy
- •28.3 vTCCS: Ultrasound Investigation Technique
- •28.4 CVST: Venous Ultrasound Findings

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481

Chapter 28
Intracerebral Venous System: Monitoring
by Transcranial Color-Coded Duplex
Sonography (TCCS)
DixonYang, MarialauraSimonetto, NellyCampo, DignaCabral,
andTatjanaRundek
Key Points
1. Cerebral venous drainage is divided into the deep and supercial venous drainage, with most reliably insonated vessels in the deep venous system.
2. Venous transcranial color-coded duplex sonography (vTCCS) imaging has good
reliability.
3. vTCCS has potential utility as a quick, bedside, complementary diagnostic and
monitoring tool.
4. Hemodynamic characteristics on vTCCS in cerebral venous sinus thrombosis
may complement the rst diagnostic line by CT or MR imaging.
5. vTCCS has clinical utility in AVM but also may be useful in ischemic stroke,
subarachnoid hemorrhage, and intracranial hypertension.
6. Further studies are needed to determine clinical value of vTCCS.
D. Yang
Department of Neurology, New York University Langone Health, New York, NY, USA
e-mail: Dixon.Yang@nyulangone.org
M. Simonetto · N. Campo · D. Cabral
Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA
e-mail: NCampo@med.miami.edu
T. Rundek (
Evelyn F.McKnight Brain Institute, Department of Neurology, Miller School of Medicine,
University of Miami, Miami, FL, USA
e-mail: trundek@med.miami.edu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_28
*)
483© Springer Nature Switzerland AG 2022

484
D. Yang et al.
28.1 Introduction
Transcranial Doppler (TCD) and transcranial color-coded duplex sonography
(TCCS) have been widely used in examination and monitoring of extra- and intracranial arterial hemodynamics [1]. Less attention has been paid to the cerebral
venous counterpart due to early technical limitations and low clinical prevalence of
known cerebral venous disease. In adults, we were not able to formally study the
cerebral venous system using sonography until 1991 because of its technical limitations [2]. Although recent technical advances in neurosonology, venous transcranial
color-coded duplex sonography (vTCCS) does not currently belong to routine clinical examination modalities. However, vTCCS has potential utility as a quick, bedside, supplementary diagnostic and monitoring tool notably for cerebral vein and
sinus thrombosis (CVST) and arteriovenous malformations (AVM), and it has a
possible clinical value in ischemic stroke, subarachnoid hemorrhage (SAH), and
raised intracranial pressure (ICP) [3]. This chapter intends to review application and
clinical usefulness of vTCCS based on available evidence.
28.2 Cerebral Venous System: Anatomy
Relevant and reliably insonated cerebral venous anatomy to sonography consists
of the deep cerebral venous drainage, contributories of the cavernous sinus, posterior fossa sinuses, inferior petrosal sinus, and vertebral plexus [4]. Beginning anteriorly, blood drained from frontal brain regions into anterior cerebral veins forms
the deep middle cerebral vein (DMCV), which is often located adjacent to the
middle cerebral artery. The DMCV drains into the basal vein (BV), which runs a
course distally to the follow in the P2 segment of the posterior cerebral artery
around the midbrain. Bilateral BVs (also known as the veins of Rosenthal) join
midline to form the unpaired great cerebral vein (GCV) or the vein of Galen
behind the pineal gland. Along with the inferior sagittal sinus (ISS), the GCV
drains mostly into the unpaired straight sinus (SRS) located at the apex of the
cerebellum tentorium [5].
The SRS ows to the conuens sinuum (COS), where it meets supercial cerebral venous drainage that is functionally separated from deep cerebral venous vasculature by a venous watershed. Notably of the supercial system, the superior
sagittal sinus (SSS) drains into the COS and then bifurcates into the transverse
sinuses (TS), which dives underneath the occipital bone to eventually forms the
sigmoid sinus and drains into the internal jugular vein. It should be noted that the
low ow velocities, unfavorable insonation windows, and frequent anatomic variations of the SSS, COS, and TS make them less detectable vessels on vTUS [6, 7]
(Fig.28.1).

Superior
ein
sinus
28 Intracerebral Venous System: Monitoring by Transcranial Color-Coded Duplex…
485
Fig. 28.1 Intracerebral
venous system anatomy
sagittal sinus
Occipital
sinus
Inferior
sagittal sinus
Straight
sinus
Sigmoid
sinus
Internal
cerebral veins
Basal vein
of Rosenthal
Great
cerebral vein
(Galen vein)
Internal
jugular v
Transverse
28.3 vTCCS: Ultrasound Investigation Technique
Intracranial venous examination with ultrasound (TCCS) generally begins with
insonation through the temporal window to identify the mesencephalon as a landmark.
From there, the deep middle cerebral vein is found adjacent to the middle cerebral artery,
with venous ow toward the center of the brain, away from the probe. Downward angulation can visualize the sphenoid bone and superior petrosal sinus with ow away from
the probe, draining into the cavernous sinus that usually cannot be insonated. Upward
angulation from the mesencephalon can visualize the basal vein of Rosenthal (Fig.28.2),
which is slightly cranial from the P2 segment of the posterior cerebral artery.
Brightness mode (B-mode) increases depth so that contralateral structures can be
insonated. The great cerebral vein (Fig.28.3) can be found behind the echogenic
pineal gland and third ventricle. The straight sinus (Fig.28.4) can be located after
upward rotation of the transducer to visualize the echogenic cerebellar tentorium. It
drains away from the transducer toward the conuens sinuum. The contralateral
transverse sinus (Fig.28.5) can be seen with downward angulation. Transforaminal
examination will reveal the vertebral venous plexus and the inferior petrosal sinus
near the basilar artery, with venous ows directed toward the transducer.
There are no consensus guidelines regarding vTCCS examination, but there are
several validated TCCS and TCD protocols that use this general approach [8].
TCCS is often preferred because it can display vascular anatomy in relation to brain
parenchyma and not only ow velocities and ow direction as in non-imaging
TCD.Further signal improvement can be achieved by intravenous administration of
echo-contrast, which is not commonly used in most TCCS or TCD protocols.
Established normative data are presented in Table28.1.

486
Fig. 28.2 Basal vein of Rosenthal
D. Yang et al.
Fig. 28.3 Great Cerebral vein (Galen)

28 Intracerebral Venous System: Monitoring by Transcranial Color-Coded Duplex…
Fig. 28.4 Straight sinus
487
Fig. 28.5 Transverse sinus

488
Table 28.1 Venous ow velocities of healthy adults using TCCS without angle-correction
Vessel Peak systolic ow (cm/s) End diastolic ow (cm/s) Visualization (%)
DMCV 8.5±2.9
8.7±2.9
8.6±1.9
BV 12.4±4.0
12.2±3.8
11.9±2.9
SRS 13.1±5.1
12.2±3.8
11.6±2.3
GCV 10.6±3.7
11.9±3.6
10.2±1.8
TS 4.9±6.7
14.0±5.9
16.4±4.4
SSS/CON 10.6±3.6
9.8±3.6
12.2±4.1
Data within each cell is listed in order from Stolz [8–10]
Percent visualization of veins is presented in range across the three studies
5.7±1.9
5.8±1.9
5.9±1.4
8.9±3.0
8.6±3.7
7.2±1.8
9.4±4.0
8.6±3.7
7.2±1.8
7.5±2.8
7.7±2.8
7.4±1.5
10.4±5.3
9.7±4.8
11.8±3.7
6.7±2.6
6.1±2.5
8.7±3.3
D. Yang et al.
76-91
89-95
71-83
89-98
67-69
52-58
28.4 CVST: Venous Ultrasound Findings
Urgent neuroimaging using magnetic resonance imaging (MRI) with venography or
computed tomography (CT) with venography are the rst choice diagnostic tools
for acute CVST, with digital subtraction angiography as the gold standard [11].
Normal sonographic ndings in vTCCS cannot positively rule out CVST even if
contrast enhancers are used; however, vTCCS may serve as a complementary tool
to MRI or CT [3]. In 1994, increased venous ow signal in bilateral DMCVs was
rst reported in SSS thrombosis, which normalized after anticoagulant therapy [12].
Smaller reports have supported changed venous hemodynamics in SSS thrombosis
though in different vessels [13, 14]. Given the absence of valves in the cerebral
venous drainage, intracranial veins may serve as collaterals and their ow may even
reverse [5]. Four sonographic ow characteristics of CVST have been described,
broadly classied as one direct criterion and three indirect criteria.
The direct criterion involves missing venous ow signals that would theoretically suggest cut-off ow from thrombosis. However, vTCCS cannot reliably distinguish between frequently encountered anatomical variations and occlusive clot.
Even with echo-contrast TCCS, occluded ow was either aplastic TS or complete
TS occlusion after MRI conrmation, while residual sonographic signals were
either hypoplastic vessel or non-occluded TS thrombosis. Examination with vTCCS
in one study missed one case of complete TS occlusion due to false-positive signal
from a dural stula [15]. Clinically, this direct criterion’s sensitivity and specicity
are too low for practical use.
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