BlueCross and BlueShield of Montana Medical Policy/Codes
Transcranial Doppler (TCD) Ultrasound
Chapter: Medicine: Tests
Current Effective Date: October 25, 2013
Original Effective Date: October 25, 2013
Publish Date: July 25, 2013
Revised Dates: This policy is no longer scheduled for routine literature review and update.

Transcranial Doppler (TCD) is a non-invasive modality for imaging blood flow in cerebral arteries and veins that is used principally in the evaluation and management of patients with cerebrovascular disease.  In TCD, a probe placed over the skull generates ultrasonic waves.  The bony plate of the skull limits TCD measurements to three primary sites (or acoustic windows).  The sites are:

  • Temporal bone along the orbito-meatal line (the opening of the boney cavity that contains the eyeball),
  • Optic foramina (a passage through the bone for the eye),
  • Foramen magnum (the large opening in the inferior and anterior part of the occipital bone interconnecting the vertebral canal and the cranial cavity) at the base of the skull.

Sound waves transmitted through these windows are reflected by blood in the intracranial vasculature. The frequency shift of the reflected sound waves recorded at the probe is used to estimate blood flow velocity or volume.

Vasomotor reactivity testing and microemboli detection are newer techniques with TCD that can assist in evaluation of impaired cerebrovascular hemodynamics. In patients with known or suspected cerebrovascular disease, TCD can aid in assessing autoregulation and vasomotor reactivity (VMR) of the distal cerebral arteriolar bed in response to small blood pressure changes and physiologic stimuli. VMR testing techniques of static (i.e., at rest) or dynamic (i.e., after provocative stimuli) cerebral autoregulation include measuring changes in flow velocities following:

  • Hemodynamic stimuli (e.g., Valsalva maneuver, head-down tilting),
  • CO2 inhalation (e.g., hyperventilation hypocapnia),
  • Breath-holding index (BHI),
  • Acetazolamide injection,
  • Transient hyperemia response and its variants.

TCD has also been used to detect microemboli signals or “high-intensity transient signals” (HITS). Particulate (solid, fat) matter and gaseous materials in flowing blood have different acoustic impedance properties than surrounding red blood cells. The Doppler ultrasound beam is both reflected and scattered at the interface between the embolus and blood, resulting in an increased intensity of the received Doppler signal. The hierarchy of backscatter of the ultrasound, in descending order, is gaseous emboli, solid emboli, and normal-flowing blood (including transient red blood cell aggregates). These signals have been detected in a variety of conditions (e.g., internal carotid stenosis, fat embolization syndrome, and others) as well as in a number of procedures (e.g., coronary catheterization, carotid endarterectomy, and others).

The foramen ovale is an opening in the heart septum between the right and left atria, which is normally present in the fetus and seals shortly after birth. Patent foramen ovale (PFO) occurs when the foramen ovale does not seal; PFO is present in up to 27% of the general population. There is debate within the neurology and cardiology communities about the role of a PFO in cryptogenic (i.e., of unknown cause) neurologic events, e.g., strokes and transient ischemia attacks—a PFO may possibly permit microemboli to bypass the pulmonary circulation and enter the intracranial circulation. A PFO can be detected noninvasively by transthoracic echocardiography (TTE), transesophageal echocardiography (TEE) or TCD imaging. In TEE and TTE, agitated saline is injected into a peripheral vein during echocardiography, and small air bubbles can be seen crossing from the left atrium to the right atrium on echocardiographic imaging; it may be possible to see bubbles travel across a PFO either at rest or during a cough. (Bubbles will only flow from right atrium to left atrium if the pressure is greater in the right than the left.) Right-to-left shunting detection by transcranial Doppler involves the recording of agitated saline bubbles mimicking microemboli as they pass through the middle cerebral artery as a series of embolic tracks seen on ultrasonography through the temporal bones. TEE is considered the gold standard for diagnosing PFO.


Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions. Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply. If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.

Medically Necessary

Blue Cross and Blue Shield of Montana (BCBSMT) may consider Transcranial Doppler (TCD) Ultrasound medically necessary when used for any of the following:

  1. Monitoring for vasospasm in patients with subarachnoid hemorrhage;
  2. Assessment of patients suspected of having steno-occlusive disease of the intracranial arteries;
  3. Assessing initial collateral blood flow and embolization during carotid endarterectomy (CEA) in order to reduce the risk of stroke by detecting severe ischemia and the possible need for a shunt to be placed;
  4. As a tool to determine risk for transient ischemic attacks (TIA) or cerebrovascular accidents (CVA) in patients with sickle cell disease;
  5. As a confirmatory test in support of a clinical diagnosis of brain death;
  6. Assessment and detection of patent foramen ovale (PFO) and/or to determine cause of cryptogenic stroke when transesophageal echocardiography (TEE) is contraindicated.  NOTE:  Examples of contraindications for TEE include, but are not limited to:
    • Unrepaired tracheoesophageal fistula;
    • Esophageal obstruction or stricture;
    • Perforated hollow viscus;
    • Poor airway control;
    • Severe respiratory depression;
    • Uncooperative, unsedated patient;
    • History prior esophageal surgery;
    • Esophageal varices or diverticulum;
    • Gastric or esophageal bleeding;
    • Vascular ring, aortic arch anomaly with or without airway compromise;
    • Oropharyngeal pathology;
    • Severe coagulopathy;
    • Cervical spine injury or anomaly.


BCBSMT considers TCD experimental, investigational and unproven when used for any other indication, including but not limited to the following:

  1. Evaluating hemodynamic significance of extracranial vascular atherosclerosis;
  2. Evaluating cerebral blood flow following trauma;
  3. Assessing migraine and tension headaches;
  4. Assessing cerebral blood flow and embolic events during cardiopulmonary bypass surgery;
  5. Evaluating blood flow patterns in central nervous system infections;
  6. Evaluating dementia;
  7. Evaluating glaucoma;
  8. Detection and assessment of the circulatory patterns of arteriovenous malformations (AVM);
  9. Assessing hydrocephalus;
  10. Testing vasomotor reactivity (VMR) to detect abnormalities of cerebral hemodynamics;
  11. Detecting cerebral microemboli signals for diagnostic uses, or for monitoring response to antithrombotic therapy;
  12. Monitoring vasodilator therapy as a treatment of behavior or developmental disorders including, but not limited to, attention deficit hyperactivity disorder (ADHD), autism, or Tourette’s syndrome.


Routine Transcranial Doppler (TCD) examination of the intracranial arteries was demonstrated to be possible in 1982. TCD is primarily a technique for measuring relative changes in flow. One fact that has to be constantly kept in mind when utilizing TCD is that the value obtained for a particular artery is the velocity of blood flowing through the vessel, and unless the diameter of the vessel is established by other means it is not possible to determine the actual blood flow.

In 1998 Adams, R.J., et al., reported on a trial of chronic blood transfusions in 130 children with sickle cell anemia and abnormal results on TCD. A total of 63 patients were randomized to receive transfusions to achieve a target hemoglobin S concentration; children received transfusions every three to four weeks. The remaining 67 patients received standard care. There was a significant decrease in the incidence of stroke in the transfusion group, leading to premature termination of the trial. In their 2004 technology assessment, the American Academy of Neurology (AAN) concluded that the clinical utility of TCD is established for assessing stroke risk in children with sickle cell disease.

Brain death is a clinical diagnosis that can be supported by TCD evidence of absent cerebral blood flow; diagnostic criteria for cerebral circulatory arrest or brain death using TCD have been published, with sensitivity and specificity of 91 to 100% and 97 to 100%, respectively. The specificity is imperfect as absence of middle cerebral artery (MCA) flow may be transient or basilar artery (BA) flow may still be present; when systolic spikes are present in multiple intracranial compartments, recovery is unlikely. TCD is especially helpful in patients with suspected brain death who have loss of brainstem function due to isolated brainstem lesions or who received sedative or paralytic agents that render clinical examination or interpretation of electroencephalogram (EEG) difficult. Based on the evidence, the AAN assessment concluded that TCD can confirm the clinical diagnosis of brain death, and is a useful adjunct test for the evaluation of cerebral circulatory arrest associated with brain death.

Intracranial atherosclerosis is responsible for up to 10% of transient ischemic attacks (TIA) and strokes. TCD ultrasound offers a noninvasive method of detecting discrete stenoses or occlusions of the intracranial vessels. The Blue Cross Blue Shield Association (BCBSA) policy, which is based partially on the BCBSA Technology Evaluation Center 1994 (TEC) Assessment, concluded that aggregate evidence suggests TCD ultrasound is moderately to highly (73-95%) sensitive and highly (90-100%) specific relative to cerebral angiography for detection of intracranial stenosis or occlusion in patients who have TIA or cerebrovascular accident (CVA) of unknown etiology, after cardiac and extracranial carotid artery evaluation; TCD results can occasionally influence the use of therapeutic options. In addition, the AAN assessment states that TCD is probably useful for the evaluation of patients with suspected intracranial steno-occlusive disease, but that data are insufficient to give a recommendation regarding replacing conventional angiography with TCD.

The principal cause of stroke following carotid endarterectomy (CEA) is embolism from the operative site. Available evidence suggests that intraoperative TCD measurements of collateral flow after carotid clamping for CEA are fairly accurate. The BCBSA TEC assessment noted at least two large studies that suggest intraoperative shunting reduces the CVA rate for patients who have poor collateral flow and increases the CVA rate for patients who have good collateral flow, as measured by TCD. These findings provide direct evidence of a reduced perioperative stroke rate for patients undergoing CEA when TCD ultrasound is used to guide selective intraoperative shunt use and severe ischemia is used as the criterion for intraoperative shunting. The AAN assessment also states that CEA monitoring with TCD can provide feedback that may help the surgeon take appropriate measures at all stages of the operation to reduce risk of perioperative stroke.

Contrast transcranial Doppler ultrasonography (cTCD) has been studied as a diagnostic technique for assessing cardiac right-to-left shunt (RLS), such as PFO. Spencer et al. reported 98% sensitivity and 94% accuracy when detecting PFO with power motion-mode transcranial imaging, compared with 91% sensitivity and 99% accuracy with transesophageal echocardiography (TEE). However, the presence of microbubbles in the cerebral circulation is not exclusive to an interatrial communication. Any cause of RLS, including ventricular septal defect and pulmonary arteriovenous malformation, can lead to a positive transcranial Doppler reading for a cardiac RLS, thus lowering the specificity of this test. The AAN technology assessment states “Data show a high correlation between contrast-enhanced TCD and contrast-enhanced TEE, with essentially 100% concordance for the “clinically significant” high number of particles shunted. Nevertheless, the sensitivity and specificity of contrast TCD for detecting right-to-left cardiac or extracardiac (pulmonary arteriovenous) shunts may vary by center, protocol, and diagnostic criteria. The routine performance of the Valsalva maneuver during testing can improve sensitivity and specificity. The sensitivity of contrast TCD can also be improved by using a higher volume of agitated saline (10 mL instead of 5 mL), use of Echovist (especially Echovist-300) instead of agitated saline, or repeating the Valsalva maneuver if the initial result is negative. Contrast TCD is comparable with contrast TEE for detecting RLS due to PFO. However, TEE is better than contrast TCD because it provides direct anatomic information regarding the site and nature of the shunt or presence of an atrial septal aneurysm. Whereas the number of microbubbles reaching the brain can be quantified by TCD, the therapeutic impact of this additional information is unknown. The AAN concluded that, although TCD is able to provide information, other tests are typically preferable for diagnosing right-to-left cardiac shunts; TEE is superior because it can provide direct information regarding the anatomic site and nature of the shunt.

The AAN technology assessment reported that there is probable evidence that vasomotor reactivity (VMR) testing techniques with TCD can detect abnormalities of cerebral hemodynamics in patients with risk factors for or symptoms of cerebrovascular disease, and is probably useful for detection of impaired cerebral hemodynamics in patients with asymptomatic severe (>70%) stenosis of the extracranial internal carotid artery, extracranial internal carotid artery occlusion, and cerebral small artery disease. However, how the results from these techniques can be used to influence therapy and affect patient outcomes remains to be determined.

The AAN also reported that new hardware and software technical capabilities may help detection of microembolic signal, and discrimination from artifact. However, accurate and reliable characterization of embolus size and composition is not possible with current technology, and data have not shown that detection of microemboli signals leads to improved patient outcomes. In addition, although TCD is probably useful to detect cerebral microemboli signals in a wide variety of cardiovascular/cerebrovascular disorders and/or procedures, current data do not support the use of microemboli detection with TCD for diagnosis, or for monitoring response to antithrombotic therapy in ischemic cerebrovascular disease.

TCD has been proposed as a technique to monitor vasodilator therapy in patients with developmental or behavioral disorders. It has been hypothesized that these disorders are related to cerebral vasospasm that can be relieved by vasodilator therapy. However, a search of the MEDLINE database failed to identify any peer-reviewed articles focused on this therapy.

Neither the BCBSA nor the AAN technology assessments found sufficient data to support the routine use of TCD for other indications including, but not limited to: migraine; cerebral venous thrombosis; evaluating hemodynamic importance of extracranial atherosclerosis; monitoring during cerebral angiography; evaluation of arteriovenous malformations (AVM); evaluation of cerebral autoregulation in other settings; evaluating hydrocephalus, dementia, or glaucoma; evaluating blood flow patterns in central nervous system infection; assessing cerebral blood flow during cardiopulmonary bypass surgery or after head trauma.

2012 Update

A search of peer reviewed literature through June 2012 identified no new clinical trial publications or any additional information that would change the coverage position of this medical policy.


Disclaimer for coding information on Medical Policies           

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive.           

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers. Only the written coverage position in a medical policy should be used for such determinations.           

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps.

ICD-9 Codes
88.71.  Refer to the ICD-9-CM Manual.
ICD-10 Codes

B040ZZZ, BH4CZZZ.  Refer to the ICD-10-CM Manual.

Procedural Codes: 93886, 93888, 93890, 93892, 93893
  1. CMS—National Coverage Determination for noninvasive tests of carotid function (20.17) (1980 November 15) Centers for Medicare and Medicaid Services. Available at (accessed on 8/29/2007).
  2. Transcranial Doppler Ultrasound. Chicago, Illinois: Blue Cross Blue Shield Association – Technology Evaluation Center Assessment Program (1994 August) 9(20):1-29.
  3. Cerebrovascular Diseases. Scientific American Medicine (February 1994) Chapter X, page 1-5.
  4. MRA of the head. Chicago, Illinois: Blue Cross Blue Shield Association – Technology Evaluation Center Assessment Program (1997 March) 11(31):1-57.
  5. Transcranial Doppler Ultrasound. American Journal of Neuroradiology. (1997 January) 18(1):127-33.
  6. Annals of Vascular Surgery. (1997 January) 11(1):9-13.
  7. Sliwka, U., Lingnau, A., et al. Prevalence and time course of microembolic signals in patients with acute stroke. A prospective study. Stroke (1997 February) 28(2):358-63.
  8. Droste, D.W., Hagedorn., G., et al. Bigated transcranial Doppler for the detection of clinically silent circulating emboli in normal persons and patients with prosthetic cardiac valves. Stroke (1997 March) 28(3):588-92.
  9. Spencer, M.P. Transcranial Doppler monitoring and causes of stroke from carotid endarterectomy. Stroke (1997 April) 28(4):685-91.
  10. Arnold, M., et. al. Continuous intraoperative monitoring of middle cerebral artery blood flow velocities and electroencephalography during carotid endarterectomy. A comparison of the two methods to detect cerebral ischemia. Stroke (1997 July) 28(7):1345-50.
  11. Anemia: Hemolysis. Scientific American Medicine (1997  April) Chapter IV, page 22.
  12. Adams, R.J., McKie, V.C., and Hsu, L., et. al. Prevention of a first stroke by transfusions in children with sickle cell anemia and abnormal results on transcranial Doppler ultrasonography. New England Journal of Medicine (1998) 339:5-11.
  13. Cohen, A.R. Sickle cell disease - new treatments, new questions (Editorial). New England Journal of Medicine (1998) 339:42-44.
  14. Babikian, V.L., Transcranial Doppler Ultrasonography. Journal of Neuroimaging. (1999)
  15. Alexandrov, Andrei V., and M. Joseph. Transcranial Doppler:  An Overview of its Clinical Applications. Journal of Emergency and Intensive Care Medicine (2000) 4(1).
  16. Anzola, G. P. Transcranial Doppler: Cinderella in the assessment of patent foramen ovale in stroke patients. Stroke (2004) 35:e137.
  17. Uzuner, N., Horner, S., et al. Right-to-left shunt assessed by contrast transcranial Doppler sonography. Journal of Ultrasound Medicine (2004) 23:1475-82.
  18. Desai, A. J., Fuller, C. J., et al. Patent foramen ovale and cerebrovascular diseases. Nature Clinical Practice Cardiovascular Medicine (2006) 3:446-55.
  19. Transcranial Doppler Ultrasound. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (2006 April) Radiology 6.01.07.
  20. Sloan, M.A., Tegeler, C.H., Assessment: Transcranial Doppler Ultrasonography—Report of the therapeutics and technology assessment subcommittee and of the American Academy of Neurology. Neurology. (2004) 62:1468-81 (Reaffirmed November 2007).
July 2013  New 2013 BCBSMT medical policy.
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Transcranial Doppler (TCD) Ultrasound