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7 — Intracranial Cerebrovascular Examination
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of 6 months’ testing experience and at least 100 ab- normal studies with correlations for proficiency.
The calculation of velocity from the Doppler-shifted frequencies depends on the angle of insonation. Using a nonimaging technique, the angle is not measured and is operator dependent, requiring skill in obtaining the signal with the highest audible pitch and therefore the highest velocity.
Patient cooperation is required to obtain an accu- rate study; some patients may be agitated and unable to remain still and quiet.
In the setting of severe stenosis, vasospasm, col- lateral flow, and hyperemia, there can be very high velocities. Aliasing of the pulsed wave Doppler can occur and should be recognized.
DIAGNOSIS
Both TCD and TCDI rely on the Doppler spectral waveforms for interpretation of normal and ab- normal exams. Normal Doppler spectral values have been established for each arterial segment. TCD interpretation requires a solid understanding of flow dynamics, systemic physiological variables that impact the cerebral circulation, and strong pattern recognition skills (see Table 7-2). The pri- mary diagnostic features of the signals include (1) alteration in velocity, (2) deviations from lami- nar flow, (3) changes in pulsatility, and (4) chang- es in the direction of flow. Adjacent artery ratios, side-to-side, and extracranial-to-intracranial indi- ces have been developed to help differentiate vari- ous findings.
The spectral waveform parameters include:
• Velocity: This is usually expressed in centimeters per second. Spectral analysis allows the quanti- fication of the PSV, EDV, and TAP-V (commonly referred to as simply “mean velocity”). The mean velocity is the primary diagnostic feature
used in TCD and TCDI.
• Pulsatility: In adults this is expressed as Gosling’s
pulsatility index (PI), which is calculated as:
PI 􏰁 (PSV 􏰃 EDV) __
TAP-V
• Disturbed or turbulent flow: This is represented in the spectral waveform as high-amplitude, low-velocity signals and flow velocities below the zero baseline. It is also apparent as a dis- ruption of the smooth contour of the waveform outer envelope.
• Systolic upstroke: This is the initial slope of the peak velocity envelope during the acceleration phase of systole.
• Lindegaard ratio: This is calculated as the MCA mean velocity divided by the submandibular ICA mean velocity. This ratio is useful in differentiating increased volume flow from a decreased diameter when high velocities are encountered in the MCA or intracranial ICA.
• Sviri ratio: This ratio is similar to the Lindegaard ratio for determining vasospasm from hyper- dynamic flow in the posterior circulation. The bilateral VA mean velocities taken at the atlas loop are added together and averaged. This ave- raged velocity is then divided into the highest BA mean velocity (Fig. 7-24).
APPLICATIONS FOR INTRACRANIAL CEREBROVASCULAR EXAMINATIONS
There are multiple applications for intracranial cerebrovascular examinations. These applications have expanded over the years. As the technology has continued to advance, this has lead to further applicability for intracranial cerebrovascular evalu- ations. Pathology Box 7-1 lists some of the com- mon abnormalities observed during TCD or TCDI examination.
TCD FINDINGS IN EXTRACRANIAL CAROTID ARTERY DISEASE—COLLATERAL FLOW
When an extracranial carotid artery stenosis reaches hemodynamic significance, the brain will compen- sate through the mechanisms of collateral flow and autoregulation. TCD is useful in identifying and as- sessing the presence and adequacy of collateral cir- culation and improving the understanding of the individual cerebral circulatory function and status. TCD assessment of cerebral collateralization also helps predict hemodynamic consequences of cross- clamping during carotid endarterectomy. There are three primary collateral patterns that can be accu- rately determined using TCD, and the diagnostic criteria for each collateral type are listed in the fol- lowing sections (Fig. 7-25).
External Carotid to Internal Carotid through a Reversed Ophthalmic Artery22,23
• Direct evidence of carotid artery disease
• Retrograde flow in the OA
• Decreased pulsatility and increased velocity in
the OA
• Obliteration, diminishment, or reversal of flow
in the OA with compression of the branches of the ECA (superficial temporal, facial, or angular arteries)