Unremarkable findings: maximum systolic velocity < 120 (–140) cm/s, with no flow disturbances detectable acoustically or in the spectral analysis.
Borderline findings: circumscribed maximum velocities around 140 cm/s (> 120 cm/s), but still with no flow disturbances.
Hyperperfusion: during recanalization after a stroke, there may be a phase of hyperperfusion. Signs arguing in favor of hyperperfusion and against a stenotic process in the middle cerebral artery are:
Similar findings are seen after carotid surgery, with hyperperfusion (an increased flow velocity of > 50% in the middle cerebral artery on side-to-side comparison) also being observed in some patients—particularly those with poor preoperative collateralization and long clamping times (Widder 1999)—as a sign that autoregulation is still disturbed.
Low-grade stenosis (50 to < 70%): circumscribed increase in the maximum systolic flow velocity to values of 140–200 cm/s, as well as in middle and possibly diastolic flow velocities. The critical velocity after which the presence of a stenosis of more than 50% can be definitely assumed is 220 cm/s (Baumgartner et al. 1999). Incipient flow disturbances, spectral widening, signs on the color Doppler signal of localized increases in flow velocity and turbulences, possibly a mixed signal with a normal main trunk signal and a stenotic signal in M2/middle artery stenoses.
Moderate stenosis (approximately 70% to < 80%): a focal increase in the maximum systolic flow velocity to values of 200–280 cm/s and also diastolic flow velocities. Clear flow disturbances, spectrum widening, blurred systolic window, retrograde flow components, marked signs on the color Doppler signal of a localized increase in flow velocity, reduced lumen size possibly visible in velocity mode and/or power mode.
High-grade stenosis (> 80%): a circumscribed increase in maximum systolic flow velocity to values of > 280 cm/s and of the diastolic flow velocities, marked flow disturbances, spectrum widening, blurred systolic window, marked retrograde flow components, clearly reduced post-stenotic flow velocity, marked signs on the color Doppler signal of a localized increase in flow velocity, also an increase in diastolic flow velocity visible particularly with variance coding (candleflame phenomenon), lumen reduction visible in velocity mode and/or power mode, possible occurrence of musical murmurs.
Middle cerebral artery main trunk occlusion (M1): no demonstrable M1 signal despite good ultrasound imaging conditions, reduced flow velocities in the proximal vessels, possibly hyperperfusion of collaterals—e.g., the anterior and posterior cerebral arteries as afferent vessels for leptomeningeal anastomoses; in cases of occlusion distal to the origins of the lenticulostriate arteries, there may be a typical prestenotic highly pulsatile signal with low flow velocity in the proximal main trunk—confirmation using ultrasound contrast enhancement.
Middle cerebral artery branch occlusion (M2): lower flow velocity in the M1 segment in side-to-side comparison, possibly higher pulsatility in M1, absent M2 imaging, possible hyperperfusion of collaterals—e.g., the anterior and posterior cerebral arteries as afferent vessels for leptomeningeal anastomoses; possible retrograde perfusion of collaterals, occlusions of small vessels not detectable; flow differences in the proximal middle cerebral artery can be identified by detecting absolute systolic/diastolic velocities and by detecting pulsatility differences.
Carotid-T processes: these are often combined with distal internal carotid artery and outflow regions of the middle and anterior cerebral arteries; carotid-T occlusion processes are the hemodynamically most severe findings, since all collateralization pathways from the middle cerebral artery are blocked with the exception of leptomeningeal anastomoses. The anterior cerebral artery may be collateralized from the contralateral side via the anterior communicating branch.
Assessment of hemodynamic consequences:
– Clarifying the indication for surgery in multiple-vessel disease (e.g., internal carotid artery stenosis with contralateral occlusion)
– Assessment of the afferent components of the various collateral pathways
– Assessment of the hemodynamic consequences of a potential vascular occlusion (e.g., progressive asymptomatic internal carotid artery stenosis)
– Testing the quality of the collateralization
– Detecting any collateral pathways that cannot be spontaneously imaged (e.g., posterior communicating branch) by inducing hyperperfusion
– Assessment of the risk of intraoperative clamping (see below) before or during carotid thromboendarterectomy or proximal embolic protection. Evidence for sufficient residual perfusion includes:
– In cases of ≤ 80% stenosis of the internal carotid artery: mean residual flow velocity in the middle cerebral artery > 30–40% of the resting value
– In cases of ≤ 80% stenosis of the internal carotid artery: mean residual flow velocity ≥ 30 cm/s
– Correlates with the risk of hemodynamic watershed infarction—corresponds to the remaining CO2-induced dilation capacity in the intracerebral vessels
– Methods:
– Breath-holding index
– Doppler CO2 testing
– Apnea–hyperventilation testing
– Acetazolamide (Diamox) testing
Fig. 1.2–6 Apnea test. Top: the power Doppler profile of the middle cerebral artery bilaterally, with massively reduced amplitude on the right, reduced pulsatility and prolonged acceleration time as signs of poor intracerebral collateralization in subtotal internal carotid artery stenosis. Bottom: inverse steal phenomenon in the apnea test as a sign of an absent autoregulation reserve and steal in a vascular area that is still capable of reacting.
The apnea–hyperventilation test is the fastest exploratory test in routine work: