Vascular Medicine. Thomas Zeller

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target="_blank" rel="nofollow" href="#fb3_img_img_6490c939-e834-5df3-98e5-854c43951ec0.jpg" alt=""/> Fibromuscular dysplasia.

      

Beaded appearance.

      

AVM feeder.

      

Typical excess flow signal, particularly in diastole.

      

Long increase in flow velocity.

      

Possibly corresponding changes in the afferent extracranial vessels.

      

Possibly pulsatile venous flow.

      

Congenital variants.

      

The vertebral artery often shows hypoplasia and also aplasia.

      

The anterior/posterior communicating branch is often hypoplastic or aplastic.

      

The P1 segment of the posterior cerebral artery is often hypoplastic (in up to 20% of cases)—then there is supply from P2 via the posterior communicating branch—i.e., from the internal carotid artery (caution: stenosis of the internal carotid artery may then be the cause of posterior infarction).

      Specific findings

       Middle cerebral artery

      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:

      

Long increased flow velocities without circumscribed turbulence phenomena.

      

Increased flow velocities, possibly also in medial branches.

      

Flow velocities not exceeding 2 m/s.

      

Quotients for maximum velocities in the middle cerebral artery/internal carotid artery < 2; values > 3 tend to suggest stenoses.

      

The intra-individual course shows a tendency toward normalization.

      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:

      

Demonstration of post-stenotic and postocclusive flow, assessment of the spectrum (steepness of increase, acceleration time, V_max systolic/diastolic)

      

Demonstration of collateralization pathways (ideally using duplex ultrasonography)

      

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