(Stroke. 2002;33:99.)
© 2002 American Heart Association, Inc.
Original Contributions |
From the University of Texas-Houston Medical School (A.E.-M., I.C., M.M., A.V.A.), and the Department of Neurology (A.E.-M., M.S.), Mansoura University, Mansoura, Egypt.
Correspondence to Dr Andrei V. Alexandrov, MSB 7.044, University of Texas, 6431 Fannin St, Houston, TX 77030. E-mail avalexandrov{at}att.net
| Abstract |
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Methods Consecutive acute ischemic stroke patients receiving intravenous tissue plasminogen activator (TPA) were studied. Pretreatment NIHSS scores and bedside transcranial Doppler (TCD) were obtained for all patients.
Results A total of 95 patients treated with intravenous TPA at 132±60 minutes from stroke onset were studied. On TCD, 48 had isolated MCA occlusion (mean NIHSS 16.8±5.8, median 17, range 5 to 28); and 16 had tandem ICA/MCA occlusion (mean NIHSS 18.8±5.8, median 22, range 8 to 29; P=NS). In the MCA occlusion and tandem ICA/MCA occlusion groups, 19% and 11%, respectively, had NIHSS scores <12 points. Compared with the NIHSS scores in patients with hemiplegia, forced gaze deviation, and complete neglect, the lower NIHSS scores were attributable to partial arm and/or leg paresis, gaze preference, and partial neglect. In those patients, TCD showed
2 major collateral channels and low-resistance flow at the M1 origin, suggesting perfusion of perforating arteries. Although TCD cannot differentiate between high-grade ICA stenosis or occlusion, collateral flow patterns and stenotic signals at the terminal ICA differentiated tandem lesions from isolated MCA occlusion (P<0.01).
Conclusions Tandem ICA/MCA occlusion was found on TCD in 17% of TPA-treated patients. NIHSS scores were similar in patients with isolated MCA and tandem occlusions. Lower NIHSS scores were seen in patients with a higher number of major collateral flow channels and higher Thrombolysis in Brain Ischemia (TIBI) flow grades at the MCA origin.
Key Words: occlusion stroke tissue plasminogen activator ultrasonography, Doppler, transcranial
| Introduction |
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Different treatment strategies are advocated for patients with acute stroke who have proximal MCA and ICA thrombi. Intravenous tissue plasminogen activator (TPA) may lyse some of these thrombi; however, recanalization of the proximal ICA occlusion almost never occurs with this therapy.3,4 Intra-arterial thrombolysis had higher recanalizations rates for M1 MCA occlusion in a recent study,5 yet even with an intra-arterial delivery of a lytic agent, ICA recanalization rates remain low. Newer thrombus-disrupting mechanical devices are undergoing pilot evaluations in patients with ICA and MCA occlusions.
Our comparative studies between transcranial Doppler (TCD) and angiography have shown that in the emergency room, TCD can reliably identify the presence and location of arterial occlusion,6,7 similar to results previously shown by others.815 TCD also has the ability to identify major collateral channels and residual flow signals in the MCA stem.8 These findings also have early prognostic significance for anterior circulation stroke, and clot localization can be helpful in selecting patients for therapeutic interventions.11,16
A few studies have attempted to correlate clinical findings with clot presence and location in acute ischemic stroke.1,2,11,17 Patients with ipsilateral motor/sensory deficit, homonymous hemianopia, and higher cortical dysfunction had MCA and/or ICA occlusion or a severe MCA stenosis, whereas pure motor or sensory symptoms without cortical signs were attributable to small perforating artery lesions without major vessel occlusion.18 Occasionally, we have observed that hyperacute stroke patients with MCA and/or ICA occlusions may present with mild stroke severity or mimic lacunar events.19
In the present study, we sought to describe the clinical and sonographic patterns in patients who arrived at the emergency department with tandem ICA/MCA occlusion and were eligible for intravenous TPA therapy.
| Subjects and Methods |
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0.2 second). Minor criteria were as follows: decreased pulsatility index (
0.6 or interhemispheric difference
30%), flow diversion signs (velocity: posterior cerebral artery>MCA, posterior cerebral artery>ICA, and contralateral anterior cerebral artery>MCA), and compensatory velocity increase (
20% increase in the contralateral hemispheric vessels or vertebrobasilar arteries). In a study of 517 stroke patients, when this broad battery was used versus angiographic findings to detect a severe stenosis or occlusion of the extracranial or intracranial ICA, sensitivity was 79% and specificity was 86%.22 Tandem ICA/MCA occlusion was diagnosed when TCD detected abnormal TIBI MCA waveforms or an asonic MCA segment in the presence of 1 major or 2 minor findings according to the broad TCD battery for an ICA obstruction (Table 1). In other words, an abnormal TIBI waveform indicates the presence of an MCA occlusion, whereas an additional finding of at least 1 collateral channel indicates a proximal hemodynamically significant lesion in the feeding vessel.6,7,22
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TCD was performed and interpreted at bedside by an experienced sonographer not involved in the clinical assessment of the patient. Pretreatment NIHSS scores were obtained for all patients by a neurologist not involved in TCD performance or interpretation.
| Results |
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Sonographic findings in patients with tandem ICA/MCA occlusions versus isolated MCA occlusions were as follows: anterior communicating artery, 62% versus 0%; posterior communicating artery, 65% versus 0%; reversed ophthalmic artery, 86% versus 0%; flow diversion, 85% versus 0%; positive diastolic flow at the MCA origin, 56% versus 30%; and contralateral flow velocity increase, 93% versus 10% (Figure 1).
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Patients with tandem occlusions had NIHSS scores similar to those with isolated MCA occlusions. In the tandem occlusion and isolated MCA occlusion groups, 19% and 11%, respectively, had NIHSS scores <12. Lower NIHSS scores were attributable to partial arm and/or leg paresis, gaze preference, and partial neglect compared with hemiplegia, forced gaze deviation, and complete neglect in patients with NIHSS scores >20. On TCD, patients with lower NIHSS scores (n=9) had positive diastolic flow at the MCA origin (Table 2) and
2 major collaterals. All patients with NIHSS scores
20 (n=7) with tandem ICA/MCA occlusion had no diastolic flow at the M1 MCA origin (Table 2, P<0.0001) and 1 or no major collaterals, indicating occlusion of perforating arteries and overall greater thrombus burden. These clinical and sonographic findings are illustrated in Figure 2.
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| Discussion |
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In 56% of the patients with tandem ICA/MCA occlusions, the NIHSS score range was 8 to 19. In these patients, TCD showed low-resistance flow at the M1 origin as well as a higher number of collateral channels compared with patients with NIHSS scores
20. Other studies showed that with an ICA occlusion, the neurological deficit and infarction volume depend on the functional capacities of collateral circulation, and an ICA occlusion without collateral flow leads to the most devastating acute ischemia.5,23,24 van Everdingen et al25 have found that in patients with an ICA occlusion, brain hemodynamics and metabolism are influenced by the presence of at least 1 collateral channel rather than a total number, ie, communicating arteries or reversed ophthalmic artery. In the present study, all patients with NIHSS scores <20 had
2 major collateral channels. Also, these patients had positive diastolic flow at the M1 MCA origin, which may suggest flow to perforators.7 In this situation, patients have less severe deficits because of partial scores in the following NIHSS sections: motor arm/leg function, best gaze, and neglect.
The limitations of the present study were the difficulty to differentiate between high-grade proximal ICA stenosis and occlusion by use of TCD studies only. Although direct carotid examination with duplex ultrasound or CT angiography can be performed in the emergency room, a sonographer should be familiar with the TCD patterns of tandem lesions. Also, rapid screening for a severe ICA stenosis or complete occlusion can be potentially helpful in selecting patients treated with intravenous TPA for subsequent urgent angiography and new experimental devices for disruption of large arterial thrombi. Another limitation is the inability of TCD to provide diagnostic information in the absence of temporal acoustic windows. The latter can be avoided with the use of ultrasound contrast agents. Finally, a relatively small number of patients may preclude generalizations regarding the utility of TCD and the accuracy of our observations. Also, the utility and accuracy of TCD were not the objectives of the present study. Finally, diagnostic TCD examinations were performed at
2 hours after stroke onset. Our results may not be reproducible at later times after stroke onset because of spontaneous recanalization or progression of infarction.
In conclusion, we report sonographic patterns of tandem ICA/MCA occlusions in patients treated with intravenous TPA therapy. Neurological deficits expressed with the NIHSS scores are similar in patients with tandem ICA/MCA occlusion and those with isolated MCA occlusions. Less severe stroke symptoms are attributable to the presence of collateral flow channels and positive diastolic flow in the proximal MCA.
Received April 16, 2001; revision received August 20, 2001; accepted October 15, 2001.
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