BACKGROUND: Transcranial Doppler (TCD) ultrasonography can detect evidence of collateral flow across the anterior communicating artery and/or the posterior communicating artery, which occurs when there is significant alteration of 'inflow' to the brain. The aim of the study was to determine the blood flow velocity produced by a carotid stenosis which produces this haemodynamic effect on the cerebral circulation and evokes collateral circulation. METHODS: Forty-eight patients with varying degrees of carotid stenosis (10 per cent to occlusion) who underwent both carotid duplex and TCD examination were reviewed. An ATL HDI 3000 ultrasound system was used for the carotid and TCD studies. The carotid examination recorded peak-systolic velocity (PSV) and end-diastolic velocity (EDV) in the carotid systems bilaterally. TCD recorded Doppler spectra from the bilateral middle cerebral, anterior cerebral, posterior cerebral, intracranial vertebral and basilar arteries. Collateral flow was assessed in two ways: 'intracranial crossover' collateral and 'posterior to anterior' collateral. Each internal carotid artery (ICA), together with the ipsilateral hemisphere, was analysed for the presence or absence of collateral flow. Data were expressed as mean(s.e.m.). RESULTS: The PSV of the group with collateral circulation was 472(14) cm s-1 and that of the group without collateral flow was 164(3) cm s-1 (P < 0.0001, Mann-Whitney test). The respective EDVs were 158(13) and 58(7) cm s-1 (P < 0.0001). CONCLUSION: PSVs and EDVs in the ICA, in conjunction with collateral flow measured by TCD, are indicators of a haemodynamically significant carotid lesion, and provide more information than two-dimensional imaging studies. In the future, parameters set by combining carotid duplex and TCD investigations may represent the 'gold standard' for evaluation of cerebral blood flow.
BACKGROUND: Transcranial Doppler (TCD) ultrasonography can detect evidence of collateral flow across the anterior communicating artery and/or the posterior communicating artery, which occurs when there is significant alteration of 'inflow' to the brain. The aim of the study was to determine the blood flow velocity produced by a carotid stenosis which produces this haemodynamic effect on the cerebral circulation and evokes collateral circulation. METHODS: Forty-eight patients with varying degrees of carotid stenosis (10 per cent to occlusion) who underwent both carotid duplex and TCD examination were reviewed. An ATL HDI 3000 ultrasound system was used for the carotid and TCD studies. The carotid examination recorded peak-systolic velocity (PSV) and end-diastolic velocity (EDV) in the carotid systems bilaterally. TCD recorded Doppler spectra from the bilateral middle cerebral, anterior cerebral, posterior cerebral, intracranial vertebral and basilar arteries. Collateral flow was assessed in two ways: 'intracranial crossover' collateral and 'posterior to anterior' collateral. Each internal carotid artery (ICA), together with the ipsilateral hemisphere, was analysed for the presence or absence of collateral flow. Data were expressed as mean(s.e.m.). RESULTS: The PSV of the group with collateral circulation was 472(14) cm s-1 and that of the group without collateral flow was 164(3) cm s-1 (P < 0.0001, Mann-Whitney test). The respective EDVs were 158(13) and 58(7) cm s-1 (P < 0.0001). CONCLUSION: PSVs and EDVs in the ICA, in conjunction with collateral flow measured by TCD, are indicators of a haemodynamically significant carotid lesion, and provide more information than two-dimensional imaging studies. In the future, parameters set by combining carotid duplex and TCD investigations may represent the 'gold standard' for evaluation of cerebral blood flow.