Transcranial color-coded duplex ultrasonography (TCCS) enables the reliable assessment of intracranial stenoses, occlusions, and cross-flow through the circle of Willis without using potentially hazardous compression tests. Transpulmonary ultrasound contrast agents (UCAs) increase the number of conclusive TCCS investigations, which suggests that UCAs may provide the conclusive evaluation of intracranial arteries in most patients with ischemic cerebrovascular disease. Further, contrast-enhanced TCCS may become an important tool both for the management of acute ischemic stroke by assessing intracranial hemodynamics and the displacement and diameter changes in supratentorial ventricles. TCCS is useful for the detection and monitoring of intracranial vasospasm, may visualize larger supratentorial hematomas with subcortical location and hemorrhagic transformation of ischemic infarcts, and provides the incidental detection of cerebral aneurysms and arteriovenous malformations. Second-generation UCAs and new ultrasound machines are very likely to further increase the frequency of conclusive TCCS studies. Power-based three-dimensional, contrast-enhanced TCCS is an important further development, which would make the method much less operator dependent. Site-targeted UCAs appear to provide a new and exciting method for ultrasonic diagnosis and management of patients with ischemic cerebrovascular disease 1).
Transcranial Doppler (TCD) and transcranial color-coded duplex sonography (TCCS) are noninvasive modalities that can be used to assess vasospasm. However, high flow velocity does not always reflect DCI. The purpose of this study was to investigate the utility of TCD/TCCS in decreasing permanent neurological deficits. METHODS: We retrospectively enrolled patients with aSAH who were treated within 72 hours after onset. TCCS was performed every day from days 4 to 14. Peak systolic velocity (PSV), mean velocity (MV), and pulsatility index were recorded and compared between DCI and non-DCI patients. In patients with DCI, endovascular therapy was administered to improve vasospasm, which led to a documented change in velocity. RESULTS: Of the 73 patients, 7 (9.6%) exhibited DCI. In 5 of the 7 patients, DCI was caused by vasospasm of M2 or the more peripheral middle cerebral artery (MCA), and the PSV and MV of the DCI group were lower than those of the non-DCI group after day 7. Intra-arterial vasodilator therapy (IAVT) was performed for all patients with DCI immediately to increase the flow volume by the next day. CONCLUSIONS: Increasing flow velocity cannot always reveal vasospasm excluding M1. In patients with vasospasm of M2 or more distal arteries, decreasing flow velocity might be suggestive of DCI. IAVT led to increases in the flow velocity through expansion of the peripheral MCA 2).
A postcraniotomy window (PCW) on a line extending from the horizontal portion of M1 using only TMP permitted flow imaging with TCCS. In external decompression, TCCS was effective only without use of Gore-tex around the postcraniotomy window. This method allows the middle cerebral artery flow to be detected easily 3).