Transcranial Doppler (TCD) and transcranial Doppler Imaging (TCDI) is a noninvasive ultrasound technique that can be used to measure blood flow velocity within the circle of Willis and the vertebrobasilar system. By providing insight into cerebral hemodynamics, TCD can be used to evaluate a wide variety of intracranial and extracranial cerebrovascular abnormalities: vasoconstriction following subarachnoid hemorrhage, intracerebral arterial stenosis or occlusion, cerebral circulatory arrest and effects of internal carotid artery lesions on collateral competency. Additional uses include the continuous monitoring of a wide variety of cerebrovascular interventions. Diagnoses made with this technology are based on increased or decreased blood flow velocity, absence of blood flow, or alterations in the pulsatility index (PI), a measurement of resistance (Fig 1).
The use of TCD to screen and document intracranial arterial stenosis represents an evolution in the non-invasive evaluation of patients at risk for ischemic infarction. TCD is widely used in the evaluation of Sickle Cell disease.
The characteristic places where intracranial stenosis can be found include the middle cerebral, internal carotid siphon and the basilar arteries.
The sonographic findings associated with intracranial stenosis are those of increased flow velocities across the narrowed vascular segment.
A total trunk occlusion is characterized by an initial absence or severe reduction of the signal at the normal depths of insonation. Intra-arterial thrombolytic therapy may be utilized to enhance the recanalization process. TCD has been used to monitor flow before, during, and after neuroradiologic interventional procedures such as this.
Intracranial Microvascular Disease
Arteriosclerotic changes can also occur in smaller vessels of the cerebrovasculature. Unlike the large vessel focal stenosis described above, microvascular disease diffusely affects all vessels throughout the brain at distal levels of the arterial tree. Blood flow velocities in the basal arteries are normal throughout the entire circle of Willis but demonstrate a high pulsatility index (Fig 2). The elevated PI (>1.20), is reflective of the distal resistance created by the small vessel disease.
The atherosclerotic process is more frequent in the extracranial portions of the cerebral circulation, particularly at certain points such as the carotid bifurcation and the origin of the vertebral arteries. The effects of stenotic extracranial lesions upon the hemodynamics of the circle of Willis can be easily detected by TCD. Comparison of flow velocities from side to side along with the flow characteristics will yield an understanding of changes taking place intracrainally.
The characteristic findings of a severe proximal internal carotid stenosis include an ipsilateral “low -flow “state measurable at the MCA in conjunction with a low PI (Fig 3).
Supportive changes in the intracranial collateral flow via communicating arterial pathways, provide the brain with protection from an ischemic insult. Alternatively, plaque at the bifurcation may still provide a source of distal emboli, which may also be detected by TCD.
Hemorrhage into the subarachnoid of the brain constitutes a dire cerebrovascular event. The presence of subarachnoid blood may trigger a severe vasospastic response during the first two weeks following hemorrhage (7-10 days). The result is often variable degrees of ischemia often proportional to the amount of blood located at the affected artery. The distribution of the vasospasm varies depending upon extension of hemorrhage. The values for vasospasm differ for the middle cerebral artery and basilar artery. The characteristic findings in vasospasm include high flow velocities usually associated with musical murmurs secondary to the spasticity of the blood vessels wall (Fig 4).
Traumatic Head Injury
Following head injury, cerebral hemodynamics may be affected in a number of ways. Post traumatic impairment of cerebral autoregulation may be identified by high systolic and diastolic mean flow velocities. The cerebral vasculature may lose their vasomotor tone resulting in a hyperemic vasodilatation. The increase of cerebral blood volume may lead to vasogenic edema with a corresponding increase in intracranial pressure. Ultimately this may lead to reduced cerebral perfusion pressure and increased intracranial pressure, ischemia or infarction. The transcranial Doppler PI can be used to diagnose increases in intracranial pressure. As pressure increases, the diastolic velocity drops to zero and the waveform appears spiked.
Cerebral Circulatory Arrest
Decisions regarding the omission or termination of life supporting care are based on specific protocols which include the demonstration of an absence of cerebral circulation by either angiography or nuclear flow studies. Transcranial Doppler can also be used to confirm cerebral circulatory arrest.
The appearance of the transcranial Doppler waveform in cerebral circulatory arrest reflects the progression of increased intracranial pressure and microvascular obstruction. The lack of peripheral perfusion results in a characteristic ”to-and-fro” pattern, called oscillatory flow reverberation (Fig 5).
Emboli identified by ultrasound are known as microembolic events (MEE) or high intensity signals (HITS). They have intensities >10dB greater than the background Doppler signal and are transient (0.01-0.1 second) in duration. The sound produced is harmonic and often described as “chirps”, “whistles”, or “plops”, depending on size and composition (Fig 6). Artifacts usually produce a rough, sonorous, non-harmonic, scratchy sound of predominantly low frequency (<400 Hz). Bubble emboli, injected for evaluation of a patent foramen ovale, have higher strength signals for their size (up to 60dB).
They can produce so much signal reflection that TCD units show an overload on the visual display (Fig 7). It is necessary to measure these showers in total seconds of duration as it is impossible to determine the exact number of microemboli.
Transcranial Doppler ultrasonography provides unique insight into a variety of intracranial and extracranial vascular pathologic conditions and their effects on cerebral hemodynamics. It is hoped that these insights will lead to improvements in the diagnosis and therapy of intracranial neurovascular diseases.
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