Transcranial Doppler (TCD) is an innovative, flexible, accessible tool for the bedside monitoring of static and dynamic cerebral flow and treatment response. Introduced by Rune Aaslid in 1982 , it has become indispensable in clinical practice.
TCD is based on the Doppler principle illustrated by Christian Andreas Doppler in 1842, which describes the apparent frequency change of a sound wave caused by relative movement between the observer and the sound source [2,3]. When stimulated by an electric current the Doppler probe emits an ultrasound wave, which is reflected by the moving red blood cells it meets: as blood flow approaches the probe, frequency of the reflected wave increases while blood flowing away from the probe produces a lower frequency compared to the original wave. The difference between the frequency of the original signal and the reflected signal is known as the Doppler shift and is directly proportional to blood flow velocity as expressed below:
where F is the Doppler shift, Ft is the frequency of the wave emitted, V is the actual velocity, C is the velocity of sound in tissue and cosℑ is the cosine of the angle between the insonated vessel and the direction of the ultrasound wave [2,4,5]. Blood flow velocity can be estimated by measuring the Doppler shift. The difference between estimated and actual velocity increases with the angle of incidence ℑ, which means that a better estimate of flow velocity may be obtained by reducing the angle.
TCD employs pulsed wave probes featuring a single piezoelectric crystal, which is alternately stimulated to produce a signal and silenced to allow the reflected wave to be read. By varying the time interval between transmission and reception, it is possible to modulate the depth of insonation and examine selectively a specific segment of the cerebral vascular tree. TCD provides information on blood flow in both acoustic and visual form. With the former an audible acoustic signal is produced whose intensity, height and pitch reflect the characteristics of blood flow of the vessel under examination. In visual mode ‘fast Fourier transform' (FFT), also known as spectral analysis, is used to produce a two-dimensional image on the screen. The curve is further elaborated to gain several important diagnostic parameters: peak systolic velocity, telediastolic velocity, mean velocity, Gosling's ‘pulsatility index (PI)' and Pourcelot's ‘resistance index (RI)'.
The main obstacle to ultrasound penetration of the skull is bone . Low frequencies, 1-2 MHz, reduce the attenuation of the ultrasound wave caused by bone. TCD also provides the advantage of acoustic windows representing specific points of the skull where the bone is thin enough to allow ultrasounds to penetrate [1,2,7].
The transtemporal window is sited at the thin portion of the temporal bone, between the external cantus of the eye and the external acoustic meatus, immediately above the zygomatic arch. It is the most frequently used window and allows investigation to be made of the proximal segment (M1) the median cerebral artery (MCA), the A1 segment of the anterior cerebral artery (ACA), the posterior cerebral artery (PCA) and the final segment of the internal carotid artery (ICA).
By compressing the carotid, it is possible to evaluate the patency of the communicating anterior and posterior arteries. This approach is unsuitable for approximately 10% of patients due to thickened bone or osteoporosis. New substances, ultrasound contrast media, have recently been introduced, which allow this approach to be used in these patients as well by amplifying the ultrasound beam reflected.
The transorbital window makes it possible to assess the ophthalmic artery, the carotid siphon and the contralateral MCA. The probe is placed above the closed eyelid. This window must not be used in patients who have recently undergone surgery to replace the lens as the effects of ultrasound on artificial lenses are as yet unknown. In addition, the signal power of the Doppler emitted by the transducer must be reduced by 20% to avoid damage to the retina.
The suboccipital window is sited posteriorly at the highest portion of the neck. The probe is placed on both sides of the spinal column and must be orientated towards the median; the ultrasound beam penetrates the cranium through the space between the atlas and the base of the skull. This window makes it possible to evaluate the suboccipital and intracranial portion of both vertebral arteries (VA) and the basilar artery (BA).
The retromandibular window is not an acoustic cranial window as such but represents an extracranial approach to assess the distal segment of the extracranial ICA, immediately before it enters the carotid foramen. The probe must be placed at the angle of the mandible and orientated cranially.
The identification of each intracranial vessel is based on the following elements: (a) velocity and direction; (b) depth of signal capture; (d) possibility of following the vessel its whole length; (e) spatial relationship with other vessels; and (f) response to homolateral and contralateral carotid compression.
Two recent publications [8,9] specified the main fields of clinical application of TCD with an assessment of the advantages and limits of the method itself.
Mean flow velocity (MFV) is directly proportional to flow and inversely proportional to the section of the vessel. Any circumstance that leads to a variation of one of these factors can thus affect mean velocity. Physiological or paraphysiological conditions that modify flow velocity are age, Ht, aPCO2 and metabolic requirement. As for pathological conditions, the main condition affecting flow velocity is the vasospasm, the reduction of the lumen of the vessel following contraction of the smooth muscles of the wall. Vasospasm is a frequent complication of subarachnoid haemorrhage (SAH) [10-15] and has an incidence of between 30% and 70%. It has a typical time-span: it is normally absent in the first 48-72 h after SAH. Onset occurs from day 3 to reach a peak between day 6 and day 12, gradually lessening at 15-20 days. The vasospasm often remains clinically silent and the factors that make it symptomatic are largely unknown .
Threshold velocities above which vasospasm comes into place are well defined as regards the MCA, while there is no consensus for the other vessels.
As far as the MCA is concerned, MFVs below 120 cm s−1 indicate the presence of a slight reduction of the vessel lumen, which cannot show up at angiography. Velocities between 120 and 200 cm s−1 indicate moderate vasospasm, which leads to a reduction of the lumen of between 25% and 50%, while velocities above 200 cm s−1 indicate serious vasospasm with a reduction of the lumen exceeding 50%.
Nevertheless, an increase in velocity alone is not sufficient to arrive at a diagnosis of vasospasm: a condition of hyperaemia also presents with an increase in flow velocity. The Lindegaard Index (LI)  has therefore been introduced, which is defined by the ratio between the MFV in the MCA and the MFV in the ICA. Thus, an LI <3 indicates hyperaemia, between 3 and 6 moderate vasospasm and >6 serious vasospasm.
Other parameters, such as velocity increases >50% in daily serial examination or the presence of an asymmetry (velocity difference exceeding 50%), can aid in the diagnosis of vasosapsm .
TCD studies also correlate well with angiography studies in vasospasm of the BA , though less so for the other arteries at the base of the skull .
Stenosis of the intracranial arteries
Criteria for diagnosis of a stenosis >50% of an intracranial vessel with TCD include: (a) segmentary acceleration of flow velocity, (b) drop in velocity below the stenotic segment, (c) asymmetry and (d) circumscribed flow disturbances (turbulence and musical murmur) [21-24]. The sensitivity and diagnostic specificity of the TCD is higher in identifying stenosis of the anterior circulation (carotid siphon and MCA in its proximal segment M1), compared with the posterior circulation (VA, BA at segment P1 of the PCA), which presents more anatomic variability and difficulty of insonation. Data to establish diagnostic criteria with TCD for stenosis <50% are insufficient.
Doppler diagnosis of occlusion in an intracranial vessel is possible when no sign of flow can be found at the normal depth and position, or when its speed is significantly reduced and none of the other vessels can be heard. There may be increases in speed in other intracranial vessels due to activation of the compensatory circles. In patients with acute cerebral ischaemia, the specificity and sensitivity of TCD in diagnosing MCA occlusions is over 90% [25,26]. Repeated or continuous TCD monitoring enables us to follow the evolution of the occlusion and to assess possible recanalization in the vessel whether that be spontaneous [27,28] or induced by fibrinolysis. Comparative studies with angiographs have shown excellent diagnostic correlation, even when there is partial recanalization [29,30]. A recent small randomized trial  compared 11 patients who underwent thrombolysis with tissue plasminogen activator (t-PA) combined with continuous TCD monitoring, and 14 patients treated with t-PA, without TCD monitoring, all of them with acute MCA occlusion. The patients who were continuously monitored with TCD had higher levels of recanalization at 1 h and better outcome at 90 days compared to those treated with t-PA alone, suggesting that ultrasound may play a role in facilitating the lysis of the thrombus. TCD showed good sensitivity and predictability with carotid siphon, VA and BA .
Cerebral autoregulation refers to the brain's intrinsic ability to maintain cerebral blood flow (CBF). When this system is compromised, patients are at risk of developing ischaemia and cerebral oedema.
Cerebral autoregulation includes pressure type regulation, which means that changes in CBF are kept to a minimum even when cerebral perfusion pressure (CPP) varies, as long as the variations are within 50 and 150 mmHg, and vasomotor reactivity, which is the response of the cerebral circle to changes in aPCO2 and aPO2.
Pressure regulation can be subdivided into dynamic regulation, involving a rapid response on the part of CBF to changes in arterial pressure or its pulsatile nature, and static regulation, involving a rapid response on the part of CBF to slow changes in average arterial pressure  (mean arterial pressure (MAP)).
The TCD enables us to assess both components of self-regulation. The static component is measured by observing changes in flow velocity caused by pharmacologically induced episodes of hypertension and hypotension. In this way, the static rate of autoregulation can be measured using the ratio between percentage variation of resistance and percentage variation of MAP. A value of 1 indicates that autoregulation is intact, whereas 0 tells us that autoregulation has stopped .
The dynamic component of autoregulation can be measured using a method devised by Aaslid known as the ‘cuff test'. Arterial hypotension is induced by placing thigh cuffs on each thigh and tightening them to 50 mmHg above the PAS for 3 min and then quickly releasing them. The dynamic rate of regulation, dRoR, whose normal value is 20% s−1 is thus calculated, indicating how quickly the velocity of cerebral flow returns to its starting level after the hypotensive stimulus. However, inducing rapid changes in systemic arterial pressure in patients who are already seriously compromised is not a good idea, so this limits the application of the cuff test.
A very effective and safe device for measuring cerebral autoregulation is the transient hyperaemic response test (THRT) [34,35].
This test is based on the compensatory vasodilatation of the arterioles, which occurs after brief compression of the common carotid. The test involves measuring systolic speed of flow in the MCA in base conditions. The common carotid is compressed homo laterally for 10 s, which causes a reduction in CPP. If autoregulation is intact, the cerebral arterioles respond to the reduction in CPP through vasodilatation to reduce resistance and keep the CBF constant. Once the compression is released, we can see that there is a temporary increase in blood flow as CPP acts on a dilatated vascular bed.
The increase in flow translates as an increase in velocity of MCA flow. Autoregulation integrity can be checked by calculating the transient hyperaemic response ratio (THRR), which is defined as the ratio between the velocity of systolic flow during the hyperaemic phase (two cycles after the compression release excluding the very first cycle) and the velocity of basic systolic flow (five cycles before compression). The normal THRR range is between 1.105 and 1.29 (average (95% CI) 1.2 (1.17-1.24)).
THRR is said to be a qualitative autoregulation indicator. The strength and duration of the carotid compression are the two variables that make THRR unreliable as a quantitative indicator. In the literature there is disagreement about how long the compression phase needs to be to get the maximum hyperaemic response. Some authors consider 5 s  whereas others consider 10 s . As far as the strength of the compression is concerned, it needs to be sufficient to cause a reduction in cerebral flow of at least 40% .
Estimating intracranial pressure
Increased ICP causes variation in CBF speed, which translates as changes in the shape of the TCD wave produced [37,38]. Differences in the Doppler wave can be quantified by calculating the pulsatility rate (PR) and resistance rate.
Various authors have demonstrated how PR increases exponentially when there is intracranial hypertension. In cranial trauma patients, raised PR is an indicator predicting worse outcome . In the second half of the 1980s, Klingelhofer [40,41] showed there was good correlation between ICP and the MAP × RI/FVm ratio (where MAP is average arterial pressure and FVm the average velocity of flow). However, many different factors can affect levels of pulsatility and resistance including hemodynamic, respiratory and haematological factors as well as vascular and tissue compliance. This is why indicators such as these cannot be used for the early identification of patients at risk for the development of endocranial hypertension.
In 1986, Aaslid  applied the Fourier analysis to the Doppler and arterial pressure waves and came up with the following formula for calculating CPP: CPP=AP1 × FVm/FV1, where AP1 is the amplitude of the first peak of the AP wave and FV1 is the amplitude of the first peak of the Doppler wave. More recently, Czsonyka and colleagues  proposed the following formula based on clinical observation: CPP=MAP × FVd/FVm+14, where FVd is the velocity of diastolic flow. In a group of 25 patients with serious cranial trauma, absolute error was less than 10 mmHg in 81% of the cases and less than 5 in 50% of the cases. Using this method, a prototype has been put forward, which allows for continuous and bilateral CPP measurement (Neuro Q TM Deltex Ltd, Chichester, UK). This technique, based on critical closing pressure (CCP), has proved to be fairly reliable in predicting CPP values, but it is not sufficiently precise where ICP is concerned in that it does not differentiate between the effects on CPP, which are caused by the increase in ICP and those produced by an increase in cerebrovascular resistence, especially in patients with intact autoregulation or in those who have intra- or extracranial stenosis.
Transcranial Doppler and ‘effective downstream pressure'
There has been a recent return to the concept of ‘effective downstream pressure (EDP)' and CCP. The concept of CCP was first mentioned in the 1950s by Burton , who defined it as the minimum transmural pressure (MAP-ICP) under which blood flow stops and the vessel collapses. Critical closing pressure corresponds to vasomotor tone .
When there is equilibrium (zero flow), transmural pressure is equal to the ratio between the wall tension, which is given by the vasomotor tone, and the radius of the vessel. A reduction in arterial pressure, an increase in ICP or in vasomotor tone can modify the balance between transmural pressure and wall tension, leading to the collapse of the vessel. The sum of CPP plus ICP gives us EDP. When EDP equals MAP, flow is zero. The difference between MAP, and EDP is effective CPP (eCPP), which CBF depends on.
EDP values can be found by analysing the beat-to-beat relationship between pressure and CBF. If we have MAP and FV for a single cardiac cycle in a single cartesian axis, we can calculate a rate of linear regression. Once we have the linear regression rate, we can extrapolate the AP value corresponding to zero flow. This value corresponds to EDP.
aPCO2 variations have the opposite effect on ICP and CCP. Increased CO2 when autoregulation is preserved leads to vasodilatation, which, on the one hand, causes an increase in cerebral blood volume and therefore ICP, and, on the other, leads to a reduction in vascular tone and therefore reduction in CCP. Weyland and colleagues  questioned what would happen if two Starling resistors were placed in sequence, one at the arteriole level so mainly influenced by CCP, and the other at vein level so influenced mainly by ICP. According to the author, if there is no endocranial hypertension, the eCPP is mainly determined by the arteriole resistor. Traditionally, we have always thought of CPP as the difference between MAP and ICP. However, it is also likely that real CPP is not determined by intracranial pressure but by CCP. In a study of 70 patients with serious trauma, these showed that in 51% of cases CPP-ICP underestimates eCPP by at least 19.8 mmHg . However, there is no evidence to suggest that the concept of eCPP is superior to that of CPP in terms of outcome. The mechanism by which the difference between EDP and ICP can be a negative also needs to be clarified. It may be due to vasoparalysis or marked dilatation at rest because of hypercapnea, hypertension or hypoxia. The literature reveals contrasting opinions on this.
Transcranial Doppler and brain death
Brain death is defined as the irreversible cessation of all functions of the whole brain . The clinical criteria are usually considered sufficient to establish a diagnosis of brain death; however, they might not be sufficient in patients who have been on sedatives or when there are ethical or legal controversies. In these circumstances, it might be useful to have tests, which could confirm a diagnosis of brain death. The use of tests is also recommended in patients with severe facial trauma, in patients with pre-existing alterations in pupillary diameter and in PBCO patients who normally have high aPCO2 levels.
The most frequently used test is EEG, even though it gives very little information about how the brain stem is, and it is not always technically possible in ICUs to conduct the test properly. Angiography is more suitable for confirming brain death. However, it remains an invasive test, which requires the use of contrast and therefore the patient needs to be taken out of Intensive Care. The same goes for computed tomography and any techniques that use radioisotopes.
TCD is a test that is relatively simple to perform, cheap and that can be done at the patient's bedside. Many authors have demonstrated the existence of a TCD pattern, which is typical of brain death . The increased ICP, which leads to the arrest of the brain circle, first causes a reduction in diastolic flow velocity, which becomes equal to 0 when ICP approximates diastolic arterial pressure. If ICP continues to increase, diastolic flow reappears but in the opposite direction (reverberating or oscillating flow), indicating a retrograde flow during the diastolic phase of the cardiac cycle. When endocranial hypertension is sufficiently high as to cause the arrest of CBF, we observe brief systolic spikes followed by the complete disappearance of the Doppler signal. A reverberating flow and systolic spikes are considered conclusive of cerebral circle arrest, because it means that both the anterior and posterior as well as the lateral ones are affected. We cannot exclude the possibility that the acoustic window is not sufficient, so if there is no signal whatsoever in any of the vessels at the base of the cranium, this is considered indicative of brain death only when previous examination showed that flow was present. To exclude temporary arrest because of hypotension, systolic arterial pressure must not be less than 70 mmHg and flow patterns need to have been monitored during at least two previous examinations at least 30 min apart.
The sensitivity of TCD is 96.5% and its specificity is 100% in the diagnosis of brain death. However, it should be used to complement rather than substitute careful clinical evaluation. It is also important to stress that central nervous system depressor drugs do not influence the diagnosis of brain death with TCD.
Patent oval foramen
Paradoxical embolism through the patent oval foramen is a possible cause of stroke in young patients. TCD enables us to diagnose the presence of a right-left cardiac shunt with almost 100% concordance if we compare it with a transoesophageal ecograph. In all, 9 cm3 of physiological solution is injected into one of the large forearm veins through a three-way tap, 1 cm3 of air. If there is right-left shunt, we can see the gaseous emboli moving in the MCA 5-15 s after the injection. If the result of the basic test is negative, we can increase the sensitivity of the test by performing it while conducting a Valsalva's  manoeuvre. Extracardiac shunt (e.g. intrapulmonary) is responsible for false positives.
1. Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg
2. McCartney JP, Thomas-Lukes KM, Gomez CR. Handbook of Transcranial Doppler
. New York, USA: Springer, 1997.
3. Aaslid R. Transcranial Doppler Sonography
. New York, USA: Springer, 1986.
4. Manno EM. Transcranial Doppler ultrasonography in the neurocritical care unit. Crit Care Clin
5. Eicke BM, Tegeler CH, Dalley G et al.
. Angle correction in transcranial Doppler sonography. J Neuroimaging
6. Grolimund P. Transmission of Ultrasound through Temporal Bone. In: Aaslid R, ed. Transcranial Doppler Sonography
. New York, USA: Springer, 1986.
7. Babikian Vl, Wechsker Lr. Transcranial Doppler Ultrasonography
. Butterworth-Heinemann 1999.
8. Babikian VL, Feldmann E, Wechsler LR et al.
. Transcranial Doppler ultrasonography: year 2000 update. J Neuroimaging
9. Sloan MA, Alexandrov AV, Tegeler CH et al.
. Assessment: transcranial Doppler ultrasonography: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology
10. Aaslid R, Huber P, Nornes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg
11. Vora YY, Suarez-Almazor M, Steinke DE et al.
. Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery
12. Sloan MA, Haley EC Jr, Kassell NF et al.
. Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage. Neurology
13. Lysakowski C, Walder B, Costanza MC et al.
. Transcranial Doppler versus angiography in patients with vasospasm due to a ruptured cerebral aneurysm: a systematic review. Stroke
14. Laumer R, Steinmeier R, Gonner F et al.
. Cerebral hemodynamics in subarachnoid hemorrhage evaluated by transcranial Doppler sonography. Part 1. Reliability of flow velocities in clinical management. Neurosurgery
15. Steinmeier R, Laumer R, Bondar I et al.
. Cerebral hemodynamics in subarachnoid hemorrhage evaluated by transcranial Doppler sonography. Part 2. Pulsatility indices: normal reference values and characteristics in subarachnoid hemorrhage. Neurosurgery
16. Grosset DG, Straiton J, McDonald I et al.
. Use of transcranial Doppler sonography to predict development of a delayed ischemic deficit after subarachnoid hemorrhage. J Neurosurg
17. Lindegaard KF. The role of transcranial Doppler in the management of patients with subarachnoid haemorrhage - a review. Acta Neurochir
18. Grosset DG, Straiton J, du Trevou M et al.
. Prediction of symptomatic vasospasm after subarachnoid hemorrhage by rapidly increasing transcranial Doppler velocity and cerebral blood flow changes. Stroke
19. Sloan MA, Burch CM, Wozniak MA et al.
. Transcranial Doppler detection of vertebrobasilar vasospasm following subarachnoid hemorrhage. Stroke
20. Lennihan L, Petty GW, Fink E et al.
. Transcranial Doppler detection of anterior cerebral artery vasospasm. J Neurol Neurosurg Psychiatry
21. Rorick MB, Nichols FT, Adams RJ. Transcranial Doppler correlation with angiography in detection of intracranial stenosis. Stroke
22. de Bray JM, Joseph PA, Jeanvoine H et al.
. Transcranial Doppler evaluation of middle cerebral artery stenosis. J Ultrasound Med
23. Schwarze JJ, Babikian V, DeWitt LD et al.
. Longitudinal monitoring of intracranial arterial stenoses with transcranial Doppler ultrasonography. J Neuroimaging
24. Wilterdink JL, Feldmann E, Furie KL et al.
. Transcranial Doppler ultrasound battery reliably identifies severe internal carotid artery stenosis. Stroke
25. Zanette EM, Fieschi C, Bozzao L et al.
. Comparison of cerebral angiography and transcranial Doppler sonography in acute stroke. Stroke
26. Camerlingo M, Casto L, Censori B et al.
. Transcranial Doppler in acute ischemic stroke of the middle cerebral artery territotories. Acta Neurol Scand
27. Kushner MJ, Zanette EM, Bastianello S et al.
. Transcranial Doppler in acute hemispheric brain infarction. Neurology
28. Toni D, Fiorelli M, Zanette EM et al.
. Early spontaneous improvement and deterioration of ischemic stroke patients. A serial study with transcranial Doppler ultrasonography. Stroke
29. Demchuk AM, Christou I, Wein TH et al.
. Accuracy and criteria for localizing arterial occlusion with transcranial Doppler. J Neuroimaging
30. Burgin WS, Malkoff M, Felberg RA et al.
. Transcranial Doppler ultrasound criteria for recanalization after thrombolysis for middle cerebral artery stroke. Stroke
31. Eggers J, Koch B, Meyer K et al.
. Effect of ultrasound on thrombolysis of middle cerebral artery occlusion. Ann Neurol
32. Lang Ew, Diehl R, Mehdorn M. Cerebral autoregulation testing after subarachnoid hemorrhage: the phase relationship between arterial blood pressure and cerebral blood flow velocity. Critical Care Med
33. Czosnyka M, Kirkpatrik P, Pickard JD. Multimodal monitoring and assessment of cerebral haemodynamic reserve after severe head injury. Cerebrovasc Brain Metab Rev
34. Giller GA. A bedside test for cerebral autoregulation using transcranial Doppler ultrasound. Acta Neurochirurgica
35. Smielewsky P, Czosnyka M, Kirkpatrik P et al.
. Evaluation of the transient hyperemic response test in head injured patients. J Nerurosug
36. Cavill G, Simpson Ej, Mahajan RP. Factor affecting assessment of cerebral autoregulation using the transient hyperaemic response test. Br J Anesth
37. McQuire JC, Sutcliffe JC, Coats TJ. Early changes in middle cerebral artery blood flow velocity after head injury. J Neurosurg
38. Ursino M, Giulioni M, Lodi CA. Relationships among cerebral perfusion pressure, autoregulation, and transcranial Doppler waveform: a modeling study. J Neurosurg
39. Chan KH, Dearden NM, Miller JD et al.
. Transcranial Doppler waveform differences in hyperemic and nonhyperemic patients after severe head injury. Surg Neurol
40. Klingelhofer J, Conrad B, Benecke R et al.
. Evaluation of intracranial pressure
from transcranial Doppler studies in cerebral disease. J Neurol
41. Klingelhofer J, Conrad B, Benecke R et al.
. Intracranial flow patterns at increasing intracranial pressure
. Klin Wochenschr
 Aaslid R. Intracranial pressure IV
. New York: Springer, 1986: pp. 226-229.
43. Czosnyka M, Matta BF, Smielewski P et al.
. Cerebral perfusion pressure in headinjured patients: a noninvasive assessment using transcranial Doppler ultrasonography. J Neurosurg
44. Burton Ac. On the physical equilibrium of small blood vessels. Am J Physiol
45. Richards HK, Czosnyka M, Pickard JD. Assessment of critical closing pressure in the cerebral circulation as a measure of cerebrovascular tone. Acta Neurochir
: 1221-1227, discussion 1226-1227.
46. Weyland A, Buhre W, Grund S et al.
. Cerebrovascular tone rather than intracranial pressure
determines the effective downstream pressure of the cerebral circulation in the absence of intracranial hypertension. J NeurosurgAnesthesiol
47. Thees C, Scholz M, Schaller MDC et al.
. Relationship between intracranial pressure
and critical closing pressure in patients with neurotrauma. Anesthesiology
48. Wijdicks EF. The diagnosis of brain death. N Engl J Med
49. Ropper AH, Kehne SM, Wechsler L. Transcranial Doppler in brain death. Neurology
50. Droste DW, Lakemeier S, Wichter T et al.
. Optimizing the technique of contrast transcranial Doppler ultrasound in the detection of right-to-left shunts. Stroke