Transcranial Doppler

Transcranial Doppler (TCD) is a non-invasive, bedside pulsed wave Doppler ultrasound examination. It measures blood flow velocity in the large intracranial arteries and the extracranial internal carotid, through natural acoustic windows in the skull. A low frequency (1 to 2 MHz) phased array probe is used.

• The transtemporal window (over the zygomatic arch) shows the middle cerebral artery (MCA, depth 45 to 65 mm), the anterior cerebral artery (ACA, 60 to 75 mm), the posterior cerebral artery (PCA, 60 to 70 mm) and the terminal internal carotid artery.
• The transorbital window shows the ophthalmic artery and carotid siphon (depth 40 to 60 mm).
• The transforaminal (suboccipital) window shows the vertebral arteries and basilar artery (depth 60 to 100 mm and beyond).

Transcranial colour coded duplex (TCCD) combines B-mode imaging of intracranial structures with colour Doppler. Measurements are mean, peak systolic and end diastolic velocity, the pulsatility index (PI), and the direction of flow. Emboli can be detected as high intensity transient signals, and a bubble study (agitated saline) can detect right to left shunting.

The examination takes 20 to 40 minutes at the bedside, with no radiation.

TCD was introduced for monitoring vasospasm after subarachnoid haemorrhage, and for stroke screening in children with sickle cell disease. Cerebral vasospasm occurs in up to 70% of angiographic cases of subarachnoid haemorrhage (symptomatic in about 30%), usually from day 3 to day 14.

In children with sickle cell anaemia, an MCA time averaged maximum velocity of 200 cm each second or more is associated with a stroke risk of around 10% each year without transfusion, and transfusion therapy reduces the risk by over 90%. TCD is operator dependent, but is repeatable, cheap and available at the bedside.

Indications. Vasospasm after subarachnoid haemorrhage (daily monitoring from day 3 to 14). Stroke risk screening in children with sickle cell disease aged 2 to 16 years. Detection and grading of intracranial arterial stenosis or occlusion in stroke and transient ischaemic attack, and monitoring of recanalisation after thrombolysis.

Detection of microembolic signals (carotid disease, cardiac sources, after procedures). Detection of right to left shunt (patent foramen ovale) with agitated saline. Assessment of cerebral autoregulation and vasomotor reactivity. Support in the diagnosis of brain death (absent diastolic flow or reverse flow, systolic spikes). Monitoring during carotid endarterectomy and cardiac surgery.

Raised intracranial pressure (high PI). Traumatic brain injury (vasospasm, hyperaemia, low flow). Cerebral venous thrombosis (limited). Meningitis (vasculopathy). Arteriovenous malformations (feeder vessels).

Contraindications and precautions. None. The temporal window is absent in 5 to 15% of people (higher in older adults, women and people of African or Asian descent). Pressure on the eye is avoided with the orbital window, using low power output (under 10% of the maximum) and short exposure. Head trauma with open wounds, scalp dressings and craniectomy need modified technique.

Normal values vary with age, sex, haematocrit, PaCO2, blood pressure and the cardiac output, and these are recorded.

Preparation and technique. The patient lies supine or sits. The probe is placed over the temporal window (anterior, middle and posterior windows), and the MCA is found at 50 to 55 mm depth with flow towards the probe. Flow direction is described by depth: MCA and ACA flow towards and away from the probe respectively at the bifurcation (about 60 to 65 mm).

The vessel is followed along its depth and the highest velocity is recorded, with angle correction minimal (TCD assumes a near parallel angle). The Lindegaard ratio (MCA mean velocity divided by the extracranial ICA mean velocity measured in the neck) is used to distinguish hyperaemia from vasospasm. Microembolic detection is done with a headset for 30 to 60 minutes.

A bubble study involves injecting agitated saline during Valsalva release while monitoring MCA for bubble signals.

Normal appearances. Normal mean flow velocities in adults:

• MCA 55 to 65 cm each second (range 40 to 80), ACA 50 cm each second (range 35 to 65), PCA 40 cm each second (range 30 to 50).
• Terminal internal carotid 40 to 50, vertebral arteries 35 to 45, and basilar artery 40 to 50.

Velocities are higher in children (MCA mean 90 to 100 cm each second at age 5 to 7 years) and fall with age. They are higher in women than in men by about 10%.

The waveform has a rapid systolic upstroke, a dicrotic notch and continuous forward diastolic flow. PI is 0.6 to 1.1. The Lindegaard ratio is under 3. Flow is symmetrical between sides (differences under 30%).

Interpretation.

• Vasospasm after subarachnoid haemorrhage: MCA mean velocity over 120 cm each second suggests mild spasm, over 160 moderate, over 200 severe, with Lindegaard ratio over 3 (3 to 6 moderate, over 6 severe).
• A rapid rise in velocity (over 50 cm each second in 24 hours) predicts delayed cerebral ischaemia. A ratio under 3 with high velocity suggests hyperaemia (increased flow) rather than spasm.
• Basilar velocities over 85 cm each second with a basilar to extracranial vertebral ratio over 2 suggest basilar spasm.
• Sickle cell disease: time averaged maximum mean velocity in the MCA or terminal internal carotid under 170 cm each second is normal, 170 to 199 conditional (repeat in 3 months), and 200 or more abnormal (high stroke risk, prompt transfusion programme).
• Two abnormal studies are usual before starting transfusion; a velocity over 220 is directly regarded as abnormal. Low velocity with anaemia is normal for the child.
• Intracranial stenosis: focal increase in velocity (MCA mean velocity over 80 to 100 cm each second with a side to side difference over 30%, or over 120 cm each second for severe), turbulence, spectral broadening.
• Intracranial stenosis also shows pre- and post-stenotic changes (a damped waveform distally). Sensitivity is about 70 to 90% for MCA stenosis.
• Occlusion: absent signal in the MCA with a good window and with preserved flow in other arteries (compensation by anterior and posterior cerebral arteries).
• A low velocity, high resistance "minimal" or "blunted" signal indicates distal occlusion, and a "stump" signal indicates proximal occlusion.
• Recanalisation after thrombolysis: grading of residual flow signal (the thrombolysis in brain ischaemia scale, from absent flow to normal flow).
• Collateral and cross-filling: reversed ophthalmic artery flow, anterior communicating artery cross-flow, and posterior communicating flow indicate severe internal carotid stenosis or occlusion.
• Raised intracranial pressure and brain death: high PI (over 1.4), decreased diastolic flow, then reverberating (oscillating) flow with equal forward and reverse flow, then small systolic spikes, and finally absent signal.
• These patterns support cerebral circulatory arrest, but do not replace a clinical diagnosis.
• Microembolic signals: transient (under 300 ms), unidirectional high intensity signals (over 9 dB over the background) with a "chirping" sound.
• Microembolic signals are found in symptomatic carotid stenosis (a marker for recurrent stroke), atrial fibrillation, prosthetic heart valves, and during procedures.
• Right to left shunt: bubble signals in the MCA within 10 seconds (early, patent foramen ovale) or later (intrapulmonary shunt), graded by number of bubbles (under 10 is small, over 25 large, or curtain).
• Arteriovenous malformation: high velocity, low resistance (low PI) feeders with turbulence and a steal effect on adjacent arteries.
• Vasomotor reactivity: impaired response to hypercapnia (breath holding index under 0.69 or less than 20% increase of velocity) predicts stroke risk in severe carotid disease.
• Cerebral hyperperfusion syndrome after carotid revascularisation: a rise in MCA velocity over 100% of baseline.

Critical values and findings needing immediate action.

• MCA mean velocity over 200 cm each second with Lindegaard ratio over 6 after subarachnoid haemorrhage, or a rapid rise: severe vasospasm; escalate to the neurointensive team for induced hypertension, endovascular treatment with intra-arterial vasodilators or angioplasty.
• Sickle cell disease child with abnormal TCD (200 cm each second or more): urgent haematology review for a chronic transfusion programme.
• Absent MCA signal in an acute stroke: possible large vessel occlusion; urgent CT angiography and stroke team activation for thrombectomy.
• Oscillating flow or systolic spikes with clinical coma: raised intracranial pressure with cerebral circulatory arrest; confirm brain death by clinical criteria and ancillary tests.
• High PI over 1.4 with deterioration after trauma: urgent CT and measures to lower intracranial pressure.
• Large right to left shunt in a patient with cryptogenic stroke: cardiology review for closure.
• Frequent microembolic signals in symptomatic carotid stenosis: urgent vascular review and antiplatelet therapy.
• Cerebral hyperperfusion after revascularisation with headache and seizures: blood pressure control.

Limitations and artefacts.

• Absent or poor temporal bone window in 5 to 15% of patients (more in older women), which prevents the study; transorbital and suboccipital approaches, ultrasound contrast, or TCCD may help.
• Velocity depends on the angle, vessel diameter, cardiac output, haematocrit (anaemia raises velocity), PaCO2 (hypercapnia raises, hypocapnia lowers, about 4% change for each mmHg), blood pressure, fever, age, pregnancy and drugs; in sickle cell disease, intercurrent illness and transfusion change results.
• TCD (non-imaging) measures velocity and not flow or vessel diameter; in vasospasm, rise in velocity can also result from hyperaemia or arteriovenous malformation, and the Lindegaard ratio helps to separate them.
• The ACA, PCA and distal branches, and the posterior circulation are less reliably studied than the MCA, and TCD has a lower sensitivity for distal stenosis and for small vessels.
• It is operator dependent, and fixed depth, probe angle and vessel identification are needed to avoid misidentification (ACA versus MCA, PCA versus basilar).
• Microembolic signal detection needs expertise to distinguish artefact (probe tapping, speech, chewing).
• Brain death support is only adjunctive, and an absent signal may be a technical error; a signal that disappears after earlier detection is meaningful.
• Vasospasm monitoring may miss vasospasm in the distal arteries and in the posterior circulation, and clinical deterioration should lead to imaging.
• Normal values vary with the laboratory and population; local reference ranges are needed.

Special groups.

• Children with sickle cell disease (2 to 16 years): screening yearly; abnormal studies lead to transfusion, and some centres continue hydroxycarbamide (hydroxyurea) therapy.
• Neonates and infants: TCD or cranial duplex through the fontanelle for hydrocephalus, haemorrhage and perfusion.
• Subarachnoid haemorrhage: daily monitoring in intensive care; nimodipine prevents delayed ischaemia but not the spasm itself.
• Pregnancy: safe, used in pre-eclampsia and eclampsia assessment, where cerebral perfusion pressure and resistance are altered.
• Older adults: the poor temporal window rate is highest; intracranial atherosclerosis is common.
• Patients undergoing cardiac and carotid surgery: intraoperative monitoring for emboli and flow.
• Regions: sickle cell disease is common, and screening can prevent stroke when transfusion or hydroxycarbamide is available; cerebral malaria, tuberculous meningitis, neurocysticercosis and HIV-related vasculopathy may cause abnormal flow; TCD may be the only vascular imaging.

Follow up tests. CT angiography, MR angiography or digital subtraction angiography for confirmation of vasospasm, stenosis and occlusion; brain CT or MR (diffusion weighted) for infarction; carotid duplex; echocardiography with bubble study or transoesophageal echocardiography for a cardiac source and patent foramen ovale;

full blood count, haemoglobin electrophoresis and haemoglobin S percentage in sickle cell disease; electroencephalography and clinical brain stem testing when brain death is considered; continuous or serial TCD for trends; intracranial pressure monitoring; and referral to neurology, neurosurgery, stroke service or haematology.