Head Position on Cerebral Haemodynamics in Acute Ischemic Stroke and Controls

Completed

Phase N/A Results N/A

Trial Description

Cerebral autoregulation is an important mechanism whereby cerebral perfusion is normally maintained at a constant level, over a relatively wide blood pressure range. It can be assessed noninvasively by the use of Trans Cranial Doppler (TCD). This means using ultrasound probes over both sides of the head to measure changes in blood flow in one of the main brain arteries (the middle cerebral artery) in response to beat to beat changes in blood pressure dynamic cerebral autoregulation (dCA). It is established that dCA is impaired following moderate to severe stroke, acting as a key role in the development of secondary brain damage related to brain swelling and further damage related to the low blood flow. The administration of clot busting therapy (thrombolysis), one of the main approved treatments of acute ischaemic stroke (AIS), results in recanalisation of the blocked artery in only approximately 50% of patients. Therefore, as well as attempts to treat major vessel blockage, improving brain blood flow, particularly to the penumbral area, through arteries that bypass the blockage is another potential therapeutic approach in AIS.One simple way of achieving this might be to lower the head of AIS patient into a lying flat (0⁰) position. However, to date, there have been very few studies exploring this. This research will use the noninvasive technique of Trans Cranial Doppler (TCD) to see how blood flow changes in different head positions, both in healthy volunteers and AIS patient. This study will provide important data regarding blood pressure management in acute stroke, an important and common clinical dilemma.

Detailed Description

In the United Kingdom (UK) alone, approximate 100,000 people suffer a stroke each year. Improved management of stroke patients not only reduces morbidity and mortality, but also reduces the cost of long term social care.
The brain has control systems (i.e.cerebral autoregulation) to maintain blood flow to the brain, over a relatively wide blood pressure range. Cerebral Autoregulation can be described as static, reflecting the integrity of such mechanisms over time, or dynamic, occurring in response to sudden fluctuations in perfusion pressure. When blood pressure drops, small arteries increase in size to restore flow levels, and when blood pressure rises, they narrow to protect the most delicate blood vessels. It is known that sudden decompensated blood pressure (BP) changes can occur after stroke, this could result in brain bleeding and swelling when there is uncontrolled increased blood flow, or reduce the viability of tissue surrounding the stroke area when there is reduced blood flow to the brain.
It is known that the clot busting agent (Alteplase), the main effective treatment used in the acute stroke can only improve blood flow in already blocked arteries in 50% of patients. Therefore, as well as attempts to treat blockage of major vessel, improving the blood flow through vessel that bypass the blocked vessel around the stroke area (penumbra) could be another potential therapeutic approach in acute ischaemic stroke patients. A simple way of increase blood flow to these penumbral area might be just lower the head of acute stroke patients into a lying flat position. Several observational studies have investigated the effects of head positioning on blood flow to the brain in a healthy population, however few studies carried out on acute ischaemic stroke patients so far.
Cerebral autoregulation can be assessed non-invasively by the use of Trans Cranial Doppler (TCD). This means using ultrasound probes over both sides of the head to measure changes in blood flow in one of the main brain arteries (the middle cerebral artery) in response to beat to beat changes in blood pressure dynamic cerebral autoregulation. This research will use the noninvasive technique of Trans Cranial Doppler to see how blood flow changes during different head position between acute ischaemic stroke patients and healthy controls, as well as over time during recovery after a stroke. This knowledge will help us to understand the changes in brain blood flow control and blood pressure in stroke patients, with implications of diagnosis, prognosis, and treatment of the disease.

Conditions

Interventions

  • Change of head position Other
    Intervention Desc: patient can be allocated to the transient change of the head position, persistent lying flat position in the first 24 hours of the hospital admission and persistent sitting up in the first 24 hours of the hospital admission
    ARM 1: Kind: Experimental
    Label: Healthy controls
    Description: healthy controls subjects who have age, sex and Blood pressure matched with the acute ischaemic stroke patient
    ARM 2: Kind: Experimental
    Label: AIS patient-transient arm
    Description: transient change of head position from lying flat (0 degree) to sitting up (30 degree)
    ARM 3: Kind: Experimental
    Label: AIS patient - persistent lying flat
    Description: lying flat (0 degree) head position for the first 24 hours in the hospital admission
    ARM 4: Kind: Experimental
    Label: AIS patient - persistent sitting up
    Description: sitting up ( 30 degree) head position for the first 24 hours in the hospital admission

Trial Design

  • Observation: Case Control
  • Perspective: Prospective
  • Sampling: Probability Sample

Trial Population

11 healthy control subjects 11 acute ischaemic stroke patient 11 acute ischaemic stroke patients in the lying flat (0 degree) head position (first 24 hours of hospital admission) 11 acute ischaemic stroke patients in the sitting up ( 30 degree) head position (first 24 hours of hospital admission)

Outcomes

Type Measure Time Frame Safety Issue
Primary cerebral blood flow velocity within 24 hours, 72 hours and 3 months of the stroke symptom onset No
Secondary dynamic cerebral autoregulation within 24 hours, 72 hours and 3 months of stroke symptom onset No
Secondary Neurovascular coupling within 24 hours, 72 hours and 3 months of stroke symptom onset No
Secondary Carbon dioxide reactivity within 24 hours, 72 hours and 3 months of stroke symptom onset No

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