Cerebral Autoregulation in Stroke

Abstract

Background and Purpose-Cerebral autoregulation may become impaired after stroke. To provide a review of the nature and extent of any autoregulation impairment after stroke and its course over time, a technique allowing repeated bedside measurements with good temporal resolution is required. Transcranial Doppler (TCD) in combination with continuous blood pressure measurements allows noninvasive continuous bedside investigation with high temporal resolution of the dynamic and the steady-state components of cerebral autoregulation. Therefore, this review focuses on all TCD studies on cerebral autoregulation in the setting of documented ischemic stroke. Methods-PubMed and EMBASE were searched for studies of stroke, autoregulation, and TCD. Studies were either acute phase (Ͻ96 hours after index stroke) or chronic phase (Ͼ96 hours after index stroke) autoregulation studies. Quality of studies was studied in a standardized fashion. Results-Twenty-three studies met the inclusion criteria. General agreement existed on cerebral autoregulation being impaired, even after minor stroke. Bilateral impairment of autoregulation was documented, particularly after lacunar stroke. Studies showed progressive deterioration of cerebral autoregulation in the first 5 days after stroke and recovery over the next 3 months. Impaired cerebral autoregulation as assessed by TCD was related to neurological deterioration, the necessity for decompressive surgery, and poor outcome. Synthesis of the data of various studies was, however, limited by studies not meeting key methodological criteria for observational studies. Conclusions-TCD

Intracranial Pressure Elevation after Ischemic Stroke in Rats: Cerebral Edema is Not the Only Cause, and Short-Duration Mild Hypothermia is a Highly Effective Preventive Therapy

“…If a similar rise in ICP does occur after small human strokes, the implications would be very important to the outcome of those patients. Blood flow to the ischemic penumbra is known to be CPP dependent as normal cerebral blood flow autoregulation is lost in the ischemic penumbra, 24 so ICP elevation would be predicted to reduce penumbral perfusion. The principle of increasing CPP to enhance collateral flow and penumbral perfusion has been exploited in several clinical trials; [25][26][27][28][29][30][31] however, to date, these have all focused on mean arterial pressure (MAP) rather than intracranial pressure (CPP = MAP − ICP).…”

Risks for Impaired Cerebral Autoregulation During Cardiopulmonary Bypass and Postoperative Stroke

“…27 Regardless, acute stroke is known to result in impaired CBF autoregulation. 23 Thus, our monitoring methods may have identified patients with stroke during surgery. It is also possible that we simply identified patients with cerebral vascular disease and impaired cerebral vasoreactivity who are at high risk for stroke.…”

Perioperative management of adult patients with a history of stroke or transient ischaemic attack undergoing elective non-cardiac surgery

“…In the days following a stroke, cerebral autoregulation is impaired and cerebral perfusion is therefore very sensitive to even modest changes in blood pressure. 17,18 The duration of this failure of autoregulation is uncertain but it has been postulated that it may last 1-3 months. [17][18][19] Furthermore, the area of infarcted cerebral tissue undergoes inflammatory processes and softens, rendering this area vulnerable to the haemodynamic stresses of anaesthesia and surgery.…”

“…17,18 The duration of this failure of autoregulation is uncertain but it has been postulated that it may last 1-3 months. [17][18][19] Furthermore, the area of infarcted cerebral tissue undergoes inflammatory processes and softens, rendering this area vulnerable to the haemodynamic stresses of anaesthesia and surgery. 19 Following a stroke, a sufficient time period should be allowed before elective surgery for the patient's neurological and haemodynamic status to stabilise and cerebral autoregulation to be restored to minimise the risk of a further stroke or worsening of the initial stroke.…”