Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, May 18, 2022

Cerebral Augmentation Effect Induced by External Counterpulsation Is Not Related to Impaired Dynamic Cerebral Autoregulation in Ischemic Stroke

 Someone with medical training needs to put this together with leg compressions and leg wraps and create a protocol.  Has your hospital implemented remote ischemic conditioning yet? I think that is another name for external counterpulsation. WHAT THE FUCK ARE THEY WAITING FOR?

 

Cerebral Augmentation Effect Induced by External Counterpulsation Is Not Related to Impaired Dynamic Cerebral Autoregulation in Ischemic Stroke

Li Xiong1,2*, Xiangyan Chen3*, Jia Liu4, Lawrence Ka Sing Wong2 and Thomas W. Leung2
  • 1Clinical Trials Centre, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, China
  • 2Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China
  • 3Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Shatin, Hong Kong SAR, China
  • 4Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China

Background and Purpose: Dynamic cerebral autoregulation is impaired after ischemic stroke. External counterpulsation (ECP) augments the cerebral blood flow of patients with ischemic stroke by elevation of blood pressure (BP). We aimed to investigate if cerebral augmentation effects during ECP were associated with impaired dynamic cerebral autoregulation in patients after acute ischemic stroke.

Methods: Forty patients with unilateral ischemic stroke and large artery atherosclerosis in the anterior circulation territory within 7 days from symptom onset and eighteen healthy controls were recruited. We monitored changes in mean flow velocity over both middle cerebral arteries (MCA) by transcranial Doppler (TCD) before, during, and immediately after ECP. Cerebral augmentation index was MCA mean flow velocity increase in percentage during ECP compared with baseline to evaluate the augmentation effects of ECP. Spontaneous arterial BP and cerebral blood flow velocity in both bilateral MCAs were recorded using a servo-controlled plethysmograph and TCD, respectively. Transfer function analysis was used to derive the autoregulatory parameters, including phase difference (PD), and gain.

Results: The cerebral augmentation index in patients with stroke was significantly higher on both the ipsilateral and contralateral sides than that in controls, while the PD in patients with stroke was significantly lower on both sides than those in controls (all P < 0.05). The cerebral augmentation index did not correlate with PD and gain on either the ipsilateral or contralateral side of patients with stroke or in controls (all P > 0.05). The cerebral augmentation index of patients with stroke was significantly related to mean BP change on the ipsilateral side (R2 = 0.108, P = 0.038).

Conclusion: The degree of ECP-induced cerebral augmentation effects as measured by the cerebral augmentation index did not correlate with the magnitude of impaired dynamic cerebral autoregulation.

Introduction

In the traditional view, cerebral autoregulation ensures the constancy of cerebral blood flow to the brain as the systemic blood pressure (BP), and hence, cerebral perfusion pressure changes over a wide range. However, considering the compelling evidence currently available, cerebral blood flow regulation is far more pressure-passive in nature than traditionally believed. Indeed, cerebral blood flow will not necessarily remain stable in some physiological/clinical conditions (1). Cerebral autoregulation is impaired after ischemic stroke (2, 3). The brain becomes more vulnerable to ischemic damage caused by changes in systemic BP or intracranial pressure. Although the management of BP following acute ischemic stroke remains controversial, the available clinical data suggest that the use of BP augmentation may improve perfusion to ischemic tissue, which can result in at least short-term neurological improvement (4, 5).

External counterpulsation (ECP) is a noninvasive and well-established method for ischemic heart disease (68). ECP operates by applying electrocardiography-triggered diastolic pressure to the lower extremities through air-filled cuffs. The diastolic augmentation of the blood flow and the simultaneously decreasing systolic afterload increases the blood flow of vital organs such as the heart, brain, and kidneys (9, 10). Our pilot study showed that ECP is feasible for patients with ischemic stroke with large artery disease by improving neurological deficits (11). ECP may improve cerebral perfusion and collateral blood supply in ischemic stroke by augmenting BP and cerebral blood flow velocity (CBFV) (12). Without cerebral autoregulation, CBFV would passively follow BP. The cerebral augmentation effects induced by ECP possibly worked via impaired cerebral autoregulation. Furthermore, we first proposed the cerebral augmentation index to evaluate the degree of cerebral augmentation effects induced by ECP. Recently, we found that the higher cerebral augmentation index on the side ipsilateral to the infarct was independently correlated with an unfavorable functional outcome after acute ischemic stroke (13).

Without too much cooperation from patients, transfer function analysis (TFA) is a frequently used method to assess dynamic cerebral autoregulation using spontaneous oscillations in BP and CBFV despite the controversies and variations in its interpretation from different research groups (14, 15). TFA quantifies cerebral autoregulation in the parameters phase difference (PD), gain, and coherence with the assumption that cerebral autoregulation is a linear control system. It is based on the concept that cerebral autoregulation minimizes the effect of dynamic BP fluctuations on CBFV, which is reflected by reduced low-frequency gain and phase-lead of CBFV over BP (16, 17). Without cerebral autoregulation, CBFV would passively follow BP, and TFA would show constant gain and zero phases across the low-frequency band. In acute ischemic stroke, recent meta-analyses of TFA parameters, obtained from spontaneous fluctuations of BP at rest, have demonstrated that PD and the autoregulation index can show highly significant differences in comparison with healthy controls, while less clear-cut results were obtained for gain (18).

Therefore, in this study, we aimed to investigate whether the degree of cerebral blood flow augmentation effects induced by ECP was related to the magnitude of impaired dynamic cerebral autoregulation in patients with ischemic stroke, assessed by cerebral augmentation index and PD and gain, respectively.

More at link.

 

No comments:

Post a Comment