Autoregulatory cerebral vasodilation occurs during orthostatic hypotension in patients with primary autonomic failure

Abstract

It is unclear whether patients with autonomic failure autoregulate cerebral blood flow during hypotension. The objective in this study was to examine cerebral autoregulatory capacity in patients with autonomic failure by studying changes in middle cerebral artery blood flow velocity using transcranial Doppler ultrasonography before, during, and after tilt-induced hypotension. Nine patients with primary autonomic failure were evaluated. Mean arterial pressure and middle cerebral artery blood flow velocity were simultaneously recorded while the patients were in the supine position, during 60 degrees head-up tilt, and after they were returned to the horizontal position. The results were as follows: during tilt-induced hypotension, mean arterial pressure decreased significantly more than middle cerebral artery mean blood flow velocity (58% versus 36%, p <0.0002). After return to the horizontal position, mean arterial pressure returned to baseline, and middle cerebral artery blood flow velocity transiently increased above pretilt value (p <0.02). It is concluded that cerebral autoregulatory vasodilation occurs in patients with autonomic failure. This was demonstrated by a more pronounced decline in mean arterial pressure than in middle cerebral artery blood flow velocity during hypotension and by a transient increase in middle cerebral artery blood flow velocity (ie, hyperemic response) after blood pressure was restored.

Contemporary Cardiovascular Concerns after Spinal Cord Injury: Mechanisms, Maladaptations, and Management

“…7 Reduced symptoms of presyncope but similar OH in the chronic phase of SCI suggests that tolerance to low blood pressure and cerebral perfusion pressure may improve with time after SCI. 44,74,75 Considering the association between OH and an elevated risk of stroke in the able bodied population, 76 as well as the fact that stroke risk is 3-4 times greater after SCI, it is logical to posit that the presence of OH after SCI plays a contributing role. 3,77 Other factors contributing to the presence of OH after SCI include reduced plasma volumes caused by hyponatremia, 72 insufficient increases in the capacity of the renin-angiotensin system to maintain blood pressure 78 and potentially cardiac deconditioning.…”

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

“…This is particularly evident in individuals suffering from autonomic failure, such as multiple system atrophy and pure autonomic failure. 21,[77][78][79] The mechanisms underlying this tolerance to hypotension are unclear, but since the ultimate cause of symptoms in these individuals is known to be due to cerebral hypoperfusion, it is likely that there is a shift in cerebral autoregulation in these individuals, whereby cerebral blood flow is maintained despite low perfusion pressures. [77][78][79] Patients with SCI who demonstrate postural hypotension also seem to have altered cerebral haemodynamics, since many of them are able to tolerate profound hypotension and remain asymptomatic, and indeed, symptoms were only reported during documented orthostatic hypotension in approximately 60% of cases.…”

The Orthostatic Hypotension Questionnaire (OHQ): validation of a novel symptom assessment scale

“…Upon standing, the release of norepinephrine from sympathetic nerve terminals is decreased or absent, vasoconstriction in the systemic circulation fails, and blood pressure falls [10]. Reduced blood supply to the brain [8,16] causes characteristic symptoms that are disabling and interfere with the ability to perform everyday physical activities [4,9,10].…”