Cerebral Autoregulation in Unconscious Patients with Brain Injury

Cold, Georg E.; Jensen, F. T.

doi:10.1111/j.1399-6576.1978.tb01301.x

Cited by 104 publications

(37 citation statements)

References 34 publications

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“…More generally, t displays a large variability in the patients of the autoregulated group, ranging from a few seconds to several 10ths of a second. The previous data confirm that autoregulation may be significantly altered in acute brain damage, a result reported by several authors (6,21). Differences between prompt and delayed autoregulation might be ascribed to damage of neural control pathways (which generally have time constants of a few seconds), which are possibly replaced by the action of slower metabolic or chemical feedback mechanisms (20).…”

Section: Discussionsupporting

confidence: 72%

Intracranial pressure dynamics in patients with acute brain damage

Ursino

Lodi

Rossi³

et al. 1997

Journal of Applied Physiology

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Section: Discussionsupporting

confidence: 72%

Intracranial pressure dynamics in patients with acute brain damage

Ursino

Lodi

Rossi³

et al. 1997

Journal of Applied Physiology

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“…[6,9,21,22,25,26] Muizelaar and colleagues [21,22] evaluated autoregulation in head-injured patients by obtaining CBF values and either raising or lowering MABP to a new steady state and repeating the CBF measurement. They defined intact autoregulation as the •% CPP/ %• CVR ¾ 2 following the change in MABP, where CVR = CPP/CBF.…”

Section: Discussionmentioning

confidence: 99%

“…[14,26] Cerebral autoregulation can be impaired or absent following severe closed head injury. [4][5][6]8,9,21,22,25,26] Impairments in autoregulation may contribute by several mechanisms to secondary neuronal injury following head injury. Lowered cerebral perfusion pressure (CPP) caused by arterial hypotension or increased intracranial pressure (ICP) can occur and may cause critical reductions in cerebral blood flow (CBF) to ischemic levels more easily in head-injured patients who have poorly functioning or absent autoregulation.…”

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confidence: 99%

Cerebral autoregulation following minor head injury

North

McNamee²,

Wu³

et al. 1997

FOC

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The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI).Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

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“…7,24 Some authors have suggested that cerebrovascular pressure reactivity could be derived from the characteristic pulse waveform from ABP, 26,27 although this has never been demonstrated to work in clinical practice. Perhaps changes in ABP are too fast (a fraction of a second) to mobilize an active vasoregulatory response.…”

mentioning

confidence: 99%

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Zweifel

Lavinio

Steiner

et al. 2008

FOC

191

112

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Object Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between mean intracranial pressure (ICP) and mean arterial blood pressure. Methods The authors analyzed a database consisting of 398 patients with head injuries who underwent continuous monitoring of cerebrovascular pressure reactivity. In 298 patients, the PRx was compared with a transcranial Doppler ultrasonography assessment of cerebrovascular autoregulation (the mean index [Mx]), in 17 patients with the PET–assessed static rate of autoregulation, and in 22 patients with the cerebral metabolic rate for O2. Patient outcome was assessed 6 months after injury. Results There was a positive and significant association between the PRx and Mx (R2 = 0.36, p < 0.001) and with the static rate of autoregulation (R2 = 0.31, p = 0.02). A PRx > 0.35 was associated with a high mortality rate (> 50%). The PRx showed significant deterioration in refractory intracranial hypertension, was correlated with outcome, and was able to differentiate patients with good outcome, moderate disability, severe disability, and death. The graph of PRx compared with cerebral perfusion pressure (CPP) indicated a U–shaped curve, suggesting that too low and too high CPP was associated with a disturbance in pressure reactivity. Such an optimal CPP was confirmed in individual cases and a greater difference between current and optimal CPP was associated with worse outcome (for patients who, on average, were treated below optimal CPP [R2 = 0.53, p < 0.001] and for patients whose mean CPP was above optimal CPP [R2 = −0.40, p < 0.05]). Following decompressive craniectomy, pressure reactivity initially worsened (median −0.03 [interquartile range −0.13 to 0.06] to 0.14 [interquartile range 0.12–0.22]; p < 0.01) and improved in the later postoperative course. After therapeutic hypothermia, in 17 (70.8%) of 24 patients in whom rewarming exceeded the brain temperature threshold of 37°C, ICP remained stable, but the average PRx increased to 0.32 (p < 0.0001), indicating significant derangement in cerebrovascular reactivity. Conclusions The PRx is a secondary index derived from changes in ICP and arterial blood pressure and can be used as a surrogate marker of cerebrovascular impairment. In view of an autoregulation–guided CPP therapy, a continuous determination of a PRx is feasible, but its value has to be evaluated in a prospective controlled trial.

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Cerebral Autoregulation in Unconscious Patients with Brain Injury

Cited by 104 publications

References 34 publications

Intracranial pressure dynamics in patients with acute brain damage

Intracranial pressure dynamics in patients with acute brain damage

Cerebral autoregulation following minor head injury

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

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