Higher Cerebral Blood Flow Velocity Research Articles

Cerebral hemodynamics before and after shunting in normal pressure hydrocephalus.

To study the relationship between cerebral hemodynamics and clinical performance in normal pressure hydrocephalus (NPH), before and after surgery. Ten patients were studied prospectively before and 3 months after shunt surgery by means of transcranial Doppler (TCD). Clinical performance was scored by means of an NPH scale and the modified Rankin scale. Peak systolic and mean cerebral blood flow velocity (MCV) were lower and cerebrovascular CO2 reactivity was higher after shunt surgery. The three patients with clinical improvement had higher preoperative end diastolic cerebral blood flow velocity and MCV. All postoperative cerebral blood flow velocities were higher in patients with clinical improvement. Our data suggest that higher cerebral blood flow velocity before surgery in patients with NPH is related to clinical improvement after shunt surgery. Cerebral hemodynamic parameters may develop into predictors of successful shunt surgery in patients with normal pressure hydrocephalus.

Anemic hypoxia in moderate intracerebral hemorrhage: the alterations of cerebral hemodynamics and brain metabolism.

To determine the influence of anemic hypoxia on cerebral hemodynamics and brain metabolism during pathological conditions of the brain, moderate-sized intracerebral hemorrhage (ICH) was created in canines with and without preoperatively inducing chronic anemia. The changes in cerebral perfusion pressure (CPP) and cerebral blood flow velocities (CBFv) were evaluated as well as the determinations for cerebral extraction fraction of oxygen (CEO2), arteriovenous oxygen content difference (AVDO2) and lactate (Lac) concentrations through the arterial and superior sagittal sinus (SSS) samples. Before ICH production, anemic animals (n = 8) showed a significant reduction in cerebral AVDO2 and arteriovenous Lac difference (AVDLac) but had higher CBFv as well as CEO2 than did nonanemic animals (n = 8). The CBFv began to decrease within 30 min after ICH in anemic but not in nonanemic animals, and the difference between the two groups was found to be significant at 2 h (P<0.05). Following ICH, anemic group also showed coupling reductions in CEO2 and AVDO2, indicating a decreased cerebral metabolic rate for oxygen (CMRO2) relative to the baseline data, compared with a constant CMRO2 in nonanemic group in which the CEO2, AVDO2, and CBFv remained relatively normal. Moreover, compared to the baseline data, a significant increase of the AVDLac was found in anemic but not in nonanemic group, although the former had lower Lac concentrations of the SSS than did the latter group throughout the whole observation period. We conclude that, in cases with chronically reduced Hct, cerebral hemodynamics and oxygenation remain in favorable conditions, thus decreasing Lac production of the brain. The findings suggest a lowered metabolic demand of the brain tissue due to reduced cerebral O2-carrying capacity. During the early phase of moderate ICH, the regulation capacity in cerebral hemodynamics and brain oxygenation tend to deteriorate in profound anemic hypoxia, which consequently leads to enhancing at least modest anaerobic glycolysis.

Cerebral blood flow velocity and perfusion in purulent meningitis: a comparative TCD and 99M-TC-HMPAO-SPECT study.

In 15 patients (median age 33 years; range 17-74 years) suffering from acute pneumococcal (10 cases) and meningococcal (five cases) meningitis, cerebral blood flow velocity (CBFV) was measured in the M1 - segment of the middle cerebral artery (MCA) by transcranial Doppler sonography, and cerebral perfusion changes were evaluated by 99m-Tc-hexamethylpropylene amine oxime single photon emission computed tomography (HMPAO SPECT). The objective of the study was to test whether increased CBFV during the acute phase of purulent meningitis reflects hyperemia, and to evaluate focal perfusion abnormalities and their correlation to CBFV changes. In eight patients with marked side-differences in CBFVs during the acute phase of the disease SPECT scans were normal in five. In three patients unilateral perfusion defects correlated with the side of higher CBFV. In seven patients presenting with symmetrically elevated CBFV, SPECT scans were normal in four and revealed focal abnormalities in the remaining three. Follow up SPECT scans were normal in 14/15 patients. The results of our study suggest that elevated CBFV in acute bacterial meningitis does not reflect cerebral hyperemia. Focal cerebral perfusion defects occur independently from functional alterations in the cerebral macrovasculature. A causative pathophysiologic relationship of high CBFV and focal perfusion defects cannot be drawn from these data.

Inflammatory cytokines in CSF in bacterial meningitis: association with altered blood flow velocities in basal cerebral arteries.

To investigate the association between release of humoral inflammatory mediators in CSF and blood and alterations of cerebral blood flow in patients with bacterial meningitis. Immunomodulatory (interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF alpha)) and vasoactive (thromboxane A, prostacyclin, endothelin-1) molecules of probable or confirmed leucocyte origin were determined in CSF and venous blood from 20 patients with bacterial meningitis, and matched control subjects. Their concentrations were related to the presence of increased blood flow velocities in the middle cerebral arteries, as recorded by transcranial Doppler sonography. Concentrations of proinflammatory cytokines and prostacyclin and leucocyte counts were significantly increased in meningitis, but concentrations of the vasoconstrictors thromboxane and endothelin-1 were not. Patients with high blood flow velocities ( > 140 cm/s) had significantly increased concentrations of IL-1 beta and IL-6 and raised cell counts in CSF. The increases of key mediators of inflammation and immunoactivation and of leucocyte count in the CSF of patients with high cerebral blood flow velocities suggest a role of excessive compartmentalised host defence in pathogenesis of disorders of cerebral blood flow in bacterial meningitis.

Severe birth asphyxia and abnormal cerebral blood-flow velocity.

Thirty-four fullterm infants with postasphyxial encephalopathy (PAE) were studied with ultrasound to assess cerebral blood-flow velocity (CBFV). A control group of 126 healthy infants also had CBFV recordings during the first week of life. Measurements for the majority of the asphyxiated group fell into two abnormal patterns in relation to the control group: four had low CBFV (less than 2 SD below the mean) and 17 had high CBFV (greater than or equal to 2 SD above the mean); all had severe PAE. Median age at the first high measurement was 26 hours. There were no statistically significant differences between infants with normal and abnormal CBFV in measurements of PaCO2 or mean arterial blood-pressure. A Pourcelot Resistance Index (PRI) less than 0.55 was common in the presence of high CBFV, but never seen with low measurements. 21 of the 34 infants died of their asphyxial insult and four of the survivors have severe cerebral palsy at a median age of two years. Three of the four with low CBFV died, and no infant with CBFV greater than 3 SD survived without severe impairment. The positive predictive value of CBFV measurements less than 2 SD or greater than 3 SD for death or severe impairment is 94 per cent, compared with 83 per cent for low PRI alone. The authors believe that high CBFV is the result of vasoparalysis of cerebral arterioles and that it represents a form of irreversible cerebral injury.

Cerebral blood flow velocity pattern in healthy and asphyxiated newborns: a controlled study.

In a controlled study serial determinations of cerebral blood flow velocity using Doppler ultrasound and repeated real-time ultrasonographic- or computerized axial tomographic studies of the brain were performed in 17 (nearly) full-term newborns who experienced perinatal asphyxia and in 17 healthy matched controls during the first week of life. A higher cerebral blood flow velocity was found during the first 4 days of life, indicating a lower cerebrovascular resistance in the asphyxiated infants compared to the control infants. These haemodynamic changes coincided with cerebral oedema and neurological abnormalities. It is speculated that the changes in the cerebral circulation in asphyxiated infants are at least partly caused by cerebral oedema-induced increase of intracranial pressure due to severe perinatal asphyxia. Serial Doppler ultrasound investigations of the brain may be a useful non-invasive method for early detection and follow-up of the consequences of severe perinatal asphyxia.

Decreased cerebrovascular resistance in small for gestational age infants

Using a transcutaneous Doppler technique we found a significantly lower cerebrovascular resistance and higher cerebral blood flow velocity indicating vasodilatation and increase of cerebral blood flow in small for gestational age infants compared with appropriate for gestational age infants during the first days of life. We speculate that these findings are due to a continuation of the fetal situation in which chronic hypoxia, mostly caused by pregnancy-induced hypertension, possibly causes a prostacyclin-induced vasodilatation.