Low Cerebral Blood Flow Velocity Research Articles

Assessment of cognitive impairment after acute cerebral infarction with T1 relaxation time measured by MP2RAGE sequence and cerebral hemodynamic by transcranial Doppler.

This study aimed to investigate early brain microstructural changes discovered using magnetization-prepared two rapid acquisition gradient echo (MP2RAGE) sequence and cerebral hemodynamic using TCD for cognitive impairment after acute cerebral infarction. We enrolled 43 patients with acute cerebral infarction and 21 healthy people in the study, who were subjected to cognitive assessments, the MP2RAGE sequence, and a cerebral hemodynamic examination. A total of 26 brain regions of interest were investigated. Furthermore, we used cerebral hemodynamics to explain brain microstructural changes, which helped us better understand the pathophysiology of cognitive impairment after acute cerebral infarction and guide treatment. T1 relaxation times in the left frontal lobe, right frontal lobe, right temporal lobe, left precuneus, left thalamus, right hippocampus, right head of caudate nucleus, and splenium of corpus callosum were substantially different across the three groups, which were significantly correlated with neuropsychological test scores. CI group patients had significantly lower cerebral blood flow velocity than those in the N-CI and Normal groups. The receiver operating curve analysis revealed that most T1 relaxation times had high sensitivity and specificity, especially on the right temporal lobe and right frontal lobe. There was a potential correlation between T1 relaxation times and MMSE scores through TCD parameters. The MP2RAGE sequence can detect alterations in whole brain microstructure in patients with cognitive impairment after acute cerebral infarction. Brain microstructural changes could influence cognitive function through cerebral hemodynamics. T1 relaxation times on the right temporal lobe and the right frontal lobe are expected to be a prospective biomarker of cognitive impairment after acute cerebral infarction.

Local cerebral blood flow assessment using transcranial Doppler ultrasonography in a dog with brain infarction in the right middle cerebral artery territory.

A 12-year-old neutered male Chihuahua was diagnosed with acute brain infarction in the right middle cerebral artery (MCA) territory. Transcranial Doppler ultrasonography (TCD) was performed to assess the local cerebral blood flow at the time of diagnosis and after 4 and 31 hr. Initially, the right MCA retained blood flow but with a lower cerebral blood flow velocity (CBFV; 14.9 cm/sec) than the left MCA (27.9 cm/sec). The TCD vascular resistance variables were higher in the right than in the left MCA. An increase in the CBFV and a decrease in TCD vascular resistance variables were observed, consistent with improvements in neurological symptoms. TCD can be a non-invasive, and easy-to-use modality for bedside monitoring of cerebral edema and infarction.

Early Cerebral Hypoperfusion in Patients with Orthostatic Intolerance Without Tachycardia During Head-Up Tilt Test is Independent of Vasovagal Response.

Cerebral hypoperfusion before syncope has been shown in patients with chronic orthostatic intolerance (OI) without tachycardia, but it is unknown if an initial decrease of cerebral blood flow velocity (CBFv) could be related to the vasovagal response (VVR) to head-up tilt test (HUTT). The objective of the study was to compare cardiovascular, cerebrovascular, and autonomic variables during HUTT in OI patients with or without a VVR. We included 74 subjects (58% female, mean age 33 ± 12 years) who underwent a 30-min HUTT and were divided into three groups: OI with VVR positive (VVR+), OI without VVR negative (VVR-), and asymptomatic healthy subjects with negative HUTT (control group). Cardiovascular, cerebrovascular, and autonomic variables were assessed beat-to-beat during HUTT with a Task Force monitor and a trans-cranial Doppler. Mean values were evaluated at baseline and throughout the first 10 min of tilting. Cardiovascular variables were similar in the three groups. Systolic, diastolic, and mean CBFv were similar in VVR+ and VVR-, but both groups had lower CBFv than the control group. Systolic and diastolic CBFv decreased from baseline since min 1 in VVR+ and VVR- and since min 5 in the control group. The mean CBFv had a significant decrease since min 1 compared to baseline in all groups. Spectral indices of heart rate and blood pressure variability showed a similar autonomic response to HUTT in all groups. Patients with chronic OI without tachycardia have early postural cerebral hypoperfusion, regardless of the VVR during HUTT.

Human Adaptations to Multiday Saturation on NASA NEEMO.

Human adaptation to extreme environments has been explored for over a century to understand human psychology, integrated physiology, comparative pathologies, and exploratory potential. It has been demonstrated that these environments can provide multiple external stimuli and stressors, which are sufficient to disrupt internal homeostasis and induce adaptation processes. Multiday hyperbaric and/or saturated (HBS) environments represent the most understudied of environmental extremes due to inherent experimental, analytical, technical, temporal, and safety limitations. National Aeronautic Space Agency (NASA) Extreme Environment Mission Operation (NEEMO) is a space-flight analog mission conducted within Florida International University’s Aquarius Undersea Research Laboratory (AURL), the only existing operational and habitable undersea saturated environment. To investigate human objective and subjective adaptations to multiday HBS, we evaluated aquanauts living at saturation for 9–10 days via NASA NEEMO 22 and 23, across psychologic, cardiac, respiratory, autonomic, thermic, hemodynamic, sleep, and body composition parameters. We found that aquanauts exposed to saturation over 9–10 days experienced intrapersonal physical and mental burden, sustained good mood and work satisfaction, decreased heart and respiratory rates, increased parasympathetic and reduced sympathetic modulation, lower cerebral blood flow velocity, intact cerebral autoregulation and maintenance of baroreflex functionality, as well as losses in systemic bodyweight and adipose tissue. Together, these findings illustrate novel insights into human adaptation across multiple body systems in response to multiday hyperbaric saturation.

Perioperative Assessment of Cerebral Oxygen Metabolism in Infants With Functionally Univentricular Hearts Undergoing the Bidirectional Cavopulmonary Connection.

The transition from single-ventricle lesions with surgically placed systemic-to-pulmonary artery shunt to the circulation following a bidirectional cavopulmonary connection results in higher pressure in the superior vena cava when compared with the preceding circulation. The aim of this study was to evaluate the impact of this transition on the perioperative cerebral oxygen metabolism. Prospective observational cohort study. Pediatric critical care unit of a tertiary referral center. Sixteen infants after bidirectional cavopulmonary connection. Cardiac surgery (bidirectional cavopulmonary connection). We measured regional cerebral oxygen saturation, amount of hemoglobin, blood flow velocity, and microperfusion immediately before, 12-24 hours, and 36-48 hours following bidirectional cavopulmonary connection. Based on these measurements, we calculated cerebral fractional tissue oxygen extraction and approximated cerebral metabolic rate of oxygen. Mean pressure in the superior vena cava increased significantly (8 vs 17 mm Hg; p < 0.001) following bidirectional cavopulmonary connection. Mean cerebral oxygen saturation increased from 49.0% (27.4-61.0) to 56.9% (39.5-64.0) (p = 0.008), whereas mean cerebral blood flow velocity decreased from 80.0 arbitrary units (61.9-93.0) to 67.3 arbitrary units (59.0-83.3) (p < 0.001). No change was found in the cerebral amount of hemoglobin and in the cerebral microperfusion. Mean cerebral fractional tissue oxygen extraction (0.48 [0.17-0.63] vs 0.30 [0.19-0.56]; p = 0.006) and approximated cerebral metabolic rate of oxygen (5.82 arbitrary units [2.70-8.78] vs 2.27 arbitrary units [1.19-7.35]; p < 0.001) decreased significantly. Establishment of bidirectional cavopulmonary connection is associated with postoperative improvement in cerebral oxygen metabolism. Cerebral amount of hemoglobin did not increase, although creation of the bidirectional cavopulmonary connection results in significant elevation in superior vena cava pressure. Improvement in cerebral oxygen metabolism was due to lower cerebral blood flow velocity and stable microperfusion, which may indicate intact cerebral autoregulation.

Determining differences between critical closing pressure and resistance-area product: responses of the healthy young and old to hypocapnia.

Healthy ageing has been associated with lower cerebral blood flow velocities (CBFVs); however, the behaviour of hemodynamic parameters associated with cerebrovascular tone (critical closing pressure, CrCP) and cerebrovascular resistance (resistance-area product, RAP) remains unclear. Specifically, evidence supports ageing being associated with greater cerebrovascular tone and resistance during exercise with elevated CrCP and RAP in older individuals at rest and during exercise. Comprehensive hemodynamic assessment of CrCP and RAP during hyperventilation-induced hypocapnia in two distinct age groups (young ≤ 49 and old > 50) has not been described. CBFV in the middle cerebral artery (CBFV, transcranial Doppler), blood pressure (BP, Finometer) and end-tidal CO2 (EtCO2, capnography) were recorded in 104 healthy individuals (43 young [age 33.8 (9.3) years], 61 old [age 64.1 (8.5) years]) during a minimum of 60s of metronome-driven hyperventilation-induced hypocapnia. Autoregulation index was calculated as a function of time, using a moving window autoregressive-moving average model. CBFV was reduced in response to age (p < 0.0001) and hypocapnia (p = 0.023) (young 57.3 (14.4) vs. 44.9cms-1 (11.1), old 51.7 (12.9) vs. 37.8cms-1 (9.6)). Critical closing pressure (CrCP) increased significantly in response to hypocapnia (young 37.6 (18.5) vs. 39.7mmHg (16.0), old 33.9 (13.5) vs. 39.3mmHg (11.4); p < 0.0001). Resistance-area product was increased in response to age (p = 0.001) and hypocapnia (p = 0.004) (young 1.02 (0.40) vs. 1.09mmHgcms-1 (11.07), old 1.16 (0.34) vs. 1.34mmHgcms-1 (0.39)). RAP and not CrCP mediates differences in cerebrovascular resistance responses to hypocapnia between the healthy young and old individuals.

Transcranial Doppler and Magnetic Resonance in Tanzanian Children With Sickle Cell Disease.

Background and Purpose- We determined prevalences of neurological complications, vascular abnormality, and infarction in Tanzanian children with sickle cell disease. Methods- Children with sickle cell disease were consecutively enrolled for transcranial Doppler; those with slightly elevated (>150 cm/s), low (<50 cm/s) or absent cerebral blood flow velocity (CBFv) were invited for brain magnetic resonance imaging and magnetic resonance angiography. Results- Of 200 children (median age 9; range 6-13 years; 105 [2.5%] boys), 21 (11%) and 15 (8%) had previous seizures and unilateral weakness, respectively. Twenty-eight (14%) had elevated and 39 (20%) had low/absent CBFv, all associated with lower hemoglobin level, but not higher indirect bilirubin level. On multivariable analysis, CBFv>150 cm/s was associated with frequent painful crises and low hemoglobin level. Absent/low CBFv was associated with low hemoglobin level and history of unilateral weakness. In 49 out of 67 children with low/absent/elevated transcranial Doppler undergoing magnetic resonance imaging, 43% had infarction, whereas 24 out of 48 (50%) magnetic resonance angiographies were abnormal. One had hemorrhagic infarction; none had microbleeds. Posterior circulation infarcts occurred in 14%. Of 11 children with previous seizure undergoing magnetic resonance imaging, 10 (91%) had infarction (5 silent) compared with 11 out of 38 (29%) of the remainder ( P=0.003). Of 7 children with clinical stroke, 2 had recurrent stroke and 3 died; 4 out of 5 had absent CBFv. Of 193 without stroke, 1 died and 1 had a stroke; both had absent CBFv. Conclusions- In one-third of Tanzanian children with sickle cell disease, CBFv is outside the normal range, associated with frequent painful crises and low hemoglobin level, but not hemolysis. Half have abnormal magnetic resonance angiography. African children with sickle cell disease should be evaluated with transcranial Doppler; those with low/absent/elevated CBFv should undergo magnetic resonance imaging/magnetic resonance angiography.

Association of small fiber neuropathy and post treatment Lyme disease syndrome.

ObjectivesTo examine whether post-treatment Lyme disease syndrome (PTLDS) defined by fatigue, cognitive complaints and widespread pain following the treatment of Lyme disease is associated with small fiber neuropathy (SFN) manifesting as autonomic and sensory dysfunction.MethodsThis single center, retrospective study evaluated subjects with PTLDS. Skin biopsies for assessment of epidermal nerve fiber density (ENFD), sweat gland nerve fiber density (SGNFD) and functional autonomic testing (deep breathing, Valsalva maneuver and tilt test) were performed to assess SFN, severity of dysautonomia and cerebral blood flow abnormalities. Heart rate, end tidal CO2, blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery using transcranial Doppler were monitored.Results10 participants, 5/5 women/men, age 51.3 ± 14.7 years, BMI 27.6 ± 7.3 were analyzed. All participants were positive for Lyme infection by CDC criteria. At least one skin biopsy was abnormal in all ten participants. Abnormal ENFD was found in 9 participants, abnormal SGNFD in 5 participants, and both abnormal ENFD and SGNFD were detected in 4 participants. Parasympathetic failure was found in 7 participants and mild or moderate sympathetic adrenergic failure in all participants. Abnormal total CBFv score was found in all ten participants. Low orthostatic CBFv was found in 7 participants, three additional participants had abnormally reduced supine CBFv.ConclusionsSFN appears to be associated with PTLDS and may be responsible for certain sensory symptoms. In addition, dysautonomia related to SFN and abnormal CBFv also seem to be linked to PTLDS. Reduced orthostatic CBFv can be associated with cerebral hypoperfusion and may lead to cognitive dysfunction. Autonomic failure detected in PTLDS is mild to moderate. SFN evaluation may be useful in PTLDS.

Cerebral Hemodynamic Changes During Migraine Attacks and After Triptan Treatments.

Migraine has been known for many years, but its mechanism remains unclear. Different cerebral hemodynamic changes have been observed at different stages of a migraine attack. Published results on cerebral hemodynamics are contradictory. For this reason, we aimed to investigate cerebral hemodynamic changes during attacks as well as the effects of frovatriptan and rizatriptan. Forty migraine patients with aura using rizatriptan (n=20) and frovatriptan (n=20) and 20 healthy individuals were included in our study. Cerebral blood flow velocities and breath-holding indices were recorded bilaterally from middle and posterior cerebral arteries. All procedures were repeated one hour after treatments and one week after attacks. We observed similar values of cerebral blood flow velocities and breath holding indices in all patients with migraine during the attack-free period compared to the control group. All cerebral vascular structures in migraine patients had significantly lower cerebral blood flow velocities and higher values in breath-holding indices during attacks. After taking rizatriptan and frovatriptan for an attack, the changes in hemodynamics disappeared. During attacks of migraineurs with aura, vasodilatation develops. In addition, higher vasomotor reactivity during attacks supports hypersensitivity in migraine pathophysiology. Triptans, acting as vasoconstrictor agents, were able to stop over-vasodilatation during attacks. In other words, it is possible that triptans show their effects by eliminating vascular hypersensitivity during acute attacks.

Hypocapnic cerebral hypoperfusion: A biomarker of orthostatic intolerance.

The objective of the study was to identify markers of hypocapnic cerebral hypoperfusion (HYCH) in patients with orthostatic intolerance (OI) without tachycardia and without orthostatic hypotension. This single center, retrospective study included OI patients referred for autonomic evaluation with the 10 min tilt test. Heart rate, end-tidal CO2 (ET-CO2), blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery were monitored. HYCH was defined by: (1) Symptoms of OI; (2) Orthostatic hypocapnia (low ET-CO2); (3) Abnormal decline in orthostatic CBFv due to hypocapnia; 4) Absence of tachycardia, orthostatic hypotension, or other causes of low CBFv or hypocapnia. Sixteen subjects met HYCH criteria (15/1 women/men, age 38.5±8.0 years) and were matched by age and gender to postural tachycardia patients (POTS, n = 16) and healthy controls (n = 16). During the tilt, CBFv decreased more in HYCH (-22.4±7.7%, p<0.0001) and POTS (-19.0±10.3%, p<0.0001) compared to controls (-3.0±5.0%). Orthostatic ET-CO2 was lower in HYCH (26.4±4.2 (mmHg), p<0.0001) and POTS (28.6±4.3, p<0.0001) compared to controls (36.9 ± 2.1 mmHg). Orthostatic heart rate was normal in HYCH (89.0±10.9 (BPM), p<0.08) and controls (80.8 ±11.2), but was higher in POTS (123.7±11.2, p<0.0001). Blood pressure was normal and similar in all groups. It is concluded that both HYCH and POTS patients have comparable decrease in CBFv which is due to vasoconstrictive effect of hypocapnia. Blood flow velocity monitoring can provide an objective biomarker for HYCH in OI patients without tachycardia.

Clinical Implications

HomeHypertensionVol. 71, No. 1Clinical Implications Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBClinical Implications Originally published1 Jan 2018https://doi.org/10.1161/HYPERTENSIONAHA.117.10603Hypertension. 2018;71:2Hypertensive Phenotypes After Preeclampsia (p 103)Download figureDownload PowerPointPreeclampsia is associated with a greater lifetime risk for cardiovascular and renal complications. International guidelines underline that women with hypertensive disorders of pregnancy should benefit from a postpartum screening and management of cardiovascular risk factors. However, specific recommendations, especially on the timing of the first medical visit and tests that need to be done, are still lacking. In this study, we performed ambulatory blood pressure monitoring 6 to 12 weeks after delivery in women who had preeclampsia and women who had not (controls). We found that preeclampsia was associated with a higher prevalence of diurnal and nocturnal ambulatory hypertension. Among women with preeclampsia, half of them were still hypertensive in the postpartum, with an increased prevalence of white coat and masked hypertension. They also had an abnormal circadian rhythm with a significant proportion of reversed rhythm. The index of salt-sensitivity risk, calculated from ambulatory blood pressure monitoring parameters, was significantly increased after preeclampsia. Individually, and in the general population, these hypertensive phenotypes are associated with a higher risk for cardiovascular disease later in life. Whether they are contributing factors or a consequence of preeclampsia is not known. Ambulatory blood pressure monitoring after preeclampsia is useful and helps to identify high-risk women. Early lifestyle modifications and regular medical follow-up should be offered to these women. The impact of these measures on future cardiovascular events remains of course to be determined in prospective trials.Myeloid-Derived Suppressor Cells, Cyclo sporine A, and Hypertension (p 199)Download figureDownload PowerPointCyclosporine A (CsA) is prescribed to reduce focal segmental glomerulosclerosis, membranous nephropathy, psoriasis, rheumatoid arthritis, and other autoimmune diseases despite the known prohypertensive side effect. Until new immunosuppressive drugs for these disorders are developed and used routinely in patients, strategies to blunt the negative cardiovascular and renal effects of CsA are needed. We demonstrate that augmenting a particular regulatory immune cell subset, myeloid-derived suppressor cells (MDSCs), is able to eradicate the hypertension, endothelial dysfunction, and vascular and glomerular injury caused by CsA in mice. The protective effects of increased MDSC levels caused by both interleukin-33 treatment and adoptive transfer of MDSCs demonstrate that CsA toxicity can be prevented and reversed. Beneficial effects of MDSCs have been reported in other forms of experimental hypertension and in various inflammatory and autoimmune diseases; therefore, autologous cell therapy with MDSCs may be feasible soon. Groups are generating MDSCs from various cells, including mouse embryonic stem cells and hematopoietic stem cells, as well as human peripheral blood mononuclear cells. Given the strong antihypertensive and organ-protective effects, MDSC therapy should be tested in patients being treated with CsA.Pregnancy History and Cerebrovascular Reactivity (p 110)Download figureDownload PowerPointHypertension during pregnancy is associated with an increased risk of developing cardiovascular or cerebrovascular disease later in life. Our group has shown that postmenopausal women who have experienced preeclampsia have lower brain volume and cognitive scores compared with women who had a normotensive pregnancy. The mechanisms underlying the interaction between pregnancy history and brain structure and function have not been elucidated. Because pregnancy-related changes in the circulation may contribute to pathological changes in the brain, we investigated cerebral blood flow reactivity and markers of vascular activation in women with a history of preeclampsia. In this study in Hypertension, women who either had a normotensive or preeclamptic pregnancy between 1976 and 1982 were recruited ≈35 years after the pregnancy. Women with a history of preeclampsia had lower cerebral blood flow velocity and reduced cerebrovascular reactivity, indicating cerebral microvascular dysfunction, compared with women with a history of normotensive pregnancy. Additionally, procoagulant circulating blood elements were associated with cerebral hemodynamic variables only in women with history of preeclampsia. Collectively, these results suggest that differences in circulating vasoactive factors in women with a history of preeclampsia might affect the reactivity of the cerebral circulation years beyond the preeclamptic pregnancy. These differences may contribute to brain atrophy and increased risk of cognitive decline in women with a history of preeclampsia. Previous Back to top Next FiguresReferencesRelatedDetails January 2018Vol 71, Issue 1 Advertisement Article InformationMetrics © 2017 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.117.10603 Originally publishedJanuary 1, 2018 PDF download Advertisement

Relationships between cerebral flow velocities and neurodevelopmental outcomes in children with moderate to severe traumatic brain injury.

This study aimed to determine relationships between cerebral blood flow and neurodevelopmental outcomes in children with moderate to severe traumatic brain injury (TBI). Children with TBI, a Glasgow Coma Score of 8-12, and abnormal brain imaging were enrolled prospectively. Cerebral blood flow velocity (CBFV) was assessed within 24h of trauma and daily thereafter through death, discharge, or hospital day 8, whichever came first. Twelve months from injury, participants completed neurodevelopmental testing. Sixty-nine patients were enrolled. Low flow velocities (< 2 SD below age/gender normal) were found in 6% (n = 4). No patient with a single low CBFV measurement had a good neurologic outcome (Pediatric Glasgow Outcome Scale (GOS-E Peds) ≤ 4)). Normal flow velocities (± 2 SD around age/gender normal) were seen in 43% of participants (n = 30). High flow velocities (> 2 SD above age and gender normal with a Lindegaard ratio (LR) < 3) were identified in 23% of children (n = 16), and vasospasm (> 2 SD above age/gender normal with LR ≥ 3) was identified in 28% (n = 19). Children with good outcomes based on GOS-E Peds scoring were more likely to have had normal flow velocity than other flow patterns. No other differences in neurodevelopmental outcomes were noted. Individual patient responses to TBI in terms of CBFV alterations were heterogeneous. Low flow was uniformly associated with a poor outcome. Patients with good outcomes were more likely to have normal flow. This suggests CBFV may serve as a prognostic indicator in children with TBI. Future studies are needed to determine if aberrant CBFVs are also a therapeutic target.

Hemodynamic correlates of transient cognitive impairment after transient ischemic attack and minor stroke: A transcranial Doppler study.

Background and aimsTransient cognitive impairment (TCI) on the Mini Mental State Evaluation score is common after transient ischemic attack/minor stroke and might identify patients at increased risk of dementia. We aimed to replicate TCI using the Montreal Cognitive Assessment (MoCA), compare it with persistent Mild Cognitive Impairment (PMCI), and to determine whether global cerebral hemodynamic changes could explain transient impairment.MethodsConsecutive patients with transient ischemic attack/minor stroke (NIHSS ≤ 3) were assessed with the MoCA and transcranial Doppler ultrasound acutely and at 1 month. We compared patients with TCI (baseline MoCA < 26 with ≥ 2 points increase at 1 month), PMCI (MoCA < 26 with < 2 points increase), and no cognitive impairment (NCI; MoCA ≥ 26).ResultsOf 326 patients, 46 (14.1%) had PMCI, 98 (30.1%) TCI, and 182 (55.8%) NCI. At baseline, TCI patients had higher systolic blood pressure (150.95 ± 21.52 vs 144.86 ± 22.44 mmHg, p = 0.02) and lower cerebral blood flow velocities, particularly end-diastolic velocity (30.16 ± 9.63 vs 35.02 ± 9.01 cm/s, p < 0.001) and mean flow velocity (48.95 ± 12.72 vs 54 ± 12.46 cm/s, p = 0.001) than those with NCI, but similar clinical and hemodynamic profiles to those with PMCI. Systolic BP fell between baseline and 1 month (mean reduction = 14.01 ± 21.26 mmHg) and end-diastolic velocity and mean flow velocity increased (mean increase = + 2.42 ± 6.41 and 1.89 ± 8.77 cm/s, respectively), but these changes did not differ between patients with TCI, PMCI, and NCI.ConclusionsTCI is detectable with the MoCA after transient ischemic attack and minor stroke and has similar clinical and hemodynamic profile to PMCI. However, TCI does not appear to be due to exaggerated acute reversible global hemodynamic changes.

Intracranial Artery Stenting May Not Improve Cognitive Function: A Preliminary Study.

Intracranial Artery Stenting May Not Improve Cognitive Function: A Preliminary Study.

Orthostatic Cerebral Hypoperfusion Syndrome.

Orthostatic dizziness without orthostatic hypotension is common but underlying pathophysiology is poorly understood. This study describes orthostatic cerebral hypoperfusion syndrome (OCHOs). OCHOs is defined by (1) abnormal orthostatic drop of cerebral blood flow velocity (CBFv) during the tilt test and (2) absence of orthostatic hypotension, arrhythmia, vascular abnormalities, or other causes of abnormal orthostatic CBFv. This retrospective study included patients referred for evaluation of unexplained orthostatic dizziness. Patients underwent standardized autonomic testing, including 10 min of tilt test. The following signals were monitored: heart rate, end tidal CO2, blood pressure, and CBFv from the middle cerebral artery using transcranial Doppler. Patients were screened for OCHOs. Patients who fulfilled the OCHOs criteria were compared to age- and gender-matched controls. From 1279 screened patients, 102 patients (60/42 women/men, age 51.1 ± 14.9, range 19-84 years) fulfilled criteria of OCHOs. There was no difference in baseline supine hemodynamic variables between OCHOs and the control group. During the tilt, mean CBFv decreased 24.1 ± 8.2% in OCHOs versus 4.2 ± 5.6% in controls (p < 0.0001) without orthostatic hypotension in both groups. Supine mean blood pressure (OCHOs/controls, 90.5 ± 10.6/91.1 ± 9.4 mmHg, p = 0.62) remained unchanged during the tilt (90.4 ± 9.7/92.1 ± 9.6 mmHg, p = 0.2). End tidal CO2 and heart rate responses to the tilt were normal and equal in both groups. OCHOs is a novel syndrome of low orthostatic CBFv. Two main pathophysiological mechanisms are proposed, including active cerebral vasoconstriction and passive increase of peripheral venous compliance. OCHOs may be a common cause of orthostatic dizziness.

Cerebral Blood Flow Velocity and Neurodevelopmental Outcome in Infants Undergoing Surgery for Congenital Heart Disease

Cerebral blood flow velocity (CBFV) measured by transcranial Doppler sonography has provided information on cerebral perfusion in patients undergoing infant heart surgery, but no studies have reported a relationship to early postoperative and long-term neurodevelopmental outcomes. CBFV was measured in infants undergoing biventricular repair without aortic arch reconstruction as part of a trial of hemodilution during cardiopulmonary bypass (CPB); CBFV (Vm, mean; Vs, systolic; Vd, end-diastolic) in the middle cerebral artery and change in Vm (rVm) were measured intraoperatively and up to 18 hours post-CPB. Neurodevelopmental outcomes, measured at 1 year of age, included the psychomotor development index (PDI) and mental development index (MDI) of the Bayley Scales of Infant Development-II. CBFV was measured in 100 infants; 43 with D-transposition of the great arteries, 36 with tetralogy of Fallot, and 21 with ventricular septal defects. Lower Vm, Vs, Vd, and rVm at 18 hours post-CPB were independently related to longer intensive care unit duration of stay (p<0.05). In the 85 patients who returned for neurodevelopmental testing, lower Vm, Vs, Vd, and rVm at 18 hours post-CPB were independently associated with lower PDI (p<0.05) and MDI (p<0.05, except Vs: p=0.06) scores. Higher Vs and rVm at 18 hours post-CPB were independently associated with increased incidence of brain injury on magnetic resonance imaging in 39 patients. Postoperative CBFV after biventricular repair is related to early postoperative and neurodevelopmental outcomes at 1 year of age, possibly indicating that low CBFV is a marker of suboptimal postoperative hemodynamics and cerebral perfusion.

Cerebral Blood Flow Velocity and Vasomotor Reactivity During Autonomic Challenges in Heart Failure

Significant alterations in autonomic nervous system (ANS) function, vasomotor reactivity, and cerebral blood flow may develop from damage to brain ANS regulatory areas in heart failure (HF). This preferentially right-sided injury occurs largely in autonomic structures perfused by the middle cerebral artery. Indications of altered, asymmetrical perfusion raise the potential for further neural damage. To determine whether the extent of middle cerebral artery blood flow velocity and vasomotor reactivity is altered on one side of the brain over the other in HF versus control subjects, three ANS challenges were administered-each challenge recruited ANS regulatory areas potentially injured in HF. Transcranial Doppler ultrasonography was used to measure cerebral blood flow velocity and vasomotor reactivity in 40 HF (mean age = 52.7 years, SD = 7.5; 27 men; left ventricular ejection fraction = 26.8, SD = 8.3) and 42 control subjects (mean age = 48.3 years, SD = 6.0; 22 men) during 5% CO2 and hyperventilation, Valsalva, and orthostatic (upper body tilt) challenges. Lower cerebral blood flow velocity and abnormal vasomotor reactivity (p < .01) were noted in HF middle cerebral arteries during all challenges. More right-sided flow velocity reductions appeared in HF, with laterality differences noted during CO2 and orthostatic (p < .05), but not Valsalva challenges. Diminished cerebral blood flow velocity and altered vasomotor reactivity were associated with HF, changes being preferentially on the right side; the asymmetry was more pronounced during CO2 and orthostatic challenges. The impaired blood flow regulation may contribute to the lateralized brain pathology in ANS areas, undermining autonomic control in HF.

Postnatal changes in cerebral blood flow velocity in term intra-uterine growth-restricted neonates

Background:Intra-uterine growth-restricted (IUGR) fetuses are prone to hypoxic changes in the brain and neurodevelopmental sequelae in later life. Chronic hypoxaemia may also lead to polycythaemia in the fetal and neonatal period.Aim:To evaluate venous haematocrit and cerebral blood flow velocity (CBFV) in term IUGR neonates in the immediate postnatal period.Methods:This was a prospective observational study of 54 clinically healthy term IUGR neonates as cases and 50 term, appropriate-for-gestational-age (AGA), healthy neonates as controls. IUGR was defined as birthweight <10th per centile for gestational age. Neonates with perinatal asphyxia, sepsis and other systemic diseases were excluded. Resistance index (RI), pulsatility index (PI), peak systolic velocity (PSV) and vascular diameter were measured in the internal carotid, vertebral and middle cerebral arteries by transcranial colour Doppler ultrasound between 48 and 72 hours of life, along with the estimation of venous haematocrit. Neonates were observed for development of any complications until discharge and followed up clinically and radiologically for a minimum 6 months.Results:Significantly higher resistance (RI and PI) and lower PSV was recorded in all the cerebral arteries of the IUGR than the AGA group whereas no difference was observed in vascular diameters. Mean haematocrit was significantly higher in the IUGR than in the AGA group [55·7 (4·22) vs 45·1 (2·79) g/dl]. Haematocrit was positively correlated with RI and PI, and negatively correlated with PSV. After discharge, three infants in the IUGR group showed hypertonia and delayed developmental milestones along with hypoxic changes in MRI of the brain.Conclusions:Compared with their AGA counterparts, higher venous haematocrit and lower CBFV were observed in clinically healthy, term IUGR neonates during the early neonatal period. Delayed developmental milestones and hypoxic changes were detected by MRI in three infants. Since the study was limited by its sample size, larger studies are required to document the clinical significance of decreased CBFV and its usefulness as a marker of poor prognosis for future neurodevelopment.

The impact of aging on cerebral vasomotor reactivity to carbon dioxide (1069.5)

The objective of this study was to determine the age‐related differences in cerebral vasomotor reactivity (CVMR) to carbon dioxide. Methods: 92 healthy adults aged 23‐77 underwent measurements of cerebral blood flow velocity (CBFV) using transcranial Doppler, mean arterial pressure, and end‐tidal CO2 (EtCO2) during baseline, hyperventilation (HVT), and modified rebreathing (RB). CVMR was determined by the maximal gain between changes in normalized CBFV (CBFV%) and EtCO2 using a 3rd order polynomial model and its derivative. Results: Lower CBFV and EtCO2 were related to increasing age at baseline. HVT decreased EtCO2 by 21±4 mmHg while RB increased by 19±3 mmHg. Increasing age was related to smaller hypocapnic but larger hypercapnic changes in CBFV% at the end of HVT and RB, respectively. The maximal gain between CBFV% and EtCO2 did not differ by age. Advanced age was associated with greater differences in EtCO2 between the baseline and the level at which the maximum gain in CBFV% occurred. Conclusions: These findings suggest that age‐related reductions in baseline CBFV and EtCO2 may lead to a decrease in hypocapnic but an increase in hypercapnic CBFV response. The larger differences in EtCO2 between baseline and the maximal gain of CBFV% with aging may lead to blunted response of CBF to given changes in arterial CO2 at levels close to baseline.Grant Funding Source: Supported by National Institute on Aging

Association of pulsatile and mean cerebral blood flow velocity with age and neuropsychological performance

Low cerebral blood flow velocity is associated with cognitive decline. However, the association between pulsatile brain blood flow velocity and cognition has not been investigated. High pulsatile hemodynamic stress in the brain may impair cognitive function through damage to small cerebral vessels. The current objective was to examine the cross-sectional association of pulsatile and mean cerebral blood flow velocity with age and neuropsychological performance. We also examined whether cerebral blood flow velocity was associated with aortic pulse pressure, a measure of arterial ageing and aortic stiffness. Cerebral blood flow velocity was measured in the middle cerebral artery using Transcranial Doppler Ultrasonography (TDU) while neuropsychological performance was measured using a computerized cognitive test battery. Aortic pulse pressure was non-invasively derived from applanation tonometry of the radial artery. The sample comprised 160 healthy adults aged 50–70years. Results indicated that increasing age correlated with lower mean (r=−0.23, p<0.01) and higher pulsatile (r=0.27, p<0.01) brain blood flow velocity. In multivariate adjusted models, both peripheral (β=0.28, p<0.05) and aortic (β=0.24, p<0.05) pulse pressure were associated with higher pulsatile flow velocity through the middle cerebral artery. In adjusted models, neither mean nor pulsatile cerebral blood flow velocity was associated with performance on any cognitive task. In conclusion, arterial ageing was associated with increased pulsatile hemodynamic stress in the brain. However, this was not associated with impaired neuropsychological performance.