Cerebral Hemodynamic Reserve Research Articles

Abstract 12782: Serial Cerebral Hemodynamic Monitoring in Patients With HeartMate 3 Left Ventricular Assist Devices

Introduction: Left ventricular assist device (LVAD) implantation improves cardiopulmonary hemodynamics and vital organ perfusion, but cerebral blood flow is not routinely measured despite the clinical significance of neurologic complications. We aimed to quantify the short and long-term impact of LVAD on cerebral hemodynamics by serially monitoring patients before and after LVAD implantation. Hypothesis: We hypothesize that LVAD implantation improves dynamic measures of cerebral blood flow: cerebral autoregulation (CA) and cerebrovascular reactivity (CVR). Methods: 20 patients with advanced heart failure with planned LVAD implantation participated in serial cerebral hemodynamic monitoring: (1) <72-hours pre-implant, (2) <72-hours post-implant, (3) 14-days post-implant, and (4) 90-days post-implant. Cerebral blood flow velocity was measured at each visit by transcranial Doppler. CA, quantified by Mx index , characterized the relationship between blood pressure and cerebral blood flow. CVR quantified the cerebral hemodynamic reserve, based on the response to a hypercapnic stimulus (5% inhaled CO 2 ). Results: As compared to the pre-implant assessment, no change was noted in absolute cerebral blood flow velocity ( Figure 1a ). However, CA improved immediately post-implant (0.47 vs 0.26; p=0.0007), at 14-days (0.47 vs 0.33; p=0.007), and at 90-days (0.47 vs 0.31; p=0.03), Figure 1b . Pre-implant CVR was not significantly altered at 14-days (1.14 vs 1.70, p=0.25) but improved at 90-days (1.14 vs 2.11, p=0.03), Figure 1c . Conclusions: Despite no change in cerebral blood flow velocity, LVAD implantation improves dynamic measures of cerebral blood flow, CA and CVR. Future studies should include longer follow-up and correlate post-LVAD cerebral hemodynamics with clinically meaningful neurologic endpoints such as stroke and cognitive decline.

Cerebral Hemodynamic Reserve Abnormalities Detected Via Transcranial Doppler Ultrasound in Recovered COVID-19 Patients.

SARS-CoV-2 infection can produce endothelial injury and microvascular damage, one cause of the multiorgan failure associated with COVID-19. Cerebrovascular endothelial damage increases the risk of stroke in COVID-19 patients, which makes prompt diagnosis important. Endothelial dysfunction can be evaluated by using transcranial Doppler ultrasound to study cerebral hemodynamic reserve, but there are few of these studies in patients with COVID-19, and the technique is not included in COVID-19 action and follow-up guidelines nationally or internationally. Estimate baseline cerebral hemodynamic patterns, cerebral hemodynamic reserve, and breath-holding index in recovered COVID-19 patients. We conducted an exploratory study in 51 people; 27 men and 24 women 20-78 years of age, divided into two groups. One group comprised 25 recovered COVID-19 patients, following clinical and epidemiological discharge, who suffered differing degrees of disease severity, and who had no neurological symptoms or disease at the time they were incorporated into the study. The second group comprised 26 people who had not been diagnosed with COVID-19 and who tested negative by RT-PCR at the time of study enrollment. Recovered patients were further divided into two groups: those who had been asymptomatic or had mild disease, and those who had severe or critical disease. We performed transcranial Doppler ultrasounds to obtain baseline and post-apnea tests of cerebral hemodynamic patterns to evaluate cerebral hemodynamic reserve and breath-holding indices. We characterized the recovered patient group and the control group through simple descriptive statistics (means and standard deviations). There were no measurable differences in baseline cerebral hemodynamics between the groups. However, cerebral hemodynamic reserve and breath-holding index were lower in those who had COVID-19 than among control participants (19.9% vs. 36.8% and 0.7 vs. 1.2 respectively). These variables were similar for patients who had asymptomatic or mild disease (19.9% vs.19.8%) and for those who had severe or critical disease (0.7 vs. 0.7). Patients recovered from SARS-CoV-2 infection showed decreased cerebral hemodynamic reserve and breath-holding index regardless of the disease's clinical severity or presence of neurological symptoms. These abnormalities may be associated with endothelial damage caused by COVID-19. It would be useful to include transcranial Doppler ultrasound in evaluation and follow-up protocols for patients with COVID-19.

Hypocapnia Induced by Hyperventilation with Indocyanine Green Kinetics Detects the Effect of Staged Carotid Angioplasty to Avoid Hyperperfusion in Patients with Impaired Cerebral Hemodynamic Reserve.

Cerebral hyperperfusion syndrome (CHS) is a serious complication following carotid artery stenting (CAS). Staged angioplasty (AP) could potentially prevent CHS and hyperperfusion phenomenon (HPP) after revascularization. However, methods for measuring the effects of staged AP on cerebral hemodynamic reserve have not been established. Here, we evaluated whether indocyanine green kinetics and near-infrared spectroscopy (ICG-NIRS) with hypocapnia induced by hyperventilation can detect the effects of staged AP on hemodynamic reserve to prevent CHS after CAS. Participants comprised 44 patients at high risk of CHS, whose ipsilateral cerebrovascular reactivity (CVR) was impaired on preoperative single photon emission computed tomography (SPECT). Patients were divided into a staged AP group (n=13) and a regular CAS group (n=31). In the staged AP group, stenting was performed 3 weeks after staged AP. In the regular CAS group, 16 cases (52%) showed HPP, and five (16%) presented with CHS after CAS, while no HPP or CHS occurred in the staged AP group (p=0.001). Changes in blood flow index (BFI) and time to peak (TTP) ratio during hypocapnia calculated from ICG-NIRS indicated a significant linear relationship with preprocedural CVR on SPECT (r=-0.710, 0.632, respectively; p<0.0001 each). BFI and TTP ratios during hypocapnia were significantly improved after staged AP (p<0.001 each). Furthermore, significant linear correlations were observed between BFI and TTP ratio during hypocapnia and postoperative asymmetry index AI (r=0.405, -0.475, respectively; p<0.01 each). Hypocapnia induced by hyperventilation under ICG-NIRS appears useful for detecting the effects of staged AP on hemodynamic reserve in patients at high risk of CHS.

Long-term outcome in extracranial-intracranial bypass surgery for severe steno-occlusive disease of intracranial internal carotid or middle cerebral artery

ObjectivesWe report the long-term outcome and rates of recurrent cerebral ischemic events in our cohort of carefully selected patients after STA-MCA bypass for severe steno-occlusive disease of intracranial ICA or MCA with exhausted cerebral vasodilatory reserve. Patients and MethodsIn this retrospective study, we reviewed the hospital records for all patients who underwent direct superficial temporal artery-middle cerebral artery bypass surgery at our institution from January 2010 to August 2017. Patients were included in the study if they presented with transient ischemic attack or non-disabling stroke due to a severe steno-occlusive lesions of the intracranial internal carotid artery or middle cerebral artery with abnormal cerebral vasodilatory reserve on imaging. The overall event rate is defined as transient ischemic attack, acute ischemic stroke, peri-operative stroke or death. Results69 patients were included in the study. The median age of cohort was 57 years (inter-quartile range 36–78). Median follow up period in our study was 73 months (range 2–90 months). The overall event rate post-treatment during the follow up period is 20.2%. In contrast, previous studies have showed that patients who underwent best medical therapy had a higher recurrent ischemic stroke rate over a 2–3-year period. ConclusionThis study suggests that carefully selected patients with severe steno-occlusive disease and significantly abnormal cerebral hemodynamic reserve who undergo extracranial-intracranial bypass surgery, may benefit from long-term prevention of symptomatic cerebral ischemic events.

The dynamics of cerebral vascular reserve in sleep apnea patients during continuous positive airway pressure therapy

To explore the possibility of cerebral hemodynamic reserve (CHR) normalization in patients with obstructive sleep apnea syndrome (OSAS), aged over fifty, who received continuous positive airway pressure (CPAP) therapy. The main group (20 patients, aged 50-65 years, with severe OSAS) and the control group (20 volunteers without snoring and OSAS matched for age and physical status) were studied. Diagnosis included cardio-respiratory monitoring of nocturnal sleep and ultrasound examination of cerebral blood flow with functional tests (breath holding and hyperventilation) and calculating the coefficient of vasomotor reactivity (CVMR) before the start of CPAP-therapy and after one month therapy. The significant CVMR decrease in vertebral (VA) and basilar arteries (BA) in patients with OSAS compared to the control group was identified: 38.9±8.5 and 55.7±11.3 for VA, 36.8±15.7 and 54.0±5.4 for BA. After one month CPAP-therapy, no significant coefficient gains was observed: 38.9±8.5 and 42.3±9.1 for VA, 36.8±15.7 and 37.2±7.7 for BA. The reduction of CVMR in patients older than 50 years with severe OSAS suggests the disturbance of CHR. The absence of its recovery within one month of CPAP-therapy may be indicative of the irreversible damage of the cerebral blood flow regulation mechanisms. Continued observations for a longer period are needed.

OBSTRUCTIVE SLEEP APNEA: THE STATE OF CEREBRAL HEMODYNAMIC RESERVE

Background: Individuals with obstructive sleep apnea syndrome (OSAS) have an increased risk of disabling disorders of the cardiovascular system, including stroke. The mechanisms of OSAS effects on cerebral blood flow and cerebral vascular autoregulation have not been clear enough. Aim: To study characteristics of cerebral blood flow in patients with OSAS and the effect of CPAP therapy on cerebral hemodynamic reserve. Materials and methods: One hundred and two patients with various OSAS severity (61 male and 41 female) and 20 healthy volunteers participated in the study. We performed ultrasound assessment of cerebral blood flow with functional tests and calculated reactivity indices. Results: With more severe OSAS, no significant differences in cerebral vascular reactivity compared to the control group were registered. However, there was a trend to some decrease in the index of constriction and dilation in the vertebral arteries and the basilar artery, as well as to its increase in the middle cerebral artery in severe and moderate OSAS. The index of vasomotor reactivity of cerebral arteries was significantly (р &lt; 0.05) lower in patients with severe OSAS: for vertebral arteries, up to 38.9 ± 8.5 and for basilar artery, up to 36.8 ± 15.7, compared to the control group (52.1 ± 9.8 and 50.1 ± 11.2, respectively). In patients who initiated CPAP therapy, there were no changes in velosity, resistance and reactivity parameters of cerebral vessels after 2 months. Conclusion: We were able to confirm a significant impairment of cerebral vascular autoregulation in patients with severe OSAS, predominantly in the posterior circulatory region. CPAP-therapy of 2 months' duration did not lead to restoration of cerebral hemodynamic reserve.

THE ROLE OF TEMPOROMANDIBULAR JOINT DYSFUNCTION AND OCCLUSAL DISORDERS IN THE PATHOPHYSIOLOGY OF SOMATOGENIC COCHLEAR AND VESTIBULAR SYNDROME

Rationale: Temporomandibular joint (TMJ) dysfunction and occlusion abnormalities can cause cochlear and vestibular disorders. This issue is at the crossroads of several disciplines: otoneurology, physiotherapy, dentistry, medical rehabilitation and posturology, which often makes it difficult to timely diagnose them and delays the onset of treatment. Aim: To assess the role of abnormal dental occlusion and TMJ disorders in the pathophysiology and clinical manifestation of cochleovestibular syndrome. Materials and methods: We examined 300 subjects with clinical signs of cochleovestibular syndrome, asymmetry of occlusion and/or TMJ dysfunction (the main group), 55 patients with signs of TMJ structural and functional disorders and occlusal disorders without a cochleovestibular syndrome (the reference group), and 35 healthy volunteers (the control group). All patients were examined by a neurologist, an ENT specialist, a dentist and a physiotherapist. A series of additional investigations of the brachiocephalic vessels, cervical spine, TMJ, auditory and vestibular function, premature tooth contacts were performed. Results: The main group patients had high values of TMJ dysfunction in the Hamburg test (5.85 vs 2.2 in the reference group) and higher proportions of patients with moderate and severe TMJ dysfunction (n = 243, 81% and n = 13, 23.7%, respectively). The functional muscle test parameters and the results of manual muscle testing in the main group patients were significantly different from those in the control group (р &lt; 0.05), whereas most values obtained in the reference group did not differ significantly (р &gt; 0.05). Patients with cochleoves-tibular syndrome had 2 to 3-fold higher rates of vertebrogenic dysfunctions than those from the reference group. The video nystamography technique detected the positional cervical nystagmus in 100% (n = 300) of patients from the main group, whereas there were no nystagmus in those from the reference group. Voluntary dental occlusion in the main group patients was associated with a deterioration of postural tests in 61.8% (n = 185) of patients; in the reference group patients these parameters deteriorated in 38.2% (n = 21) of cases. According to T-SCAN assessment, 300 (100%) patients from the main group had in imbalance of total distribution of the occlusion force (р &lt; 0.05 compared to the control group). The biggest number of patients from the main group (73.7%, n = 221) had an imbalance of occlusion force within 20 to 40%, and in most patients from the reference group this parameter was in the range of 10 to 30% (85.5%, n = 47), with 14.5% (n = 8) of this group having a normal balance of the occlusion force. Cerebrovascular reactivity parameters measured by ultrasound Doppler technique demonstrated a moderately significant (р &lt; 0.05) strain of the cerebral hemodynamic reserve in the posterior arterial system in patients with cochleovestibular syndrome. Conclusion: Cochleovestibular disorders can be caused by a dysfunction of the dentoman-dibular system and/or cervical / masticatory myofascial syndrome. After exclusion of any otogenic pathology in patients with cochleovestibular syndrome, their neurological examination should include a visual assessment of the occlusion and mandibular movements, as well as testing of the cervical and masticatory muscles. If any abnormalities of occlusion and/or TMJ and local muscle dysfunction are revealed, then a dentist and a physiotherapist consultation should be performed.

Carotid bypass for carotid occlusion.

The 2-year risk of ipsilateral ischemic stroke following internal carotid artery occlusion (ICAO) in a patient undergoing maximal medical therapy is 5-8% per year. While medical therapy may reduce the risk of stroke, it does not completely eliminate it. Since the 1985 extracranial-intracranial (EC-IC) bypass study, additional trials have been conducted to further investigate the usefulness of EC-IC bypass surgery in more selected patients with cerebral ischemia and impaired hemodynamic reserve. These important studies will be briefly reviewed in this article, as well as a discussion regarding the utility of bypass surgery for ICAO in current clinical practice. In addition, a short discussion regarding the pathophysiology of carotid occlusion will be presented. We will also highlight our own institutional patient selection criteria based on the latest methods for hemodynamic assessment, as well as our intraoperative flow assisted surgical techniques (FAST), and post-operative patient follow-up.

Cerebral Hemodynamic Reserve and Vascular Remodeling in C57/BL6 Mice Are Influenced by Age

Age is the most important risk factor for ischemic stroke. Recent experiments evidenced an age-associated rarefaction of the native collateral vasculature. The purpose of this study was to assess in what way age and arteriogenesis influence cortical perfusion and recovery of hemodynamic impairment in aged and young C57/BL6 mice. After model establishment of chronic cerebral hypoperfusion in the C57/BL6 strain, sustained hemodynamic impairment was induced by permanent unilateral internal carotid artery occlusion in animals aged 4 to 6 weeks, 12 weeks, and 18 months. Functional and morphological outcome was assessed by laser speckle imaging before and during acetazolamide challenge on Days 0, 3, 7, and 14 and latex/carbon black angiography and immunohistochemistry on Day 21. Although internal carotid artery occlusion did not result in a reduction of baseline perfusion, it led to significant hemodynamic impairment in all age groups. Furthermore, baseline perfusion in sham and cerebrovascular reactivity after internal carotid artery occlusion were significantly lower in animals aged 18 months (468±57 Flux; 20.8%±17%) compared with mice aged 4 to 6 weeks (568±120 Flux; 30.3%±17%) and 12 weeks (591±72 Flux; 34.2%±12%) from the beginning until Day 7 of the monitoring period. Functional outcome was in line with a 27% reduction of native leptomeningeal anastomoses in aged mice and only limited collateral outgrowth compared with young animals. Strikingly, all age groups reached spontaneous functional compensation by Day 14. Next to limited collateral remodeling, our results suggest that a hampered cerebrovascular response with age could intensify the risk for hemodynamic stroke in the elderly.

Neurocritical Care of a Reperfused Brain

Cerebral hyperperfusion and reperfusion injuries are not infrequently encountered following in reperfusion of ischemic or hypoperfused brain. Mechanism of injury could be related to tissue plasminogen activator toxicity, oxidative stress, and hyperperfusion due to impaired cerebral autoregulation in already maximally dilated cerebral vasculature and compromised cerebral hemodynamic reserve. Reperfusion injury can present as headaches and seizures in mild forms and as subarachnoid hemorrhage, intracranial hemorrhage, cerebral edema, and encephalopathy in its most severe manifestation. Prevention and identifying those at risk of hyperperfusion syndromes are the best strategy. Active treatment includes basic neurocritical care with reduction of blood pressure to a reperfused brain and timely neuroprotection and cerebral edema control measures are the mainstay of its management approach.

Leptin Augments Cerebral Hemodynamic Reserve after Three-Vessel Occlusion: Distinct Effects on Cerebrovascular Tone and Proliferation in a Nonlethal Model of Hypoperfused Rat Brain

The adipocytokine leptin has distinct functions regulating vascular tone, inflammation, and collateral artery growth. Arteriogenesis is an inflammatory process and provides a mechanism to overcome the effects of vascular obstruction. We, therefore, tested the effects of leptin in hypoperfused rat brain (three-vessel occlusion). Systemic leptin administration for 1 week after occlusion surgery increased cerebral hemodynamic reserve similar to granulocyte-macrophage colony-stimulating factor (GM-CSF), as indicated by improved CO(2) reactivity (vehicle 0.53%±0.26% versus leptin 1.05%±0.6% per mm Hg arterial pCO(2), P<0.05). Infusion of microspheres under maximal vasodilation failed to show a positive effect of leptin on cerebral perfusion (vehicle 64.9%±4.5% versus leptin 66.3%±7.0%, occluded/nonoccluded hemisphere). Acute treatment with GM-CSF led to a significant increased CO(2) reactivity and cerebral perfusion (79.2%±8.1% versus 64.9%±4.5%, P<0.05). Vasoconstrictive response of isolated rat carotid artery rings, after phenylephrine was attenuated at 24 hours following preincubation with leptin, was unaffected by removal of endothelium but abrogated by coculture with N-(omega)-nitro-L-arginine methylester, pointing toward an inducible nitric oxide synthase-mediated mechanism. In chronic cerebral hypoperfusion, acute leptin treatment restored the hemodynamic reserve of the cerebral vasculature through its effects on vascular tone, while leaving vascular outward remodeling unaffected. Our results, for the first time, reveal a protective role of leptin on vascular function in hemodynamically compromised brain tissue.

Cerebral hemodynamics in vertebrobasilar pathology, as for the issue of vertebrobasilar insufficiency

A study of the functional state of cerebral hemodynamics (blood flow velocity and hemodynamic reserve in the basilar artery) using transcranial Doppler with nitroglycerine test has been carried out in 18 patients with ischemic stroke in vertebrobasilar circulation and 20 patients with and/or symptoms suggestive of posterior circulation disease. Significant decrease of the parameters of cerebral hemodynamic reserve was shown in patients with a history of ischemic stroke and also in patients with atherosclerotic obstructive lesions of the vertebral arteries. On the other hand in patients with the anomalies of the vertebral arteries (kinking, hypoplasia) blood flow in vertebrobasilar circulation was normal. Therefore these patients need not of the surgical preventive treatment

Urgent Endarterectomy Using Pretreatment With Free Radical Scavenger, Edaravone, and Early Clamping of the Parent Arteries for Cervical Carotid Artery Stenosis With Crescendo Transient Ischemic Attacks Caused by Mobile Thrombus and Hemodynamic Cerebral Ischemia-Case Report-

A 68-year-old man with left cervical internal carotid artery stenosis suffered crescendo transient ischemic attacks caused by mobile thrombus detected by carotid echography and secondary impairment of cerebral hemodynamic reserve demonstrated by positron emission tomography. Urgent carotid endarterectomy (CEA) was performed following pretreatment with edaravone and early clamping of the carotid arteries without intraluminal shunting. The postoperative course was uneventful, and postoperative magnetic resonance imaging and single-photon emission computed tomography revealed no new cerebral ischemic lesions and no findings of cerebral hyperperfusion, respectively. The risks associated with CEA are higher for patients with evolving stroke or crescendo transient ischemic attacks than that for patients with stable disease. This case demonstrates that urgent endarterectomy for cervical carotid artery stenosis with crescendo transient ischemic attacks caused by mobile thrombi and hemodynamic cerebral ischemia can be successfully performed following pretreatment with edaravone and early clamping of the carotid arteries.

Hemodynamic and Metabolic Changes After Carotid Endarterectomy in Patients With High-Degree Carotid Artery Stenosis

In symptomatic stenosis of the internal carotid artery (ICA), the predominant mechanism of ischemic event is considered thromboembolic. Carotid endarterectomy (CEA) removes the embolic source and is accepted as the major benefit from the surgery. Even in high-degree stenosis, hemodynamic compromise as a causal factor for cerebral ischemia remains controversial, however. We used positron emission tomography (PET) to evaluate possible hemodynamic and/or metabolic changes caused by a severe ICA stenosis and the subsequent changes after CEA. Subjects consisted of 10 patients with recent transient ischemic attack and/or minor stroke whose carotid stenosis exceeded 80% (mean, 92%). We measured regional cerebral blood flow (CBF), oxygen extraction fraction (OEF), oxygen metabolic rate (CMRO2), and regional cerebral blood volume (CBV) before and after the CEA. In addition, we calculated CBF/CBV value as an indicator of tissue perfusion reserve. We compared these PET values to those of 15 age-matched normal controls. Significant reductions in CBF, CBF/CBV, and CMRO2 values were observed in the hemisphere not only ipsilateral, but also contralateral to the stenosis. In 4 patients, an increase in OEF and decrease in CBF/CBV were also detected. These variables significantly recovered after CEA. High-degree carotid stenosis in the tested range reduces cerebral hemodynamic and metabolic reserve and forms a vulnerable environment in the brain. Successful CEA benefits not only by removing embolic source, but also by improving hemodynamic status, which may be seen in even the contralateral hemisphere.

Superficial Temporal Artery-to-Middle Cerebral Artery Bypass

The superficial temporal artery-to-middle cerebral artery bypass represents the mainstay of bypass operations for cerebral revascularization. The role of this operation in the setting of cerebrovascular occlusive disease, with compromised cerebral hemodynamic reserve, is a topic of current investigation. In this report, we describe technical nuances to avert potential pitfalls in the performance of this procedure. The use of intraoperative quantitative blood flow measurements as a reliable method of assessing the success of the bypass is also described.

Cerebral Hemodynamic Reserve and Early Neurologic Deterioration in Acute Ischemic Stroke

Early neurological deterioration (END) is associated with increased mortality and morbidity. Although several predictive factors have been reported, there are little data about the hemodynamic factors. Our aim was to determine the capacity of cerebral hemodynamic reserve (CHR) to predict END. We studied 100 hospitalized patients with a first ever ischemic stroke of the middle cerebral artery (MCA) within the first 24 hours of symptoms onset. END was defined as a drop of at least one point in the Canadian Stroke Scale between admission and 72 hours. The mean flow velocity (mV) in the MCA and the CHR were measured by means of transcranial Doppler within the first 24 hours of admission. The CHR was expressed as the percentage increase in the MCA mV divided by the absolute increase in the end-tidal CO2 pressure in mm Hg after carbogen inhalation. END was observed in 23 patients. Reduced values of the mV in the symptomatic MCA (P = 0.043) and of the CHR in the symptomatic hemisphere (P < 0.001) were significantly associated with END. A CHR of less than 2%/1 mm Hg was independently associated with END (OR 8.45, 95% CI 1.82-39.2) after adjusting for potential confounders. CHR impairment within the first 24 hours of acute ischemic stroke is associated with a higher risk of END. This technique may be useful in selecting patients requiring a more intensive management.

Asymmetry of cerebral autoregulation following head injury.

To investigate asymmetry of cerebra autoregulation in head-injured patients with lateral brain contusions. Sixty five patients were admitted to Addenbrooke's Hospital suffering from head injuries with mean Glasgow Coma Score 6 (range 3 to 10). The patients were paralyzed, sedated and ventilated to achieve mild hypocapnia. Intracranial pressure (ICP), arterial pressure (ABP) were monitored directly. The left and right Middle Cerebral Arteries were insonated daily and flow velocity (FV) was recorded. Correlation coefficients between slow waves in cerebral perfusion pressure (CPP) and FV were calculated for every 3 minute period. Positive value of Mx denotes a positive association between waves in FV and CPP, therefore deranged autoregulation. Zero or slightly negative value of Mx denotes a good autoregulatory capacity. In each patient all CT scans were reviewed to assess a dominant side of brain contusion and a level of brain compression. The side-to-side difference in FV, pulsatility indices or critical closing pressures, did not correlate with the side of contusion or midline shift. In contrary, the side-to-side difference in Mx indices were significantly (p < 0.05) worse at a side of contusion and at the side of brain expansion in patients presenting with a midline shift (p < 0.05). Of those patients who died in hospital, significantly more presented within meaningful (ABS(Mx) > 0.2) asymmetry in cerebral autoregulation (40% versus 12%; p < 0.05). Side-to-side difference in cerebral hemodynamic reserve of injured brain is a predictor of fatal outcome following head injury and correlates with the side of contusion or brain expansion.

A case of adult moyamoya disease showing progressive angiopathy on cerebral angiography

In moyamoya disease, progression of carotid occlusive lesion in an adult patient is very rare. We report a case of adult moyamoya disease with acute angiographical stage progression and hemodynamic deterioration. A 56-year-old female complaining of left motor weakness visited our department. On MRI, infarct lesion was found in the right white matter. On cerebral angiography, occlusive lesions in the bilateral internal carotid arterial siphons and moyamoya vessels were found. The right side was stage V and the left side was stage III. On IMP-SPECT, decreased cerebral hemodynamic reserve of the right cerebral hemisphere was found. In this patient, right STA-MCA anastomosis was performed. After operation, she became possible to walk and discharged to home. Five months after operation, good collateral formation and improvement of hemodynamic reserve in the right hemisphere were found. However, on left carotid arteriography, the anterior and middle cerebral arteries were only slightly imaged, and the disease state progressed to stage IV. In addition, decreased blood flow and hemodynamic reserve were appeared in the left hemisphere.

Response to hypercapnia in moyamoya disease. Cerebrovascular response to hypercapnia in pediatric and adult patients with moyamoya disease.

We have previously reported that cerebral blood flow decreased and oxygen extraction fraction and cerebral blood volume increased in pediatric patients with moyamoya disease, whereas these values did not change significantly in adult patients. In this study, we measured the cerebrovascular response to hypercapnia using 15O H2O positron emission tomography (PET) in each group of patients. These data were also compared with the oxygen extraction fraction and transit time (cerebral blood volume/cerebral blood flow) measured by 15O PET. The subjects consisted of 20 patients with moyamoya disease (7 pediatric and 13 adult patients). Cerebral blood flow was measured by the 15O H2O bolus injection method at the resting state and during the inhalation of 5% CO2. Cerebrovascular CO2 response was estimated as the percentage change of cerebral blood flow per 1 mm Hg change of PaCO2. Oxygen extraction fraction and transit time were measured by the 15O steady-state method. Cerebrovascular response to hypercapnia severely decreased over the cerebral cortices in both pediatric and adult patients with moyamoya disease when compared with those of normal control subjects, and there was no significant difference between pediatric and adult patients. A significant correlation was observed between the CO2 response and transit time, whereas no significant correlation was seen between the CO2 response and oxygen extraction fraction. Our study revealed that the cerebral hemodynamic reserve capacity decreased to an equal degree in both pediatric and adult patients with moyamoya disease. This finding may thus help to explain the occurrence of transient ischemic attack in adult patients.

Cerebral blood flow and vascular response to hypercapnia in hypertensive patients with leukoaraiosis.

Both arteriosclerosis and leukoaraiosis have a close relationship with hypertension, but the relationship between cerebral hemodynamics and leukoaraiosis in hypertensive patients has not been fully examined. To clarify this issue, we measured the regional cerebral blood flow (rCBF) and cerebrovascular response to hypercapnia in hypertensive patients with various degrees of leukoaraiosis. The subjects consisted of 7 normotensive normal controls and 17 hypertensive patients. The hypertensive patients were divided into three groups according to the severity of white matter lesions (leukoaraiosis) on MRI and the presence of dementia, namely, (1) negative or mild leukoaraiosis without dementia, (2) moderate to severe leukoaraiosis without dementia and (3) severe leukoaraiosis with dementia. Both the rCBF and the cerebrovascular response to hypercapnia were measured by the O-15 H2O bolus-injection method and positron emission tomography. The rCBF in hypertensive patients without dementia did not decrease when compared with the normotensive controls, but the rCBF in hypertensive patients with dementia markedly decreased in the cerebral cortices and white matter. On the other hand, the cerebrovascular response to hypercapnia declined with the severity of leukoaraiosis, and it decreased most severely in patients with severe leukoaraiosis and dementia. Our results indicate that the reduction in the cerebral hemodynamic reserve capacity has a close relationship with the severity of leukoaraiosis in hypertensive patients, although the rCBF is maintained in hypertensive patients without dementia, and suggest that arteriosclerotic change reduces cerebrovascular CO2 response and causes a leukoaraiosis in hypertensive patients.