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PubMed2004

Isoflurane preconditioning induces neuroprotection against ischemia via activation of P38 mitogen-activated protein kinases.

A brief exposure to the volatile anesthetic isoflurane (preconditioning) induces ischemic tolerance in rat brain. However, whether isoflurane preconditioning improves long-term neurological outcome after brain ischemia and the mechanisms for this neuroprotection are not known. Here, we report that isoflurane preconditioning (2% isoflurane for 30 min at 24 h before brain ischemia) reduced brain infarct sizes and improved neurological deficit scores assessed 6, 24, and 72 h after permanent right middle cerebral arterial occlusion (MCAO) in adult male rats. More morphologically intact neurons and fewer dying cells existed in the ipsilateral frontal cortex area 1 and rostral subventricular zone of caudate putamen of isoflurane-preconditioned rats than rats undergoing MCAO alone at 14 days after the MCAO. This neuroprotection was abolished by an inhibitor of p38 mitogen-activated protein kinases (MAPK), 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580) (the percentages of infarct volumes in the ipsilateral hemisphere volumes were 34 +/- 7% for MCAO, 24 +/- 6% for isoflurane preconditioning plus MCAO, and 30 +/- 6% for SB203580 plus isoflurane preconditioning plus MCAO, n = 8, P < 0.05 for isoflurane preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus isoflurane preconditioning plus MCAO) and mimicked by an activator of these kinases, anisomycin. Isoflurane induced a rapid and prolonged increase of the phosphorylated p38 MAPK in cerebral neocortex. These active kinases distributed mainly in perikaryal regions of neurons. These results suggest that isoflurane preconditioning may improve long-term neurological outcome after focal brain ischemia and that the effects may be mediated by activating p38 MAPK.

Animals↗
PubMed1996

Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects.

Cholesterol, triglyceride (TG), and apolipoprotein (apo) B were determined in plasma and in lipoprotein subfractions (VLDL, intermediate-density lipoproteins [IDL], LDL, and HDL) in nonobese NIDDM subjects, who were classified into well-controlled, fairly controlled, or poorly controlled states with or without macrovascular complications (macroangiopathy [MA]). The same analyses were also performed on subjects who had coronary artery disease (CAD) with stable angina pectoris (SA) or unstable angina pectoris (UA) and acute myocardial infarction, cerebrovascular disease (CVD) with atherothrombotic or lacunar infarction, and arteriosclerosis obliterans (ASO). In nonobese NIDDM subjects, the number of apoB-containing lipoproteins (VLDL, IDL, and LDL) increased. This alteration was more prominent in subjects with poorly or fairly controlled disease as well as in subjects with MA, but not in those with well-controlled NIDDM. Cholesterol/apoB in LDL decreased in subjects with poorly or fairly controlled diabetes or with MA and was correlated with low HDL cholesterol. The disorder is characterized by hyperbetalipoproteinemia with elevated LDL cholesterol and small dense LDL. In obese NIDDM subjects, the similar disorder was more pronounced. Glycemic control had less effect and hyperinsulinemia, if present, aggravated the lipid disorder. In those with CAD, the number of IDLs increased and the LDL fraction had the properties of small dense LDL. HDL cholesterol decreased. In those with UA, the LDL number increased without elevation of LDL cholesterol, indicating typical hyperbetalipoproteinemia. The subjects with atherothrombotic brain infarction, an increased number of small-sized LDLs was noted. In those with ASO, the number of VLDL and IDL increased with small LDL. HDL cholesterol decreased in those with CAD, cerebrovascular disease, and ASO. Since similar quantitative and qualitative alterations of apoB-containing lipoprotein have been observed in NIDDM patients as well as in those with macrovascular diseases, diabetic patients are thought to be more susceptible to the initiation and progression of atheromatous lesions in coronary, brain, and peripheral arteries.

Adult↗
PubMed2005

Risk of falls in Alzheimer's disease: a prospective study.

OBJECTIVE: Falls are common in patients with Alzheimer's disease (AD). Identification of the potential risk factors and developing preventive strategies for falls will have a significant impact in maintaining the quality of life in AD. PATIENTS: Clinical follow-up of 124 (74.1+/-6.1 years, range 62-88) mild to moderate AD patients in an outpatient memory clinic. METHODS: Postural sway, cognitive function, use of neuroleptics, severity of periventricular and deep white matter lesions, and the presence or absence of silent brain infarctions on magnetic resonance imaging were assessed at baseline. RESULTS: A total of 104 patients (84%) completed the study. Fall events were confirmed in 42.3% (44/104). After adjustment for age, gender, and cognitive status, a high grade of periventricular white matter lesions (odds ratio 8.7 [95%CI 1.5 to 51.8], p = 0.017) and neuroleptic drug use (odds ratio 3.5 [95%CI 1.2 to 10.5], p = 0.027) were significantly associated with an increased risk of falls. CONCLUSION: Our results suggest that periventricular white matter lesions and the use of neuroleptics may be related to falls in mild to moderate AD. A comprehensive risk management of brain ischemia as well as the use of the smallest efficacious dose of neuroleptics in the treatment of behavioral and psychiatric symptoms of AD should be recommended to help reduce the risk of unexpected falls.

Accidental Falls↗
PubMed1997

Cognitive deficits in peripheral vascular disease. A comparison of mild stroke patients and normal control subjects.

BACKGROUND AND PURPOSE: Evidence indicates that peripheral vascular disease (PVD) and cerebrovascular disease (CVD) coexist and therefore reflect a generalized pattern of atherosclerotic disease in an individual. Given the known deleterious effects of CVD on cognitive function, it was hypothesized that patients with PVD may have impaired cerebral function due to concomitant but clinically unrecognized CVD. The purpose of this study was to determine whether neuropsychological tests would reveal this potential dysfunction. METHODS: Neuropsychological test scores (n = 25) were compared across three groups: (1) 29 PVD patients (13 amputees, 16 nonamputees), (2) 29 age- and education-matched patients with atherothrombotic brain infarcts (ie, CVD), and (3) 30 age- and education-matched control subjects. RESULTS: PVD patients performed significantly worse (P < .002) than control subjects on eight neuropsychological measures of executive function, attention, and visuopatial function. The pattern and, in certain instances, the magnitude of impairment was highly similar between PVD and CVD subjects. Regression analysis revealed that PVD severity and ischemic heart disease were significant negative predictors of test performance. Depression and atherosclerotic risk factors did not explain neuropsychological deficits after the effects of PVD and ischemic heart disease were considered. CONCLUSIONS: PVD patients exhibit neuropsychological deficits that suggest the presence of mild vascular-related brain dysfunction. Patients with multiple manifestations of generalized atherosclerosis (ie, severe PVD, ischemic heart disease) appear to be particularly at risk. Clinicians should be alert to these potential deficits and to the possibility of further vascular-related cognitive decline.

Affect↗
PubMed2001

Hyperglycemic but not normoglycemic global ischemia induces marked early intraneuronal expression of beta-amyloid precursor protein.

Preischemic hyperglycemia is known to accentuate acute ischemic injury to neurons, microglia, and endothelia. In the present study, we used a monoclonal antibody to the N-terminal portion of beta-APP to examine how the immunoreactivity of this normal membrane glycoprotein is differentially influenced by transient cerebral ischemia when carried out under normoglycemic vs. hyperglycemic conditions. Anesthetized, physiologically regulated rats received 12.5 min of global forebrain ischemia by bilateral carotid artery occlusions plus systemic hypotension. Hyperglycemia was induced by intraperitoneal dextrose administration prior to ischemia. One or three days later, brains were examined by beta-APP immunohistochemistry. Ischemia under hyperglycemic conditions led to the robust, widespread intraneuronal expression of beta-APP immunoreactivity in neocortex, hippocampus, thalamus, and striatum of all 11 rats; this was most prominent at 24 h postischemia. Compared to rats with normoglycemic ischemia, numbers of beta-APP-immunopositive neurons in the parietal cortex of hyperglycemic rats were increased by 5.9 fold at 24 h, and by 10.6 fold at 3 days postischemia. beta-APP-immunopositive neurons in hyperglycemic rats often exhibited striking morphological alterations typical of ischemic necrosis; however, no beta-APP immunoreaction was observed in zones of frank infarction. Brains of normoglycemic rats (n=11), by contrast, showed only weak beta-APP immunostaining in occasional non-necrotic pyramidal neurons of parietal neocortex; no necrosis was present in thalamus. In sham-operated hyperglycemic rats, beta-APP immunostaining of thalamic neurons was somewhat increased at 24 h. Western analysis revealed that the hyperglycemia-induced intraneuronal overexpression of beta-APP was not associated with an overall increase in tissue levels. The results of this study demonstrate that transient forebrain ischemia under hyperglycemic conditions leads to the early intraneuronal expression of beta-APP within neuronal populations showing a heightened susceptibility to hyperglycemia-induced accentuation of ischemic injury. Our data suggest that beta-APP or its metabolites may be involved in the injury process.

Amyloid beta-Protein Precursor↗
PubMed1994

MRI in acute cerebral ischaemia: perfusion imaging with superparamagnetic iron oxide in a rat model.

An imaging technique capable of detecting ischaemic cerebral injury at an early stage could improve diagnosis in acute or transient cerebral ischaemia. We compared the ability of superparamagnetically contrast-enhanced MRI and conventional T2-weighted MRI to detect ischaemic injury early after unilateral occlusion of the middle cerebral artery in 12 male Wistar rats. Permanent vessel occlusion was achieved by a transvascular approach, which has the advantage of not requiring a craniectomy. At 45-60 min after the procedure, the animals had conventional T2-weighted MRI before and after administration of a superparamagnetic contrast agent (iron oxide particles). Unenhanced images were normal in all animals. After administration of iron oxide particles, the presumed ischaemic area was clearly visible, as relatively increased signal, in all animals; this high signal area corresponded to the area of ischaemic brain infarction seen on histological studies. Magnetic susceptibility effects of iron particles cause low signal in normally perfused cerebral tissue, whereas tissue with reduced or absent blood flow continues to give relatively high signal. Our results suggest that superparamagnetic iron particles may significantly reduce the interval between an ischaemic insult and the appearance of parenchymal changes on MRI.

Acute Disease↗
PubMed2004

A therapeutic window for intravenous administration of autologous bone marrow after cerebral ischemia in adult rats.

The primary objective of this study was to test the hypothesis that intravenous administration of autologous bone marrow cells could improve functional recovery after middle cerebral artery occlusion (MCAO) for 45 min in the rat and to determine specific time windows for efficacy. Mononuclear cells from autologous bone marrow were transfected with the LacZ reporter gene, and injected intravenously into rats at 3-72 h after induction of MCAO. Histological analysis of the ischemic lesion at 14 days after transplantation revealed reduced ischemic lesion volume. Lesion volume was 250+/-45 mm(3) (n=6) after MCAO without cell transplantation. Lesions were minimally detected by absence of 2,3,5-triphenyltetrazolium chloride (TTC) staining when bone marrow cells were infused 3 h after lesion induction. Lesions were clearly detected beginning with the 6-h postlesion group and became progressively larger at 12, 24 and 72 h (80+/-25, 140+/-18, and 180+/-22 mm(3), respectively; n=6 for each group). Transplanted LacZ(+) bone marrow cells accumulated extensively in and around the ischemic lesions, and immunohistochemistry suggests some neuronal and glial lineage differentiation. Behavioral testing (Morris water maze and Treadmill stress test) indicated greater functional recovery in the treated group. These findings suggest that early intervention with intravenous administration of autologous mononuclear cells from bone marrow can reduce lesion size in the MCAO model in the rat, and improve functional outcome.

Animals↗
PubMed2003

Reversible posterior leukoencephalopathy syndrome in a postpartum woman without eclampsia.

We report a patient who developed reversible posterior leukoencephalopathy syndrome (RPLS) in puerperium without preeclampsia-eclampsia or chronic hypertension. The woman suddenly complained of visual loss and headache 10 days after delivery caused by edematous lesions mainly distributed in the bilateral occipital lobe. Apparent diffusion coefficient map was useful for distinction of this vasogenic edema from cytotoxic edema due to brain infarction. Under the diagnosis of RPLS, we successfully treated her disease using a trinitroglycerin as an antihypertensive, a hyperosmolar agent, methylprednisolone, and a free radical scavenger. Postpartum women may have the risk of development of RPLS even without preeclampsia-eclampsia. Vascular endothelial dysfunction may trigger RPLS, in addition to acute and modest increase in systemic pressure.

Adult↗
PubMed1995

When do brain abnormalities in cerebral palsy occur? An MRI study.

The authors used MRI to analyse retrospectively the brain images of patients with cerebral palsy (CP) to evaluate its the role in the assessment of brain abnormalities and injury, and the relationship of pre-, peri- and postnatal events to CP. 70 patients with CP aged two to 16 years who underwent MRI were divided into four groups: group 1 (26 patients) comprised subjects whose CP was considered to have been caused by neuronal migration disorders in the embryonal stage; group 2 (30 patients) contained subjects whose cause was vascular disorders; in group 3 patients (five) the cause was intra-uterine infection; and CP clearly attributable to birth asphyxia (group 4) was noted in only nine patients. The results indicate that CP of term infants is often the result of prenatal factors, and their MRI findings indicated migration and cerebral infarction. Brain MRI is an essential examination in identifying the factors causing brain damage in CP.

Adolescent↗
PubMed1995

Intra- and postoperative cerebral complications of open-heart surgery.

A consecutive series of 1400 patients who had undergone open-heart surgery was retrospectively reviewed concerning postoperative cerebral dysfunction. The 30-day mortality was 1.6%. Forty-one patients (2.9%) showed signs of cerebral dysfunction, which proved fatal in seven cases. Neurologic symptoms were observed immediately after surgery in 14 patients, suggesting intraoperative damage. In 20 others there was an interval between surgery and the onset of cerebral symptoms, which in 12 cases were preceded by supraventricular tachycardia. Computed tomographic scans were performed on 27 patients and showed recent brain infarction in 22. No bleeding was found. At follow-up 34 of the 41 patients were alive, 21 of them with neurologic sequelae and 13 reporting complete recovery. Nineteen of the 34 survivors experienced no diminution of quality of life. Since half of the cerebral complications occurred postoperatively, more aggressive prevention and management of supraventricular tachyarrhythmia and anticoagulation therapy should be considered.

Adolescent↗
PubMed1998

Proton MR spectroscopy in inflammatory and infectious brain disorders.

This article reviews the proton MR spectroscopy literature regarding brain infarction and inflammatory diseases. We examine the salient findings reported for bacterial abscesses, intracranial tuberculomas, Creutzfeldt-Jakob disease, herpes simplex encephalitis and HIV. These processes demonstrate specific metabolic profiles which may be useful in differential diagnosis. The results reported in the literature support the view that MR spectroscopy can be employed in longitudinal studies to monitor the response to therapy and therefore may lead to individual optimized treatment effectiveness.

AIDS Dementia Complex↗
PubMed2001

[Different vascular risk factor profiles in ischemic stroke versus intracerebral hemorrhage: a study in 1,702 consecutive patients with acute stroke].

BACKGROUND: To characterize the vascular risk factor profiles in ischemic stroke and in intracerebral hemorrhage. PATIENTS AND METHOD: The study population consisted of 1,473 consecutive ischemic stroke patients and 229 consecutive intracerebral hemorrhagic patients collected in the Sagrat Cor Hospital of Barcelona Stroke Registry over a 10-year period. The prevalence of vascular risk factors in ischemic stroke and in intracerebral hemorrhage was analyzed by means of univariate analysis and a logistic regression model. RESULTS: Hypertension was present in 52% of ischemic stroke patients and in 60.7% of intracerebral hemorrhagic patients. The pattern of risk factors associated with ischemic stroke included valve heart disease (OR = 5.96; 95% CI, 1.42-24.88), transient ischemic attack (OR = 4.16; 95% CI, 2-8.64), atrial fibrillation (OR = 2.95; 95% CI, 1.88-4.64), previous brain infarct (OR = 2.58; 95% CI, 1.53-4.35), ischemic heart disease (OR = 2.55; 95% CI, 1.41-4.62), hyperlipidemia (OR = 2.12; 95% CI, 1.32-3.4), hypertension (OR = 0.64; 95% CI, 0.48-0.87), chronic liver disease (OR = 0.32; 95% CI, 0.14-0.73), previous cerebral hemorrhage (OR = 0.24; 95% CI, 0.09-0.64) and oral anticoagulant therapy (OR = 0.11; 95% CI, 0.03-0.36). CONCLUSIONS: Different potentially modifiable vascular risk factors profiles were identified in ischemic versus hemorrhagic stroke.

Aged↗
PubMed2004

Randomized comparison of intra-arterial and intravenous thrombolysis in a canine model of acute basilar artery thrombosis.

We compared the rates of recanalization cerebral infarct and hemorrhage between intra-arterial (i.a.) reteplase and intravenous (i.v.) alteplase thrombolysis in a canine model of basilar artery thrombosis. Thrombosis was induced by injecting a clot in the basilar artery of 13 anesthetized dogs via superselective catheterization. The animals were randomized in a blinded fashion, 2 h after clot injection and verification of arterial occlusion, to receive i.v. alteplase 0.9 mg/kg over 60 min and i.a. placebo, or i.a. reteplase 0.09 units/kg over 20 min, equivalent to one-half the alteplase dose, and i.v. placebo. Recanalization was studied for 6 h after treatment with serial angiography; the images were later graded in a blinded fashion. Blinded interpretation of postmortem MRI was performed to assess the presence of brain infarcts and/or hemorrhage. At 3 h after initiation of treatment, partial or complete recanalization was observed in one of six dogs in the i.v. alteplase group and in five of seven in the i.a. reteplase group (P = 0.08). At 6 h, no significant difference in partial or complete recanalization was observed between the groups (two of six vs. five of seven; P = 0.20). Postmortem MRI revealed infarcts in four of six animals treated with i.v. alteplase and three of seven treated with i.a. reteplase (P = 0.4). Intracerebral hemorrhage was more common in the i.v. alteplase group (four of six vs. none of seven; P = 0.02). This study thus suggests that i.a. thrombolysis affords a recanalization rate similar to that of i.v. thrombolysis, but with a lower rate of intracerebral hemorrhage.

Animals↗
PubMed2005

Neuroprotection by tetramethylpyrazine against ischemic brain injury in rats.

In traditional Chinese medicine, Ligusticum wallichii Franchat (Chuan Xiong) and its active ingredient tetramethylpyrazine (TMP) have been used to treat cardiovascular diseases and to relieve various neurological symptoms such as ischemic deficits. However, scientific evidence related to their effectiveness or precise modes of neuroprotective action is largely unclear. In the current study, we elicited the neuroprotective mechanisms of TMP after focal cerebral ischemic/reperfusion (I/R) by common carotid arteries and middle cerebral artery occlusion model in rats. TMP was administrated 60 min before occlusion via intraperitoneal injection. TMP concentration-dependently exhibited significant neuroprotective effect against ischemic deficits by reduction of behavioral disturbance. Neuronal loss and brain infarction in the ischemic side of rats were markedly lowered by treatment with TMP. Cerebral I/R-induced internucleosomal DNA fragmentation, caspase-8, caspase-9, and caspase-3 activation, and cytochrome c release were reduced by TMP treatment. Western blot analysis revealed the down-regulation of Bcl-2 and Bcl-xL and the up-regulation of Bax and Bad by cerebral I/R insult. Among them, only the alteration in Bcl-xL expression was reversed by TMP treatment. Moreover, the activation of microglia and/or recruitment of inflammatory cells within the ischemic side and the consequent production of monocyte chemoattractant protein 1 (MCP-1) were suppressed by TMP pre-treatment. Our findings suggest that TMP might provide neuroprotection against ischemic brain injury, in part, through suppression of inflammatory reaction, reduction of neuronal apoptosis, and prevention of neuronal loss.

Animals↗
PubMed1999

Recent heavy drinking of alcohol and embolic stroke.

BACKGROUND AND PURPOSE: Epidemiological evidence suggests that heavy alcohol consumption increases the risk for ischemic stroke, whereas light-to-moderate alcohol intake decreases the risk, but the role of different drinking patterns has remained unclear. We investigated recent light, moderate, and heavy alcohol drinking and former heavy drinking as risk factors for acute ischemic brain infarction by etiological subtype of stroke. METHODS: We compared 212 consecutive patients aged between 16 and 60 years, who were completely evaluated for the etiology of their ischemic stroke, with 274 control subjects admitted to the emergency unit of the same hospital. ORs, as estimates of multivariate relative risks (RRs), and 95% CIs after adjustment for possible confounding variables were calculated by logistic regression. The ORs were adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipemia, current smoking, and history of migraine. RESULTS: Recent heavy drinking but not former heavy drinking was an independent risk factor for stroke (RR 1.82, 95% CI 1.08 to 3.05). Consumption of 151 to 300 g and >300 g alcohol within the week preceding the onset of stroke significantly increased the risk for cardioembolic and cryptogenic stroke. Consumption of >40 g alcohol within the preceding 24 hours increased the risk for cardiogenic embolism to the brain among those who had a high-risk source (RR 4.75, 95% CI 1.23 to 18.4), the risk for tandem embolism among those who had prominent large-artery atherosclerosis (RR 7.68, 95% CI 1.82 to 32.3), and the risk for cryptogenic stroke (RR 3.84, 95% CI 1.69 to 8.71). Light drinking did not increase the risk for stroke. CONCLUSIONS: We conclude that acute drinking of intoxicating amounts of alcohol may trigger the onset of embolic stroke among subjects who have a source of thrombus in the heart or the large arteries.

Adolescent↗
PubMed2005

Dynamics of cytochrome c oxidase activity in acute ischemic stroke.

We have investigated the dynamics of cytochrome c oxidase (COX) activity in the cerebrospinal fluid (CSF) and the erythrocyte haemolysate (EH) in 85 patients suffering from brain infarction (BI), reversible (RIA), or transient (TIA) ischemic attack from the perspective of mitochondrial affection in ischemia. In all patients, the COX activity was decreased in the CSF, especially within the first two days, indicating an acute inactivation or modification of mitochondrial proteins, probably mediated by free radicals. The gradual elevation of COX activity until the seventh day suggested that these changes may be reversible. The increase in the COX activity was established in the EH, with the highest values found in the BI, somewhat lower in the RIA, and the lowest in the TIA group, respectively. This could indicate a systemic compensatory response to an acute ischemia. Thus, COX activity in the CSF and EH in acute ischemia could be an indicator of brain metabolic dysfunction.

Acute Disease↗
PubMed1984

Common carotid artery stump pressure in the gerbil stroke model.

In 106 slightly anaesthetised adult mongolian gerbils one common carotid artery (CCA) was ligated and the blood pressure in the distal and in the proximal stump was monitored for 8 minutes. The mean distal CCA stump pressure of the 39 nonsurvivors was 15 (+/- 6) mm Hg, that of the 25 survivors with retinocerebral infarcts was 25 (+/- 6) mm Hg, and that of the 42 intact survivors was 31 (+/- 7) mm Hg. The corresponding mean arterial blood pressures (MABP), as measured in the proximal CCA stump, were 81 (+/- 12) mm Hg, 84 (+/- 13) mm Hg, and 87 (+/- 11) mm Hg, respectively. There were no differences between the samples concerning sex, body weight, rectal temperature, arterial blood gases, arterial pH, and haematocrit. Measurements in a second series of 10 awake gerbils showed that the mean values of MABP, heart rate, and respiratory rate of the nonsurvivors were less than those of the survivors during 90 minutes after CCA ligation. It is inferred that in the mongolian gerbil the lower threshold of the arterial blood pressure for the development of brain infarcts ranges within 22 and 25 mm Hg, that is, within the values found in monkeys and cats. The longlasting depression of respiration and circulation in the nonsurvivors is considered to be related to the phenomenon of diaschisis .

Animals↗
PubMed1996

[Perfusion studies with paramagnetic contrast media and rapid pulse sequences in cerebrovascular diseases and brain tumors].

The combination of fast MR sequences and rapid i.v. injection of paramagnetic contrast media provides information on cerebral perfusion. MR-perfusion imaging primarily depicts the relative cerebral blood volume. The aim of this study was to test whether MR-perfusion imaging with a clinical MR scanner using a standard 2D-FLASH sequence provides clinically relevant information on patients with cerebrovascular diseases and brain tumors. Brain infarctions, lesions in cerebral microangiopathy and occlusions of the carotid artery with very poor collateralization showed definite differences in perfusion imaging compared with normal controls. However, our results show that acceleration of the imaging sequence and optimization of the contrast bolus and data processing are prerequisites for the clinical use of this method, which in principle may provide information on the absolute cerebral blood volume and even blood flow.

Adult↗