Biomedical subjects

Michael Neveling

Publications and source records attributed to Michael Neveling.

6 recordsLinked to original sources

PubMed2006

Early ischemic edema on cerebral computed tomography: its relation to diffusion changes and hypoperfusion within 6 h after human ischemic stroke. A comparison of CT, MRI and PET.

BACKGROUND: Brain tissue hypoattenuation on early computed tomography is frequently included in decision making in acute stroke management. However, its pathophysiological counterpart needs further evaluation. METHODS: By comparative imaging with diffusion-weighted imaging and 15O-water positron emission tomography we aimed to interpret early (<6 h) hypoattenuation. RESULTS: In 11 patients, the hypoattenuation corresponded to a decreased proton diffusion (median 115.9% relative DWI value) measured by magnetic resonance imaging and to a severe hypoperfusion (below 12 ml/100 g/ min) assessed by positron emission tomography. The volume of parenchymal hypoattenuation correlated to the tissue with disturbed diffusion (Spearman's rho=0.73), but largely underestimated the hypoperfusion below 20 ml/100 g/min. CONCLUSIONS: Early hypoattenuation reflects the coupling of the severity of ischemia and resulting diffusion changes. It allows an estimate of the infarct core but underestimates the penumbral hypoperfusion.

Adult↗

PubMed2005

Does the mismatch match the penumbra? Magnetic resonance imaging and positron emission tomography in early ischemic stroke.

BACKGROUND AND PURPOSE: In ischemic stroke, diffusion-weighted (DW) and perfusion-weighted (PW) magnet resonance imaging (MRI) is used to define the mismatch as the therapeutic target. With positron emission tomography (PET), we characterized the metabolic patterns of tissue compartments identified by MRI and compared the volumes of mismatch to those of PET-defined penumbra. METHODS: In 6 acute (median, 5.2 hours) and 7 chronic (median, 10 days) stroke patients in whom a mismatch was defined by PW/DW MRI, PET was performed (median, 120-minute delay). Cerebral blood flow (CBF), oxygen metabolism (CMRO2), and oxygen extraction fraction (OEF) was determined in the areas of DWI lesion, mismatch, and oligemia. Then, the mismatch volume was compared with the volume of penumbra. RESULTS: DWI lesions showed impaired tissue integrity (low CMRO2 and low OEF). Mismatch areas were viable (normal CMRO2) but showed largely varying OEF. Oligemic areas had metabolic patterns comparable to normal tissue. A mismatch volume was found in all 13 patients. However, only 8 of 13 had a corresponding penumbra volume that covered only a part of the mismatch. CONCLUSIONS: Our comparative PET/MRI study confirmed the current pathophysiological hypothesis for the DWI lesion and for the oligemic areas. However, the mismatch area did not reliably detect elevated OEF and overestimated the penumbra defined by PET.

Adult↗

PubMed2005

Value of gradient-echo magnetic resonance imaging in the diagnosis of familial cerebral cavernous malformation.

BACKGROUND: Cerebral cavernous malformations (CCMs) are congenital vascular anomalies that can cause seizures, intracranial hemorrhages, focal neurological deficits, and migrainelike headaches. Magnetic resonance (MR) imaging has substantially facilitated diagnosis of CCM. It is now widely accepted that familial clustering with an autosomal dominant inheritance pattern should be suspected in cases of multiple lesions. OBJECTIVE: To determine by MR imaging the penetrance of cavernous malformations in a 3-generation family that included 5 members with typical clinical signs and diagnostic findings. METHODS: All family members underwent routine MR T1-weighted and T2-weighted spin-echo sequences in addition to MR T2-weighted gradient-echo sequences. RESULTS: Four family members had been symptomatic with either brainstem bleeding, headaches, or focal neurological signs. The gradient-echo sequences yielded a dramatically higher sensitivity with regard to lesion number and distribution. As in previous reports of familial CCM, an increase in lesion number with increasing age, changes in lesion characteristics, de novo occurrence in serial MR imaging over time, and the phenomenon of anticipation could be confirmed in this family. CONCLUSION: Magnetic resonance gradient-echo sequences should be considered the method of choice for diagnosis of familial CCM.

Adult↗

PubMed2003

Extracellular concentrations of non-transmitter amino acids in peri-infarct tissue of patients predict malignant middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Space-occupying brain edema is a life-threatening complication in patients with large middle cerebral artery (MCA) infarction. To determine predictors of this detrimental process, we investigated alterations of extracellular non-transmitter amino acid concentrations in peri-infarct tissue. METHODS: Thirty-one patients with infarctions covering >50% of the MCA territory in early cranial CT scans were included in the study. Probes for microdialysis, intracranial pressure, and tissue oxygen pressure were placed into the noninfarcted ipsilateral frontal lobe. Positron emission tomography imaging was performed in 16 of these patients to measure cerebral blood flow in the tissue around the neuromonitoring probes. RESULTS: Fourteen of the 31 patients developed a malignant MCA infarction, and 17 did not. The patients in the malignant group had significantly lower extracellular concentrations of non-transmitter amino acids than those in the benign group in the first 12 hours of neuromonitoring. At this time, CBF values determined in regions of interest around the probes by positron emission tomography and tissue oxygen pressure showed that the monitored tissues were not yet infarcted, and no differences in transmitter amino acids concentrations were found between the 2 groups. Furthermore, extracellular concentrations of non-transmitter amino acids were negatively correlated with size of infarction. CONCLUSIONS: We assume that reduction of non-transmitter amino acid concentrations reflects an expansion of the extracellular space by vasogenic edema formation in peri-infarct tissue of patients with malignant MCA infarction. Our findings facilitate early prediction of malignant edema formation and may help to increase knowledge of the pathophysiology of the peri-infarct zone of large MCA infarction.

Amino Acids↗

PubMed2003

Prediction of malignant course in MCA infarction by PET and microdialysis.

BACKGROUND AND PURPOSE: To predict malignant course in patients with large middle cerebral artery (MCA) infarction, we combined PET imaging and neuromonitoring, including microdialysis. METHODS: Thirty-four patients with stroke of >50% of the MCA territory in early cerebral CT scan were included. Probes for microdialysis and measurement of intracranial pressure and tissue oxygen pressure (Pto2) were placed into the ipsilateral frontal lobe. PET was performed with 11C-flumazenil to assess CBF and irreversible neuronal damage. RESULTS: PET measurements within 24 hours after stroke showed larger volumes of ischemic core (mean, 144.5 versus 62.2 cm3) and larger volumes of irreversible neuronal damage (157.9 versus 47.0 cm3) in patients with malignant course (ie, edema formation with midline shift) than in patients with benign course. Mean cerebral blood flow values within the ischemic core were significantly lower and the volume of the ischemic penumbra was smaller in the malignant than in the benign group. In patients with malignant course, cerebral perfusion pressure dropped to <50 to 60 mm Hg 22 to 72 hours (mean, 52.0 hours) after onset of symptoms; subsequently, Pto2 dropped and glutamate increased, indicating secondary ischemia. Maximal changes in the monitored variables reached significant levels for glutamate, aspartate, GABA, glycerol, lactate-to-pyruvate ratio, hypoxanthine, intracranial pressure, cerebral perfusion pressure, and Pto2. CONCLUSIONS: PET allowed prediction of malignant MCA infarction within the time window suggested for hemicraniectomy. Neuromonitoring helped to classify the clinical courses by characterizing pathophysiological sequelae of malignant edema formation. In contrast to PET, however, it did not predict fatal outcome early enough for successful implementation of invasive therapies.

Biomarkers↗

PubMed2003

Nosocomial pneumonia after acute stroke: implications for neurological intensive care medicine.

BACKGROUND AND PURPOSE: Pneumonia has been estimated to occur in about one third of patients after acute stroke. Only limited data are available on stroke-associated pneumonia (SAP) in specialized neurological intensive care units (NICUs). METHODS: We enrolled 124 patients with acute stroke who were treated at our university hospital NICU in a prospective observational study. Incidence rates and risk factors of SAP and long-term clinical outcome were determined. RESULTS: SAP incidence was 21% with a spectrum of pathogens, which is comparable to previously published data on general ICU patients. Mechanical ventilation, multiple location, and vertebrobasilar stroke, as well as dysphagia and abnormal chest x-ray findings, were identified as risk factors for the disease. SAP patients showed higher mortality rates than nondiseased subjects (acute, 26.9% versus 8.2%; long-term, 35.3% versus 14.3%) and a significantly poorer long-term clinical outcome (Barthel Index, 50.5+/-42.4 versus 81.5+/-27.8; Rankin Scale, 3.5+/-1.7 versus 2.2+/-1.6). CONCLUSIONS: Our data underline the considerable epidemiological and prognostic impact of SAP for the treatment of acute stroke patients in a specialized NICU setting. They demonstrate that the occurrence of SAP deteriorates clinical outcome in these patients. Our results allow us to identify high-risk stroke patients at time of NICU admission in whom the use of preventive treatment strategies is most promising.

Acute Disease↗