Biomedical subjects

René Knab

Publications and source records attributed to René Knab.

6 recordsLinked to original sources

PubMed2005

Magnetic resonance imaging and clinical patterns of patients with 'spectacular shrinking deficit' after acute middle cerebral artery stroke.

BACKGROUND: Rapid resolution of neurological deficits after severe middle cerebral artery (MCA) stroke has been coined spectacular shrinking deficit (SSD). We studied clinical and MRI patterns in patients with SSD. METHODS: Patients with acute MCA stroke <6 h were examined by stroke MRI (perfusion- and diffusion-weighted imaging (PWI, DWI), MR angiography (MRA)) at admission, day 1 and day 7. SSD was defined as a > or =8-point-reduction of neurological deficit in the National Institute of Health Stroke Scale (NIHSS) to a score of < or =4 within 24 h. PWI and DWI lesion volumes were measured on ADC (ADC < 80%) and time to peak maps (TTP > +4 s). Recanalization was assessed by MRA after 24 h. Final infarct volumes were defined on T2 weighted images at day seven. Outcome was assessed after 90 days using modified Rankin Scale (mRS) and Barthel Index (BI). RESULTS: SSD was present in 14 of 104 patients. Initial DWI and PWI lesion volumes were smaller in SSD patients - ADC < 80%: 8.9 (4.3-20.5) vs. 30 (0-266.7) ml; TTP > +4 s: 91.6 (29.7-205.8) vs. 131.5 (0-311.5) ml. Early recanalization was associated with SSD resulted in smaller final infarct volumes (11.9 (2.4-25.9) vs. 47.7 (1.2-288.5)). All SSD patients were independent at day 90 (mRS 0 (0-2); BI 100). CONCLUSION: The clinical syndrome of SSD is reflected by a typical MRI pattern with small initial DWI and PWI lesion volumes, timely recanalization and small final infarct volumes.

Acute Disease↗

PubMed2005

Tissue at risk is overestimated in perfusion-weighted imaging: MR imaging in acute stroke patients without vessel recanalization.

BACKGROUND AND PURPOSE: The volume of decreased cerebral blood flow (CBF) in acute stroke perfusion-weighted imaging frequently overestimates final infarct volume. We hypothesized that surviving tissue exists even in patients without recanalization and tried to determine perfusion thresholds from initial MR imaging. METHODS: Stroke MR imaging including MR angiography was carried out at days 0, 1, and 7 after stroke onset in 19 patients without recanalization at least until day 1. The following lesions were defined: L0 = diffusion restriction at day 0; LG1 = lesion growth until day 1; LG7 = lesion growth until day 7; ST7 = initially hypoperfused, but surviving tissue. These lesions were transferred on initial MR imaging within 4.7 hours and perfusion values at day 0 were determined. RESULTS: Median lesion volume L0 at day 0 was 18.2 mL and increased to 39.4 and 43.8 mL at days 1 and 7. Volume of decreased rCBF not progressing to infarction was 148.5 mL (ST7). Mean ST7 perfusion values were different from L0 and LG1, but only mean relative cerebral blood volume (rCBV) was different from LG7, discriminating survival against death of tissue. A threshold value of 0.82 CBV for death versus survival was determined with a sensitivity of 0.56 and specificity of 0.95. Carotid T occlusions showed the greatest potential of lesion growth. CONCLUSION: Even when vessel occlusion persists, hypoperfused tissue on MR imaging does not necessarily progress toward infarction. The most conclusive inferences can be drawn from CBV images. The site of arterial occlusion also determines progression to infarction.

Adult↗

PubMed2004

Transient ischemic attacks before ischemic stroke: preconditioning the human brain? A multicenter magnetic resonance imaging study.

BACKGROUND AND PURPOSE: We investigated whether transient ischemic attacks (TIAs) before stroke can induce tolerance by raising the threshold of tissue vulnerability in the human brain. METHODS: Sixty-five patients with first-ever ischemic territorial stroke received diffusion- and perfusion-weighted MRI within 12 hours of symptom onset. Epidemiological and clinical data, lesion volumes in T2, apparent diffusion coefficient (ADC) maps and perfusion maps, and cerebral blood flow and cerebral blood volume values were compared between patients with and without a prodromal TIA. RESULTS: Despite similar size and severity of the perfusion deficit, initial diffusion lesions tended to be smaller and final infarct volumes were significantly reduced (final T2: 9.1 [interquartile range, 19.7] versus 36.5 [91.2] mL; P=0.014) in patients with a history of TIA (n=16). This was associated with milder clinical deficits. CONCLUSIONS: The beneficial effect of TIAs on lesion size in ADC and T2 suggests the existence of endogenous neuroprotection in the human brain.

Blood Flow Velocity↗

PubMed2004

Cerebral perfusion impairment correlates with the decrease of CT density in acute ischaemic stroke.

Within the first 6 h of ischaemic stroke, changes on computed tomography (CT) scans are known as early ischaemic signs. We tested the hypothesis that the severity of perfusion impairment correlates with the degree of CT density decrease. Water uptake in ischaemic brain tissue results in a subtle decrease of CT density, and was quantified by delineation of the corresponding decrease of the apparent diffusion coefficient (ADC). Regions of decreased ADC and CT density in 29 acute-stroke patients were superimposed on the corresponding magnetic resonance perfusion images. Mean values of ADC and CT density decrease were correlated with the corresponding relative changes of cerebral blood flow (rCBF) and volume (rCBV), mean transit time (rMTT) and time-to-peak (rTTP). The decrease of CT density was 1.2 +/- 0.6 Hounsfield units and showed a linear correlation with rCBF (0.42, p < 0.01) as well as rCBV (0.62, p < 0.01), but not with the prolongation of rMTT (1.43, p = 0.78) or rTTP (1.34, p = 0.26). Therefore, the reduction of rCBF determines the severity of the early ischaemic oedema (EIOE) on CT, as well as reduction of the ADC. These findings provide a coherent view on the pathophysiology of the EIOE.

Adult↗

PubMed2003

The influence of extra- and intracranial artery disease on the BOLD signal in FMRI.

Functional MRI is based on the vascular response due to neuronal activation. The underlying mechanism of fMRI is the blood oxygenation level-dependent (BOLD) effect-a complex interplay between changes in the cerebral metabolisation rate of oxygen (CMRO2), neurovascular coupling, and the resulting hemodynamic response. An intact neurovascular coupling is essential for the detection of the BOLD signal and it seems likely that a disturbed cerebrovascular reserve capacity (CVRC) alters the BOLD response. We tested the hypothesis that extra- or intracranial artery disease influences the BOLD signal. Twenty-one patients with extra- or intracranial stenosis were studied with BOLD sensitive T2*-weighted MRI. All patients presented with transient or prolonged reversible ischemic symptoms ipsilateral to the artery disease but were asymptomatic at the time point of the MRI study. fMRI was performed employing a simple motor task (fist closure right and left). Additionally, the CVRC was assessed applying carbogen gas during serial T2*-weighted MRI for the calculation of CO(2) reactivity maps of the relative signal change. Signal differences between both hemispheres were compared in individual subjects and with healthy subjects. Patients with disturbed CVRC in the CO(2) reactivity maps showed either a significantly reduced (n = 5) or a negative (n = 1) BOLD signal in the affected compared to the unaffected primary sensorimotor cortex during fist closure. Patients with intact CVRC showed no significant BOLD signal differences between affected and unaffected hemisphere. Extra- or intracranial artery disease influences CVRC and consequently the BOLD signal. This observation is important for the clinical application of fMRI paradigms.

Adult↗

PubMed2002

Cerebral blood flow predicts lesion growth in acute stroke patients.

BACKGROUND AND PURPOSE: We sought to study the role of MRI-derived cerebral blood flow (CBF) measurements for the prediction of lesion development in acute stroke patients. METHODS: Thirty-two patients were treated with tissue plasminogen activator. Diffusion-weighted (DWI) and perfusion-weighted MRI, T2-weighted imaging, and MR angiography were performed before treatment (2.8+/-0.9 hours after symptom onset) and on follow-up (days 1 and 7). CBF thresholds (12 and 22 mL/100 g per minute) were applied to bolus tracking MRI maps to determine predictive cutoff levels. RESULTS: In 21 patients (group A), the terminal lesion volume (T2-weighted imaging) was larger than the initial DWI lesion volume (89+/-93 versus 21+/-38 mL). In 11 patients (group B), the terminal lesion volume was smaller than the initial DWI lesion volume (7+/-27 versus 15+/-29 mL). The initial DWI lesion volume did not differ between both groups. The presence of a tissue volume > or =50 mL with a CBF value < or =12 mL/100 g per minute was predictive for lesion enlargement to day 7 in T2-weighted imaging (positive predictive value, 0.80). CONCLUSIONS: The presence of a tissue volume > or =50 mL with a CBF value < or =12 mL/100 g per minute predicts further lesion growth in hyperacute stroke patients. MRI-derived CBF values, with all their present limitations, are valuable in early estimation of prognosis of stroke patients.

Acute Disease↗