Biomedical subjects

Johannes Weber

Publications and source records attributed to Johannes Weber.

4 recordsLinked to original sources

PubMed2003

Brain diffusion after single seizures.

PURPOSE: Diffusion-weighted magnetic resonance imaging (DWI) after focal status epilepticus has demonstrated focal alterations of the apparent diffusion coefficient (ADC) in the epileptogenic zone. We hypothesized that localized dynamic alterations of brain diffusion during the immediate postictal state will be detectable by serial DWI and correlate with the epileptogenic zone. METHODS: Nine adult patients (four men, five women) with medically intractable epilepsy were prospectively examined with a total of 25 DWI scans taken 2-210 min after a seizure. RESULTS: The interictal ADC was significantly (p < 0.05) elevated in the ictogenic hippocampus in all patients with temporal lobe epilepsy. The following postictal changes of the ADC were seen: (a) decreases by maximally 25-31%, which were most pronounced in the epileptogenic zone (n = 2); (b) generalized ADC changes after generalized seizures (n = 1) or prolonged complex partial seizures (n = 2); (c) no major changes after short-lived seizures or if the time to first DWI scan was >15 min or both (n = 3); and (d) widespread bilateral ADC increases after a flumazenil-induced seizure (n = 1). CONCLUSIONS: ADC changes seen during serial postictal DWI are complex and appear to reflect origin and spread of the preceding seizure. A delineation of the epileptogenic zone appears to be possible only in complex-partial seizures of >60 s duration that do not secondarily generalize.

Adult↗

PubMed2003

Presurgical evaluation of epilepsy by brain diffusion: MR-detected effects of flumazenil on the epileptogenic focus.

PURPOSE: After focal status epilepticus, focal alterations of the apparent diffusion coefficient (ADC) have been demonstrated in the epileptogenic zone by using diffusion-weighted magnetic resonance (MR)imaging (DWI). Effects of flumazenil on an epileptogenic focus have been demonstrated by EEG recordings, but not by functional MRI. We hypothesized that dynamic spatiotemporal alterations of brain diffusion of the epileptogenic focus after application of flumazenil will be detectable by DWI and correlate with the epileptogenic zone. METHODS: Twelve adult patients considered for epilepsy surgery with medically intractable temporal lobe epilepsy (TLE; n = 7), extratemporal lobe epilepsy (ETE; n = 2), and TLE+ETE (n = 3) were prospectively examined with DWI interictally (serving as baseline) and 10 min after application of 1 mg flumazenil i.v. RESULTS: The baseline interictal ADC was significantly elevated in the hippocampus on the ictogenic side in the patients with TLE (p = 0.002) as compared with healthy volunteers. The following changes of the mean ADC were seen in different regions of interest (ROIs) after injection of flumazenil: decreases in the hippocampus on the seizure-onset side by 14.8% (p = 0.005); decreases in the parahippocampal gyrus on both sides by 6.8% (epileptogenic side; p = 0.044) or 7.9% (nonepileptogenic side; NS), respectively; decreases in the cortex on the nonictogenic side by 7.9% (p = 0.047); and no significant changes of the ADC in the other ROIs. CONCLUSIONS: ADC decreases measured after application of flumazenil were seen in the seizure-onset zone as revealed by EEG and structural MRI and are an indicator of focus localization in patients with TLE.

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PubMed2002

Eyeblink-related areas in human cerebellum as shown by fMRI.

Classical eyeblink conditioning is used frequently to study the role of the cerebellum in associative learning. To understand the mechanisms involved in learning, the neural circuits that generate the eyeblink response should be identified. The goal of the present study was to examine cerebellar regions that are likely to control the human eyeblink response using event-related functional magnetic resonance imaging (fMRI). In 14 healthy volunteers eyeblinks were evoked by unilateral air-puff stimulation (total of 30 stimuli, inter-trial interval 27-44 sec). With eyes closed throughout the experiment, eyeblinks were recorded using a video-based system with infrared reflecting markers being attached to the upper eyelids. From each subject 500 scans were taken (TR = 2.2 sec, 22 slices per scan, slice thickness = 3 mm) using an echo planar imaging sequence (EPI). The statistical parametric maps of the experimental volume images were estimated with SPM99 specifying an appropriate event-related design matrix. Two main regions of significant activation were found in the ipsilateral posterior lobe of the cerebellar hemisphere. In the more anterior region the maxima of activation were located in hemispheral lobules VI and Crus I, and in the more posterior region in hemispheral lobules VIIb, Crus II and VIIIa (nomenclature according to Schmahmann et al. [2000]: MRI Atlas of the Human Cerebellum). Although less pronounced, activity was found also in corresponding areas of the contralateral cerebellar hemisphere. These eyeblink-related areas agree with trigeminal projection areas and blink reflex control areas shown in previous animal studies.

Adult↗

PubMed2002

Brain representation of hemifield stimulation in poststroke visual field defects.

BACKGROUND AND PURPOSE: Plasticity in extended, parallel, or reciprocal operating networks is well recognized. Changes in neuronal activity after lesions to distinct localized structures, such as the primary visual cortex, are less well characterized. We investigated the cortical reorganization in patients with poststroke visual field defects using blood oxygen level-dependent functional MRI. METHODS: Brain activation was measured in 7 patients with a single occipital cortical lesion and partially recovered hemianopia and in 7 age-matched control subjects. Differences in activation between rest and visual hemifield stimulation were assessed with statistical parametric mapping (SPM'99). RESULTS: In normal subjects, significant activation was found in the contralateral primary visual cortex and bilaterally in the extrastriate cortex. During hemifield stimulation of the unaffected side of stroke patients, a similar pattern was found compared with that seen in control subjects. During stimulation of the hemianopic side, bilateral activation was seen within the extrastriate cortex, stronger in the ipsilateral hemisphere. The primary visual cortex was not significantly activated in either hemisphere during stimulation of the hemianopic side. CONCLUSIONS: Visual field defects after stroke are associated with bilateral activation of the extrastriate visual cortex. This pattern of activation indicates altered neuronal activity in the visual system. Further investigation is necessary to determine the relationship between functional reorganization and recovery of lost visual function after poststroke hemianopia.

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