Search PubMed⌕ Search

Biomedical subjects

W Reiche

Publications and source records attributed to W Reiche.

29 records · Page 2Linked to original sources
PubMed1993

The case of aphasia or neglect after striatocapsular infarction.

The occurrence of aphasia or neglect was related to anatomo-structural (CT/MRI), functional [regional cerebral blood flow (rCBF)] and pathogenetic features [duration of middle cerebral artery (MCA) occlusion and degree of cortical leptomeningeal anastomoses] in 57 cases (26 with and 31 without aphasia or neglect) with strictly subcortical infarcts of one defined type, i.e. striatocapsular infarcts. No distinct pattern of language disturbances was found. Aphasic syndromes did not differ in the amount of involvement of the putamen, pallidum, head of caudate nucleus and white matter. Patients with aphasia or neglect had larger infarcts than those without. However, there was no specific involvement of the basal ganglia, the internal capsule or the deep white matter in patients with aphasia or neglect. Patients with aphasia or neglect had a significantly longer duration of MCA occlusion and mostly poor leptomeningeal collaterals. The cortical rCBF was significantly decreased in the cortical MCA territory in the patients with aphasia or neglect only. The rCBF remained low at follow-up after 1 year and corresponded to focal cortical atrophy on MRI, although neglect had subsided completely in all patients and aphasia had improved considerably in almost 75% of the cases. Aphasia or neglect after striatocapsular infarcts are most likely due to selective neuronal loss of the cerebral cortex due to prolonged MCA occlusion and insufficient collateral blood flow. Individual differences in recovery from aphasia after striatocapsular infarction can be explained in terms of the number of surviving cortical neurons.

Adolescent↗
PubMed1991

Patterns of brain infarctions in internal carotid artery dissections.

In 15 patients with internal carotid artery (ICA) dissections, patterns of brain infarctions visible on CT were categorized according to a pathogenetically oriented classification system. This differentiated ischemic brain damage due to low flow from thromboembolic infarctions. Simultaneously, cerebral hemodynamic reserve was evaluated by means of both CO2-dependent vasomotor reactivity and HMPAO- and 99mTc-RBC-SPECT. Six out of 11 patients with ischemic infarctions had the territorial type of brain lesion, suggesting distal embolism. Five patients revealed the pattern of hemodynamically induced low-flow infarctions. Cerebral hemodynamic reserve was significantly decreased only in these latter patients. In ICA dissections the frequencies of hemodynamically and thromboembolically induced brain infarctions is approximately equal. This finding suggests that only half of the patients with symptoms of symptomatic dissections had brain emboli, whereas in the other half the dissections lead to a low-flow effect in terminal supply areas which is so severe that non-embolic brain infarctions occur. This differentiation can help decide whether antithrombotic or hemodynamic treatment should be given.

Adult↗
PubMed1991

Clinical and hemodynamic aspects of low-flow infarcts.

We used single-photon emission computed tomography to measure cerebral blood flow, cerebral blood volume, and cerebral perfusion reserve and transcranial Doppler sonography with CO2 stimulation to assess hemispheric vasomotor reactivity in 37 patients and in normal controls. Computed tomography and magnetic resonance imaging were performed to differentiate morphologically low-flow infarcts (n = 17) from territorial infarcts (n = 20). In patients with either type of infarct, blood flow was decreased and blood volume was increased in the infarcted areas compared with the same areas in the controls. Perfusion reserve and vasomotor reactivity were significantly reduced in patients with territorial infarcts and carotid artery occlusions (n = 12) and even more reduced in patients with low-flow infarcts (p less than 0.001). Both parameters were normal in patients with cardiac embolic territorial infarcts (n = 8). In patients with territorial infarcts, blood flow and perfusion reserve changes were restricted to the infarcted areas, whereas in patients with low-flow infarcts, regions of decreased perfusion reserve considerably exceeded the area of the infarct. Low-flow infarcts are related to the hemodynamic effects of severe extracranial carotid artery disease.

Adult↗
PubMed1991

[A comparison of MRT and SPECT findings in patients with cerebral microangiopathy].

Lacunar infarctions and periventricular hypodensity are assumed to be typical CT patterns of cerebral microangiopathy (MA). In 17 patients with such findings and in 6 controls without any signs of central nervous system disease cranial CT, MRT and 99mTc-HMPAO-SPECT were employed. Seven patients with CT findings of minor MA demonstrated in comparison to controls no significant difference. In 10 cases with CT findings of pronounced MA periventricular rCBF was significantly reduced compared to controls. rCBF of temporal and parietal cortex was not diminished compared to controls. In 14 patients studied with MRT deep white matter lesions were found which appeared solitary, multiple or confluent. Employing 99mTc-HMPAO-SPECT, cerebral MA revealed rCBF reduction in periventricular brain tissue by cerebellar standardization.

Aged↗
PubMed1990

The large striatocapsular infarct. A clinical and pathophysiological entity.

We examined 29 patients with strictly subcortical large striatocapsular infarctions. Eight of them had aphasia or neglect. All patients underwent transcranial Doppler ultrasonography or selective carotid angiography, magnetic resonance imaging, and single photon emission tomography for assessment of cerebral blood flow, blood volume, and cerebral perfusion reserve. The signs were compatible with cortical territorial infarctions rather than lacunes. On both magnetic resonance imaging and computed tomographic scans, the lesions corresponded to the territories of the medial and lateral group of the lenticulostriate arteries, Heubner's artery, or the anterior choroidal artery. The infarctions were either due to cerebral embolization into the M1 segment of the middle cerebral artery or due to stenosis at the same site, ie, lesions that acutely and simultaneously occluded the orifices of the lenticulostriate or neighboring arteries. Persistent occlusion of the middle cerebral arteries and a decrease of cortical regional cerebral blood flow were only found in patients with aphasia or neglect. All patients without aphasia or neglect showed a rapid recanalization of the middle cerebral artery occlusion or a stenosis of the M1 segment and no cortical regional cerebral blood flow decrease. Large striatocapsular infarctions occur due to occlusive disease of the middle cerebral artery (large-vessel disease) and not due to a disseminated in situ occlusion of the long penetrating arteries (small-vessel disease), as in lacunes. Neuropsychological deficits can be explained by decreased cortical blood flow due to a persistent occlusive lesion of the middle cerebral artery.

Adult↗
PubMed1990

[Determination of regional cerebrovascular perfusion reserve (rCPR) using quantitative flow/volume (F/V)-SPECT. Results in patients with subcortical ischemic brain lesions with or without neuropsychological symptoms].

NPS (aphasia or neglect) are a regular concomitant symptom of cortical, and, occasionally, subcortical ischemic lesions. In 19 patients with subcortical lesions (eight with NPS, 11 without NPS), F/V-SPECT was employed to search for changes in rCPR in both, lesions and ipsilateral cortex. Results were correlated with NPS and MRI findings. Compared to the unaffected hemisphere, all subcortical lesions showed reduced regional cerebral blood flow (rCBF) (-16 to -23%), increased regional cerebral blood volume (rCBV) (+34 to +62%), and decreased or missing rCPR (-27 to -28%). Compared to MRI, there was no difference in lesion size in the thromboembolic lesions. Hemodynamic low-flow infarcts, however, were greater with SPECT than in MRI. In patients without NPS, the adjacent cortex was normal in SPECT and MRI. In addition, patients with NPS revealed reduced rCBF (-18%), increased rCBV (+19%), and decreased rCPR (-22%) in the adjacent cortex. MRI was normal in the same cortical area. These results indicate that NPS in subcortical lesions may be caused by a hemodynamic mechanism causing reduction of rCPR in the adjacent cortex.

Adult↗
PubMed1990

[A method of adjusting and evaluating MRT and SPECT tomograms for comparing cerebral morphology with cerebrovascular regulation].

A method is introduced which yields computerized correlations of topographically identical morphological and functional orbito-meatal slices of the brain by employing the specific local resolutions and a simple adaptation algorithm. In addition, a ROI-overlay method is described which may be used to evaluate semiquantitatively (interhemispherical ratios or ratios hemisphere/cerebellum) identical planes to assess rCBF, rCBV and regional vascular regulation. It appears to be advantageous that ROIs can be superimposed on MRI images as well as on SPECT images.

Brain↗
PubMedDate not supplied

Cerebroretinal vasculopathy and leukoencephalopathy mimicking a brain tumor. Report of two early-onset cases with Fanconi's anemia-like phenotypes suggesting an autosomal-recessive inheritance pattern.

We report two sisters affected with a unique disorder characterized by recurrent space-occupying brain lesions and retinal vasculopathy since their early twenties. Affection status was associated with abnormalities characteristic of Fanconi's anemia, i.e. aplastic anemia, microcephaly, short stature, an unusual face and pigmentation abnormalities of skin. In cytogenetic analyses performed in childhood signs of chromosome fragility or any chromosomal aberration were lacking. Histopathological examination of brain biopsy samples in both cases demonstrated identical histomorphological features of an unusual occlusive vasculopathy with multilayered basement membranes and coagulation necroses which were confined to the white matter. A veno-occlusive retinopathy with neovascularization attributed to progressive visual loss. One of the sisters died at an age of just 24 years, the other is now 27 years old. Unlike any other published cases of hereditary cerebroretinal vasculopathy, the sisters' complex early-onset vaso-occlusive CNS-/eye-disease seems to be genetically associated with their Fanconi's anemia-like phenotypes and is suggested to constitute an autosomal-recessive variant. Patchy white matter calcifications, an incidental finding in either of the affected sisters, may represent preclinical manifestation of disease onset in childhood.

Adult↗