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Biomedical subjects

C Weiller

Publications and source records attributed to C Weiller.

At least 109 records · Page 6Linked to original sources
PubMed1993

Individual patterns of functional reorganization in the human cerebral cortex after capsular infarction.

We have previously shown bilateral activation of motor pathways and the recruitment of additional motor areas in studies of groups of patients with recovery from motor stroke. We have now developed a new positron emission tomographic technique to measure the changes in regional cerebral blood flow elicited during a motor task in individual patients, relative to the cerebral activation found in normal subjects. The patterns of cerebral activation in each of 8 individual patients with capsular lesions of the pyramidal tract and complete recovery from hemiplegia are described by comparison with the pattern found in a representative sample of 10 normal subjects. We found a large ventral extension of the hand field of the contralateral (sensori)motor cortex in all patients with lesions of the posterior limb of the internal capsule. Greater activation than in normal subjects was found in variable combinations of the supplementary motor areas, the insula, the frontal operculum, and the parietal cortex. Structures belonging to motor pathways ipsilateral to the recovered limb were also more activated in the patients than in normal subjects. However, additional activation of the ipsilateral (sensori)motor cortex was only found in the 4 patients who exhibited associated movements of the unaffected hand when the recovered hand performed the motor task. We conclude that recovery from motor stroke due to striatocapsular damage is associated with individually different patterns of functional reorganization of the brain. These patterns are dependent on the site of the subcortical lesion and the somatotopic organization of the pyramidal tract, both of which may determine the precise potential for recovery of limb function following this type of brain injury.

Adult↗
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↗
PubMed1992

Functional reorganization of the brain in recovery from striatocapsular infarction in man.

We used positron emission tomography (PET) to study organizational changes in the functional anatomy of the brain in 10 patients following recovery from striatocapsular motor strokes. Comparisons of regional cerebral blood flow maps at rest between the patients and 10 normal subjects revealed significantly lower regional cerebral blood flow in the basal ganglia, thalamus, sensorimotor, insular, and dorsolateral prefrontal cortices, in the brainstem, and in the ipsilateral cerebellum in patients, contralateral to the side of the recovered hand. These deficits reflect the distribution of dysfunction caused by the ischemic lesion. Regional cerebral blood flow was significantly increased in the contralateral posterior cingulate and premotor cortices, and in the caudate nucleus ipsilateral to the recovered hand. During the performance of a motor task by the recovered hand, patients activated the contralateral cortical motor areas and ipsilateral cerebellum to the same extent as did normal subjects. However, activation was greater than in normal subjects in both insulae; in the inferior parietal (area 40), prefrontal and anterior cingulate cortices; in the ipsilateral premotor cortex and basal ganglia; and in the contralateral cerebellum. The pattern of cortical activation was also abnormal when the unaffected hand, contralateral to the hemiplegia, performed the task. We showed that bilateral activation of motor pathways and the recruitment of additional sensorimotor areas and of other specific cortical areas are associated with recovery from motor stroke due to striatocapsular infarction. Activation of anterior and posterior cingulate and prefrontal cortices suggests that selective attentional and intentional mechanisms may be important in the recovery process. Our findings suggest that there is considerable scope for functional plasticity in the adult human cerebral cortex.

Adult↗
PubMed1992

The cortical localization of the lexicons. Positron emission tomography evidence.

Positron emission tomography was used to investigate changes in regional cerebral blood flow (rCBF) in neurologically normal subjects during word reading and word repetition. The blood flow in these conditions was compared with control conditions where subjects were presented with stimuli of comparable auditory and visual complexity to real words and said the same word on presentation of each stimulus. The control condition for word repetition (hearing spoken words presented backwards) resulted in bilateral activation of the superior temporal gyrus. Word repetition caused a significant increase in rCBF over this control condition in the left superior and middle temporal gyri. The control condition for word reading (seeing stimuli written in 'false fonts', i.e. non-existent letter-like forms) resulted in significant changes in rCBF bilaterally in the striate and extrastriate cortex. Word reading caused a significant increase in blood flow relative to this control in the posterior part of the left middle temporal gyrus. The implications of these results are discussed, and it is argued that they are consistent with localization of a lexicon for spoken word recognition in the middle part of the left superior and middle temporal gyri, and a lexicon for written word recognition in the posterior part of the left middle temporal gyrus.

Adult↗
PubMed1992

Type and extent of hemispheric brain infarctions and clinical outcome in early and delayed middle cerebral artery recanalization.

We evaluated the influence of time of recanalization or degree of initial leptomeningeal collateral blood flow in cardioembolic or arterio-arterial middle cerebral artery (MCA) occlusion on infarct size and clinical outcome in a series of 34 consecutive acute stroke patients with main stem (N = 31) or major branch (N = 3) occlusions using CT, initial cerebral arteriography (N = 21), repetitive close-meshed transcranial Doppler ultrasonography, and a neurologic stroke scale. We treated 15 patients with tissue plasminogen activator intravenously within the first 6 hours. The type and size of infarction depended on the location of the occluding lesions within the MCA trunk. Proximal MCA occlusion always led to infarction involving the striatum and internal capsule. Sixty-five percent of patients showed recanalization of the occluded MCA within 1 week. Following MCA recanalization, hyperperfusion was present in 38 to 44% of cases. There was a marginally significant relation between size of infarction on CT and recanalization time within the first 24 hours. The more rapidly recanalization occurred, the smaller the size of the infarct. When recanalization time was greater than 8 hours, the lesions always extended to the cortex. An additional good leptomeningeal collateral blood flow significantly reduced the size of the infarct and improved clinical outcome after 17 days and after 10 months. Early recanalization of embolic MCA occlusions within up to 8 hours, in conjunction with good transcortical collateralization, has a favorable impact on infarct size and outcome and may constitute the therapeutic window of opportunity.

Aged↗
PubMed1991

The functional anatomy of recovery from brain injury.

The functional neuroanatomical basis for recovery from ischaemic brain injury is not known. We have used positron emission tomography (PET) to study changes in the functional organization of the brain in patients recovering from striatocapsular motor strokes. Significant changes in regional cerebral blood flow (rCBF) were found during repetitive sequential opposition movements of the fingers in normal subjects and in patients with recovery from motor deficits. There was a difference in the pattern of cerebral activation when patients performed the motor task with the unaffected hand (when the activation was lateralized to contralateral sensorimotor and premotor cortex and ipsilateral cerebellum) and when the task was performed with the recovered, previously plegic hand (when the activation was bilateral and involved novel areas of cortex, especially area 40). Comparisons of rCBF maps at rest in the patient group and in normal subjects showed areas with significantly decreased rCBF in the patients (contralateral to the plegic hand in the basal ganglia, thalamus, insular cortex, brainstem and ipsilateral cerebellum), which reflected the distribution of dysfunction caused by the ischaemic lesions. A significantly increased activation over and above that in normal subjects was found in patients during movement of the recovered fingers in ipsilateral premotor cortex and bilateral frontal opercular/insular regions and area 40, the ipsilateral basal ganglia (the ischaemic lesion lying contralaterally) and the contralateral cerebellum. We postulate that these findings may be explained by the generation of movements by pathways that are different from those that normal subjects use to perform what are ordinarily fairly simple, automated tasks. We suggest that this is a direct demonstration of cerebral plasticity resulting in the resolution of acquired motor deficits.

Brain Ischemia↗
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

Infarctions and non-invasive diagnosis in moyamoya disease: two case reports.

An 31-year-old female and a 32-year-old male had clinical signs and angiographical confirmation of adult Moyamoya disease (MMD). Bilateral carotid siphon (C1), middle cerebral artery (M1), and anterior cerebral artery (A1) stenoses were diagnosed by means of transcranial Doppler sonography (TCD) and visualized during angio Magnetic Resonance Imaging (angio-MRI). In the woman, a 'rete mirabile' of dilated and tortuous lenticulostriate arteries could be visualized during proton weighted and T1-weighted MRI sequences. CO2-dependent vasomotor reactivity was bilaterally reduced and completely exhausted in the territory of right middle cerebral artery in both patients. Cerebral perfusion reserve, defined as the ratio of cerebral blood flow (CBF) to cerebral blood volume (CBV) was assessed by SPECT, and was found to be dramatically reduced in the anterior region of the male patient. Both patients had bilateral small subcortical infarctions in the corona radiata. TCD and MRI are important noninvasive techniques for a preliminary diagnosis of Moyamoya disease. Infarctions in Moyamoya disease may be hemodynamically produced low-flow infarctions.

Adult↗
PubMed1991

Hereditary motor and sensory neuropathy (HMSN) and optic atrophy (HMSN type VI, Vizioli).

Clinical and electrophysiological findings are described in three patients with hereditary motor and sensory neuropathy in association with optic atrophy (HMSN VI). The optic atrophy was of the Leber type in a 15-year-old boy. In a 70-year-old patient, as in three members of his family, optic atrophy was associated with tapetoretinal degeneration. In addition to HMSN and optic atrophy a 20-year-old man suffered from sensorineural deafness. Electrophysiological studies indicated a neuronal form of neuropathy, as in HMSN II. Brainstem auditory evoked potentials also revealed subclinical involvement of the central auditory pathways in the patients without hearing defects.

Adolescent↗
PubMed1991

[Dissections of the internal carotid artery--new diagnostic and pathogenetic aspects].

Initial and follow-up investigations were done systematically in 15 cases of internal carotid artery (ICA) dissections by means of angiography, computerized tomography, Magnetic Resonance Imaging, extracranial and transcranial Doppler sonography, as well as B-mode imaging. Cerebral hemodynamic reserve was evaluated by means of both SPECT and CO2-dependent vasomotor reactivity. The findings are focussed on two major issues: Do modern diagnostic tools permit to make the diagnosis of ICA dissection without angiographical proof? What is the pathogenesis of brain infarctions due to ICA dissections? Our findings demonstrate that the diagnosis of carotid artery dissection can reliably be done noninvasively by means of ultrasound techniques and MRI. These methods also allow for frequent follow-up investigations without any inconvenience for the patient. Embolic brain infarctions caused by carotid artery dissections are equally frequent as low flow induced lesions. Acute and follow-up findings suggest that surgical intervention is contraindicated in the acute phase, but may be considered for chronic pseudoaneurysms. Initial anticoagulation with high dose heparin is safe and seems to be efficacious. In certain cases, subsequent cumarine therapy may be indicated for a maximum of six months. Measures improving hemodynamics, e. g. induced hypertension, are reasonable, as long as the vasomotor reserve is exhausted.

Carotid Artery Diseases↗
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↗