Matches in SemOpenAlex for { <https://semopenalex.org/work/W2015484848> ?p ?o ?g. }
- W2015484848 endingPage "94" @default.
- W2015484848 startingPage "43" @default.
- W2015484848 abstract "Abstract In this study we examined the input-output relations of the somatosensory system in 94 patients having unilateral, circumscribed lesions of one hemisphere. The lesions were verified during operation. Their localization and extent were measured in relation to gyri and sulci. In addition stereotaxical measurements were taken during the operation and post-operatively. Lesions of the anterior deep part of SI, the overt part of SI, SPC, SS, 5L, RI-PO and the supero-lateral part of the prefrontal cortex introduced noise in detection and discrimination of somatosensory signals. Lesions of anterior deep part of SI gave rise to noise in detection of a particular combination of somato-sensory signals: sense of passive movement, kinesthesia, and detection of size and shape. The noise in kinesthetic discrimination was band-limited. Similarly, lesions of the other somatosensory areas each gave rise to noise in a differentiated way in detection of kinesthesia, microgeometry, size and shape. For certain lesions the noise in kinesthetic detection and microgeometric detection was band-limited. The noise in size and shape detection was never band-limited. The degree of noise also varied amongst lesions of the different somatosensory areas. Lesions of SI caused in general large amounts of noise, whereas lesions of SS, 5L were associated with small amounts of noise. Only within the SI-hand area was it possible to establish a region of maximal overlap within which lesions always elicited discrimination loss for size or shape. No such region could be established for discrimination loss in microgeometry and kinesthesia. No such region could be established elsewhere in the brain. In order to delimit the structures to which damage caused discrimination loss we maximized the space of equiterritorial lesions associated with discrimination loss and simultaneously we maximized the equiterritorial lesions associated with normal discrimination. The result was that damage to the anterior 2 3 of the superior and middle frontal gyrus, the SI-hand area, the cortex lining the postcentral sulcus (SPC), the supplementary sensory area (SS), the anterior and lateral part of the superior parietal lobule (5L) and the retroinsular cortex—parietal operculum caused somatosensory discrimination loss. All lesions of the SI-hand area were exclusively associated with contralateral discrimination loss, and all but two lesions of the somatosensory association areas and frontal cortex, respectively, were associated with contralateral discrimination loss. There were no differences in the effect of lesions to the right and the left hemisphere. Damage to a part of one of the delimited areas above were without effect. At least 3 4 or more had to be damaged to cause an effect. Moreover, within the somatosensory association areas and the frontal cortex any subfield within the delimited field could be damaged without effect. This implied that the information was uniformly represented within the delimited field. It was demonstrated that the discrimination loss was not due to non-specific factors such as aphasia, disturbances of general attention etc., It was quite remarkable that even major motor disturbances and abnormalities in sampling of somatosensory information did not cause any discrimination loss. The abnormalities in sampling arose from lesions of claustrum, putamen, premotor cortex, primary motor cortex, supplementary motor area, SII and SS-5L. Discrimination loss of kinesthesia appeared after lesions of the contralateral primary somatosensory hand area, the supplementary sensory area, the cortex lining the postcentral sulcus and the retroinsular cortex. Anesthesia of the skin uncovered kinesthetic discrimination loss in patients with lesions of the supplementary sensory area and lateral part of the superior parietal lobule and in patients with larger lesions of the cortex lining the postcentral sulcus and the retroinsular cortex. Additional joint anesthesia induced a severe, sometimes total, kinesthetic discrimination loss in the latter group of patients. Lesions of the contralateral overt part of the SI-hand area caused discrimination loss for microgeometry over the whole stimulus energy range. Another subgroup of patients with lesions of RI-PO had moderate discrimination loss for large amplitude long wavelength surfaces. Patients with lesions of the SS had a slight discrimination loss for microgeometry. Lesions of the contralateral anterior part of the SI-hand area caused size discrimination loss, but no shape discrimination loss. Lesion of the anterior part plus the overt part of the SI-hand area provoked a severe size discrimination loss and a total loss of shape discrimination. Lesions confined to the overt part of the SI-hand area only elicited a moderate size discrimination loss; whereas total lesions of the overt part made the subjects unable to discriminate any shape. In addition, larger lesions of SPC, SS, RI-PO and the superior and middle frontal gyrus caused a mild discrimination loss for shape. Some somatosensory functions were more vulnerable than others. The vulnerability was assumed to be due to a lack of physiological redundancy of detection processors. In contrast to kinesthesia and size information which most likely could be signaled from afferents in skin, joints and muscles having parallel projections to SI and a secondary wide distribution to somatosensory association areas. The anterior (buried) part of SI was believed to participate in the initial demodulation of macrogeometric and kinesthetic signals. In a few successive steps of integration information about size was recovered. The overt part of SI was believed to participate in the reconstruction of curvature and microgeometric surface characteristics and of kinesthetic signals from the skin. The SPC probably is a convergence area for kinesthesia. It was, however, impossible to demonstrate any importance of kinesthetic information in the discrimination of the shapes although lesions of SPC affected both kinesthesia and shape discrimination. Kinesthesia per se does not provide any information about curvature or the shape of objects. Kinesthesia is too inaccurate to account for shape and size discrimination in normals. The lack of correlation between kinesthesia and size and shape thresholds in patients with lesions of the somatosensory areas showed that kinesthetic information was not used in either of these circumstances. Akinesthesia, thus does not lead to shape or size discrimination loss. Although kinesthetic and cutaneous information might be integrated in SPC, the contribution of the SPC in shape detection is probably an integration of curvature information from multiple cutaneous fields rather than a contribution of kinesthesia to shape detection22,88,92. The present investigation thus does not give support to the idea that kinesthesia must be normal for size and shape detection to be normal. Neither was there from the present results any support for the idea that detection of somatosensory threshold stimuli must be normal for size and shape detection to be normal83. It is possible that the secondary somatosensory area also participates in the analysis of somatosensory information in man, although unilateral lesions here did not affect discrimination of neither simple nor complex somatosensory signals. Unilateral lesions of SII caused abnormal manipulation. This points more to a role for SII in sensory-motor integration than a role in the analysis of somatosensory information. For the microgeometric stimuli some additional filtering outside the SI is necessary for the final reconstruction. The neurons in RI-PO were supposed to participate in this and perhaps also recover information about phase angle. For the macrogeometric shape stimuli some filtering outside the SI was also necessary. It is possible that the somatosensory areas SPC, SS and 5L participate in the final reconstruction although their exact contribution is still unclear. The results indicated that the macro- and microgeometric is collated with kinesthetic information in SS and 5L. The superior and middle frontal gyri probably participated in the organization and decision processes associated with two-alternative forced-choice discriminations. The pattern of localization of lesions associated with noisy kinesthetic, micro- en macrogeometric discrimination indicated that there was a general organization of somatosensory perception in the human cerebral cortex in which the SI, some of the somatosensory association areas (SPC, SS, RI-PO, 5L), and the middle and superior prefrontal gyrus participated." @default.
- W2015484848 created "2016-06-24" @default.
- W2015484848 creator A5008736543 @default.
- W2015484848 date "1987-03-01" @default.
- W2015484848 modified "2023-09-24" @default.
- W2015484848 title "Somatosensory detection of microgeometry, macrogeometry and kinesthesia after localized lesions of the cerebral hemispheres in man" @default.
- W2015484848 cites W10739509 @default.
- W2015484848 cites W1565771609 @default.
- W2015484848 cites W1802213054 @default.
- W2015484848 cites W1894615969 @default.
- W2015484848 cites W1945542429 @default.
- W2015484848 cites W1973422620 @default.
- W2015484848 cites W1975492207 @default.
- W2015484848 cites W1977170192 @default.
- W2015484848 cites W1981356310 @default.
- W2015484848 cites W1984446252 @default.
- W2015484848 cites W1985538061 @default.
- W2015484848 cites W1994865952 @default.
- W2015484848 cites W1997616310 @default.
- W2015484848 cites W1998716595 @default.
- W2015484848 cites W1999237895 @default.
- W2015484848 cites W2003400004 @default.
- W2015484848 cites W2004716627 @default.
- W2015484848 cites W2015558198 @default.
- W2015484848 cites W2016297315 @default.
- W2015484848 cites W2016309184 @default.
- W2015484848 cites W2018823329 @default.
- W2015484848 cites W2022424636 @default.
- W2015484848 cites W2026826357 @default.
- W2015484848 cites W2026920237 @default.
- W2015484848 cites W2029178717 @default.
- W2015484848 cites W2034036816 @default.
- W2015484848 cites W2034897939 @default.
- W2015484848 cites W2035511416 @default.
- W2015484848 cites W2040200937 @default.
- W2015484848 cites W2042335527 @default.
- W2015484848 cites W2042619570 @default.
- W2015484848 cites W2042716264 @default.
- W2015484848 cites W2042962599 @default.
- W2015484848 cites W2043841338 @default.
- W2015484848 cites W2045029966 @default.
- W2015484848 cites W2054549571 @default.
- W2015484848 cites W2063345723 @default.
- W2015484848 cites W2064759785 @default.
- W2015484848 cites W2065663844 @default.
- W2015484848 cites W2072968663 @default.
- W2015484848 cites W2073854051 @default.
- W2015484848 cites W2079138836 @default.
- W2015484848 cites W2085238721 @default.
- W2015484848 cites W2088556906 @default.
- W2015484848 cites W2091788365 @default.
- W2015484848 cites W2096442115 @default.
- W2015484848 cites W2101766009 @default.
- W2015484848 cites W2102949060 @default.
- W2015484848 cites W2105808890 @default.
- W2015484848 cites W2136131831 @default.
- W2015484848 cites W2158815034 @default.
- W2015484848 cites W2159923572 @default.
- W2015484848 cites W2163686172 @default.
- W2015484848 cites W2165476478 @default.
- W2015484848 cites W2172702357 @default.
- W2015484848 cites W2240607264 @default.
- W2015484848 cites W2286615781 @default.
- W2015484848 cites W2289104698 @default.
- W2015484848 cites W2325728128 @default.
- W2015484848 cites W2342105818 @default.
- W2015484848 cites W2415880730 @default.
- W2015484848 cites W2419659546 @default.
- W2015484848 cites W2431103624 @default.
- W2015484848 cites W2441135453 @default.
- W2015484848 cites W3087756695 @default.
- W2015484848 cites W4250638771 @default.
- W2015484848 doi "https://doi.org/10.1016/0165-0173(87)90018-x" @default.
- W2015484848 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/3552126" @default.
- W2015484848 hasPublicationYear "1987" @default.
- W2015484848 type Work @default.
- W2015484848 sameAs 2015484848 @default.
- W2015484848 citedByCount "70" @default.
- W2015484848 countsByYear W20154848482012 @default.
- W2015484848 countsByYear W20154848482013 @default.
- W2015484848 countsByYear W20154848482014 @default.
- W2015484848 countsByYear W20154848482015 @default.
- W2015484848 countsByYear W20154848482016 @default.
- W2015484848 countsByYear W20154848482017 @default.
- W2015484848 countsByYear W20154848482019 @default.
- W2015484848 countsByYear W20154848482020 @default.
- W2015484848 countsByYear W20154848482021 @default.
- W2015484848 countsByYear W20154848482022 @default.
- W2015484848 crossrefType "journal-article" @default.
- W2015484848 hasAuthorship W2015484848A5008736543 @default.
- W2015484848 hasConcept C105702510 @default.
- W2015484848 hasConcept C15744967 @default.
- W2015484848 hasConcept C169760540 @default.
- W2015484848 hasConcept C172497186 @default.
- W2015484848 hasConcept C71924100 @default.
- W2015484848 hasConceptScore W2015484848C105702510 @default.
- W2015484848 hasConceptScore W2015484848C15744967 @default.
- W2015484848 hasConceptScore W2015484848C169760540 @default.