The Pyramidal Tract

Wiesendanger, M.

doi:10.1007/978-1-4684-3884-0_8

Cited by 18 publications

(4 citation statements)

References 296 publications

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“…1, section 34 in Matelli et al, 1985). Previous architectonic studies have reported consistent medio-lateral variations in the size of layer V pyramids, with the largest ones found within the medial portion of the primary motor cortex (Stepniewska et al, 1993;Wiesendanger, 1981), and our present results confirm these observations. However, since cytoarchitectonic differences were accompanied by differences in laminar distribution patterns of multiple receptors, we defined the mesial portion of the primary motor cortex as a distinct region, i.e.…”

Section: Comparison With Previous Subdivisions Of Macaque Motor and Psupporting

confidence: 91%

Multimodal 3D atlas of the macaque monkey motor and premotor cortex

Rapan¹,

Niu²,

et al. 2020

Preprint

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In the present study we reevaluated the parcellation scheme of the macaque frontal agranular cortex by implementing quantitative cytoarchitectonic and multireceptor analyses, with the purpose to integrate and reconcile the discrepancies between previously published maps of this region.We applied an observer-independent and statistically testable approach to determine the position of cytoarchitectonic borders. Analysis of the regional and laminar distribution patterns of 13 different transmitter receptors confirmed the position of cytoarchitectonically identified borders. Receptor densities were extracted from each area and visualized as its “receptor fingerprint”. Hierarchical and principal components analyses were conducted to detect clusters of areas according to the degree of (dis)similarity of their fingerprints. Finally, functional connectivity pattern of each identified area was analyzed with areas of prefrontal, cingulate, somatosensory and lateral parietal cortex and the results were depicted as “connectivity fingerprints” and seed-to-vertex connectivity maps.We identified 16 cyto- and receptor architectonically distinct areas, including novel subdivisions of the primary motor area 4 (i.e. 4a, 4p, 4m) and of premotor areas F4 (i.e. F4s, F4d, F4v), F5 (i.e. F5s, F5d, F5v) and F7 (i.e. F7d, F7i, F7s). Multivariate analyses of receptor fingerprints revealed three clusters, which first segregated the subdivisions of area 4 with F4d and F4s from the remaining premotor areas, then separated ventrolateral from dorsolateral and medial premotor areas. The functional connectivity analysis revealed that medial and dorsolateral premotor and motor areas show stronger functional connectivity with areas involved in visual processing, whereas 4p and ventrolateral premotor areas presented a stronger functional connectivity with areas involved in somatomotor responses.For the first time, we provide a 3D atlas integrating cyto- and multi-receptor architectonic features of the macaque motor and premotor cortex. This atlas constitutes a valuable resource for the analysis of functional experiments carried out with non-human primates, for modeling approaches with realistic synaptic dynamics, as well as to provide insights into how brain functions have developed by changes in the underlying microstructure and encoding strategies during evolution.HighlightsMultimodal analysis of macaque motor and premotor cortex reveals novel parcellation3D atlas with cyto- and multireceptor architectonic features of 16 (pre)motor areasPrimary motor area 4 is cyto- and receptor architectonically heterogeneous(Pre)motor areas differ in their functional connectivity fingerprints

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Section: Comparison With Previous Subdivisions Of Macaque Motor and Psupporting

confidence: 91%

Multimodal 3D atlas of the macaque monkey motor and premotor cortex

Rapan¹,

Niu²,

et al. 2020

Preprint

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“…There were no significant differences in myelinated axon number between any of the 5 rostral sampling sites, although axon number was slightly higher in the rostral-most site. This may be explained by corticonuclear fibers leaving the pyramid as this does correspond to the region where the facial nucleus and nucleus ambiguous are located near the pons-medulla border (Zimmerman et al, 1964; Reh and Kalil, 1981; Wiesendanger, 1981; FitzGerald et al, 2007). Fewer axons were present at the caudal site (site 6), which is just rostral to the pyramidal decussation (p < 0.001); this is probably a reflection of the fact that CST axons are beginning to leave the pyramid to ascend dorsally and cross over prior to joining the dorsal CST in the spinal cord.…”

Section: Resultsmentioning

confidence: 99%

Unexpected Survival of Neurons of Origin of the Pyramidal Tract after Spinal Cord Injury

Nielson¹,

Sears-Kraxberger²,

Strong³

et al. 2010

J. Neurosci.

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There is continuing controversy about whether the cells of origin of the corticospinal tract (CST) undergo retrograde cell death after spinal cord injury (SCI). All previous attempts to assess this have used imaging and/or histological techniques to assess upper motoneurons in the cerebral cortex. Here, we address the question in a novel way by assessing Wallerian degeneration and axon numbers in the medullary pyramid of Sprague Dawley rats after both acute SCI, either at cervical level 5 (C5) or thoracic level 9 (T9), and chronic SCI at T9. Our findings demonstrate that only a fraction of a percentage of the total axons in the medullary pyramid exhibit any sign of degeneration at any time after SCI-no more so than in uninjured control rats. Moreover, design-based counts of myelinated axons revealed no decrease in axon number in the medullary pyramid after SCI, regardless of injury level, severity, or time after injury. Spinal cord-injured rats had fewer myelinated axons in the medullary pyramid at 1 year after injury than aged matched controls, suggesting that injury may affect ongoing myelination of axons during aging. We conclude that SCI does not cause death of the CST cell bodies in the cortex; therefore, therapeutic strategies aimed at promoting axon regeneration of the CST in the spinal cord do not require a separate intervention to prevent retrograde degeneration of upper motoneurons in the cortex.

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“…Histological and imaging studies have shown massive shrinkage in the midbrain, pons, and pyramids after hemispheric lesions causing hemiparesis. 33,34 One patient, 14 examined more than 2 years after stroke, had a large cortical lesion with moderate motor deficit but no NAA loss from the capsule on the side of the lesion. Atrophy of the damaged motor pathways in this patient may have caused the volume originally occupied by the damaged pathways to be replaced by the surrounding normal tissue, resulting in no measured loss of NAA signal from the voxel.…”

Section: Discussionmentioning

confidence: 99%

Axonal Injury in the Internal Capsule Correlates With Motor Impairment After Stroke

Pendlebury

Blamire

Lee

et al. 1999

Stroke

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Background and Purpose-Magnetic resonance spectroscopy (MRS) in ischemic stroke has shown a correlation between N-acetylaspartate (NAA) loss from the infarcted region and disability. We tested the hypothesis that NAA loss in the descending motor pathways, measured at the level of the posterior limb of the internal capsule, would determine motor deficit after a cortical, subcortical, or striatocapsular stroke. Methods-Eighteen patients with first ischemic stroke causing a motor deficit were examined between 1 month and 5 years after stroke. T2-weighted imaging of the brain and localized proton (voxel, 1.5ϫ2ϫ2 cm 3 ) MRS from the posterior limb of each internal capsule were performed and correlated to a motor deficit score. Results-Mean internal capsule NAA was significantly lower in the patient group as a whole compared with the control group (PϽ0.001). Reductions in internal capsule NAA on the side of the lesion were seen in cases of cortical stroke in which there was no extension of the stroke into the voxel as well as in cases of striatocapsular stroke involving the voxel region. There was a strong relationship between reduction in capsule NAA and contralateral motor deficit (log curve, r 2 ϭ0.9, PϽ0.001). Conclusions-Axonal injury in the descending motor pathways at the level of the internal capsule correlated with motor deficit in patients after stroke. This was the case for strokes directly involving the internal capsule and for strokes in the motor cortex and subcortex in which there was presumed anterograde axonal injury. (Stroke. 1999;30:956-962.)

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The Pyramidal Tract

Cited by 18 publications

References 296 publications

Multimodal 3D atlas of the macaque monkey motor and premotor cortex

Multimodal 3D atlas of the macaque monkey motor and premotor cortex

Unexpected Survival of Neurons of Origin of the Pyramidal Tract after Spinal Cord Injury

Axonal Injury in the Internal Capsule Correlates With Motor Impairment After Stroke

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