Lateral Corticospinal Tract


Using a preparation method composed of secondary chromic acid fixation, nitrocellulose embedding and Luxol fast blue-PAS-hematoxylin stain (a discriminative staining method) for the purpose of axonal discrimination, we examined 43 human spinal cords (31 males and 12 females) at the C5 level to find the differences due to gender and aging in axons of the lateral corticospinal tract.  

After 10 days, the MRI lesion became clear; it involved the left lateral spinothalamic tract and the lateral corticospinal tract; however, her muscle strength and deep tendon reflexes were normal.  

Furthermore, L-DOPA-induced PAG608 expression on motor neurons in the contralateral side of the ventral horn of the spinal cord and the lateral corticospinal tract without cell loss.  

Immunohistological studies showed profound CD68 immunoreactivity in the lesion area and the contralateral lateral corticospinal tract in the spinal cord at all time points, demonstrating that microglia/macrophage remain reactive at the sites of injury and axonal degeneration/survival for at least 12 months.  

These include the ipsilateral motor pathway from the unaffected motor cortex to the affected hand, peri-lesional reorganization, the recovery of a damaged lateral corticospinal tract, and contribution of the secondary motor area.  

Myelin pallor of the lateral corticospinal tract was observed in two of the 10 cases.  

Intensely gamma1 laminin-positive, aggressive-looking reactive astrocytes of the lateral columns of both cervical and thoracic spinal cord surround the lateral ventral horns and roots and extend into the area of the lateral corticospinal tract.  

Furthermore, the anterior horn cells and lateral corticospinal tract are located in the highly vulnerable region of spinal cord, either possibly due to venous engorgement or arterial insufficiency..  

To investigate the functional organization in the lateral corticospinal tract (LCST), the cervical white matter was stimulated with multiple penetrations in the mediolateral direction at the C5/C6 and C6/C7 segmental borders in cats.  

The lateral corticospinal tract is the major motor pathway in humans. In the present study, we undertook to demonstrate that some stroke patients can walk despite complete lateral corticospinal tract injury. Ten stroke patients who were able to walk with evidence of complete unilateral lateral corticospinal tract injury, as determined by clinical course, brain magnetic resonance imaging, and diffusion tensor tractography, were recruited. We conclude that some stroke patients can walk despite complete lateral corticospinal tract injury of the affected hemisphere..  

Six adult monkeys (Macaca mulatta) received a unilateral lesion of the lateral corticospinal tract (CST) in the thoracic spinal cord.  

Myelinated axons in the human lateral corticospinal tract (LCST) at the C6 and L4 levels were examined on 16 male cadavers, with age ranging from 41 to 88 years.  

Electrophysiological recordings revealed lack of the direct lateral corticospinal tract (LCST) volley, monosynaptic extracellular field potentials in the motor nuclei, and monosynaptic CM excitation.  

The core neuropathology of HSP is distal degeneration of the lateral corticospinal tract and of fasciculus gracilis, but there are few neuropathological studies of cases with a defined mutation.  

Neuropathologic examination revealed anterior horn cell loss and lateral corticospinal tract degeneration in spinal cord, with marked muscular atrophy.  

In this case, we suppose that the mechanism of spinal cord injury was due to direct injury by a knife avoiding the lateral corticospinal tract because his right hemiparesis obviously improved..  

Axons in the lateral corticospinal tract (LCST) were analyzed morphometrically on 37 cadavers (24 males and 13 females).  

The use of somatosensory evoked potentials (SEP) began at late 70's, as a method to monitorize spinal cord function during surgery; years later, motor evoked potentials (MEP) joined this option, giving us direct information about the functioning of posterior spinothalamic tract (posterior column) and lateral corticospinal tract (pyramidal tract), respectively.  

RESULTS: beta2 adrenergic receptors were visualized on astrocytes in white matter of controls, and they were prominently expressed in reactive astrocytes at the boundary of cerebral infarctions and in the lateral corticospinal tract in ALS.  

Concerning the regional concentrations of CNTF, in homozygotes, CNTF contents in the lateral corticospinal tract were markedly lower (p < 0.001) in ALS patients than in controls. The decrease in CNTF expression in the lateral corticospinal tract of the spinal cord from ALS patients may be a feature of ALS and could be related to motor neuron loss..  

We performed quantitative amino acid analyses in the posterior funiculus, the lateral corticospinal tract, and the anterior horn of cervical enlargement of the spinal cord from seven ALS patients, and the results were compared with those of seven patients with other neurologic diseases (control A) and seven patients without neurologic diseases (control B). The levels of collagen-associated amino acids, hydroxyproline, proline, glycine, and hydroxylysine, were markedly lower in the lateral corticospinal tract and the anterior horn of ALS patients than in controls A and B. The contents of the acidic amino acids glutamate and aspartate were also significantly decreased in the lateral corticospinal tract and the anterior horn of ALS patients as compared with those of controls A and B.  

High signal in the anterolateral column of the spinal cord on T1 weighted images was seen in 14, and high signal in the lateral corticospinal tract on T2 weighted images was seen in 7 of the 21 patients.  

Six cases of middle cerebral artery occlusion are presented in which the cellular changes accompanying descending degeneration of the lateral corticospinal tract were studied at different time points (5 days-10 years) following the insult.  

Morphometric analyses were carried out to reveal a relation between age and axonal changes in the lateral corticospinal tract (LCST) at the L1 level of the human spinal cord.  

These results suggest that lateral corticospinal tract descending dorsolateral fasciculus in the spinal cord is main corticospinal pathway and spatial distribution of D and I-waves are similar in the human cervical cord..  

The responses of 175 identified corticospinal axons (conduction velocities of 24-95 m/s) were recorded from the lateral corticospinal tract at the T12-L3 spinal level.  

Increased signal intensity areas were present in the lateral corticospinal tract of the brain and cervical spinal cord on a T2-weighted image.  

T2 weighted MRI demonstrated high signal intensity of the lateral corticospinal tract of the spinal cord in two, high signal intensity of the intracranial corticospinal tract in five, and low signal intensity of the motor cortex in six of the 14 patients.  

The myelinated fiber density of the lateral corticospinal tracts at the T7 cord level was well preserved for both large and small myelinated fibers.  

It follows that fibres from the brainstem that enter the cord in the anterior column may be in the lateral column anterior to the lateral corticospinal tract at lower levels. Reticulospinal fibres within the lateral column lie anterior to the lateral corticospinal tract. In addition, they are present in a more compact group, forming a triangle on transverse section on the periphery of the lateral column, immediately anterior to the lateral corticospinal tract.  

Small myelinated fibers in the lateral corticospinal tract (LCST) were selectively diminished as compared with large myelinated fibers in a patient with an old paramedian midbrain infarct involving the red nuclei, oculomotor nuclei, and inferior olivary pseudohypertrophy.  

In 9 patients, areas of high signal intensity located in the dorsolateral columns coinciding with the lateral corticospinal tracts, were detected on axial T2*-weighted MR imaging of the cervical spinal cord using a gradient echo technique. In two patients, these spinal cord MR abnormalities corresponded well to the postmortem pathological findings of lateral corticospinal tract degeneration.  

We carried out a morphometric study on the myelinated fibers in the anterolateral funiculus (ALF) and lateral corticospinal tract (LCS) in the cervical segment of the spinal cord of 13 patients with classic amyotrophic lateral sclerosis (ALS), 6 of whom had been on a respirator; 5 age-matched subjects were used as controls.  

In addition, lesions were found throughout the spinal cord; degenerative changes were found in the lateral corticospinal tract, posterior colum (especially the fasciculus gracilis), and anterior and posterior spinocerebellar tracts.  

Magnetic resonance imaging by gradient echo method demonstrated lesions of the lateral corticospinal tract at cervical cord levels in three ALS patients.  

A large unilateral lesion dividing most of the lateral corticospinal tract, and the descending fibres anterior to it, caused flaccid paralysis of the ipsilateral lower limb. An incision in the thoracic cord cutting through one lateral corticospinal tract and 85-90% of the opposite tract and reticulospinal fibres anterior to that tract caused total paralysis of the lower limbs. Recovery of some flexor and extensor movements of the ipsilateral fingers and toes occurred within 6 h of an incision being made in the upper cervical cord that divided the lateral corticospinal tract unilaterally. Division of only the anterior fibres of the lateral corticospinal tract above the cervical enlargement did not affect the motility of the ipsilateral upper limb. Correlation of the clinical with the histological evidence of a lesion of the lateral corticospinal tract was carried out. The Babinski response was found, in general, to occur with lesions of the lateral corticospinal tract and not with lesions elsewhere in the cord.(ABSTRACT TRUNCATED AT 400 WORDS).  

This selective distribution pattern of immunoreactivity of alpha- and beta-antibodies in the rat was also present in the monkey spinal cord, although the alpha-immunopositive corticospinal tract fibers in the monkey descended in the lateral funiculus as the lateral corticospinal tract instead of passing through the dorsal funiculus, as is the case in the rat.  

A quantitative analysis was made of the myelinated fibers in the lateral corticospinal tract (LCST) at the levels of the 6th cervical, 7th thoracic and 4th lumbar spinal segments in 20 patients between 19 and 90 years old, and who died of non-neurological diseases.  

These results suggest that N4 of the MEPs-S originates from the sensorimotor cortex and conducts in the lateral corticospinal tract.  

The myelinated fibers in the lateral corticospinal tract at the C6, T7, L4 levels in amyotrophic lateral sclerosis (ALS) and control cases were morphometrically examined.  

The pattern of fibre degeneration in the lateral corticospinal tract (LCST) was studied in a case of Friedreich's ataxia (FA).  

A large band of horseradish peroxidase (HRP) positive fibers was found crossing at the pyramidal decussation to reach the contra-lateral corticospinal tract and the deeper part of the funiculus, in the cervical cord. However, a small band of HRP positive fibers was noticed to reach the ipsilateral corticospinal tract without crossing at the pyramidal decussation.  

The population of myelinated fibers in the lateral corticospinal tract at the thoracic segment, and in the fourth ventral roots, and motor neurons in the fourth ventral horns were morphometrically quantified. Fiber size profile of the myelinated fibers in the lateral corticospinal tracts at T7 segments and L4 lumbar ventral roots were estimated on the epon-embedded transverse sections as previously described (Sobue et al, 1981). The large myelinated fibers in the lateral corticospinal tract were extensively and predominantly depleted in all three cases.  

Recordings were made from within the lateral corticospinal tract, either from axonal populations or with a microelectrode from individual axons.  

The following features of the lateral corticospinal tract are emphasized in the cervical cord: (1) the large extent of the white matter of the cord covered by the tract, and the anterior extent of the tract, the border being anterior to the central canal; (2) in the lower cervical cord, the separation of fibres from the main mass of the tract, which reach the periphery of the cord in the anterolateral sector; (3) the presence in many cords of the ventral crossed bundle; and (4) the relationship of the denticulate ligament to the tracts in the cervical segments.  

The neurological deficit was revealed on neurophysiological, neuroradiological and in 2 cases on neuropathological tests (gross demyelinisation of the posterior column, mainly of the fasciculus gracilis, less in the lateral corticospinal tract and in some spinal roots).  

At autopsy there was old necrosis of most of the gray matter in the middle thoracic segment of the spinal cord and severe hypotrophy of the posterior columns in the lumbar spinal cord, of the posterior and anterior spinocerebellar tracts, and of the lateral corticospinal tract, unilaterally, in the entire thoracolumbar spinal cord from the middle thoracic segment on.  

Displaced neurons were most numerous in the ventral outflow and lateral corticospinal tract regions of all cord levels.  

Glial cells in the lateral corticospinal tract were classified and quantified directly on the electron microscope. This study shows that the population of immature glial cell precursors, abundant at birth in the lateral corticospinal tract, appear to be differentiating primarily into oligodendroglia, because this population exhibits a rapid increase in size, and relatively little change occurs in the astrocyte population.  

As a lesion of the upper motor neuron, the degree of lateral corticospinal tract degeneration in the spinal cord were classified into 4 groups. Total fascicular area (TFA), total myelinated fibers (TF) and large fibers (LF) of the ventral roots were significantly (p less than 0.001) decreased in CVD patients who revealed severe degeneration in the lateral corticospinal tracts in affected sides compared with those of controls. The apparent unilateral fiber loss in the ventral root was also observed in some cases whose lateral corticospinal tracts were degenerated with ipsilateral predominance. Therefore, the degree of degeneration of the lateral corticospinal tracts seemed to parallel that of fiber loss of the ventral roots. These findings suggest a trans-synaptic effect of the degenerated upper motor neuron (lateral corticospinal tract) in CVD patients facilitating fiber loss in the ventral roots..  

Some labeled axons from the damaged pyramidal tract crossed the midline, descended with fibers in the intact pyramidal tract through the pyramidal decussation, and entered the lateral corticospinal tract.  

The pyramidal and lateral corticospinal tract response in monkey or cat to a surface stimulus applied to area 4 is a direct (D) wave conducted in fast axons followed by several indirect (I) waves with a period of greater than 1 ms.  

Neurological and symptomatic considerations are discussed in relation to the topographical anatomy of the lateral corticospinal tract..  

However, well-myelinated fibres were scattered above the pyramidal decussation and they were also present below the decussation in both the anterior and the lateral corticospinal tract.  

some contralateral lateral corticospinal tract fibers apparently recross to end in the ipsilateral Onuf's nucleus..  

Autoradiographs revealed a strong contralateral lateral corticospinal tract.  

The organization of the corticospinal system has been studies, in the cat, using electrophysiological techniques (stimulation of the lateral corticospinal tract at different spinal levels, recording in the contralateral cortex by means of transcortical bipolar electrodes) and anatomical techniques (HRP injection localized in the grey matter of a chosen spinal level).  

70% of the slow and 82% of the fast PT neurons within this cortical area were found to send their axons into the contralateral, lateral corticospinal tract.  

According to its clinical symptoms and pathomorphological substrate of this main neurological syndrome (peculiar lower spastic paraparesis as a result of systemic ascending degeneration of lateral corticospinal tract of spinal cord), VE belongs to hereditary heterogenous group of diseases which are referred to Strümpell's spastic paraplegia.  

Myelinated fibres were found in the dorsal, ventral and peripheral lateral tracts, while the lateral corticospinal tract was completely unmyelinated.  

The tract is composed of thick and thin fibers, extends the length of the cord in the lateral funiculus, and is located ventral and ventrolateral to the lateral corticospinal tract and medial to the dorsal spincerebellar tract.  


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