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Absence of impairments or recovery mediated by the uncrossed pyramidal tract in the rat versus enduring deficits produced by the crossed pyramidal tract.

The pyramidal tract of the rat consists of at least two components. A majority of the fibers cross in the lower medulla and descend through the spinal cord in the ventral portion of the dorsal funiculus. The remaining 5% of the corticospinal projection does not cross and descends in the ipsilateral ventral funiculus into the cervical spinal region where its projections terminate in the internuncial portions of the spinal gray matter. The anatomical origin and terminal distribution of the ipsilateral component suggests that it may be involved in the control of the ipsilateral limb, but the possible contribution of the ipsilateral corticospinal tract has not been systematically examined. To determine whether the ipsilateral corticospinal tract makes a contribution to skilled movement, the corticospinal tract was severed unilaterally at the medullary level rostral to the decussation, thus severing both the crossed component of the tract as well as the ipsilateral component. Performance of the ipsilateral and the contralateral limbs of rats were then evaluated on tests of limb posture, preference, placing, and use in two skilled reaching tasks. No impairments on any quantitative or qualitative measure of performance were detected in the use of the limb ipsilateral to the lesion but severe, enduring impairments on all qualitative and quantitative measures were obtained in use of the limb contralateral to the lesion. Thus, the study finds: (1) no evidence that the ipsilateral portion of the corticospinal tract makes a contribution to skilled movement of the kind made by the contralateral portion of the corticospinal tract, and (2) no evidence that the remaining uncrossed portion of the tract contributes to recovery of symptoms produced by severing the crossed portion of the tract.

Animals↗

Subcortical topography and proportions of the pyramidal tract.

The pyramidal tract (PT) was dissected in 30 normal human hemispheres according to the method of Klingler. The various dimensions as well as the cerebral landmarks were studied. The pyramidal tract is built up like a fan in the white matter by a thin layer of fibers of 2.8-3.5 mm in thickness. The fibers converge toward the internal capsule to a solid fiber tract with a lateral and apdiameter of 7.8 +/- 1.6 mm and 17.5 +/- 2.1 mm, respectively. This configuration of the PT presents different possibilities of damage during surgery. The evaluation of the three-dimensional course of the PT is possible by using three cerebral landmarks, the precentral gyrus, the entrance into the internal capsule and the posterior limb of the internal capsule. Their topography is described. Additionally the pyramidal tract can be defined medially by the sulcus cinguli and the roof of the lateral ventricle and laterally by the superior sulcus circularis Insulae. The possible displacement of the PT by space occupying lesions and the intra-operative orientation is discussed.

Adult↗

[Development and maturation of the pyramidal tract].

The pyramidal tract contains axons that originate from neurons located in layer 5 of the neocortex of the frontal areas 4 and 6 and of the parietal lobe. These neurons are generated during the first half of gestation in humans. The growth of these axons is highly regulated and the mechanisms that control this growth begin to be unravelled. For example, netrins could serve as chemattractants, the adhesion molecule L1 plays a crucial role in the control of axonal decussation at the level of the medulla, the ephrin B3-Eph A4 couple prevents the axons from crossing the midline. During development, the total number of pyramidal axons increases progressively and then decreases by regression of exuberant collaterals. The pyramidal tract is the sole unmyelinated tract in the human spinal cord at birth. This accounts for the protracted central conduction time in newborns. This immaturity of the pyramidal system could explain the existence of specific motor reflexes in newborns (the so-called primary reflexes) that disappear as the pyramidal system matures.

Animals↗

Selective collateral elimination in early postnatal development restricts cortical distribution of rat pyramidal tract neurones.

The pyramidal tract, comprising those axons which pass from the neocortex to the medulla and spinal cord, is among the most thoroughly studied projections of the mammalian cortex. Recent studies using anterograde axon tracing techniques have provided information concerning the time course of the growth of pyramidal tract fibres, yet much remains to be learned about its development. We have now begun to study the distribution of the neurones of origin of the pyramidal tract during the postnatal development of the rat neocortex using the recently introduced retrogradely transported fluorescent marker, True blue. During the first postnatal week, injections of True blue into the pyramidal decussation result inthe labelling of pyramidal tract neurones which are distributed virtually throughout the tangential extent of layer V of the neocortex, whereas after comparable injections during the fourth postnatal week the distribution of such cells is much more restricted and remains restricted into adult life. This developmental restriction is most dramatic in the occipital cortex: during the first postnatal week many pyramidal tract neurones are found throughout the visual cortex while none is seen in this area of the adult. When True blue is injected into the pyramidal decussation during the first postnatal week and the animals are allowed to survive until the fourth postnatal week, the distribution of pyramidal tract neurones is as widespread as in the immediate postnatal period and includes the entire visual cortex. This implies that many of the neurones in the occipital cortex initially send a collateral into the pyramidal tract which is later eliminated, although the neurones themselves persist. These findings, together with similar recent observations on the development of the callosal connections, indicate that the elimination of axon collaterals may be a general feature of the development of cortical projection systems, and that such transitory collaterals may traverse considerable distances.

Animals↗

Pyramidal tract function and the clinical "pyramidal syndrome".

In this review, I wish to reconcile clinical usage of terminology and experimental concepts of pyramidal tract function. The traditional view, based essentially on neurological observations in stroke patients, was that this tract provides the structural basis of volitional movements. This concept is too simple and understanding of pyramidal tract function needs a considerably larger perspective. The view is discussed that the pyramidal tract is composed of subsystems with different cortical origin, fibre terminations and fibre sizes. The system shares its motor control function with other descending pathways and it also contributes to the phenomenon of descending control of sensory inflow. The pyramidal system plays a special role in the control of digital skill and speed of movements. However, there are also somewhat neglected observations that point to its function in postural control.

Adult↗

Responses of the pyramidal tract to stimulation of the baboon's motor cortex.

1. The arm area of the baboon's precentral motor cortex was stimulated by brief surface-anodal pulses, and the discharge of the corticospinal tract (the ;pyramidal tract waves') was recorded by an electrode resting on the dorsolateral surface of the cervical spinal cord.2. Some properties of the pyramidal tract waves were described, and they were also studied in relation to the firing of single cortico spinal fibres.3. The results led to the conclusion that the later pyramidal tract waves (the ;I waves') were almost exclusively due to a semi-synchronous repetitive discharge of the same fast cortico spinal fibres as those responsible for the initial wave (the ;D wave').4. Some problems concerning the origin and significance of the I waves were discussed.

Action Potentials↗

Functional role of regrowing pyramidal tract fibers.

When pyramidal tract axons are severed in the infant hamster, the damaged fibers regrow via a new pathway to their normal terminal sites in the medulla and spinal cord and there form synaptic connections (Kalil and Reh, '79, '82). We studied the behavior of animals with infant and adult lesions of the medullary pyramid to determine the functional significance of the new pathway in maintaining normal motor behavior. Examination of behaviors normally mediated by the pyramidal tract, particularly the manipulation of sunflower seeds during feeding, revealed a correlation between the presence of the new tract and the preservation of function. Furthermore, in the adult animal with an infant lesion, the spared behaviors were lost when the new pathway was destroyed.

Age Factors↗

Rostral wulst in passerine birds. I. Origin, course, and terminations of an avian pyramidal tract.

An avian "pyramidal tract" was defined in zebra finches and green finches by making injections of neuronal tracers into the hyperstriatum accessorium (HA) of the rostral Wulst. Extratelencephalic projections of rostral HA traveled in the septomesencephalic tract (TSM) and gave rise to nuclear-specific terminal fields in the precerebellar medial spiriform nucleus of the posterior thalamus, the red nucleus in the mesencephalon, the medial pontine nucleus in the pons, and the subtrigeminal, external cuneate, cuneate, gracile, and inferior olivary nuclei in the medulla. Extensive but more diffuse terminal fields were also present in the stratum cellulare externum of the posterior hypothalamus, the central periaqueductal gray, the prerubral field, and the lateral and ventrolateral tegmentum of the pons and medulla. There was also a sparse projection to the dorsal thalamic nucleus intermedius ventralis anterior, which supplies the somatosensory input to the rostral Wulst, and distinct projections to the intercollicular region surrounding the central nucleus of the inferior colliculus, where they partly overlapped the projections of the dorsal column nuclei. Projections from HA to the cerebellum via the TSM are described separately. In the brainstem the ventral ramus of TSM was situated ventral to the medial lemniscus at the base of the brain, entered the spinal cord in the inner margin of the lateral funiculus, predominantly ipsilaterally, and terminated bilaterally but predominantly contralaterally in the medial part of the base of the dorsal horn of the upper six or seven cervical segments. After injections of tracers into putative targets, numerous retrogradely labeled cells were found in the rostral HA, predominantly ventrally. The results confirm the presence of a major descending fiber system in passerine birds that resembles in its brainstem course and several of its terminations the pyramidal tract of mammals. The reciprocal projections of HA with the hypothalamus suggest that rostral HA may also incorporate neuronal components that in mammals would be considered parts of prefrontal cortex.

Animals↗

[Adrenoleukodystrophy with high signal intensity areas in bilateral pyramidal tracts from internal capsule through medullary pyramids on MRI].

We reported a case of adrenoleukodystrophy in which MRI showed high signal intensity areas in the pyramidal tracts from the internal capsule through the medullary pyramids. A 20-year-old man was admitted with complaints of slowly progressive spastic paraparesis of one and a half year duration. He had no mental deterioration, visual disturbance or sensory impairment. His maternal cousin died of adrenoleukodystrophy at the age of 13 years old, after showing progressive visual disturbance, dementia and quadriplegia. On admission, neurological examination revealed spastic tetraparesis and exaggerated deep tendon reflexes with pathological reflexes. Examination of the mental function and cranial nerves were normal. There were no sensory abnormalities in all modalities. Routine laboratory data including hematological studies, urinalysis, serum electrolytes and enzymes were all normal. Endocrinological examinations showed no adrenocortical insufficiency, and testicular function was normal. Cerebrospinal fluid, EEG, needle EMG and nerve conduction studies were also normal. CT scan showed a mild ventricular enlargement and no low density areas were seen in the cerebral white matter. Spin-echo MRI (SE 2,000/100, 2,000/40) revealed continuous high signal intensity areas in the pyramidal tracts from the internal capsule through medullary pyramids bilaterally. There were no abnormal findings in the spinal cord on MRI. Electrophysiologically, the brain-stem auditory evoked potentials (BAEPs) were abnormal and suggested the presence of bilateral dorsal brain stem lesions. Short latency somatosensory evoked potentials (SEPs) obtained by the bilateral tibial nerve stimulation revealed slowing of the central conduction time, showing delayed P37 latency and normal peripheral conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenoleukodystrophy↗

Feasibility study of single region lambda chart analysis for pyramidal tract physiology.

Diffusion characteristics of the pyramidal tract were assessed in nine patients who had clinical evidence of pyramidal tract dysfunction, utilizing lambda chart analysis (LCA). The underlying pathologic process of tract dysfunction was varied and included Pelizaeus-Merzbacher disease (PMD), Alexander disease, adrenoleukodystrophy (adrenomyeloneuropathy (AMD) type and cerebral type), amyotrophic lateral sclerosis (ALS), and Wallerian degeneration (WD). While pyramidal tract diffusion characteristics in WD indicated a pathological process characterized by replacement of normal fibers by smaller cellular component such as degenerated small fibers and/or gliosis, pyramidal tract diffusion characteristics in patients with PMD, Alexander disease, and adreno leukodystrophy of the cerebral type indicated a pathological process characterized by replacement of normal fibers by larger cellular components such as spheroids or edematous space. Pyramidal tract diffusion characteristics of patients with ALS or adrenoleukodystrophy of AMD type were relatively intact suggesting a pathological process characterized by relatively preserved structural architecture. These findings are highly consistent with known pathophysiological indices and indicate the feasibility of the clinical utility of LCA for assessing pyramidal tract physiology.

Adolescent↗

Retrograde cortical aand axonal changes following lesions of the pyramidal tract.

Following lesions of the pyramidal tract in hamsters, retrograde changes were studied in the sensorimotor cortex and in the pyramidal tract axons proximal to the lesion, at survival times ranging from 2 weeks to 14 months. Severe cell shrinkage occurred in layer 5 pyramidal neurons as early as 2 weeks, but there was no cell loss among these neurons even with long survival times. Use of the Fink-Heimer method for degenerating axons revealed that the pyramidal tract proximal to the lesion had undergone a retrograde axon degeneration which, in some respects, resembled anterograde degeneration. The retrograde axon degeneration began at the lesion site and advanced slowly rostralwards with time involving increasingly greater numbers of fibers. However, even at the longest survival times the degeneration fell off markedly at pontine levels. The results indicate that this process represents a true retrograde fiber degeneration (as opposed to an indirect Wallerian degeneration) which appears to reach a point of equilibrium such that a partially shrunken pyramidal cell is maintaining a partially degenerated axon.

Animals↗