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PubMed1994

[Effect of pyramidal tract stimulation on segmental spinal cord potentials].

The author reports his results of the effect of pyramidal tract stimulation on the segmental spinal cord potentials (seg-SCP) using a total of 50 Wistar rats. Forty two Wistar rats were used to observe the effects of a pyramidal tract stimulation on the seg-SCP evoked by hindpaw stimulation. Another 5 Wistar rats were used to observe dorsal column stimulation as the conditioning stimuli instead of pyramidal tract stimulation. And the other 3 Wistar rats were used for both pyramidal tract and dorsal column stimulation as a separate trial. The seg-SCP of the rats consisted of three major peaks, P1, N1 and P2. P2 was separated into a first (P2F) and second component (P2S). The P2F peak was constantly preceded by a small notch, considered to be the onset of P2F, and named the P2F initial peak. The P2F peak amplitude of the seg-SCP was significantly decreased by pyramidal tract stimulation, while the P2F initial peak amplitude remained unchanged. This effect persisted until the concentration of sevoflurane was reduced to below 1.5% or until the peak arterial blood pressure was decreased to below 80 mmHg. The amplitude of both the P2F initial peak and the P2F peak were decreased significantly by dorsal column stimulation. These findings indicated that inhibition of the P2F peak amplitude was a characteristic effect of the pyramidal tract stimulation on the seg-SCP, while inhibition of the overall P2F amplitude was characteristic of the dorsal column stimulation.

Animals↗

PubMed1982

A reanalysis of the ventrolateral input in slow and fast pyramidal tract neurons of the cat motor cortex.

In deeply anesthetized cats the temporal characteristics of ventro-lateral (thalamic) excitatory postsynaptic potentials (EPSPs) induced in pyramidal tract cells were studied with an averaging technique. Stimulation of the ventrolateral thalamus induced EPSPs in all pyramidal tract neurons at latencies of 1-5 ms. It was found that there was a positive relationship between the latency and rise time of stimulation-induced EPSPs and the latency of antidromic invasions of pyramidal tract neurons. In response to two closely spaced shocks the second EPSP had the same latency and amplitude as the first one in both slow and fast pyramidal tract neurons. Moreover, the span of antidromic latencies of ventrolateral thalamic relay cells to motor cortex stimulation showed that these thalamic neurons had the necessary conduction velocities to account for the distribution EPSP latencies recorded in pyramidal tract neurons. From these electrophysiological results, it has been concluded that slow and fast pyramidal tract morphological evidence, obtained at the electron-microscopic level, supporting this conclusion. Terminal degeneration induced by a lesion in the ventrolateral thalamus was found on the apical dendrite of a slow pyramidal tract neurons that had been injected with horseradish peroxidase. It is proposed that the matching between the latencies of EPSPs evoked from the ventrolateral thalamus and the latencies of antidromic invasions of pyramidal tract neurons may reflect a matching between the conduction velocity of thalamocortical and cortico-spinal neurons and/or it may be due to the electrotonic properties of the apical dendrites.

Animals↗

PubMed1994

Very early demonstration of secondary pyramidal tract degeneration by computed tomography.

BACKGROUND: While magnetic resonance imaging has revealed progressive changes in the pyramidal tract in accordance with histopathologic stages of wallerian degeneration secondary to a supratentorial lesion, computed tomography (CT) has only demonstrated a shrinkage of the pyramidal tract in the midbrain or pons during the chronic stage. We present a patient with frontoparietal subcortical hemorrhage in whom serial CT scans clearly demonstrated wallerian degeneration along the axis of the pyramidal tract early in the acute stage. CASE DESCRIPTION: A 63-year-old man with a history of hypertension suddenly developed a deterioration of consciousness, transcortical mixed aphasia, and dense hemiplegia on the right side. CT scans revealed a massive intracerebral hematoma in the frontoparietal subcortices of the left hemisphere. Although initial CT did not detect any hypodense areas along the left pyramidal tract below the hematoma, ill-defined areas of decreased density appeared in the posterior limb of the internal capsule, cerebral peduncle of the midbrain, and pontine base of the left side on day 13 after the stroke. These areas became well demarcated on day 22 and persisted thereafter. CONCLUSIONS: An extensive hematoma can interrupt the pyramidal tract fibers that arise not only from the motor cortex and caudal premotor cortex but also from the somatosensory and parietal cortices, allowing very early CT demonstration of wallerian degeneration of the pyramidal tract.

Cerebral Hemorrhage↗

PubMed1991

Effects of infant versus adult pyramidal tract lesions on locomotor behavior in hamsters.

The role of the pyramidal tract in locomotion was studied in hamsters by analyzing their locomotor behavior after lesions of the medullary pyramidal tract. Animals with lesions either as adults or as infants were compared to determine whether early pyramidotomy results in greater functional recovery. Normal and pyramidotomized animals were filmed during locomotion on a runway consisting of either smooth or rough terrain to assess whether the uneven surface would accentuate locomotor deficits. Frame-by-frame analysis of the filmed behavior during all phases of the step cycle was carried out to determine positions of the joints of the forelimb and hindlimb during locomotion. Accuracy of limb placement on the rough terrain was determined by observations of consecutive step cycles. The results show that lesions of the pyramidal tract in both infant and adult hamsters affect locomotion first by causing a reduction in the yielding phase of the step cycle and second by producing inaccuracies of forelimb placement. Rough terrain accentuates deficits in forelimb placement during locomotion. Animals with lesions as infants and those with lesions as adults show surprisingly similar deficits in locomotion, with the exception that animals with lesions as infants show some behavioral compensation in hindlimb movement by developing a normal degree of yielding at the knee. In contrast, hamsters with lesions as either adults or infants never recover normal forelimb behavior in either yielding at the elbow or accuracy of forelimb placement. These results emphasize the sensorimotor role of the pyramidal tract, even in a relatively stereotyped behavior such as locomotion.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMedDate not supplied

Evoked responses of pyramidal tract neurons to stimulation of the lateral hypothalamus.

The evoked responses of identified pyramidal tract neurons of the pericruciate region of the cortex arising on stimulation of the posterior, tuberal, and anterior sections of the lateral hypothalamus were investigated in acute experiments on cats anesthetized with chloralose. THe pyramidal tract neurons recorded were situated at a depth of 0.75-2.5 mm and on stimulation of the hypothalamus discharged with a latent period of 1.6-52.5 msec. They discharged most efficiently in the case of stimulation of the caudal half of the lateral hypothalamus. The pyramidal tract neurons activated by the hypothalamus were also tested by electrocutaneous stimulation of the four limbs. Of the neurons 75% responded to stimulation of several limbs, i.e., they had a broad bilateral receptive field, while 15% reacted to stimulation of one contralateral limb (either the anterior limb or the posterior limb), i.e., they had a small contralateral receptive field. Comparison of the latent periods of the anti- and orthodromic responses of the pyramidal tract neurons did not reveal any relationship between the magnitude of the latent period of the orthodromic response (on hypothalamic or electrocutaneous stimulation) and the type of pyramidal tract neuron (according to the axonal transmission velocity). No relationship between the latent period of hypothalamic stimulation and the magnitude of the latent period of the response to a peripheral stimulus was detected either.

Animals↗

PubMed1993

The pyramidal tract of the hedgehog (Erinaceus europaeus) and its relationship with the olfactory bulb.

The pyramidal tract of the hedgehog has been investigated. The motor cerebral cortex was first located electrophysiologically and subsequently ablated. Ablation of the motor cortex did not apparently cause motor deficits. The cerebral hemisphere of the operated side, brain stem and spinal cord were removed for histological examination. The Nauta-Gygax and the horseradish peroxidase methods were employed to study the course and origin of the above mentioned tract. The pyramidal tract runs ipsilaterally in the cerebral peduncle, and does not go beyond the first cervical segments of the spinal cord (C3-C4); moreover, their fibers do not cross at spinal level. The close relation between this anatomical pathway and the olfactory bulb of the same side is also reported.

Animals↗

PubMed2003

DTI-based three-dimensional tractography detects differences in the pyramidal tracts of infants and children with congenital hemiparesis.

PURPOSE: To test the hypothesis that there is greater asymmetry in diffusion properties between right and left pyramidal tracts in patients with congenital hemiparesis than in patients with normal motor function. MATERIALS AND METHODS: Four congenitally hemiparetic patients and four age-matched controls underwent magnetic resonance diffusion tensor imaging (DTI)-based three-dimensional tractography of the pyramidal tracts. Relative anisotropy, individual eigenvalues, and directionally averaged apparent diffusion coefficient were measured and degree of asymmetry was calculated. RESULTS: Compared with age-matched controls, congenitally hemiparetic patients had greater asymmetry in all measured diffusion properties. The asymmetry was characterized primarily by lower anisotropy, lower parallel diffusion, higher transverse diffusion, and slightly higher mean diffusivity in the pyramidal tract contralateral to the hemiparesis (i.e., affected pyramidal tract) compared with the unaffected pyramidal tract. CONCLUSIONS: There appears to be greater diffusion asymmetry between the pyramidal tracts in congenitally hemiparetic patients compared to controls. These differences suggest that there are alterations in the microstructure of the pyramidal tract that controls the motor function of the hemiparetic side. Our results suggest that DTI-based three-dimensional tractography is potentially useful in the assessment of motor dysfunction in infants and children with congenital hemiparesis.

Anisotropy↗

PubMed1985

Neuronal chromatin changes in layer V pyramidal cells of somatomotor cortex after pyramidal tract lesions as demonstrated by [3H]actinomycin D binding.

Changes in chromatin structure of pyramidal tract neurons after medullary pyramidal tract lesions were examined autoradiographically utilizing [3H]actinomycin D (Act D) binding to nuclei in frozen sections of brain. After a right pyramidal tract lesion, the binding of Act D to nuclei of axotomized pyramidal neurons of somatomotor cortex layer V increased sharply at 1 and 5 days postoperation, compared with pyramidal cells of the left side or hippocampal control cells of the left hemisphere. At 3, 7, 9, and 11 days the axotomized cells showed significantly decreased binding compared with controls. The unoperated pyramidal cells showed a significantly decreased Act D binding at 2 h and 9 days postoperation compared with the ipsilateral hippocampal control cells. The data suggested that intrinsic neurons of the central nervous system had a response pattern of chromatin changes to axotomy that was basically similar to that of peripheral neurons (sensory ganglion cells). However, the response was compressed into the 1st week postoperation with only a brief reaction which might be correlated to axonal regeneration. This reaction was followed by a prolonged depression of Act D nuclear binding which may be associated with cellular atrophy.

Analysis of Variance↗

PubMed1999

Imaging the pyramidal tract in patients with brain tumors.

The clinical usefulness of diffusion-weighted magnetic resonance imaging (DWI) of the pyramidal tract was evaluated in patients with brain tumors. Five normal volunteers and seven patients with glioma (n = 4) or meningioma (n = 3) near the pyramidal tract underwent coronal echo planar DWI. Greyscale DWIs in each of the three orthogonal diffusion gradients were transformed into graduations, color-coded as red, green or blue, respectively, and then composited to form a combined color image. The entire pyramidal tract was visualized on a single fiber mapping image by combining the upper half of the image slice including the primary motor cortex, the corona radiata and the internal capsule with the lower half of the image slice including the internal capsule, the cerebral peduncle and the ventral brain stem. Fiber mapping images demonstrated the pyramidal tract as a distinct band indicating nerve fiber integrity in all volunteers. The entire pyramidal tract from the primary motor subcortex to the ventral brain stem could be traced. Fiber mapping images showed the ipsilateral pyramidal tract as either discontinuous due to impaired anisotropy or compressed due to mass effect in patients with brain tumors. These findings corresponded well with the pre- and postoperative motor functions. Fiber mapping images are useful for evaluating the white matter neuronal tracts and can provide indications for determining surgical strategy.

Adult↗

PubMed1990

Immunoelectron microscopic localization of cell adhesion molecule L1 in developing rat pyramidal tract.

The glycoprotein L1 is a cell adhesion molecule that has been proposed to function in the peripheral nervous system in axon fasciculation and onset of myelination. In this report we localize L1 during the development of a major central pathway: the pyramidal tract. The (sub)cellular localization of L1 was determined both by pre-embedding staining on Vibratome sections and by immunogold labelling on ultracryosections in developing rat pyramidal tract at the fifth cervical segment. On arrival at the fifth cervical segment, i.e. at postnatal day 1, growth cones of pioneer fibres did not exhibit L1-immunoreactivity. In the contact zone between pyramidal tract growth cones and glial processes no L1-immunoreactivity was observed. A clear L1-immunoreactivity was noted on small unmyelinated other axons situated in the entrance area of the pyramidal tract growth cones. Also on later arriving, i.e. between postnatal days 2 and 10, small unmyelinated fasciculating pyramidal tract axons L1 were present. It is our impression that L1 is localized in an irregular patchy way on the outer side of the axonal membrane. During the onset of myelination, i.e. between postnatal days 10 and 14, L1 could not be detected on axons ensheathed by oligodendrocytic processes. When myelination is largely completed, i.e. at postnatal day 21, the L1 antigen could be localized within the axoplasma of both unmyelinated and myelinated pyramidal tract axons. Furthermore, L1 could be observed occasionally on small unmyelinated pyramidal tract axons. Whereas compact myelin was always L1-negative, L1 was noted periaxonally between the axolemma and compact myelin and at (para)nodal regions at the contact zone between axolemma and oligodendrocytic processes. From these results it may be deduced that: (1) L1 is involved in fasciculation of outgrowing later arriving pyramidal tract fibres: (2) L1 is not involved in the onset of myelination in this central tract; (3) L1 might play an additional adhesive role in myelinated rat pyramidal tract.

Aging↗

PubMed1994

Effects of prenatal exposure to ethanol on the number of axons in the pyramidal tract of the rat.

We examined the effect of gestational ethanol exposure on the number of axons in the caudal pyramidal tract. Between gestational day (G) 6 and G21, inclusive, pregnant rats were fed a liquid ethanol-containing diet (Et), an isocaloric liquid control diet (Ct), or a diet of chow and water (Ch). On postnatal day 30, the offspring of these rats were killed and their caudal medullas were processed for electron microscopy. The overall size of the pyramidal tract and the space occupied by the axons was smaller in the Et-treated rats than in the Ct-treated rats. The myelinated axons were smaller and the myelin was thinner in the Et-treated rats than in the Ct-treated rats. These decreases produced an ethanol-induced increase in the density of axons in the pyramidal tract. In particular, the density of myelinated axons (but not nonmyelinated axons) was greater in Et-treated rats. The net result was that the estimated number of axons in the pyramidal tracts of the Et-treated rats was not significantly different than the number in the Ch- and Ct-treated rats. The present data demonstrate that ethanol does not affect the absolute number of axons in the pyramidal tract. As a result of the ethanol-induced microencephaly, however, the data translate into a relative increase in the number of pyramidal tract axons. This relative increase matches the ethanol-induced increase in the density of corticospinal projection neurons that may result from the retention of a developmentally exuberant projection.

Animals↗

PubMedDate not supplied

[Absence of pyramidal signs in pyramidal tract postischemic Wallerian degeneration].

INTRODUCTION: Wallerian degeneration (WD) is the irreversible axonal and myelin damage after the injury to the proximal portion of the axon or its cell body. The most frequent cause of WD in the central nervous system is ischemic stroke. Various studies have related the presence of pyramidal tract WD with the severity of motor deficit and partial motor improves. We present a patient with pyramidal tract WD without motor sequelae. CLINICAL CASE: A 55 years old man, hypertense and heavy smoker, suffered a sudden episode of dysarthria and left hemiparesis. Routine analysis showed hypercholesterolemia and an aortic valvular sclerosis on an echocardiogram. Cranial magnetic resonance imaging (MRI) showed multiple supratentorial lacunar infarctions. He was discharged without deficits, antiaggregated with aspirin. Six months later, he suffered a sudden episode of dysarthria. A new cranial MRI disclosed WD of the right pyramidal tract without pyramidal signs on neurologic exam. CONCLUSIONS: Presence of WD on the pyramidal tract is related with pyramidal disability in diverse degree but can develop a complete motor rehabilitation. We present a case of WD of the pyramidal tract without pyramidal deficits that supports the role of supplementary motor areas on motor rehabilitation.

Brain Ischemia↗

PubMed1985

Occipital cortical neurons with transient pyramidal tract axons extend and maintain collaterals to subcortical but not intracortical targets.

During the early postnatal development of the rat large numbers of pyramidal tract neurons are present in layer V of the occipital cortex, but by the end of the third postnatal week the distribution of pyramidal tract neurons becomes restricted to the more rostral cortical areas. This restriction is brought about by selective collateral elimination rather than by cell death. We have found, by using retrogradely transported fluorescent dyes as either short-term or long-term markers, that occipital cortical neurons which had transiently extended pyramidal tract axons maintain subcortical axonal connections to either the superior colliculus or the pons, and, at least in the case of the corticotectal projection, that the maintained collateral is present prior to the elimination of the transient pyramidal tract collateral. Further, it appears that at no time during postnatal development do the occipital pyramidal tract neurons form either callosal or ipsilateral cortico-cortical collaterals. Thus in the early postnatal occipital cortex the neurons which project through the pyramidal tract constitute a population of cells which is separate from neurons which make cortico-cortical connections, but which largely overlaps with the population of corticotectal and corticopontine neurons.

Amidines↗

PubMed2004

Development and malformations of the human pyramidal tract.

The corticospinal tract develops over a rather long period of time, during which malformations involving this main central motor pathway may occur. In rodents, the spinal outgrowth of the corticospinal tract occurs entirely postnatally, but in primates largely prenatally. In mice, an increasing number of genes have been found to play a role during the development of the pyramidal tract. In experimentally studied mammals, initially a much larger part of the cerebral cortex sends axons to the spinal cord, and the site of termination of corticospinal fibers in the spinal grey matter is much more extensive than in adult animals. Selective elimination of the transient corticospinal projections yields the mature projections functionally appropriate for the pyramidal tract. Direct corticomotoneuronal projections arise as the latest components of the corticospinal system. The subsequent myelination of the pyramidal tract is a slow process, taking place over a considerable period of time. Available data suggest that in man the pyramidal tract develops in a similar way. Several variations in the funicular trajectory of the human pyramidal tract have been described in otherwise normally developed cases, the most obvious being those with uncrossed pyramidal tracts. A survey of the neuropathological and clinical literature, illustrated with autopsy cases, reveals that the pyramidal tract may be involved in a large number of developmental disorders. Most of these malformations form part of a broad spectrum, ranging from disorders of patterning, neurogenesis and neuronal migration of the cerebral cortex to hypoxic-ischemic injury of the white matter. In some cases, pyramidal tract malformations may be due to abnormal axon guidance mechanisms. The molecular nature of such disorders is only beginning to be revealed.

Animals↗

PubMed1984

[The pyramidal tract. Recent anatomic and physiologic findings].

The cortical origin of the pyramidal tract is first considered. Contributions of retrograde degeneration studies as well as fiber counting method following different cortical lesions are presented and discussed. The results of these classical neuro-anatomical methods are compared with those of the more recent retrograde transport tracing method. The number and the diameter spectrum of pyramidal tract fibers differ in various mammals. In more evolved species the number of pyramidal fibers increase and their diameter span becomes wider. The thickest fibers are found in man. Along their diencephalic, mesencephalic, pontine and medullary course, axonal collaterals of corticospinal axons may terminate onto cells of origin of other descending pathways, onto relay cells of ascending pathways, and onto neurons projecting to the cerebellum. At the spinal level, the rostrocaudal extent and the termination area of corticospinal fibers may differ in various mammals. In a first group of mammals, the corticospinal fibers extend only to cervical or mid-thoracic segments and terminate in the dorsal horn. In a second group of mammals, the corticospinal fibers extend throughout the spinal cord and terminate in the dorsal horn and the intermediate zone. In a third group of mammals, the corticospinal fibers extend throughout the spinal cord and terminate in the dorsal horn, the intermediate zone and the dorsolateral part of the lateral motoneuronal cell group. In a fourth group of mammals, the corticospinal fibers also extend throughout the spinal cord and terminate in the dorsal horn, the intermediate zone and the dorsolateral as well as the ventral parts of the lateral motoneuronal cell group. A comparison is made between these different types of spinal terminations and the motor capacities of these different species. The motor deficits observed after pyramidal lesions are summarized and a comparison is made between the corticospinal tract and the descending brain stem pathways. According to electrophysiological studies in conscious animals different pyramidal units can be activated during different types of movements and at different times during the preparation or execution of a movement. Recent neuro-anatomical data suggest that the pyramidal tract is composed of many structural subsystems. Recent physiological data suggest that the pyramidal tract can be involved in various aspects of the motor control.

Animals↗

PubMed2000

Constant involvement of the Betz cells and pyramidal tract in multiple system atrophy: a clinicopathological study of seven autopsy cases.

We investigated clinicopathologically the pyramidal signs, including spasticity, hyperreflexia, and Babinski's sign, and the involvement of the pyramidal tract and primary motor cortex, in seven Japanese autopsy cases of multiple system atrophy (MSA). Pyramidal signs were observed in six (86%) of the seven autopsy cases. Hyperreflexia and Babinski's sign were each evident in five patients, but spasticity was observed in only one patient. Loss of Betz cells and presence of glial cytoplasmic inclusions in the primary motor cortex were noticed in all seven cases. Astrocytosis in the fifth layer of the primary motor cortex was noticed in five cases, but its presence was not related to the duration of the disease. Involvement of the pyramidal tract in the spinal cord, particularly of the small myelinated fibers, was observed in all seven cases, but no involvement of the pyramidal tract in the midbrain was evident in any of the six cases in which this structure was examined. In MSA, pyramidal signs were shown to be present more frequently than believed before, and the clinicopathological correlation between pyramidal signs and involvement of the pyramidal tract was obvious. Constant involvement of Betz cells in MSA has not been reported. Our clinicopathological findings may also make a contribution to the understanding of the clinicopathological hallmarks of MSA.

Female↗

PubMedDate not supplied

[The pyramidal tract: new pathways].

OBJECTIVE: To review some anatomofunctional aspects of the pyramidal tract which are relevant in clinical practice, especially the newer concepts. DEVELOPMENT: a) Although the motor function is best known, the pyramidal tract also has sensory functions, modulating the transmission of impulses in the spinal cord. In fact, motor function is a recent acquisition on the evolutionary scale. b) Other descending pathways, such as the cortico reticulospinal path, participate in voluntary movements. However, the pyramidal pathway is necessary for fine movements of the hand. c) Most of the pyramidal fibres control movements of the contralateral side of the body, but there are a few fibres which do not cross to the other side and play a part in ipsilateral body movements. These fibres seem to contribute to motor recovery following a brain lesion. d) Classically it is recognized that the motor cortex and pyramidal fibres follow a somatotopical distribution. Nevertheless territories corresponding to different parts of the body are superimposed to a considerable extent and may be modified on very diverse occasions. e) Experimentally it has been proved that a circumscribed lesion of the pyramidal pathway does not cause hyper reflexia or spasticity. The hyper reflexia and spasticity habitually seen in patients with pyramidal syndrome is due to lesions of other descending pathways. CONCLUSION: The pyramidal tract is anatomically and functionally related to other nerve structures and its activity is therefore integrated within the nervous system.

Animals↗

PubMed1982

A light and electron microscopic study of regrowing pyramidal tract fibers.

Autoradiographic and EM techniques were used to study the regenerative capacity of severed axons in the mammalian CNS. In infant and adult hamsters the pyramidal tract was severed unilaterally in the medulla several millimeters rostral to the decussation. After survival to adulthood, the animals received injections of [3H] proline in the sensorimotor cortex ipsilateral to the lesion. Autoradiography showed that labeled pyramidal tract axons in the medulla did not cross the lesion site. Instead, in animals with infant lesions there was massive new axonal growth arising from the severed pyramidal tract several millimeters rostral to the cut. Most of these labeled fibers crossed to the contralateral brainstem, coalesced into a compact bundle, descended just medial to the spinal trigeminal nucleus, and grew caudally for 6-7 mm. Although the trajectory of the regrowing axons was completely abnormal, their pattern of termination in the dorsal column nuclei and dorsal horn of the cervical spinal cord was normal. Synapse formation by the anomalous regrowing pyramidal tract axons in their appropriate terminal areas was confirmed by electron microscopy of terminal degeneration in animals with infant pyramidotomies followed by adult cortical lesions. Autoradiographic labeling of the new pathway at short postlesion survival times showed that the fibers grew out rapidly at about 1 mm/day, a rate somewhat slower than normal (2-4 mm/day). There was a dramatic difference in the capacity of the pyramidal axons to regrow in animals operated as infants vs. those operated as adults. The regrowth was maximal with lesions at 4-8 days of age. Capacity for new growth declined sharply thereafter such that after 20 days of age, pyramidal tract lesions elicited no new growth but instead a progressive axon degeneration retrograde to the lesion. These results, in contrast to many previous findings, show that significant regrowth of severed axons can occur in the neonatal CNS. Most importantly pyramidal tract fibers regrowing by anomalous routes can nevertheless establish synaptic connections in appropriate terminal areas and thus, as we show in the following paper, play a functional role in maintaining normal motor behavior.

Age Factors↗