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[The riddle of the pyramidal tract].
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[Aberrant pyramidal tract: a study with Sudan III stain].
The aberrant pyramidal tracts in the pontine medial lemnisci were studied, using standard Sudan III stain, in six cases of chronic pyramidal tract degeneration. Three of the six cases had bilateral or unilateral cerebral destructive lesions, one cervical hematomyelia with rare retrograde pyramidal tract degeneration, one classical amyotrophic lateral sclerosis, and one atypical motor neuron disease with striatonigral degeneration. Except for the latter two cases the aberrant pyramidal tract degeneration was confirmed bilaterally or on the side ipsilateral to the pyramidal tract degeneration in the pontine base. This degeneration could also be found, on careful examination, with other stains, i.e., H & E, Luxol fast blue-periodic acid Schiff and modified Bielschowsky. Significant change was not observed in the medullary medial lemniscus in any case. The different results observed in the aberrant pyramidal tract between the destructive and degenerative disorders might be pathogenetically important. Reservation, however, may be required since the number of the cases of degenerative disorders in this study was limited. A possible factor for this difference is the survival length which might have erased degradation products altogether. Another factor is the sensitivity of Sudan III in comparison with the Marchi's method which might demonstrate more subtle evidence of degeneration but with its intrinsic capricious staining characteristics. The physiological role of the aberrant pyramidal tract, which has been neglected in the recent textbooks of neuroanatomy, may become of clinical interest with high-quality MRI in cases such as isolated cranial motor nerve palsy without concomitant paralysis of the extremities.
Interpositus nucleus influences on pyramidal tract neurons in the cat.
The influences of the interpositus nucleus on pyramidal tract neurons were investigated by stimulating, in unanesthetized cats, interpositus nucleus foci which activated single muscles in limbs, while recording unitary discharges of pyramidal tract neurons located in foci (area 4 gamma) from which contraction was obtained in the same muscles as those excited from interpositus nucleus (agonist pyramidal tract neurons), in their antagonist (antagonist pyramidal tract neurons), or in heteronymous muscles (heteronymous pyramidal tract neurons). It was found that agonist pyramidal tract neurons were inhibited from the interpositus nucleus, whereas antagonist pyramidal tract neurons displayed a pure excitatory or an excitatory-inhibitory pattern, and the heteronymous neurons were not significantly influenced. A direct activation of interposito-thalamic efferents could be responsible for these effects. In fact, unitary discharge changes of pyramidal tract neurons, elicited from interpositus nucleus stimulation, persisted after chronic intermediate cortex ablation and dentate nucleus lesions, and disappeared following coagulations in the ventrolateral nucleus of the thalamus. These results suggest that interpositus nucleus efferents, which activate a given muscle, via the rubrospinal pathway, could inhibit the discharge of pyramidal neurons controlling that muscle, via collaterals direct to the thalamic ventrolateral nucleus.
Development of the pyramidal tract in the hamster. I. A light microscopic study.
The development of the pyramidal tract and other projections from the sensorimotor cortex was studied in the postnatal hamster with both (3H) proline and horseradish peroxidase (HRP) as anterograde tracers. In the 1-day-old animal labeled axons extend as far as the pons. Other corticofugal fibers have penetrated into the corpus striatum and the thalamus. By 2 days postnatally, the pyramidal tract has grown to midmedullary levels and there is substantial retrograde (HRP) and anterograde labeling in the thalamus. The pyramidal decussation is formed at 3 days of age and by 4 days the pyramidal tract has descended in the dorsal funiculus as far as midcervical spinal cord. Corticofugal fibers invade the pontine nuclei at 4 days and both the dorsal column nuclei and the superior colliculus at 6 days of age. At 6 days the pyramidal tract can be traced to mid-thoracic levels of the spinal cord, by 8 days the tract reaches lumbar levels, and by 14 days it has completed its caudal growth to the coccygeal spinal cord. Fibers first penetrate the gray matter of a given spinal cord level approximately 2 days after the tract has grown past that level in the dorsal funiculus. Pyramidal fibers continue their lateral growth into the dorsal horn at all levels of the cord throughout the third postnatal week such that by 21 days of age the pyramidal tract appears similar to that of the adult. The projections from sensorimotor cortex to the pontine nuclei, the superior colliculus, and the dorsal column nuclei appear to have a pattern similar to that of the adult soon after the fibers grown into these structures. There is a consistent delay of 2 to 3 days between the arrival of the pyramidal tract axons in the white matter adjacent to target structures and their innervation of a given terminal field. The pyramidal tract grows more quickly through the dorsal funiculus of the spinal cord than it does along the ventral surface of the medulla. Extensive elongation of pyramidal tract axons is achieved long before the growth and differentiation of the sensorimotor cortical neurons from which they originate. Finally, the pyramidal tract appears to grow as a compact bundle and not by the addition of temporally staggered groups of fibers. The relatively protracted period of innervation of the spinal cord by the pyramidal tract coupled with the immaturity of the cortical neurons at birth may be factors contributing to the significant regrowth of pyramidal tract axons severed early in development.
Proximal and distal impairments in rat forelimb use in reaching follow unilateral pyramidal tract lesions.
Although it was once thought that the corticospinal (pyramidal) tract was the main substrate of voluntary movement, the extent to which it is involved in the control of proximal vs. distal musculature, independent finger movements, and movements characteristic of different species of animals now is unclear. The objective of this study was to examine the effects of pyramidal tract lesions on skilled forelimb use in rats. In addition, cell morphology in motor cortex following lesions was examined. Naive and trained rats received unilateral pyramidal sections just rostral to the pyramidal decussation. Performance was assessed and filmed on two reaching tasks. Measures of reaching consisted of success in obtaining food, kinematic analysis of limb trajectory and velocity, and qualitative evaluation of 10 movement components comprising a reach. Pyramidal tract lesions only impaired reaching for single food pellets. Almost all movements comprising a reach, except digit opening, were impaired, including lifting, aiming, pronating and supinating the limb, and releasing food. Although success in limb use was unchanged over the 180 day observation period, there were significant improvements in the qualitative features of limb use. Histologically, the morphology of pyramidal cells in the forelimb area ipsilateral to the lesion seemed normal. Rats with additional damage to adjacent structures, such as the medial lemniscus and olivary complex, were much more severely impaired on the reaching tasks, and displayed similar impairments as judged by qualitative and kinematic measures. The results demonstrate that a number of movements involved in independent limb use are chronically impaired by pyramidal tract lesions in the rat. Nevertheless, significant use of the limb is possible, due perhaps to both the contribution of extrapyramidal motor systems and the influence of the remaining pyramidal system through its extrapyramidal connections. The results not only show that the rat pyramidal tract supports functions very similar to those of primates and thus might provide a good model for some aspects of pyramidal tract dysfunctions, but also they argue that the pyramidal tract is involved in both proximal and distal limb movements.
[Synaptic processes in neurons of the cat pericruciate cortex evoked by pyramidal tract stimulation].
The influences of pyramidal tract stimulation on the activity of neurons in the pericruciate cortex were investigated on 423 neurons (81 neurons were studied intracellularly and 342--extracellularly), 78 of them having background activity. Pyramidal stimulation is shown to evoke not only antidromic spikes (0.5-16.0 ms latency) in the pyramidal cells, but also lateral and recurrent PSPs in the pyramidal and unidentified units of all cortical layers. IPSPs were observed in 46.7% of the investigated neurons, EPSPs--in 21.0%, mixed responces--in 26.0%. The latency of IPSPs was 1.5-14.0 ms, their amplitude ranged from 1.3 to 17.0 mV, the duration of the rising phase varied from 4 to 18 ms and the whole duration was 18-120 ms reaching sometimes 250-500 ms. In 30% of cases it was possible to divide the IPSPs into two phases: a fast one with a duration of 10-20 ms and a slow one. The latency of IPSPs was 2.6-19.0 ms, their amplitude--1.0--7.8 mV and duration--from 10.0 to 50.0 ms. The antidromic discharge in the pyramidal tract inhibited the background activity for 200-400 ms in 51.2% of spontaneously active units; acceleration was observed in 19.5% and mixed effect in 7.4% of units. The participation of pyramidal axonal collaterals and cortical interneurons in generation of the described processes is discussed.
Redirected growth of pyramidal tract axons following neonatal pyramidotomy in cats.
After the pyramidal tract at the pontomedullary junction in neonatal cats had been cut and the ipsilateral frontoparietal cortex injected with intra-axonal markers at 40 to 74 days of age, cortical axons were labeled in aberrant pathways that descended into the caudal medulla and spinal cord. 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. Another group of aberrant projections descended bilaterally along the ventrolateral edge of the medulla and either ended in the lateral reticular nuclei or continued into the spinal cord. Finally, some axons descended individually through the central medullary tegmentum and ended bilaterally in the spinal trigeminal, dorsal column, and lateral reticular nuclei. Although these findings suggest that pyramidal tract axons regenerate after injury, the findings from a second series of experiments refute this conclusion. In 2- to 5-day-old cats, the fluorescent dye Fast Blue was injected into the spinal cord, and 7 to 8 days later the contralateral pyramidal tract was cut. In these animals, there were never any cortical neurons retrogradely labeled with Fast Blue in the frontoparietal cortex ipsilateral to the pyramidotomy, although numerous neurons were labeled contralaterally. Control experiments confirmed that the interval between the Fast Blue injections and the pyramidotomies was long enough for retrogradely labeling cortical neurons, that the spinal cord injections did not adversely affect the retrogradely labeled cortical neurons, and following axotomy dying cortical neurons could be demonstrated directly using silver impregnation techniques. We conclude that neonatal pyramidotomy causes the death of all axotomized cortical neurons in kittens, and, therefore, the aberrant cortical projections seen caudal to the lesion must be redirected, late-developing, and undamaged cortical axons, and not regenerated axons.
Changes in the axonal conduction velocity of pyramidal tract neurons in the aged cat.
The present study was undertaken to determine whether age-dependent changes in axonal conduction velocity occur in pyramidal tract neurons. A total of 260 and 254 pyramidal tract neurons were recorded extracellularly in the motor cortex of adult control and aged cats, respectively. These cells were activated antidromically by electrical stimulation of the medullary pyramidal tract. Fast- and slow-conducting neurons were identified according to their axonal conduction velocity in both control and aged cats. While 51% of pyramidal tract neurons recorded in the control cats were fast conducting (conduction velocity greater than 20 m/s), only 26% of pyramidal tract neurons in the aged cats were fast conducting. There was a 43% decrease in the median conduction velocity for the entire population of pyramidal tract neurons in aged cats when compared with that of pyramidal tract neurons in the control cats (P < 0.001, Mann-Whitney U-test). A linear relationship between the spike duration of pyramidal tract neurons and their antidromic latency was present in both control and aged cats. However, the regression slope was significantly reduced in aged cats. This reduction was due to the appearance of a group of pyramidal tract neurons with relatively shorter spike durations but slower axonal conduction velocities in the aged cat. Sample intracellular data confirmed the above results. These observations form the basis for the following conclusions: (i) there is a decrease in median conduction velocity of pyramidal tract neurons in aged cats; (ii) the reduction in the axonal conduction velocity of pyramidal tract neurons in aged cats is due, in part, to fibers that previously belonged to the fast-conducting group and now conduct at slower velocity.
The mode of activation of pyramidal tract cells by intracortical stimuli.
1. Direct and indirect effects of intracortical stimulattion on pyramidal tract cells were compared in the monkey and in the cat under barbiturate or chloralose anaesthesia. The hind-limb motor areas were explored, that in the monkey only within the convex part of the precentral gyrus. The intracortical stimuli were applied in the nearest vicinity of pyramidal tract cells, where antidromic spike potentials of single cells were recorded. 2. Average records of descending volleys in corticospinal tract fibres were taken from the surface of the lateral funiculus or from its dissected fascicles. The sensitivity of the recording was sufficient to detect responses in single fibres. 3. The latencies of the earliest descending volleys evoked by weak intracortical stimuli were compared with the latencies of the antidromic spike potentials of pyramidal tract cells evoked by stimulation of the lateral funiculus at a low lumbar level (same conduction distance). Only in about one third of cases these latencies were similar and compatible with a direct activation of pyramidal tract cells. In the remaining cases they indicated mono- or polysynaptic activation of pyramidal tract cells. 4. Latencies of the later components of the descending volleys indicated that they were due to indirect activation of pyramidal tract cells in practically all cases. 5. The components of the descending volleys attributable to the indirect activation of pyramidal tract cells were greatly increased when repetitive intracortical stimuli were applied instead of single ones. 6. The investigation leads to the conclusion that a weak intracortical stimulation is relatively ineffective in a direct excitation of pyramidal tract cells and that the effects of such a stimulation are mainly indirect, especially when repetitive stimuli are used.
Course and termination of the pyramidal tract in the pig.
To study the pyramidal tract in the pig, the motor cerebral cortex of one side was defined electrophysiologically and subsequently excised. The animals operated were killed after 7, 11 and 14 days, and the cerebral hemisphere of the operated side, brain stem and spinal cord were removed for histological examination. The pyramidal tract proved to run ipsilaterally as far as the oral extremity of the 12th cranial nerve nucleus. The decussation, which exhausted itself almost completely at the level of the rostral extremity of the 1st cervical metamere, started here. After the limit just mentioned only rare isolated fibres were visible. Along its course, the pyramidal tract sent a small number of axons to the ipsilateral and contralateral nucleus of the 7th cranial nerve, while the fibres running from the opposite side to the reticular formation and to the hypoglossal nerve nucleus, cuneatus, gracilis and trigeminal spinal tract nuclei were more numerous.
Immunocytochemical localization of cell adhesion molecule L1 in developing rat pyramidal tract.
L1 is a representative of a family of carbohydrate neural cell adhesion molecules. The expression of L1 was studied during postnatal development of the rat pyramidal tract by immunohistology using polyclonal antibodies to L1 in spinal cord cervical intumescences. On postnatal day 1 (P1), L1 immunoreactivity was present in the entire dorsal funiculus, consisting of the ascending fasciculus gracilis and fasciculus cuneatus and the descending pyramidal tract. At that time the cervical pyramidal tract contains the first outgrowing corticospinal axons. At P4 both the fasciculus gracilis and the pyramidal tract are immunoreactive whereas the fasciculus cuneatus is negative. At P10 the pyramidal tract is intensely labelled whereas both ascending bundles are negatively stained. In the period between P4 and P10 the pyramidal tract is characterized by a massive outgrowth of corticospinal axons. During pyramidal tract myelination, between P10 and the end of the third postnatal week (P21), L1 immunoreactivity is progressively reduced. These observations suggest that L1 may play a prominent role in outgrowth, fasciculation and the onset of myelination of rat pyramidal tract axons. The differential L1 immunoreactivity of the pyramidal tract and the earlier developing ascending systems in rat dorsal funiculus indicate that this polyclonal antiserum is a useful differentiating marker for outgrowing fibre tracts.
Constant involvement of the Betz cells and pyramidal tract in amyotrophic lateral sclerosis with dementia: a clinicopathological study of eight autopsy cases.
We investigated clinicopathologically pyramidal signs, including hyperreflexia, Babinski sign, and spasticity, and the involvement of the primary motor cortex and pyramidal tract, in eight Japanese autopsy cases of amyotrophic lateral sclerosis (ALS) with dementia. Pyramidal signs were observed in seven (88%) of the eight autopsy cases. Hyperreflexia and Babinski sign were evident in seven (88%) and three (38%) patients, respectively, but spasticity was not observed in any of the eight patients. Loss of Betz cells in the primary motor cortex was evident in the seven cases in which this structure was examined. Astrocytosis in the fifth layer of the primary motor cortex was noticed in three cases. In all eight cases, involvement of the pyramidal tract was obvious in the medulla oblongata, but no involvement of the pyramidal tract was found in the midbrain. Involvement of the pyramidal tract in the spinal cord, particularly of large myelinated fibers, was observed in all six cases in which the spinal cord was examined. In ALS with dementia, pyramidal signs were shown to be present more frequently than previously believed, and the clinicopathological correlation between pyramidal signs and involvement of the pyramidal tract was obvious. Constant involvement of Betz cells and the pyramidal tract in ALS with dementia has not been reported. Our clinicopathological findings may make a contribution to the understanding of the clinicopathological hallmarks of this disorder. Furthermore, we believe that this study will also contribute to the elucidation of the nosological status of ALS with dementia.
Fetal occipital cortical neurones transplanted to the rostral cortex can extend and maintain a pyramidal tract axon.
In adult rats, cortical neurones that send axons through the pyramidal tract are confined to layer V, over the rostral two-thirds of the cerebral hemisphere. However, during the first postnatal week, many neurones in layer V in the occipital cortex (including the visual cortex) also extend axon collaterals through the pyramidal tract and into the spinal cord. These occipital corticospinal collaterals are completely eliminated over the subsequent 2 weeks, although their cells of origin do not die. We now report that when portions of the occipital cortex from fetal rats are transplanted to more rostral cortical regions of newborn rats, some of the transplanted neurones not only extend axons through the pyramidal tract, but also maintain these axons beyond the stage at which they are normally eliminated. These results suggest that normally-eliminated cortical axons can be 'rescued' and, in the case of pyramidal tract neurones, the position of the neurones within the tangential plane of the cortex is a critical factor in determining which neurones retain and which lose their pyramidal tract collaterals.
[Role of diffusion tensor imaging in neuronavigation surgery of brain tumors involving pyramidal tracts].
OBJECTIVE: To explore the role of diffusion tensor imaging (DTI) in neuronavigation surgery of brain tumors involving pyramidal tracts. METHODS: Forty-nine patients with brain tumors involving pyramidal tracts were randomly divided into trial group (DTI navigation) and control group (traditional navigation). The patients in trial group underwent DTI and T1 weighted 3D navigational magnetic resonance imaging (MRI) studies. The main white matter tracts were constructed by the DTI datasets, and merged to the anatomical structure, which was delineated by the T1-weighted three-dimensional fast spoiled gradient recalled sequence (3D/FSPGR). The relationship between the tumors and adjacent pyramidal tracts were segmented and reconstructed for three-dimensional visualization. RESULTS: In 25 patients of trial group and 24 patients of control group, the statistic analysis confirmed well balance of main variations. The tumors were completely resected in 12 patients (50.0%) of control group and in 20 patients (80.0%) of trial group (P < 0.05). Postoperative aggravated contralateral extremities weakness or hemiplegia due to pyramidal tract injury occurring in 75.0% cases of control group whereas only 20.0% patients in trial group (P < 0.01). The mean Karnofsky scale were 69.58 +/- 23.49 and 84.80 +/- 23.49 respectively in control and trial groups (P < 0.05). The excellent outcome ratio (Karnofsky scale = 90 - 100) was 37.5% in control group and 72.0% in trial group respectively (P < 0.05). CONCLUSIONS: DTI allows individual estimation of large fiber tracts of brain. Furthermore, to integrate spatial three-dimensional information concerning the white matter tracts into traditional neuronavigation images during surgery, was valuable in presenting topographical character of involving (shift or erosive) pyramidal tracts and relationship with the margins of neighboring tumors. The mapping of large fiber tracts was a safe, efficient, reliable technique. DTI should be routinely used in neuronavigation surgery of brain tumor involving pyramidal tracts to plan the optimal trajectory and ensure total resection of the lesions during operation, as well as to decrease potential disability after operation and to shorten the length of hospitalization.
Cortical pyramidal tract interneurones and their sensitivity to L-glutamic acid.
1. Pyramidal tract interneurones, defined as neurones which are activated synaptically as a result of pyramidal tract stimulation, have been identified in the rat cerebral cortex. The number of evoked spikes depended upon stimulus strength, and stimulation in a specific thalamic nucleus produced a burst of activity lasting for up to 1 sec.2. These cells are readily excited by a brief (50 msec) pulse of glutamate applied by micro-iontophoresis. Other, unidentified cells are not so responsive.3. Synaptically evoked spikes resulting from pyramidal tract stimulation can be blocked by the iontophoretic and I.P. administration of substances shown to antagonize glutamate excitation of cells.4. The results support suggestions that glutamic acid is a neurotransmitter in the cerebral cortex. The evidence presented further indicates that glutamic acid could be the transmitter released by the pyramidal tract.
[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.
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.