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PubMed1976

Further study on the excitation of pyramidal tract cells by intracortical microstimulation.

The effective spread of stimulating current for pyramidal tract (PT) cells and fibers was studied using a method of cancelling the shock artifacts and the following results were obtained: 1. The excitability of PT axon collaterals was as high as that of PT cells. 2. These axon collaterals extended as far as 1.0 mm horizontally from the PT cells. 3. The low threshold area for activation of a given PT cell was as wide as 3--4 mm2 on the surface of the cortex. 4. Intracortical microstimulation (ICMS) delivered to the PT cell layer produced direct (D) and indirect (I) descending volleys in the pyramidal tract, but ICMS to the superficial layer (III) produced only I-waves. 5. These I-waves grew significantly larger after 15--20 msec from the start of the train of stimuli. 6. It is concluded that either surface stimulation, or short train of ICMS is inadequate for delineating fine localization of motor function within the cortex. Longer train (30--40 msec) with high frequency pulses (300--400 cy/sec) can produce muscle contraction with much smaller currents, increasing the accuracy of measuring the localization of motor function.

Animals↗

PubMed1994

Extent of pontine pyramidal tract Wallerian degeneration and outcome after supratentorial hemorrhagic stroke.

BACKGROUND AND PURPOSE: Pyramidal tract Wallerian degeneration has been detected on magnetic resonance imaging (MRI) as T2-weighted high-intensity areas. We analyzed the relation between the extent of brain stem Wallerian degeneration and activities of daily living (ADL) after supratentorial hemorrhagic stroke. METHODS: Twenty-six patients with supratentorial hemorrhage were examined on the coronal T2-weighted image of the pons 3 months or later after stroke, and the percentage of Wallerian degeneration in the pons was calculated. The patients were divided into three groups. In group A (n = 6), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 2 months from the MRI. In group B (n = 11), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 10 months from the MRI (mean, 15.5 months from the onset). In group C (n = 9), MR films were taken after 10 to 17 months (mean, 12.0 months) from the ictus, and the ADL assessment was done simultaneously. Barthel Index score was used for quantitative ADL assessment. RESULTS: All patients showed various degrees of pontine pyramidal tract Wallerian degeneration associated with capsular involvement by the hematoma. In group A, the percentage of degeneration did not correlate with the Barthel Index score (r = .2101, P = .6895). An inverse relation between percentage of degeneration and Barthel Index score was seen in groups B (r = .7354, P = .0099) and C (r = .888, P = .0014). In groups B and C, Wallerian degeneration was higher in patients with Barthel scores less than 60 (P = .005). CONCLUSIONS: The extent of pontine Wallerian degeneration on MRI 3 months or later after the stroke correlated with the patient's Barthel Index score 1 year after the stroke.

Activities of Daily Living↗

PubMed1989

Differences in the fiber composition of the pyramidal tract in two- and 14-month-old rats.

The present study is aimed at an electron-microscopic morphometrical analysis of the pyramidal tract of 14-month-old rats at the level of the pyramis medullae and the second cervical segment, and a comparison with data obtained for rats of two months of age. Between 2 and 14 months of age there is, at the level of the pyramis medullae of the left pyramidal tract, a statistically significant increase of the number of myelinated fibers, from 91,000 to 118,000, whereas the total number of unmyelinated fibers decreases from 133,000 to 101,000. On the right side at the same level there is no statistically significant change in the number of myelinated fibers, whereas there is a significant decrease of unmyelinated fibers at this side, from 148,000 to 89,000. At the second cervical level, a statistically significant increase in the number of myelinated fibers has been noted at both sides (from 43,000 to 60,000) between 2 and 14 months, whereas the mean total number of unmyelinated fibers at this level decreases somewhat (from 35,000 to 28,000), but is not statistically significant. Several processes which might be involved in the age-related changes observed are discussed, including the possibility of a shift from unmyelinated fibers to myelinated ones, withdrawal of corticobulbar fibers and ongoing outgrowth of myelinated corticofugal fibers after two months of age, and a summarizing scheme is presented. We conclude that the pyramidal tract of the rat changes in composition after the age of two months and that continuing outgrowth of myelinated corticospinal fibers is an important aspect of this continuing development.

Aging↗

PubMed1990

Wallerian degeneration of the pyramidal tract in capsular infarction studied by magnetic resonance imaging.

Using magnetic resonance imaging, we studied 24 patients with ischemic infarction of the internal capsule. Magnetic resonance imaging detected wallerian degeneration of the pyramidal tract below the capsular lesion in 11 patients (45.8%); all 11 had clinical evidence of pyramidal tract damage. In six additional patients magnetic resonance imaging findings, present only on axial slices, were considered to indicate possible wallerian degeneration. When motor deficit was associated with posterior limb lesions, magnetic resonance imaging detected wallerian degeneration of the pyramidal tract in 78.6% (11) of 14 patients.

Aged↗

PubMed1994

Motor cortex and pyramidal tract axons responsible for electrically evoked forelimb flexion: refractory periods and conduction velocities.

Double-pulse methods are used here to measure the refractory periods and conduction velocities of the pyramidal tract axons which cause forelimb flexion in pentobarbital anesthetized rats. In the refractory period experiments, conditioning and test pulses were delivered to the motor cortex, the ipsilateral internal capsule, or the ipsilateral pyramid, and the maximum force exerted by the contralateral forelimb was measured at various conditioning-test intervals. The movements increased as conditioning-test interval increased from 0.5 to 1.0 ms in pyramid sites, from 0.6 to 1.5 in internal capsule sites, and from 0.6 to 2.0 ms in surface cortical sites, suggesting longer refractory periods for the substrates at more rostral sites. In cortical sites, as the conditioning-test interval increased from 4.0 to 20.0 ms, the movements decreased gradually to the single-pulse level, suggesting decreasing temporal summation at longer conditioning-test intervals. In the collision experiments, when conditioning pulses were delivered to one site and test pulses to a second site, the movements increased at conditioning-test intervals that were longer by 0.5-1.3 ms than the refractory periods in either site. This suggests that collisions occurred between orthodromic and antidromic action potentials in the pyramidal tract axons responsible for the limb movement. The collision-like increase was greater between internal capsule and pyramid than between cortex and pyramid, or between cortex and internal capsule. The estimated conduction times were 0.9-1.5 ms between cortex and pyramid, 0.4-0.8 ms between cortex and internal capsule, and 0.5-0.8 ms between internal capsule and pyramid. The range of conduction velocities, therefore, was quite narrow between all pairs (8.8-16.8 m/s). The largest pyramidal tract axons appear to be responsible for most of the force of forelimb flexion in pentobarbital anesthetized rats.

Animals↗

PubMed1991

[A case of HTLV-1 associated myelopathy with diffuse white matter lesion of the frontal lobe and continuous lesion of the pyramidal tract on cranial MRI].

In this report, the characteristic findings of cranial MRI of a case with HTLV-1 associated myelopathy (HAM) is described. The patient was a 62-year-old woman with 6 years history of paraplegia. Her main clinical signs were bilateral spastic paraplegia in the lower limb girdle muscles and extremities, paresthesia below the tenth thoracic cord level and urinary disorder. There was bilateral blepharoptosis. Hyperreflexia was observed in the examination of the cranial nerves and upper extremities. She showed no dementia or any other higher cortical dysfunctions. Positive anti-HTLV-1 antibody in the serum and cerebrospinal fluid established a diagnosis of HAM. T2 weighted MRI study revealed the symmetrical diffuse hyperintensity in the subcortical white matter of the frontal lobe and temporal lobe. The hyper-intensity was also observed in the bilateral internal capsule-peduncular base junction and pontine base, which indicated the continuous lesions in the intracranial pyramidal tracts. These MRI findings were different from those of reported cases of scattered lesion in central nervous system. There are some speculations for the nature of the diffuse lesion in the white matter, i.e., fusion of solitary gliosis and/or perivascular cuffing, or diffusely advanced spongy state. The continuous lesion of the pyramidal tract is suspected a systemic demyelination. Although the pathomechanism still remains uncertain, HTLV-1 infection generally affects the spinal pyramidal tract. It seems that this case is selectively affected in the pyramidal tracts in CNS.

Female↗

PubMed1995

Pyramidal tract and corticospinal neurons with branching axons to the dorsal column nuclei of the cat.

Extracellular single activity was recorded from pericruciate neurons in anaesthetized, paralysed, artificially ventilated cats. A total of 309 neurons were identified antidromically by stimulation of the dorsal column nuclei (229 from the nuneate nucleus and 80 from the gracile nucleus). The study addressed the question whether pericruciate-dorsal column nuclei neurons (corticonuclear cells) sent collaterals to the ipsilateral red nucleus and/or to the contralateral nucleus reticularis gigantocellularis. Also, the ipsilateral pyramidal tract was stimulated at mid-olivary level, as was the crossed corticospinal tract at C2, Th2 and L2 levels in order to know whether the corticonuclear cells sent their axons to the spinal cord and if so to which level. It was found that more than 95% of the corticonuclear fibres coursed through the pyramidal tract. A significant (28.4%; 88/309) proportion of the the corticonuclear neurons sent collaterals to the red nucleus and/or to the nucleus reticularis gigantocellularis. About 68% (209/309) of the corticonuclear cells did not send their axons to the spinal cord and the remainder were corticospinal neurons. Most of the corticospinal fibres terminated at the cervical level (72/100) and the remaining ended at thoracic (18/100) and lumbar (10/100) segments of the cord. While 63.4% (123/194) of the corticonuclear fibres coursing through the pyramidal tract and ending at supraspinal levels were slow conducting, the great majority of the corticospinal neurons were fast conducting (91/100). The non-corticospinal neurons were significantly slower conducting than the corticospinal cells. The corticogracile neurons were slower conducting than the corticocuneate cells. Of the 88 corticonuclear neurons that sent at least a branch to the sites tested, 50% branched into the red nucleus, 35.2% into the nucleus reticularis gigantocellularis and 14.7% into both nuclei, without significant difference between non-corticospinal and corticospinal cells. Most of the main axons of the corticonuclear cells ended at bulbar and cervical levels (281/309 or 90.9%). The data indicate that pericruciate-dorsal column nuclei neurons form a particular substrate within pyramidal tract cells. They can serve precise functions in motor coordination associated with the selection of their own sensory input. The results are discussed from this point of view.

Animals↗

PubMed1994

Effects of 2,5-hexanedione on rat spinal pyramidal tract.

The present study was undertaken to investigate central axonal neuropathy caused by 2,5-hexanedione (2,5-HD) administration. The effects of 2,5-HD on rat pyramidal tract were studied electrophysiologically and histopathologically. Male rats were given 0.5% 2,5-HD in their drinking water for 4, 6 or 8 wk. Spinal motor conduction velocity was measured by direct electrical stimulation and was examined histopathologically by electron microscopy. Rats treated with 2,5-HD had reduced spinal motor conduction velocity at 6 wk and their pyramidal tract axons had decreased cross-sectional areas at 4 wk. The mean number of neurofilaments in myelinated axons of rats treated with 2,5-HD for 8 wk was 42.1% of that found in control rats, but the number of microtubules was not significantly different. The ratio of neurofilaments to microtubules in rats treated with 2,5-HD for 4 wk was less than 1.0 in 30.9% of myelinated fibers, while in control rats it was greater than 1.0 in all axons. These changes in spinal pyramidal tract were detected relatively early after 2,5-HD administration. These results in rats indicate the need for further studies of 2,5-HD neurotoxicity in the human central nervous system.

Animals↗

PubMed1978

Dystopic myelination with hypertrophy of pyramidal tract.

In a case of hypertrophy of the pyramidal tract the cross section of the hypertrophic pyramids was 174% of controls with an increase (148%) in the total population of myelinated fibers. However, there was no commensurate increase in the density of Betz cells. Confined to the hypertrophic tract there was a peculiar anomaly consisting of tubes of thick myelin sheaths that encompassed columns of glial nuclei instead of axons. This type of change, along with the clinical data, may indicate that the lesion originated in the perinatal period when myelin formation is in progress and is susceptible to derangement.

Cell Count↗

PubMed1989

Corticostriatal cells in comparison with pyramidal tract neurons: contrasting properties in the behaving monkey.

Antidromically identified neurons projecting to the putamen (CPNs) and pyramidal tract neurons (PTNs) were recorded from motor and premotor cortex of a monkey which performed a load-bearing task with the wrist. CPNs appeared as a uniform population with very slowly conducting axons and low spontaneous activity. In contrast to PTNs, they exhibited weak, mostly insignificant correlation with graded steady-state forces, responded to torque perturbations with remarkably long latency, and seemed to discharge much later with active movement. Collateral branching of PTNs to the putamen was found to be infrequent (1%). We suggest that the putamen receives a cortical message that is strikingly different from that sent down the pyramidal tract.

Animals↗

PubMed1984

Diameter of axons and thickness of myelin sheaths of the pyramidal tract fibres in the adult human medullary pyramid.

After perfusion fixation with a mixture of paraformaldehyde, glutaraldehyde, and potassium-chromate 4 adult human medullary pyramids were examined with the electron microscope. The myelin sheaths showed only mild signs of post mortal destructions. The periodicity of the lamellae is preserved and varies about 17 nm. For quantitative purposes specimens were taken at random from regions with an extend of half a mm2 on the cross section of the pyramid. On the average 62 lamellae (s = 5, n = 200) built up 1 micron myelin sheath in the 4 brains. The myelin sheath thickness and the inner circumference of the myelin sheath are measured. The axon diameter is calculated from the inner circumference. We obtained an average number of 66,000 fibres, s = 11,000 per mm2. Fibres with a total diameter below 4 microns amount to 87.9%, fibres from 4 to 10 microns to 10.77%, and larger than 10 microns to 1.4%. An axon diameter of about 0.5 micron combined with a thickness of the myelin sheath of 0.3 micron was most often found in all 4 cases. The fibres showed a broad variation of myelin thickness. In a given group of the small axons the thickest myelin sheath exceeded 3 to 4 times the value of the thinnest one. The coefficient of correlation between axon diameter and myelin sheath thickness was calculated as r2 = 0.56. No correspondence exists between frequency maxima and the ratio g, axon diameter to total diameter. Below a total fibre diameter of 5 microns the ratio g scatters broadly about 0.6, fibres larger than 5 microns exceed the value of 0.6. From the morphological data only large sized fibres can evoke a strong effect on compound action potentials if the method of reconstruction of the action potential from fibre size frequency distribution is employed.

Adult↗

PubMed1986

A transient pyramidal tract projection from the visual cortex in the hamster and its removal by selective collateral elimination.

During the early postnatal development of the neocortex in rats there is an axonal projection from the occipital cortex (which includes the visual cortex) to the spinal cord which is subsequently completely removed through a process of selective collateral elimination. In order to determine whether a similar phenomenon occurs during the development of the hamster cortex, we have injected the retrogradely transported fluorescent dye Fast Blue (FB) into the pyramidal decussation of hamsters at various ages. In adult hamsters such an injection results in a band of labeled neurons confined to layer V and to about the rostral two-thirds of the neocortex; no labeled cells are seen in the occipital cortex. However, a similar FB injection made during the first postnatal week results after a 4-day survival in a continuous band of FB-labeled layer V neurons spread throughout the tangential extent of the neocortex, including the occipital cortex. A similar continuous band of FB labeled layer V neurons is seen throughout the tangential extent of the neocortex including the occipital region in hamsters injected during the first postnatal week but allowed to survive until the fourth week (i.e., after the restriction of the widespread neonatal pattern has occurred). Injections of the anterograde tracer wheat germ agglutinin conjugated to horseradish peroxidase made into the occipital cortex, or for comparison, into more rostral cortical regions in hamsters ranging in age from neonates to adults, reveal that the extension of pyramidal tract axons is staggered along the anterioposterior axis of the cortex such that axons originating from the posterior regions lag behind those arising from more rostral areas. The transient occipital projection appears to reach a maximum around the end of the first postnatal week: a large number of labeled occipital axons is seen in the medullary pyramidal tract, and some of these can be followed through the pyramidal decussation and into the dorsal funiculus of the spinal cord. Injections into the occipital cortex on P16 label only a few fibers in the medullary pyramidal tract, and none is labeled in hamsters injected as adults.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1986

Direct synaptic linkage of ventrolateral nucleus of thalamus terminal with cat fast pyramidal tract neuron.

An electron microscopic study on the synaptic connections between neurons of ventrolateral nucleus of thalamus (VL) and pyramidal tract neurons (PTNs) in cat motor cortex was conducted by means of the anterograde degenerating procedure coupled with horseradish peroxidase (HRP) intracellular staining. Following VL lesions, a large majority of the degenerating terminals were found to terminate on dendritic spines and a few on the dendritic shaft. An asymmetric type synapse formed by a VL degenerating terminal and the dendritic shaft of a branch of apical dendrite of a labeled fast pyramidal tract neuron was demonstrated.

Animals↗

PubMed1993

[A case of hereditary motor and sensory neuropathy type I with optic atrophy, neural deafness and pyramidal tract signs].

A case of hereditary motor and sensory neuropathy (HMSN) type I with optic atrophy, neural deafness and pyramidal tract signs was described. The patient was a 53-year-old man who had suffered from difficulty in walking, decreased visual acuity since age 16 years. These symptoms were slowly progressive. At the age of 37, he was pointed out optic atrophy, positive pyramidal tract signs. Distal muscle weakness with atrophy of four limbs was prominent at the age of 50. Since then, he noticed progressive hearing loss with blindness. His elder sister was diagnosed Charcot-Marie-Tooth disease. On neurological examination, he showed to have optic atrophy without retinitis pigmentosa and neural deafness. Also he showed mild degree of muscle weakness and atrophy in four limbs, severe in the distal part of lower limbs. Deep tendon reflexes were absent in all limbs with right Babinski sign. Superficial sensation was decreased slightly in the distal parts of four limbs. Deep sensation was markedly decreased in the leg. There were no cerebellar signs. Audiometric examination revealed bilateral neural hearing loss. There were no findings of spinal cord compression on spinal MRI. On the nerve conduction studies, sensory nerve action potential was not elicited in all nerves tested. Motor nerve conduction velocity of the right median was 41.1 M/sec, also ulnar nerve 44.7 M/sec, but M-wave was not elicited with the electrical stimulation of other tested nerves. On sural nerve biopsy, the density of myelinated fibers was severely decreased. Well-myelinated axon surrounded by onion bulb formation was observed in electron microscopic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Charcot-Marie-Tooth Disease↗

PubMed1991

Junctional specializations between growth cones and glia in the developing rat pyramidal tract: synapse-like contacts and invaginations.

The ultrastructure of contacts between axonal growth cones and glial cells in the developing pyramidal tract was examined by serial sectioning at the third cervical spinal cord segment in 0-, 2-, and 4-day-old rats. Junctional specializations, composed of synapse-like contacts and invaginations, were frequently observed at the contact zone between growth cones and glial elements. The synapse-like contacts consist of clear, round vesicles of 43 +/- 6 nm in the presynaptic growth cone, a pre- and a postsynaptic density, separated by a cleft of 12.1 +/- 0.9 nm. The invaginations consist of small protrusions of the growth cone into the glial element. The invaginated glial membrane is coated. Within the glial element, close to the invagination, frequently organelles were observed that closely resemble endosomes and prelysosomes. Therefore, it is suggested that the invagination represents a stage in endocytosis or possibly phagocytosis of the protruding part of the growth cone by the glial cell. The junctional specializations are formed by growth cones and, less frequently, by axon shafts. The targets of these specialized contacts are, in general, immature glial cells located within the tract area. Occasionally, however, invaginations were also observed into myelinating oligodendrocytes, suggesting that the population of immature target cells includes oligodendrocyte precursors. With regard to the functional significance of these temporary growth cone-glial contacts, several possibilities are discussed, including the suggestion that outgrowing pyramidal tract axons provide immature glial cells with chemical messages, which may influence the timing of glial cell maturation in the tract.

Animals↗

PubMed1990

A quantitative analysis of axon outgrowth, axon loss, and myelination in the rat pyramidal tract.

A quantitative analysis of the development of the pyramidal tract (PT) was carried out at the level of the caudal medulla oblongata and at the sixth cervical spinal segment (C6), in rats ranging in age from embryonic day 20 (E20) to the adult of 90 days postnatally (P90). The axon number in the right medullary PT rises from 27,000 axons at E20 to 391,000 axons at P4. Growth cones are abundant during this period, but can still be observed occasionally at P7. After P4, the axon number is reduced by 62%, to 150,000 in the adult. A rapid axon loss until P14 is followed by a gradual axon loss, continuing beyond the third postnatal week. A similar biphasic axon loss was observed in the cervical PT. At P2 and at P7, concentrations of electron-dense material were observed in 0.5-0.7% of the axon profiles in the medullary PT. Since at P21 this feature was only observed in 0.2% of the axons, it might represent an early sign of axon loss. Myelination starts in the medullary PT at P7. Especially during the third postnatal week, the number of myelinated axons increases rapidly. In the adult rat PT, both at medullary and cervical levels, about one third of the axons are still unmyelinated. The results indicate that the development of the rat PT is characterized by a gradual outgrowth of its fibers and by a protracted, biphasic axon loss. Furthermore, comparing the PT at the medulla, at C3, and at C6, a rostrocaudal decrease in axon number was observed during development as well as at the adult stage. Therefore, no evidence was found for increased axon branching in the tract in the cervical intumescence.

Aging↗

PubMed1980

[Role of the pyramidal tract in the mechanism of dyspnea and hyperventilation].

Hypoxia evoked by mechanical asphyxia first of all disturbs the generation of potentials in pyramidal tract neurons. Hypoxic work, therefore, causes inadequate contraction of somatic muscles, a difficulty in work performance and respiratory discomfort. Concurrently, the disturbance of the pyramidal tract disinhibits the respiratory center of the brain stem with a result of excessive hyperventilation during hypoxic work.

Afferent Pathways↗

PubMed1982

A re-evaluation of the question of ascending fibers in the pyramidal tract.

In 1952 we published a study in the cat with the Glees method, demonstrating the occurrence of degenerating fibers in the pyramidal tract rostral to transections of the tract in the spinal cord. These fibers were interpreted as spinocortical fibers, which have also been described in man. However, other authors have disputed the existence of such fibers. In an attempt to provide more information about this subject, multiple injections of horseradish peroxidase (free and lectin-labeled) were made in the sensorimotor cortex of 4 cats. No retrogradely labeled cells were found in the spinal cord in these cases. Our present and previously reported findings are discussed in the light of other studies of pathological changes in fiber tracts within the central nervous system. Although the present experiments were negative, the degenerating axons previously observed by us in silver sections from the pyramid, pons and internal capsule after lesions of the pyramidal tract in the spinal cord, can not be satisfactorily explained as evidence of retrograde, indirect Wallerian, degeneration of corticospinal fibers.

Animals↗