Pattern of myelination in the pyramidal tract of the rat

The size and myelination of midbulbar pyramidal tract axons were measured by electron microscopy in the rat. We found that myelin thickness did not increase linearly with fiber size; rather, it took on certain preferred thicknesses almost independently of fiber size. This pattern of growth and development is fundamentally different from that of peripheral nerve and may be important for the physiology of the pyramidal tract.     

Fiber spectrum and functional propertis of pyramidal tract neurons in the American opossum

The number and size of pyramidal tract (PT) axons and the functional properties of cerebral PT neurons were examined in the American opossum. The pyramidal tract contains 30,000–40,000 axons, none greater than 5 μ in diameter and 99% of 3 μ or less in diameter. Cerebral neurons were isolated and classified as PT or non-PT according to standard antidromic spike criteria in response to stimulation of the medullary pyramid. Response to natural stimulation and to electrical stimulation of the four paws was tested. PT neurons displayed a wider convergence than non-PT neurons, but the more superficially isolated PT neurons showed only weak or nonexistent excitation from the skin. Response to stimulation of one paw could be blocked by prior stimulation of another paw, whether or not the conditioning stimulus evoked a discharge. At least some of the blocking may be due to intracortical inhibitory synapses, for weak conditioning shocks applied to the pyramidal tract could block the peripherally evoked response in half of the neurons tested, both PT and non-PT. During high-frequency stimulation of the pyramidal tract, antidromic spikes readily separated into distinct A and B components, the B spike frequently failing altogether. The slow antidromic conduction speeds, 4–14 m/sec, agreed well with the small axon diameters found by histological methods.     

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.     

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.     

Unmyelinated fibers in the pyramidal tract of the rat: a new view

An electron microscopical morphometric analysis has been carried out at the medullary level of the pyramidal tract of the rat in order to quantify both myelinated and unmyelinated fibers: it was found that unmyelinated fibers outnumber myelinated ones substantially (133,000 ± 18,000 versus 91,000 ± 11,000, respectively). The unmyelinated fibers range from 0.05 to 1 μm in a monomodal distribution (mean 0.16 μm). For myelinated axons also a monomodal distribution was observed (ranges: axon 0.10–4 μm, mean 0.80 μm; myelin sheath 0.25–5 μm, mean 1.19 μm).     

A quantitative electron microscopic study of myelination in the pyramidal tract of rat

The ultrastructure of fibers during myelin formation in the pyramidal tract of rats is described. The distribution of fiber classes based on counts of myelin lamellae was determined for newborn, young and mature rats. In newborn rats (2–12 days), growth of the axon was extremely rapid in fibers undergoing early myelination, resulting in greater variation in the relation between axon circumference and sheath thickness and, also, in the presence of myelin sheaths that were unusually thin in relation to the size of the axons. In young rats (12 days to 8 weeks), the numbers of myelin lamellae present in the sheaths increased in proportion to the increase in axon circumference. In adult rats, the numbers of myelin lamellae present in the sheaths was in linear relation to axon circumference for all sizes of myelinated fibers. Approximately 20% of the fibers were nonmyelinated. The number of glia cells per axon at the onset of myelination was approximately 20% of the adult ratio. During growth, myelination gliosis resulted in a steady increase in the number of glia cells per axon until adult levels were ultimately achieved. Our observations suggest that formation of myelin lamellae by oligodendroglia cells may be controlled by the caliber of the axon.     

The pyramidal syndrome and the pyramidal tract: a brief historical note

The discovery of the pyramidal syndrome and tract is briefly reviewed with emphasis on a few key historical aspects. The pursuit of the relationship between the lateralized deficits resulting from contralateral head trauma begins in the fourth century BC with the Hippocratic School and continues until the present day.     

Development and malformations of the human pyramidal tract

Abstract 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.     

A morphometric analysis of pyramidal tract structures during postnatal undernourishment and recovery

Rats were postnatally undernourished during the suckling period (up to 20 days) and the brainstems of the perfused rats were dissected and prepared for electronmicroscopy at 21, 35 and 63 days of age. The effects on myelin were relatively mild and consisted primarily of a slight reduction in the relative numbers of myelinated fibers, most likely caused by a lag in the rate of loss of non-myelinated fibers, and fewer lamellae in myelinated axons of less than 2.5 micron circumference. Organelles were examined in the interfasicular oligodendroglia and in paragigantocellular reticular neurons immediately dorsal to the pyramidal tract. The numbers of mitochondrial particles in neuronal perikarya were significantly increased by postnatal undernourishment, although the numbers of other organelles appeared normal. Increased numbers of mitochondria persisted in nutritionally rehabilitated rats. Mitochondrial particles in oligodendroglia were not altered.     

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

Abstract. 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.