Magnetic stimulation with a double-cone-coil over the back of the head activates the motor tracts at the level of pyramidal decussation (brainstem stimulation: BST).
CONCLUSION: The VBM study did not show significant white matter changes in patients with KS but showed gray matter alterations in keeping with a hypertrophic response to a deficient pyramidal decussation in patients with MM.
By analyzing mutant mice, we show that motor CST axons that turn dorsally to cross the midline at the pyramidal decussation require plexin-A3 and plexin-A4 signaling. Further expression pattern study and mutant analysis indicate that Sema6A is one of the local cues for motor CST axon turning at the pyramidal decussation. CONCLUSION: Dorsal turning and midline crossing at the pyramidal decussation is a crucial step to properly direct CST axons into the dorsal spinal cord.
Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation.
Although the diagnostic reliability and sensitivity of various parameters of central motor conduction measurement differ, central motor conduction time measurement using brainstem stimulation is potentially useful for determining UMN dysfunction by distinguishing lesions above the pyramidal decussation.
Here we describe the technique in detail using the injection of biotinylated-dextran amine (BDA) in the rat cuneate nucleus and its projection through the pyramidal decussation as an example.
The elucidation of the various tracts in the spinal cord actually began with demonstrations of pyramidal decussation by Mistichelli (1709) and Pourfoir du Petit (1710).
Axons of the DLCST diverge from the main tract at the pyramidal decussation, gather in fascicles in the dorsolateral gray matter below the spinomedullary junction, and project in a gradual trajectory laterally toward the dorsolateral column over the first few cervical segments.
The stimulus probably activates the corticospinal tract at the cervicomedullary junction (pyramidal decussation) and evokes large, short-latency motor responses in the arm muscles.
After injecting unchelated MnCl2 into the forelimb area of sensorimotor cortex of 18 healthy and 10 lesioned rats corticofugal projections could be traced through the internal capsule to the cerebral peduncle and the pyramidal decussation.
At the pyramidal decussation, fibers to the lower extremities cross caudal to the fibers going to the upper extremities, therefore right below the decussation, fibers to the lower extremities run medial side of the fibers to the upper extremities, but later the former run lateral side of the latter. In this patient, the authors considered that the lesion initially damaged the pyramidal decussation at a slightly lower level, involving the tract to left lower extremity, and then extended to right lower extremity, to the left upper extremity, finally to the right upper extremity.
Following nicotine and capsaicin, there was a significant increase in fos-like immunoreactivity (FLI) compared with controls in the following areas: nucleus of the solitary tract from the level of the pyramidal decussation caudally to the level of the area postrema rostrally; dorsomedial aspect of trigeminal subnucleus caudalis (Vc); and paratrigeminal islands interspersed in the spinal trigeminal tract.
The CST was transected bilaterally at its entry into the pyramidal decussation.
At the pyramidal decussation of mutant mice, some corticospinal axons either stayed ventrally and extended laterally, or axons turned dorsally, but instead of growing to the contralateral dorsal column, a significant fraction of axons projected ipsilaterally. We also observed that corticospinal axons of NCAM mutants entered the pyramidal decussation significantly later than axons of wild-type littermates.
This micromapping study pinpointed the precise location of caudal pressor area (CPA) neurons in a restricted region lateral to the caudal end of the lateral reticular nucleus and ventromedial to the medullary dorsal horn near the level of the pyramidal decussation.
We attribute the observed diplegia to a medullary lesion at the level of the pyramidal decussation, presumably caused by an intraoperative embolic occlusion of the anterior spinal artery.
Origination in the primary motor cortex, convergence in the centrum semiovale, the posterior limb of the internal capsule, the cerebral peduncles, the splitting at the level of the pons, and the pyramidal decussation were identified in all subjects.
The dentate nuclei were broken into islands and showed a few heterotopias within the superior cerebellar pedunculi, the inferior olives were plump and dysplastic, and an almost complete absence of the pyramidal decussation was found.
Also, after their axons crossed the pyramidal decussation, continued expression of L1 but no expression of TAG-1 in the CS projection neurons was shown by an additional double-labeling experiment involving DiI injection into the spinal cord at postnatal day (P) 1.
Even more striking was dysplasia of the caudal medulla at the cervicomedullary junction, which was characterized by the absence of a posterior median sulcus, neuronal swelling and axonal spheroids in the region of malformed nuclei gracilis and cuneatus, and absence of pyramidal decussation.
Fluoro-Gold injections into the C4 ventral horn labeled bulbospinal neurons within a densely packed column within the ventrolateral intermediate reticular nucleus from the level of the pyramidal decussation to the facial nucleus.
Cortical cells projecting to the caudal medulla were confined to the contralateral layer V with their descending axons crossing the midline at the level of pyramidal decussation.
We hypothesized that such reinnervation may be supplied from newly formed fibers sprouting at the level rostral to, or at, or caudal to the pyramidal decussation.
Successful elongation of these sprouts through the pyramidal decussation and into the cervical spinal cord was also dependent on the presence of this antibody.
After administration of vasopressin SPR-LI structures became denser, especially at levels of pyramidal decussation (PYX) and area postrema (AP).
A paired-pulse protocol was used, in which motor-evoked potentials (MEPs) were produced by cortical transcranial magnetic stimulation (cTMS) or by electrical stimulation of the pyramidal tract at the level of the pyramidal decussation (pdTES), in both preactivated and relaxed hand muscles.
CONCLUSIONS: L1 function is necessary for the guidance of corticospinal axons across the pyramidal decussation in mice. Some of the defects in the corticospinal tract of humans with mutations in L1 could be due to errors in axon guidance at the pyramidal decussation..
We have examined these pathways to determine the fibre relationships along the extent of their course through the internal capsule, cerebral peduncle, longitudinal pontine fasciculus, pyramid, pyramidal decussation, and dorsal column of the spinal cord. By the medullary pyramid, the pyramidal decussation, and the dorsal column of the spinal cord, the representations of all the cortical regions injected overlap completely; in these structures, the axons arising from each cortical area are widely intermingled.
Five patients had an infarction above the pyramidal decussation. Two patients had infarction below the pyramidal decussation, with ipsilateral hemiparesis and lemniscal sensory loss.
However, the motor evoked potential (MEP) study revealed the pyramidal tract dysfunction above the levels of the pyramidal decussation.
Bilateral lesions of the lateral projections had no effect on the distribution of labeled neurons in the spinal cord and dorsal column nuclei following injections of Fluoro-Gold (FG) into the thalamus, and a small unilateral lesion of the lateral projection reduced the ipsilateral labeling in the motor cortex following injections of FG into the pyramidal decussation.
After the injection of carbocyanine dye DiI into the hindlimb area of the primary motor cortex of the rat, corticospinal axons and their terminal arbors were anterogradely labeled: DiI-labeled corticospinal fibers proceeded caudally in the ipsilateral internal capsule, cerebral peduncle and medullary pyramid, crossed at the pyramidal decussation and descended in the ventralmost area of the contralateral dorsal funiculus of the spinal cord.
The descending motor tracts were activated using a high voltage electrical stimulation technique at four levels: the motor cortex, brainstem (around the pyramidal decussation), and the first and sixth thoracic vertebral levels (T1, T6).
Formation of the aberrant neuronal pathway has been confirmed to be contributed mainly by new axons, which ramified at the level of the pyramidal decussation from healthy corticospinal fibers. A few fibers also contributed to the aberrant pathway by changing their direction on the way of extension at the level of the pyramidal decussation.
They continued caudally as a compact bundle along the ventral surface of the medulla, passed through the pyramidal decussation at the spinomedullary junction and entered the contralateral dorsal funiculus of the spinal cord.
It is concluded that transcranial electrical stimulation of the motor cortex at high intensities can access corticospinal neurones at the pyramidal decussation, and that stimulation of the brainstem (and the spinal cord) preferentially accesses corticospinal axons.
At the craniovertebral junction, neural compression and traumatic injury typically occur anteriorly at the pyramidal decussation producing cruciate paralysis with considerable weakness in both arms and minimal leg involvement.
These results indicate that activation occurs at the foramen magnum level (just below the pyramidal decussation).
To eliminate the descending influences from medullary respiratory neurons to phrenic motoneurons, bulbospinal conduction paths were temporarily blocked by focal cooling applied to the ventral caudal medulla at the pyramidal decussation level by means of a cooling thermode (1 mm tip diam).
Some visual cortical axons extended transiently beyond their permanent targets in the pontine nuclei, by growing through the pyramidal decussation and in some cases extending as far caudally as the lumbar enlargement.
Ramifications of the axons in the pyramidal tract were found to contribute to the ipsilateral tract at the level of the pyramidal decussation, suggesting that ramification of immature axons play an important role in the formation of the ipsilateral corticospinal tract..
The mature synaptic junctions and the protosynapses were found above and at the level of the pyramidal decussation..
Transient corticospinal axons from the presumptive primary visual cortex did not grow caudal to the pyramidal decussation.
Retrograde tracers Fast Blue and Diamidino Yellow were injected in the subcortical path at the pyramidal decussation and in the contralateral cortex, respectively, of adult and newborn rats.
Naive and trained rats received unilateral pyramidal sections just rostral to the pyramidal decussation.
Bell's cruciate paralysis with severe paresis or paralysis of the upper extremities and no or minimal paresis of the lower extremities represents a rare lesion of the pyramidal decussation of the lower brain-stem.
Clinical manifestation of the injury to the pyramidal decussation with resulting cruciate paralysis has been described.
These observations suggest that activation occurs at the level of the cervical-medullary junction where the pyramidal decussation lies. We conclude that the brainstem stimulation technique would be clinically useful for localization of lesions in the corticospinal tract; the primary lesion can be localized whether above or below the pyramidal decussation..
Tracers were injected into the superior colliculus, the principal midbrain target of layer 5 neurons, at times before, during, and after the arrival of cortical axons, or into the subcortical pathway of primary layer 5 axons at two points, the cerebral peduncle caudal to the internal capsule, and the pyramidal decussation at the junction of the hindbrain and spinal cord, at times shortly after the passing of cortical axons.
The underlying mechanism of this paralysis is commonly thought to be selective damage affecting the upper-extremity nerve fibers in the pyramidal decussation.
To determine whether or not the intracortical distribution pattern of pyramidal tract (PT) neurons in the motor cortex (hindlimb area) of normal and reeler mutant mice changes during early postnatal development of the cortex, we injected HRP into the pyramidal decussation of postnatal day (P) 8 and adult animals of the normal and reeler strains, and killed the animals 2 days later.
A large band of horseradish peroxidase (HRP) positive fibers was found crossing at the pyramidal decussation to reach the contra-lateral corticospinal tract and the deeper part of the funiculus, in the cervical cord. However, a small band of HRP positive fibers was noticed to reach the ipsilateral corticospinal tract without crossing at the pyramidal decussation.
Therefore, the focal ischemia in the region below the pyramidal decussation due to the occlusion of both VA and PICA, regardless of thrombotic or embolic episode, was considered to be responsible for ipsilateral hemiparesis..
Detailed morphological analysis of PHA-L labeled corticospinal axons revealed that sprouting from the intact corticospinal pathway into the contralateral denervated spinal cord occurred only at local spinal levels and not at the pyramidal decussation.
The presence of the pyramidal decussation during the embryonic period is noted for the first time.
Corticospinal neurons in primary somatosensory cortex were examined by intracellularly recording and filling cells that were driven by antidromic stimulation of the pyramidal decussation.
Injections into SI barrel cortex-labeled pyramidal fibers that decussated at all levels of the V brain stem complex, though crossing fibers were most numerous in the pyramidal decussation and pons.
AC motoneurons supplying the sternocleidomastoid (SC) and trapezius (TZ) muscles form a single slender cell column extending from the most rostral level of the pyramidal decussation to the middle levels of the C6 cord segment. SC motoneurons are distributed from the most rostral level of the pyramidal decussation to the middle levels of the C3 cord segment, while TZ motoneurons are distributed from the upper levels of the C2 cord segment to the lower levels of the C6 cord segment.
Also, this patient exhibited signs of "hemiplegia cruciata," which is thought to be due to damage to the pyramidal decussation..
Her clinical picture, as well as radiographic evidence of a fracture at C1, led to the diagnosis of Bell's cruciate paralysis, caused by a small lesion in the rostral part of the pyramidal decussation.
At P40, following FB injections into the pyramidal decussation on P34, pyramidal tract neurons are labeled within the O----R transplants, but none can be labeled within R----O transplants, although in the same R----O cases transplanted neurons are labeled by an injection of DY in the superior colliculus. In a second series of host rats, on P34 FB was injected in the pyramidal decussation of the O----R cases, or in the superior colliculus of the R----O cases, and in both groups DY was injected into the region of contralateral cortex homotopic for the new location of the transplant.
The most responsive area was located just dorsal to the lateral aspect of the lateral reticular nucleus at the level of the pyramidal decussation and the caudalmost pole of the inferior olives.
Labeled fibers projected heavily to the transitional zone between caudal pars interpolaris and rostral pars caudalis (i.e., the "periobex" region of the TBNC) and moderately to the trigeminal main sensory nucleus, pars oralis, and caudal pars caudalis at the level of the pyramidal decussation.
On the contrary, its stimulation in the pyramidal decussation caused inhibition of the D and contraction of the AOM.
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.
Their descending axons issued 8 and 13 collaterals (left and right EN-RSN, respectively) at different rostro-caudal levels, between the abducens nucleus and the pyramidal decussation.
Traced motor neurons were observed at spinal levels and a portion of the brain stem slightly below the pyramidal decussation to a plane where the inferior olivary nucleus begins to disappear..
Cortical axons form a cerebral peduncle by at least postnatal day (PD) 10, a medullary pyramid by estimated PD (EPD) 17, a pyramidal decussation by EPD 26, and reach the first cervical segment of the spinal cord by EPD 29.
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. 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.
Cruciate paralysis is characterized by midline involvement of the rostral portion of the pyramidal decussation, resulting in paralysis of the upper extremity without lower extremity involvement.
The authors speculated that such a peculiar pattern of paralysis was due to the injury of the rostral part of the pyramidal decussation and to the acute central cord injury at the C2 level of the spinal cord.
A continuous band of retrogradely labeled layer V neurons which spans the entire cortex including the occipital cortex is seen following injections of the fluorescent marker Fast Blue into the pyramidal decussation during the first postnatal week. However, if the Fast Blue injection is made on P2 and the animal is allowed to survive until P25 a large number of Fast Blue-labeled layer V neurons is found in the occipital cortex, even though an acute, second injection of the retrograde tracer Nuclear Yellow made into the pyramidal decussation shortly before the animal is killed results in no occipital cortical labeling.
At the most caudal medullary level these longitudinally passing fibres became displaced ventrally to a position just laterally to the pyramidal decussation.
All parts of the central gray substance are supplied by ipsi-and contralateral fibres which emerge from the PT at the level of the pyramidal decussation.
Rostro-caudally, silver grain accumulation within the LPRF extends from the level of the motor trigeminal nucleus (VM) to the pyramidal decussation, exhibiting a cephalocaudal decrease of grain density.
Following injections of tritiated leucine restricted to occipital (visual) regions of cerebral cortex during the first postnatal week (days 3--6), labeled corticofugal axons were followed caudally through the pons, medullary pyramid, pyramidal decussation and into the cervical spinal cord.
Its rostral tip coincides with the first appearance of sensory fibres of the glossopharyngeal nerve, the caudal end extends into the pyramidal decussation. The rostral tip lies dorsal to the facial nucleus, and the caudal tip extends to the level of the pyramidal decussation. The medial column begins at the caudal aspect of the pyramidal decussation and terminates in C2 spinal cord segment.
During the first postnatal week, injections of True blue into the pyramidal decussation result inthe labelling of pyramidal tract neurones which are distributed virtually throughout the tangential extent of layer V of the neocortex, whereas after comparable injections during the fourth postnatal week the distribution of such cells is much more restricted and remains restricted into adult life. When True blue is injected into the pyramidal decussation during the first postnatal week and the animals are allowed to survive until the fourth postnatal week, the distribution of pyramidal tract neurones is as widespread as in the immediate postnatal period and includes the entire visual cortex.
They lie at the level of the pyramidal decussation.
The ultrastructure of pyramidal fibres at the level of the pyramidal decussation was studied in a 23 week-old human fetus (220 mm. However, well-myelinated fibres were scattered above the pyramidal decussation and they were also present below the decussation in both the anterior and the lateral corticospinal tract.
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.
These projections ar bilateral, and those fibers destined for the contralateral medial subdivision cross over below the level of the pyramidal decussation..
The findings consisted of an almost total aplasia of the cerebellar vermis; dysplasias and numerous heterotopias of cerebellar nuclei; an almost total absence of pyramidal decussation; and anomalies in the structure of the inferior olivary nuclei, the descending trigeminal tract, solitary fascicle and of the dorsal column nuclei.
The anomalous fibres reached their specific target cells either by deflecting ipsilaterally at the pyramidal decussation to reach the spinal cord and the caudal medulla or by running across the mid-line to the contralateral pons, superior colliculus, pretectal area and the thalamic ventrobasal complex.
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