			Home About us Contact

Pyramidal Tract (pyramidal + tract)

Distribution by Scientific Domains

Medical Sciences	54%
Life Sciences	45%

Selected Abstracts

Diffusion Tensor Tractography-based Analysis of the Pyramidal Tract in Patients with Amyotrophic Lateral Sclerosis

JOURNAL OF NEUROIMAGING, Issue 3 2008
Yoon-Ho Hong MD
ABSTRACT BACKGROUND AND PURPOSE We attempted to measure DTI parameters of the brainstem pyramidal tract using two approaches, ie, simple ROI and tract-specific analyses. Results obtained for healthy subjects and ALS patients were compared. METHODS DTI was performed using a single shot SE-EPI with 25 noncollinear diffusion gradient directions (b= 1000 second/mm2) and with no diffusion gradient on a 3.0-T MR system in 10 ALS patients and in 8 age- and sex-matched normal controls. To delineate the brainstem pyramidal tract, tractography was performed using two ROIs, ie, a seed ROI at the cerebral peduncle (ROI-1) and a target ROI at the lower pons (ROI-2). ROI-1 was subsequently restricted to voxels that contained streamlines in the tract reconstruction, thus creating a sub-ROI. RESULTS Mean fractional anisotropy (FA) and mean diffusivity values were highly reproducible by tract specific analysis, whereas simple ROI analysis yielded larger variabilities between operators. FA values were significantly lower in ALS patients than in normal controls in the tractography-derived sub-ROI (P= .01), but not in the seed or target ROIs. CONCLUSIONS These results suggest, compared with simple ROI analysis, that tract-specific analysis using DTI fiber-tracking is more reliable and sensitive for detecting upper motor neuron pathology in ALS. [source]

Development of the pons in human fetuses

CONGENITAL ANOMALIES, Issue 2 2007
Toshihisa Hatta
ABSTRACT Morphometric and histological studies of the pons were performed by light microscopy in 28 cases of externally normal human fetuses ranging from 90 to 246 mm in crown-rump length (CRL) and from 13 to 28 weeks of gestation. The brainstems of fetuses were embedded in celloidin or paraffin, and transverse sections were prepared. The pons was divided into two regions at the most ventral margin of the medial lemniscus at the level of the motor trigeminal nucleus. The relationships between the total dorsoventral length, ventral length, and dorsal length of the pons versus CRL and gestational ages were calculated, and empiric formulas were fitted. It was found that the ventral portion increased in size more rapidly than the dorsal portion. The proportion of the ventral portion in the total dorsoventral length was constitutively higher than that of the dorsal portion in the present range of CRL. In the pontine nuclei, from 235 mm in the CRL, some large cells with rich cytoplasm, pale nuclei, and a distinct nucleolus appeared on the dorsal side of the pyramidal tract. According to Weigert stained preparations, the first myelinated fibers in each motor root of the trigeminal, abducent, and facial nerves were recognized at 130,140 mm in CRL and the medial lemniscus at 230,235 mm. [source]

Coherent corticomuscular oscillations originate from primary motor cortex: Evidence from patients with early brain lesions

HUMAN BRAIN MAPPING, Issue 10 2006
Christian Gerloff
Abstract Coherent oscillations of neurons in the primary motor cortex (M1) have been shown to be involved in the corticospinal control of muscle activity. This interaction between M1 and muscle can be measured by the analysis of corticomuscular coherence in the ,-frequency range (,-CMCoh; 14,30 Hz). Largely based on magnetoencephalographic (MEG) source-modeling data, it is widely assumed that ,-CMCoh reflects direct coupling between M1 and muscle. Deafferentation is capable of modulating ,-CMCoh, however, and therefore the influence of reafferent somatosensory signaling and corresponding neuronal activity in the somatosensory cortex (S1) has been unclear. We present transcranial magnetic stimulation (TMS) and MEG data from three adult patients suffering from congenital hemiparesis due to pre- and perinatally acquired lesions of the pyramidal tract. In these patients, interhemispheric reorganization had resulted in relocation of M1 to the contralesional hemisphere, ipsilateral to the paretic hand, whereas S1 had remained in the lesioned hemisphere. This topographic dichotomy allowed for an unequivocal topographic differentiation of M1 and S1 with MEG (which is not possible if M1 and S1 are directly adjacent within one hemisphere). In all patients, ,-CMCoh originated from the contralesional M1, in accordance with the TMS-evoked motor responses, and in contrast to the somatosensory evoked fields (SEFs) for which the sources (N20m) were localized in S1 of the lesioned hemisphere. These data provide direct evidence for the concept that ,-CMCoh reflects the motorcortical efferent drive from M1 to the spinal motoneuron pool and muscle. No evidence was found for a relevant contribution of neuronal activity in S1 to ,-CMCoh. Hum Brain Mapp, 2006. © 2006 Wiley-Liss, Inc. [source]

Diffusion Tensor Tractography-based Analysis of the Pyramidal Tract in Patients with Amyotrophic Lateral Sclerosis

An autopsy case of Fabry disease with neuropathological investigation of the pathogenesis of associated dementia

NEUROPATHOLOGY, Issue 5 2008
Riki Okeda
The pathogenesis of dementia associated with Fabry disease was examined neuropathologically in an autopsy case. The patient was a 47-year-old computer programmer who developed renal failure at the age of 36, necessitating peritoneal dialysis, and thereafter suffered in succession episodic pulmonary congestion, bradyacusia, heart failure, and dementia, before dying of acute myocardial infarction. MRI of the brain demonstrated leuko-araiosis. The CNS parenchyma showed widespread segmental hydropic swelling of axons in the bilateral cerebral and cerebellar deep white matter in addition to neuronal ballooning due to glycolipid storage in a few restricted nuclei and multiple tiny lacunae. Hydropic axonal swelling was also sparsely distributed in the pyramidal tract, pedunculus cerebellaris superior and brachium colliculi inferioris, but wallerian degeneration of these tracts was absent. Additional features included angiopathy of the subarachnoidal arteries due to Fabry disease, such as medial thickening resulting from glycolipid deposition in smooth muscle cells (SMCs) and adventitial fibrosis with lymphocytic infiltration, together with widespread subtotal or total replacement of medial SMCs by fibrosis, associated with prominent intimal fibrous thickening and undulation of the internal elastic membrane of medium-sized (1000,100 ,m diameter) arteries. The findings in this case suggest that axonopathic leukoencephalopathy due to multisegmental hydropic swelling of axons in the bilateral cerebral deep white matter is responsible for the dementia associated with Fabry disease, and may be caused by ischemia resulting from widespread narrowing and stiffening of medium-sized subarachnoidal arteries and progressive heart failure. [source]

Hypoxia-sensing properties of the newborn rat ventral medullary surface in vitro

THE JOURNAL OF PHYSIOLOGY, Issue 1 2006
N. Voituron
The ventral medullary surface (VMS) is a region known to exert a respiratory stimulant effect during hypercapnia. Several studies have suggested its involvement in the central inhibition of respiratory rhythm caused by hypoxia. We studied brainstem,spinal cord preparations isolated from newborn rats transiently superfused with a very low O2 medium, causing reversible respiratory depression, to characterize the participation of the VMS in hypoxic respiratory adaptation. In the presence of 0.8 mm Ca2+, very low O2 medium induced an increase in c-fos expression throughout the VMS. The reduction of synaptic transmission and blockade of the respiratory drive by 0.2 mm Ca2+,1.6 mm Mg2+ abolished c-fos expression in the medial VMS (at the lateral edge of the pyramidal tract) but not in the perifacial retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) VMS, suggesting the existence of perifacial RTN/pFRG hypoxia-sensing neurons. In the presence of Ca2+ (0.8 mm), lesioning experiments suggested a physiological difference in perifacial RTN/pFRG VMS between the lateral VMS (beneath the ventrolateral part of the facial nucleus) and the middle VMS (beneath the ventromedial part of the facial nucleus), at least in newborn rats. The lateral VMS lesion, corresponding principally to the most rostral part of the pFRG, produced hypoxia-induced stimulation, whereas the middle VMS lesion, corresponding to the main part of the RTN, abolished hypoxic excitation. This may involve relay via the medial VMS, which is thought to be the parapyramidal group. [source]

Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque

THE JOURNAL OF PHYSIOLOGY, Issue 1 2006
A. Jackson
The efficacy of sensory input to the spinal cord can be modulated presynaptically during voluntary movement by mechanisms that depolarize afferent terminals and reduce transmitter release. It remains unclear whether similar influences are exerted on the terminals of descending fibres in the corticospinal pathway of Old World primates and man. We investigated two signatures of presynaptic inhibition of the macaque corticospinal pathway following stimulation of the peripheral nerves of the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticospinal axon terminals as revealed by changes in antidromically evoked cortical potentials, and (2) changes in the size of the corticospinal monosynaptic field potential in the spinal cord. Conditioning stimulation of the pyramidal tract increased both the terminal excitability and monosynaptic fields with similar time courses. Excitability was maximal between 7.5 and 10 ms following stimulation and returned to baseline within 40 ms. Conditioning stimulation of peripheral nerves produced no statistically significant effect in either measure. We conclude that peripheral afferents do not exert a presynaptic influence on the corticospinal pathway, and that descending volleys may produce autogenic terminal depolarization that is correlated with enhanced transmitter release. Presynaptic inhibition of afferent terminals by descending pathways and the absence of a reciprocal influence of peripheral input on corticospinal efficacy would help to preserve the fidelity of motor commands during centrally initiated movement. [source]

Multimodal microglia imaging of fiber tracts in acute subcortical stroke,

ANNALS OF NEUROLOGY, Issue 6 2009
Basia A. Radlinska BSc
Objective Case series with 11C-PK11195 and positron emission tomography (PET) in stroke patients suggest that activated microglia may be detected in remote brain regions with fiber tract connections to the lesion site as an indicator of poststroke neuroinflammation. However, the specificity of these imaging findings remains to be demonstrated. Methods In a prospective controlled study, we measured microglia activity using 11C-PK11195-PET along the pyramidal tract, as defined by diffusion tensor imaging, in 21 patients with first-time acute subcortical ischemia within 2 weeks of stroke. Uptake ratios (affected vs unaffected side) were determined for a set of standardized volumes of interest along the pyramidal tracts (PT). Uptake ratios from patients in whom the PT was affected were compared with those in whom the PT was not affected. Uptake ratios were related to motor deficit and lesion size according to correlation analyses. Results Increased uptake ratios were only found in patients in whom the PT was affected by stroke. In the affected hemisphere, uptake was increased at the level of pons, midbrain, and internal capsule, but not in the oval center. The extent of remote microglia activation was independent of infarct size or clinical measures of stroke severity. Interpretation A specific activation of microglia was only found in patients in whom the PT was affected by the stroke and only caudal (anterograde) to the lesion; no activation was found in the retrograde direction or in those patients in whom the PT was not affected. These findings were independent of infarct size and may represent changes secondary to early Wallerian degeneration. Ann Neurol 2009;66:825,832 [source]

Pyramidal tract imaging in multiple-system atrophy

MOVEMENT DISORDERS, Issue 11 2005
Nicole Limberg MBBS
Abstract A new radiological finding of T2 FLAIR hyperintensities in the pyramidal tracts is described in a patient clinically thought to have idiopathic Parkinson's disease but histologically proven to have multiple-system atrophy. © 2005 Movement Disorder Society [source]