Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PYRAMIDAL TRACT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,441 records · Page 80Linked to original sources
PubMed2000

Influence of GAA expansion size and disease duration on central nervous system impairment in Friedreich's ataxia: contribution to the understanding of the pathophysiology of the disease.

OBJECTIVE: To verify if GAA expansion size could account for the severity of the central nervous system involvement in Friedreich's ataxia (FA). METHODS: Retrospective study of 52 FA patients (mean age 26.9+/-12.1 years; mean disease duration 10.6+/-7.6 years) homozygous for GAA expansion. Median nerve somatosensory evoked potentials (SSEPs) were available in 36 FA patients, upper limb motor evoked potentials (MEPs) to transcranial magnetic stimulation in 32, brainstem auditory evoked potentials (BAEPs) in 24, and visual evoked potentials (VEPs) in 34. N20, P100, MEP amplitude, SSEP and MEP central conduction time (CCT and CMCT), P100 latency and I-III and I-V interpeak latency, and a BAEP abnormality score were correlated with disease duration and GAA expansion size on the shorter (GAA1) and larger (GAA2) allele in each pair. RESULTS: The GAA1 size inversely correlated with the N20 amplitude (r = -0.49; P<0. 01). Disease duration directly correlated with CMCT (r = 0.57; P<0.01) and BAEP score (r = 0.61; P<0.01) and inversely with MEP (r = -0.40; P<0.05) and P100 amplitude (r = -0.39; P<0.05). CONCLUSIONS: Our data suggest that central somatosensory pathway involvement in FA is mainly determined by GAA1 expansion size. Vice versa, degeneration of pyramidal tracts, auditory and visual pathways seems to be a continuing process during the life of FA patients.

Adolescent↗
PubMed2003

Control of hand movements after striatocapsular stroke: high-resolution temporal analysis of the function of ipsilateral activation.

OBJECTIVE: Hemiparesis due to infarction of the middle cerebral artery has become an increasingly important focus of research on cortical plasticity. Positron emission tomography and functional magnetic resonance imaging studies in such patients found involvement of the hemisphere ipsilateral to the affected hand related to movements of this hand. To understand the function of this ipsilateral activation, the present study investigated movement-related electroencephalogram (EEG) potentials in patients and healthy control subjects to measure timing of ipsi- and contralateral activation relative to movement onset. METHODS: Thirteen patients were investigated in their chronic stage. Their pyramidal tracts were affected by infarctions of the middle cerebral artery at striatocapsular level. EEG potentials were recorded from 26 scalp electrodes while patients were pressing a key with their right or left index finger within a warned choice-response task. RESULTS: Beginning 200 ms before responses of the affected hand, there was normal contralateral preponderance of EEG negativity. Briefly after response onset, however, the other unaffected hemisphere, ipsilateral to the responding hand, became additionally active. This pattern did not occur with responses made by the unaffected hand nor in healthy participants. CONCLUSIONS: The timing of the onset of ipsilateral activity precludes its role in response initiation. Rather, this activity may indicate reflex-like activation of the unaffected motor system to compensate for possible failure of the affected hand.

Aged↗
PubMed2003

Disturbed transcallosally mediated motor inhibition in children with attention deficit hyperactivity disorder (ADHD).

OBJECTIVE: The aim of this study was to investigate mechanisms of motor-cortical excitability and inhibition which may contribute to motor hyperactivity in children with attention deficit hyperactivity disorder (ADHD). METHODS: Using transcranial magnetic stimulation (TMS), involvement of the motor cortex and the corpus callosum was analysed in 13 children with ADHD and 13 sex- and age-matched controls. Contralateral silent period (cSP) and transcallosally mediated ipsilateral silent period (iSP) were investigated. RESULTS: Resting motor threshold (RMT), amplitudes of motor evoked potentials (MEP) and cSP were similar in both groups whereas iSP-latencies were significantly longer (p<0.05) and their duration shorter (p<0.01) in the ADHD group. For the ADHD group iSP duration tended to increase and iSP latency to decrease with age (n.s.). Conners-Scores did neither correlate with iSP-latencies and -duration nor with children's age. CONCLUSIONS: The shortened duration of iSP in ADHD children could be explained by an imbalance of inhibitory and excitatory drive on the neuronal network between cortex layer III-the projection site of transcallosal motor-cortical fibers-and layer V, the origin of the pyramidal tract. The longer iSP-latencies might be the result of defective myelination of fast conducting transcallosal fibers in ADHD. iSP may be a useful supplementary diagnostic tool to discriminate between ADHD and normal children.

Adolescent↗
PubMed1999

Motor neuron disease: usefulness of transcranial magnetic stimulation in improving the diagnosis.

Clinical upper motor neuron (UMN) involvement is sometimes difficult to detect in motor neuron disease (MND). For this reason we performed transcranial magnetic stimulation (TMS) to find out whether this technique may be useful in revealing signs of pyramidal tract impairment. Fifty-five MND patients, clinically divided into 22 amyotrophic lateral sclerosis (ALS), 18 ALS with probable UMN signs (ALS-PUMNS), 10 pure lower motor neuron syndrome (LMNS), and 5 progressive bulbar palsy (PBP), underwent standard TMS, recording from abductor digiti minimi and flexor allucis muscles. Prolongation of cortical motor evoked potential (MEP) latency and central conduction time (CCT) and absent MEP were considered as pathologic. ALS-PUMNS and LMNS patients were clinically reclassified after 1 year. TMS was abnormal in 95.4% of ALS, 72.2% of ALS-PUMNS, 50% of LMNS and 20% of PBP. Correlations between TMS parameters and both clinical signs of UMN involvement and disease severity were highly significant. TMS showed a high sensitivity, but lacked specificity. After 1 year, 11 patients among the ALS-PUMNS group were clinically reclassified as definite ALS: all of them had shown TMS abnormalities at the first examination. In conclusion, TMS provides important diagnostic information for an early prediction of ALS in those MND patients presenting with clinically equivocal UMN impairment.

Adult↗
PubMed2006

Oculomotricity in childhood: is the normal range the same as in adults?

UNLABELLED: The study of oculomotricity is done by the evaluation of three systems: saccade eye movements (MOS), optokinetic nystagmus (NO) and smooth pursuit eye movement (MORL). The joint action of these three systems allows the visual field's establishment in different movement situations. AIM: To compare the value of oculomotricity in normal adults and children to confirm, or not if it is viable to use the same parameters of adults normality to children's exams interpretation. STUDY DESIGN: Clinical with transversal cohort. MATERIAL AND METHOD: We studied MOS, NO and MORL in 50 normal children and in 35 adults and the results were compared by the t Student test. RESULTS: The data analysis showed significant difference between children and adults (significance at level +/- = 0.05) DISCUSSION: In the literature we have found evidence that myelinization of the vestibular pathways happen at about 16 weeks and the pyramidal tracts, at 24 months. Oculomotricity is finished at this time. Other papers describe the importance of these tests in the diagnostic of neurological diseases, visual alterations and as predictors of the risk of schizophrenia development but they do not report the normal range in children. In our study we found increased latency of MOS, increase in gain of NO, reduction in gain and increase in the distortion of MORL in children if compared to adults, which is in accordance with the literature. These alterations can be explained by the low attention during the tests and the immaturity of ocular movements' control in children. CONCLUSION: Therefore, the establishment of a parameter of normality to the oculomotricity in childhood is necessary for the correct analysis of the oculography to avoid misinterpretation of the exam.

Adult↗
PubMed2003

Brainstem dysgenesis: report of five patients with congenital hypotonia, multiple cranial nerve involvement, and ocular motor apraxia.

This paper reports three females and two males with a distinctive congenital syndrome characterized by severe congenital hypotonia, facial diplegia, jaw ankylosis, velo-pharyngeal incoordination, pyramidal tract signs, and ocular motor apraxia. Patients were followed up at ages ranging from 20 months to 16 years. All cases of this syndrome are sporadic, without dysmorphological features, chromosomal, or MRI brain abnormalities. Electrophysiological studies indicate the brainstem as the site of the neurological dysfunction. Post-mortem CNS study of one of the patients demonstrated neuronal depletion of the IV, VII, VIII, and IX cranial nerve nuclei and intact morphology of the cerebral hemispheres. A vascular accident, early in foetal life, is the most likely cause of the clinical picture. The extent of brainstem involvement and its related clinical findings distinguishes these patients from those with Moebius, Pierre Robin, or Cogan syndromes. Outcome is better than what could be anticipated during the first few months of life given the severity of symptoms. Intelligence or developmental quotients are within the normal range for their age. Facial hypomimia, feeding, and speech articulatory performance difficulties are the main disabilities observed in these patients at follow-up.

Abnormalities, Multiple↗
PubMed2001

Distributed grey and white matter deficits in hyperkinetic disorder: MRI evidence for anatomical abnormality in an attentional network.

BACKGROUND: Previous neuroimaging studies of children with attention deficit hyperactivity disorder (ADHD) have demonstrated anatomic and functional abnormalities predominantly in frontal and striatal grey matter. Here we report the use of novel image analysis methods, which do not require prior selection of regions of interest, to characterize distributed morphological deficits of both grey and white matter associated with ADHD. METHODS: Eighteen children with a refined phenotype of ADHD, who also met ICD-10 criteria for hyperkinetic disorder (mean age 10.4 years), and 16 normal children (mean age 10.3 years) were compared using magnetic resonance imaging. The groups were matched for handedness, sex, height, weight and head circumference. Morphological differences between groups were estimated by fitting a linear model at each voxel in standard space, applying a threshold to the resulting voxel statistic maps to generate clusters of spatially contiguous suprathreshold voxels, and testing cluster 'mass', or the sum of suprathreshold voxel statistics in each 2D cluster, by repeated random resampling of the data. RESULTS: The hyperkinetic children had significant grey matter deficits in right superior frontal gyrus (Brodmann area (BA) 8/9), right posterior cingulate gyrus (BA 30) and the basal ganglia bilaterally (especially right globus pallidus and putamen). They also demonstrated significant central white matter deficits in the left hemisphere anterior to the pyramidal tracts and superior to the basal ganglia. CONCLUSIONS: This pattern of spatially distributed grey matter deficit in the right hemisphere is compatible with the hypothesis that ADHD is associated with disruption of a large scale neurocognitive network for attention. The left hemispheric white matter deficits may be due to dysmyelination.

Adolescent↗
PubMed1998

Is subcortical disease associated with a poor response to antidepressants? Neurological, neuropsychological and neuroradiological findings in late-life depression.

BACKGROUND: Late-life depression is associated with increased subcortical white matter hyperintensities. There is some evidence that they are associated with a poorer response to acute treatment. Neurological signs and neuropsychological dysfunction are further evidence of abnormalities in the brain, but they have not been studied in relation to therapy resistance. METHODS: A prospective study of 24 normal controls and 75 consecutive elderly (aged 65 to 85) patients with DSM-III-R major depression entered a naturalistic study of treatment. Assessment of response to monotherapy and then lithium augmentation or ECT created three outcome groups. Investigations included magnetic resonance brain imaging, neuropsychological and neurological examination. RESULTS: Response to monotherapy within 12 weeks was shown by 42.7%, a further 37.3% responded to lithium augmentation or ECT within 24 weeks and 20% had responded poorly to all treatments at 24 weeks. Subcortical hyperintensities were significantly increased in the more resistant patients. These included confluent deep white matter, multiple (> 5) basal ganglia lesions and pontine reticular formation lesions. Most of the neuropsychological impairment was restricted to the resistant groups and was of a subcortico-frontal type. Extrapyramidal, frontal and pyramidal neurological signs characterized the resistant groups. The combination of extrapyramidal signs, pyramidal tract signs and impairment of motor hand sequencing strongly predicted resistance to 12 weeks of antidepressant monotherapy with 89% sensitivity and 95% specificity. CONCLUSION: In late-life depression a poor response to antidepressant monotherapy can be expected in those patients with a frontal lobe syndrome, extrapyramidal signs or if MRI T2-weighted lesions are present in both the basal ganglia and the pontine reticular formation.

Aged↗
PubMed1982

Pilot study of threonine supplementation in human spasticity.

Threonine supplementation (500 mg/day) was given to 6 patients with genetic spasticity syndromes for a period of 12 months, followed by a 4-month observation period without medication. All 6 patients showed partial improvement of spasticity, intensity of knee jerks and muscle spasms without changes in true pyramidal tract signs. The improvement in motor performance, objectively measured, averaged 29% (19% in upper limbs and 42% in lower limbs). The range of overall improvement was 19--35% (7--30% for upper limbs; 25--67% for lower limbs). No toxic clinical or biochemical side effects were encountered. Thus threonine, a precursor of glycine, produced the same effect on spasticity than that previously observed with glycine. It is concluded that threonine supplementation is feasible and safe and that it deserves a controlled trial in well defined (preferably genetic) cases of spasticity.

Adult↗
PubMed1998

Demyelination of retinal myelinated nerve fibers in Behcet's disease.

A 39 year-old Behcet's patient had demyelination of retinal myelinated nerve fibers after recurrent papillitis and vitritis. Oral Prednisolone, cyclosporine, and later periocular corticosteroids and oral colchicine were used but demyelination continued over a 5 year-period. A pseudobulbar palsy with urinary incontinence and pyramidal tract signs developed and azathioprine and corticosteroids were used. Demyelination of retinal nerve fibers stopped and while treatment was underway, the central nervous system (CNS) signs were stable. While the ocular pathology of Behcet's can mirror the CNS signs, indeed optic nerve ischemic demyelination may signal the potential for CNS involvement; azathioprine with prednisone may be more effective in the long-term for optic nerve and CNS involvement than cyclosporine with prednisone.

Adult↗
PubMed1999

Dipole source analysis in persistent mirror movements.

To elucidate the pathomechanism underlying persistent mirror movements (MM), we modelled the origin of electric brain activity associated with these movements. Movement-related cortical potentials (MRCP) in a group of subjects affected by persistent mirror movements were compared with those of a control group. The data of the normal subjects were best explained with two bilaterally active electric sources in the sensorimotor cortices with a clear preponderance of the hemisphere contralateral to the movement. In contrast, the MM subjects presented a fairly symmetric source activity in both hemispheres during unilateral intended movements. In the control group, the source representing the activity of the motor cortex ipsilateral to the moving finger reduced activity before the beginning of the movement; this was interpreted as an inhibition of the ipsilateral motor cortex during unilateral movement. In the MM group, however, this inhibition was not seen. Furthermore, while normal subjects demonstrated no relevant activity of an additional source placed near midline motor structures (supplementary motor area; SMA), subjects with MM showed considerable activity of this dipole source. These findings suggest that subjects with persistent MM have abnormal bilateral activation of the primary motor areas, probably together with an additional activation of mesial motor structures. This assumption fits well with the observation of an incomplete decussation of the pyramidal tract. The bilateral activation is then explained as a compensatory strategy in order to achieve sufficient force in the innervated target muscles.

Adolescent↗
PubMed1985

Grooming reflexes and Brown-Séquard epilepsy in cats with pontile lesions.

The literature on the relation between the scratch reflex and Brown-Séquard epilepsy in the guinea pig indicates that the scratch reflex is a stimulus-induced myoclonus that is the first component of a complete seizure. Cats with pontile lesions and cats with frontal neocortical lesions exhibit the scratch reflex and other grooming reflexes. The grooming reflexes in cats with pontile lesions develop over a period of a year or more into complete seizures that are similar to Brown-Séquard epilepsy as described for the guinea pig by Brown-Séquard and others. Cinematographic analyses revealed that the scratch reflex in cats with pontile lesions and in cats with frontal neocortical lesions has the same frequency and the same complex spatial and temporal pattern as normal scratching behavior. In addition, the myoclonus of the complete seizures is identified as the scratch reflex, representing a very vigorous and long-lasting afterdischarge. Reconstruction of the pontile lesions indicate that the lateral and rostral portions of the paralemniscal tegmental fields were destroyed along with portions of the pontile gray and pyramidal tract.

Animals↗
PubMed1983

Focal increases of white matter glucose utilization produced by electrical stimulation of rat motor cortex.

The right motor cortex was electrically stimulated in adult, awake rats for 45 min. Local cerebral glucose utilization (LCGU) was measured in white matter pathways with the (14C)-2-deoxyglucose method. Stimulation increased LCGU in focal regions of the right internal capsule to 51.3 mumol/100 g/min, compared to 39.8 on the control left side. Stimulation also increased LCGU in the right, medial pontine pyramidal tract to 36.2 mumol/100 g/min, compared with 27.3 on the control left side. The data demonstrate that electrical stimulation of motor cortex neurons increases LCGU 30 to 40% in the efferent myelinated axons of those neurons.

Animals↗
PubMed1995

Persistence of distal motor control in the locked in syndrome. Review of 11 patients.

We report 11 patients with the locked in syndrome (LIS). The functional outcome was good in four patients with notable motor recovery, but motor deficit remained seriously disturbed in seven patients. All of the patients regained some distal control of finger and toe movements, often allowing functional use of a digital switch. The independence thereby gained is worthwhile, in some patients allowing environment control, communication by means of a computer, and electric wheelchair ambulation. When motor recovery occurs, the progression is disto-proximal with dramatic axial hypotonia. In five patients clinical insomnia was noted and polysomnography showed a reduction of REM sleep. The implications of systems other than the pyramidal tracts in the physiopathology of LIS are discussed.

Adolescent↗
PubMed1996

Neurographic assessment of intramedullary motoneurone lesions in cervical spinal cord injury: consequences for hand function.

Examination of hand function and neurography of the median- and ulnar nerves was performed in 15 patients with acute and 26 patients with chronic tetraplegia due to cervical spinal cord injury (SCI). 30% of patients showed a mild and 20% a severe axonal lesion of motor fibres of both nerves. The latter is caused by intramedullary damage of ventral horn cells and anterior nerve roots as neurographic examination of sensory nerve fibres was normal in these patients. The most frequent and severe nerve lesion was present in those with lower cervical spinal cord injuries (C6/7-Th1) where the median and ulnar nerves originate. In the latter patients the development of active hand function, which enables the patient to perform active grasping movements, was closely related to the result of neurography, already early after trauma. The results of median and ulnar neurography in tetraplegia due to cervical SCI allow to differentiate between intramedullary damage of motoneurones and the anterior nerve roots (peripheral nervous system) or the pyramidal tract fibres (central nervous system) within the spinal cord responsible for the paresis of the intrinsic hand muscles. Neurography is of prognostic value in cervical SCI to predict the outcome of hand function and therefore influences the appropriate occupational therapy and the program and aims of rehabilitation.

Action Potentials↗
PubMed2005

Longitudinal diffusion changes in cerebral hemispheres after MCA infarcts.

Diffusion tensor imaging can be used in vivo to assess the longitudinal and regional microstructural changes occurring after middle cerebral artery (MCA) infarcts in humans. Nine patients were investigated 1 week (D7), 1 (M1), 3 (M3), and 6 months (M6) after the occurrence of an isolated MCA infarction. First, an overall analysis was performed using histograms of mean diffusivity (MD) and fractional anisotropy (FA) in each hemisphere. Thereafter, the regional pattern of diffusion changes was investigated voxel by voxel with statistical parametric mapping 99. In the hemisphere ipsilateral to the infarction, histogram analysis revealed a significant decrease in FA between D7 and M6 associated with a progressive increase in MD from D7 to M3. Remote from the MCA territory, the voxel by voxel analyses detected a significant increase in MD within the thalamus at M3 and M6 and a reduction in FA along the pyramidal tract at M6. In the contralateral hemisphere, between D7 and M6, a significant hemispheric atrophy was observed in association with a global reduction in anisotropy, in the absence of distinctive regional diffusion changes. These results suggest that micro- and macrostructural tissue modifications can be detected with diffusion tensor imaging in regions remote from the ischemic area in both hemispheres.

Adult↗
PubMed2003

Autopsy verifies demyelination and lack of vascular damage in partially reversible radiation myelopathy.

STUDY DESIGN: Case report of recovering radiation myelopathy. OBJECTIVE: To present autopsy and functional imaging findings on a unique case of slowly recovering radiation myelopathy with the aim of the clarification of the underlying mechanism. PATIENT: The cervical spinal cord and the distal part of the medulla oblongata of a 36-year-old thyroid cancer patient had been incorrectly irradiated with a total dose of 61 Gy and a fraction size of 3.4 Gy (J Neurol Sci 1999; 163:39-43), resulting in incomplete cervical transection with a 5-month latency period following the termination of radiotherapy. This was followed by a 9.5-year spontaneous improvement until her demise, during which the check-ups were supplemented by positron emission tomography (PET) investigations; these indicated increased [18F]deoxyglucose and [15O]butanol uptakes, but a diminished [11C]methionine accumulation by the irradiated spinal cord segment. RESULTS: Autopsy revealed demyelination (with axonal loss) and neuronal damage in the cervical spinal cord and the distal part of the medulla oblongata. In the same region, only minimal vascular injury (thickening of some of the capillary walls) was detected, but not cell proliferation or chronic inflammation. Bilateral, secondary pyramidal tract degeneration caudal to the irradiated segment was observed. The PET and autopsy findings, although separated by 2 years, are consistent. CONCLUSIONS: The pathological state of the spinal cord revealed by the autopsy is concordant with the incomplete cervical transection, implying that the functional recovery is supported by a process that probably differs from the restoration of the mechanism destroyed by the radiotherapy. For the restoration of the function, we suggest an altered conduction mechanism of the action potential, involving an increased number of sodium channels along the demyelinated segments of the injured axons, which is fully congruent with the PET findings.

Adult↗
PubMed2001

Autopsy case of autosomal recessive hereditary spastic paraplegia with reference to the muscular pathology.

An autopsied case of autosomal recessive hereditary spastic paraplegia with severe neurogenic muscular atrophy is described herein. This patient, a 16-year-old woman, presented with gait disturbance. She developed progressive spastic paralysis of the upper and lower limbs and mental deterioration. She became bedridden at approximately 40years of age. Dysarthria worsened at 45 years of age. She died of pneumonia at 50 years of age. Her younger sister has shown similar clinical symptoms and became bedridden at 37 years of age. Their parents were second cousins. Autopsy revealed a severely atrophic brain, weighing 720 g. The cerebral cortex was thin, and the white matter was extremely reduced in volume. Microscopically, neuronal loss and variable astrogliosis with diffuse spongy changes were evident at the cerebral cortex, thalamic nuclei, basal ganglia and hippocampus. The remaining neurons were atrophied with heavy deposition of lipofuscin. In the spinal cord, the pyramidal tracts as well as the dorsal spinocerebellar tracts were degenerated. In addition, marked loss of the anterior horn cells was seen. Severe neuronal loss of the nucleus gracilis was also detected. In contrast, only mild degeneration of the ventral spinocerebellar tracts and fasciulus cuneatus in the spinal cord were observed. In the frozen sections of skeletal muscle, severe neurogenic atrophy and fatty infiltration were evident. In addition, several rimmed vacuoles were observed in the atrophic fibers, and cytochrome coxidase-deficient fibers were present in part. Reduced nicotinamide adenine dinucleotide (NADH)-tetrazolium reductase reaction revealed abnormal accumulation of mitochondria around the center of the non-atrophic muscle fibers. It is suggested that an analysis of mitochondrial function of Japanese autosomal recessive hereditary spastic hemiplegia may provide additional information to clarify the pathogenesis.

ATPases Associated with Diverse Cellular Activitie↗