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Pyramidal tract

Z Graggen, W. J., Fouad, K., Raineteau, O., Metz, G. A. S., Schwab, M. E. and Kartje, G. L. Compensatory sprouting and impulse rerouting after unilateral pyramidal tract lesion in neonatal rats. /. Neurosci. 20 6561-6569, 2000. [Pg.527]

The nigrostriatal pathway participates in the production of smooth physical motion. It is not the brain area that works to initiate movement, which is in the cerebral cortex (pyramidal tract) it is the region that helps one to have fluid motion (extrapyramidal tract). Although many neurotransmitters are found in this latter system, two neurotransmitters—dopamine and acetylcholine—are predominantly involved in this pathway. The brain normally maintains a relatively stable ratio of dopamine and acetylcholine in the pathway. However, when something happens to upset this ratio, problems arise. [Pg.109]

With severe intoxication, lesions of the anterior horn cells and the pyramidal tracts may also occur. Muscular weakness may increase over a period of several weeks or months recovery may take months or years and in 25-30% of cases, permanent residual effects remain, usually confined to the lower limbs. Gait impairment, characterized by high steps and footdrop and permanent in some, was called Jake Walk. ... [Pg.716]

Tire neuronal events that occur within the cerebral cortex are extraordinarily complex and little understood 409 In what way the brain is able to initiate voluntary movement of muscles is obscure. However, it is established that the signals that travel out of the brain down the efferent fibers to the muscles arise from large motor neurons of the motor cortex,410 a region that extends in a band across the brain and adjacent to the sensory cortex (Fig. 30-14). The axons of these cells form the pyramidal tract that carries impulses downward to synapses in the spinal cord and from there to the neuromuscular junctions. These are specialized synapses at which acetycholine is released, carrying the signal to the muscle fibers themselves. Passing over the cell surface and into the... [Pg.1766]

In addition to the somatic motor system that operates the voluntary (striated) muscles via the pyramidal tract, there is the autonomic system, which controls the involuntary (smooth) muscles, glands, heartbeat, blood pressure, and body temperature. This system has its origins in both the cerebral cortex and... [Pg.1767]

Motor control that does not involve the pyramidal tracts. It originates in the basal ganglia. [Pg.471]

Finally, one of the most interesting extensions of DTI is the potential to track fibers [ in vivo MR tractography (Bammer et al. 2003 Mori and van Zijl 2002)], by using the information on anisotropic directionality contained in the diffusion tensor. With these mathematically complex methods, it has become possible to track fibers from an initial set of seed points, which can be used to track the pyramidal tract or corpus callosum as shown in Fig. 7.5b. [Pg.122]

Thomalla G, Glauche V, Koch MA, Beaulieu C, Weiller C, Rother J (2004) Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke. Neuroimage 22 1767-1774... [Pg.158]

Recently, using color-coded diffusion tensor imaging five different patterns of corticospinal tract stroke were identified that fall into two clinical subgroups with either little recovery or good recovery. Patients with poor motor recovery had lesions centered in the pyramidal tract (anterior choroidal artery). Patients with good recovery had either very small lesions or lesions located anteriorly or medially (Lie et al. 2004). [Pg.212]

The STh receives also direct excitatory input from the cerebral cortex, especially from the frontal cortical areas the primary motor cortex, with a minor contribution of prefrontal and premotor areas (see for review Nambu et al., 2002). Cortical afferents from the primary motor cortex in rodents and cats are composed of collaterals of the pyramidal tract or of corticostriatal fibers (reviewed by Hamani et al., 2004). The hyperdirect pathway is a cortico-STN-pallidal pathway, which conveys excitatory input from the motor-related cortical areas to the GP bypassing the striatum, and therefore with shorter conduction time. According to the model of the hyperdirect pathway, the activity of the cortico-STh-pallidal route could result in a wide inhibitory effect on motor programs, with adjustments of signals through the direct cortico-striato-pallidal pathway (Nambu et al., 2002). [Pg.43]

A 37-year-old man, with a short history of heroin and cocaine use, presented with spasticity of all limbs, a confusional state, and mutism (28). The electroencephalogram, CT scan, and MRI scan showed predominantly positive frontal pathology, with other lesions in the pyramidal tracts and corpus callosum. The diagnosis was leukoencephalopathy. The symptoms gradually abated after 4 weeks, and repeat tests after 6 months shown to be normal. [Pg.545]

A 24-year-old man, who had sniffed toluene-containing compounds since he was 17, developed a syndrome that included psychiatric impairment, signs of bilateral pyramidal tract damage, altered cerebellar and sensory functions, and a peripheral neuropathy (19). [Pg.618]

A spastic pyramidal tract syndrome of the legs has been reported. In young children the features of an extrapyr-amidal syndrome include abnormal eye movements, trismus, torticollis, and torsion dystonia. [Pg.723]

Restlessness, agitation, queer sensations, difficulty in memorizing (40), and vertigo and convulsions (50) have also been reported. In nearly aU cases there was a concomitant polyneuropathy. Muscle weakness or cramps, mild ataxia, carpal tunnel syndrome, and signs of pyramidal tract involvement have also been described (51). [Pg.3346]

Extrapyramidal Outside the pyramidal tracts, with origin in the basal ganglia. These cell bodies are involved with starting, stopping, and smoothing out movements (Chapter 13). [Pg.442]

Main symptoms involve the nervous system. The initial symptoms are characterized by muscle weakness in the arms and legs that may occur days or weeks after exposure. Eventually, symptoms include symptoms of spinal cord injury, including a clumsy shuffling gait, spasticity, hyperreflexia, and permanent damage to the pyramidal tracts and upper motor neuron syndrome. This syndrome is known as OPIDN. [Pg.1253]

The types of nervous system effects described in the Minamata outbreak included mental retardation retention of primitive reflexes cerebellar symptoms dysarthria hyperkinesia hypersalivation atrophy and hypoplasia of the cerebral cortex, corpus callosum, and granule cell layer of the cerebellum dysmyelination of the pyramidal tracts and an abnormal neuronal cytoarchitecture. It has been suggested that the widespread damage involved derangement of basic developmental processes, such as neuronal migration (Choi et al. 1978 Matsumoto et al. 1965) and neuronal cell division (Sager et al. 1983). [Pg.162]

Late lateral cervical nucleus LSp lateral spinal nucleus pyD pyramidal tract... [Pg.118]

We have identified the parapyramidal nucleus as the cell group dorsolateral to the pyramidal tract, which is outlined but not named in the second edition of this atlas (Paxinos and Watson, 1986). [Pg.132]

Py pyramidal cell layer of the hippocampus 35, 87, 106 py pyramidal tract 53-76, 79-81, 117a,b pyx pyramidal decussation 77-80... [Pg.497]


See other pages where Pyramidal tract is mentioned: [Pg.176]    [Pg.70]    [Pg.59]    [Pg.29]    [Pg.287]    [Pg.366]    [Pg.139]    [Pg.140]    [Pg.386]    [Pg.123]    [Pg.110]    [Pg.545]    [Pg.545]    [Pg.139]    [Pg.140]    [Pg.1394]    [Pg.407]    [Pg.224]    [Pg.276]    [Pg.407]    [Pg.1098]    [Pg.1098]    [Pg.1796]    [Pg.157]   
See also in sourсe #XX -- [ Pg.1766 ]

See also in sourсe #XX -- [ Pg.212 ]

See also in sourсe #XX -- [ Pg.43 ]




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Pyramidal tracts, degeneration

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