Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Cortex motor

ALS is a disorder of the motor neurons and the cortical neurons that provide their input. The disorder is characterized by rapidly progressive weakness and muscle atrophy. Most affected patients die of respiratory compromise and pneumonia after 2 to 3 years. There is prominent loss of motor neurons in the spinal cord and brainstem although the oculomotor neurons are spared. Large pyramidal motor neurons in layer V of motor cortex, which are the origin of the descending corticospinal tracts, are also lost. [Pg.74]

Localization CNS Hippocampus (CA1, CA3, DG), septum, amygdala, raphe nuclei CNS Striatum, hippocampus (CA1), substantia nigra, globus pallidus, superior colliculi, spinal cord, raphe nuclei CNS like 5-HT1B but at lower densities. CNS Caudate putamen, parietal cortex, fronto-parietal motor cortex, olfactory tubercle, amygdala CNS Cortex, Thalamus, olfactory bulb (rat), claustrum (g-pig), hippocampus (CA3), spinal cord. [Pg.1121]

One might have thought that d Arsonval s discovery would be sufficient to generate further studies of brain function by magnetic stimulation, but the technical solutions to this had to wait for the best part of the twentieth century until 1985 when Anthony Barker and colleagues at the University of Sheffield successfully stimulated the motor cortex and pro-... [Pg.176]

Fig. 8.1 Rostrocaudal neuroanatomical distribution of CCR5-immunoreactivity in the telencephalon, diencephalon and mesencephalon using a CCR5 antibody (Santa Cruz Biotechnology, Santa Cruz, CA, USA). Regions corresponding to pictures are depicted in coronal diagrams taken from the Paxinos and Watson (1998). (a, b) M Motor cortex, (c, d) CPu caudate putamen (striatum), (e,t)SID substantia innominata dorsal part, (g, h) GP globus pallidus, (i, j)Me medial amygdaloid... Fig. 8.1 Rostrocaudal neuroanatomical distribution of CCR5-immunoreactivity in the telencephalon, diencephalon and mesencephalon using a CCR5 antibody (Santa Cruz Biotechnology, Santa Cruz, CA, USA). Regions corresponding to pictures are depicted in coronal diagrams taken from the Paxinos and Watson (1998). (a, b) M Motor cortex, (c, d) CPu caudate putamen (striatum), (e,t)SID substantia innominata dorsal part, (g, h) GP globus pallidus, (i, j)Me medial amygdaloid...
Following the development of the motor program, neurons originating in the multimodal motor association areas transmit impulses by way of association tracts to neurons of the primary motor cortex. The primary motor cortex is located in the precentral gyrus, which is the most posterior region of the frontal lobe adjacent to the multimodal motor association areas (see Figure 6.3) this area initiates voluntary contractions of specific skeletal muscles. Neurons whose cell bodies reside here transmit impulses by way of descending projection tracts to the spinal cord, where they innervate the alpha motor neurons (which innervate skeletal muscles). [Pg.54]

The corticospinal tracts originate in the cerebral cortex. Neurons of the primary motor cortex are referred to as pyramidal cells. Most of these neurons axons descend directly to the alpha motor neurons in the spinal cord. In... [Pg.70]

Emerick, A. J., Neafsey, E. J., Schwab, M. E. and Kartje, G. L. Functional reorganization of the motor cortex in adult rats after cortical lesion and treatment with monoclonal antibody IN-1. /. Neurosci. 23 4826-4830, 2003. [Pg.527]

Phenotype determined by cortical region activated (e.g. if motor cortex representing left thumb is activated, then left thumb jerking results). Consciousness is preserved Impaired consciousness lasting seconds to minutes, often associated with automatisms such as lip smacking Simple or partial complex seizure evolves into a tonic-clonic seizure with loss of consciousness. There are sustained muscular contractions (tonic) followed by periods of relaxation (clonic) lasting 1-2 min... [Pg.630]

Motor neuron disease is characterized clinically by weakness, muscle atrophy and spasticity. This illness, often termed Lou Gehrig s disease in the United States, is the most common adult-onset form of MND with a prevalence of approximately 2-3 per 100,000 people [1-3,10, 25, 28]. Each year in the United States, in excess of 5,000 people are diagnosed with ALS. In parts of the United Kingdom, 1 in =500 deaths are attributed to some form of MND. The principal clinical signs of ALS include progressive limb weakness, which may be symmetrical or asymmetrical atrophy of appendicular, bulbar and respiratory muscles and spasticity [1,2,26,28]. The paralysis/muscle atrophy and spasticity are the result of degeneration of motor neurons in the spinal cord/brain stem and motor cortex respectively. The onset of this illness is typically in the fifth or sixth decade of life affected individuals usually... [Pg.732]

Excitotoxicity (see Chs 15 and 32) has been suggested to be a mechanism by which motor neurons are damaged in ALS [25,48,49]. About 60-70% of sporadic ALS patients have a 30-95% reduction in the levels of the astroglial glutamate transporter EAAT2 (excitatory amino acid transporter 2), also termed GLT-1, in motor cortex and spinal cord [25, 48, 49]. Reduction in level of activity of this major glutamate transporter leads to increased extracellular concentrations of glutamate at synapses and evidence of excitotoxicity exists in some patients with ALS. [Pg.732]

Basal ganglia output is directed from GPi and SNr to the thalamus. Movement-related basal ganglia output projects from GPi almost exclusively to the ventrolateral nucleus of the thalamus which, in turn, projects to the primary motor cortex, the cortical supplementary motor area, and other premotor cortical areas. Movement-related output from SNr terminates in the ventral anterior and in... [Pg.761]

Reduced activation of dopamine-1 and dopamine-2 receptors results in greater inhibition of the thalamus. Clinical improvement may be more tied to restoring activity at the dopamine-2 receptor than at the dopamine-1 receptor. Loss of presynaptic nigrostriatal dopamine neurons results in inhibition of thalamic activity and activity in the motor cortex. Degeneration of nigrostriatal dopamine neurons results in a relative increase of striatal cholinergic activity, which contributes to the tremor of PD. [Pg.642]

Arriza, J. L., Fairman, W. A., Wadiche, J. I., Murdoch, G. H., Kavanaugh, M. P., and Amara, S. G. (1994) Functional comparisons of three glutamate transporter subtypes cloned from human motor cortex../. Neurosci. 14, 5559-5569. [Pg.157]

W. N. Colier, V. Quaresima, B. Oeseburg, and M. Ferrari. Human motor-cortex oxygenation changes induced by cyclic coupled movements of hand and foot. Experimental Brain Research, 129 457-461, 1999. [Pg.365]

M. Wolf, U. Wolf, J. H. Choi, R. Gupta, L. P. Safonova, and L. A. Paunescu. Functional frequency-domain near-infrared spectroscopy detects fast neuronal signal in the motor cortex. Neuroimage, 17 1868-1875, 2002. [Pg.371]

An inevitable consequence of ageing is an elevation of brain iron in specific brain regions, e.g. in the putamen, motor cortex, pre-frontal cortex, sensory cortex and thalamus, localized within H- and L-ferritin and neuromelanin with no apparent adverse effect. However, ill-placed excessive amounts of iron in specific brain cellular constituents, such as mitochondria or in specific regions brain, e.g. in the substantia nigra and lateral globus pallidus, will lead to neurodegenerative diseases (Friedreich s ataxia and Parkinson s disease (PD), respectively). We discuss here a few of the examples of the involvement of iron in neurodegenerative diseases. From more on iron metabolism see Crichton, 2001. [Pg.307]

Motor cortex Controls movement of the face, arms, and legs... [Pg.15]

Difficulty moving, impaired coordination Motor cortex, basal ganglia, cerebellum... [Pg.67]


See other pages where Cortex motor is mentioned: [Pg.461]    [Pg.126]    [Pg.163]    [Pg.185]    [Pg.172]    [Pg.174]    [Pg.179]    [Pg.180]    [Pg.180]    [Pg.174]    [Pg.176]    [Pg.54]    [Pg.23]    [Pg.273]    [Pg.210]    [Pg.52]    [Pg.54]    [Pg.54]    [Pg.55]    [Pg.276]    [Pg.287]    [Pg.525]    [Pg.525]    [Pg.525]    [Pg.630]    [Pg.732]    [Pg.882]    [Pg.103]    [Pg.367]    [Pg.31]    [Pg.170]   
See also in sourсe #XX -- [ Pg.70 ]

See also in sourсe #XX -- [ Pg.1766 ]

See also in sourсe #XX -- [ Pg.354 , Pg.356 ]

See also in sourсe #XX -- [ Pg.289 ]

See also in sourсe #XX -- [ Pg.43 , Pg.46 , Pg.52 , Pg.69 , Pg.78 , Pg.306 , Pg.529 ]

See also in sourсe #XX -- [ Pg.172 , Pg.173 , Pg.176 ]

See also in sourсe #XX -- [ Pg.229 ]




SEARCH



Brain regions motor cortex

Cortex

Cortexal

Motor cortex stimulation

Sensory-motor cortex

Supplementary motor cortex

© 2024 chempedia.info