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Motor cortex stimulation

Pagni C.A., Altibrandi M.G., Bentivoglio A., Caruso G., Cioni B., Fiorella C., Insola A., Lavano A. et al. Extradural motor cortex stimulation (ECMS) for Parkinson s disease. History and first results by the study group of the Italian neurosurgical society. Acta Neurochir Suppl, 2005, 93, 113-119. [Pg.371]

Pagni, C.A., S. Zeme, and F. Zenga, Further experience with extradural motor cortex stimulation for treatment of advanced Parkinson s disease. Report of 3 new cases. /. Neurosurg. Sci, 2003,47 189-193. [Pg.463]

Brown, J.A. et al. Motor cortex stimulation for enhancement of recovery after stroke case report. Neurol. Res., 2003,25 815-818. [Pg.463]

Motor cortex stimulation is reserved for the treatment of complex central and neuropathic pain syndromes that have proven refractory to medical treatment, including post-stroke pain, deafferentation pain, and some neuropathic pain states of peripheral origin. [Pg.35]

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]

Figure 13.26 The motor control pathway for stimulation of voluntary contractions. The motor control pathway begins in the motor cortex in the brain and the sequence continues through the spinal cord to the muscle and the myofibrils. It has two components, central and peripheral. One or both components can be involved in biochemical mechanisms of fatigue (see below). Figure 13.26 The motor control pathway for stimulation of voluntary contractions. The motor control pathway begins in the motor cortex in the brain and the sequence continues through the spinal cord to the muscle and the myofibrils. It has two components, central and peripheral. One or both components can be involved in biochemical mechanisms of fatigue (see below).
The cerebral cortex is conventionally subdivided into four main regions that may be delineated by the sulci, or large clefts, termed the frontal, temporal, parietal and occipital lobes. These names are derived from the bones of the skull which overlay them. Each lobe may be further subdivided according to its cellular structure and composition. Thus Brodmarm has divided the cortex into approximately 50 discrete areas according to the specific cellular structure and function. For example, electrical stimulation of the strip of cerebral cortex in front of the central sulcus (see Figure 1.3) is responsible for motor commands to the muscles. This is termed the primary motor cortex and can be further subdivided according to which muscles are controlled in different parts of the body. [Pg.5]

Pascual-Leone A, Valls-Sole J, Wassermann EM, et al Responsiveness to rapid-rate transcranial magnetic stimulation of the human motor cortex. Brain 117 847-858, 1994... [Pg.715]

Other structures have recently been stimulated including the motor cortex [52], the pedunculopontine nucleus in the brain stem [54] and the zona incerta (a structure adjacent to the STN) [55]. This indicates that the stimulation of various structures along the motor loop can lead to improvement of parkinsonian signs but spreading to other adjacent structures cannot be excluded. In the present chapter we focus on DBS of the STN. [Pg.355]

The mechanisms of motor recovery vary according to location of the lesion cortical iirfarcts are associated with activation of the contralateral primary sensorimotor cortex, whereas subcortical infarcts appear to activate the bilateral primary sensorimotor cortex (Kwon et al. 2007). Several studies indicate that worse motor performance is related to a greater amount of contralesional activation (Calautti et al. 2007) and that patients who activate the ipsilesional primary motor cortex early had a better recovery of hand function (Loubinoux et al. 2007). Repetitive peripheral magnetic stimulation increases the activation of the parieto-premotor network and thereby might have a positive conditioning effect for treatment (Struppler et al. 2007). In addition to changes in the activation pattern of the... [Pg.280]

Epilepsy is a neurological disorder characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition, with a tendency towards uncontrolled excitability (Papandreou et al., 2006). Recurrent severe seizures can lead to death of brain cells. Phenytoin (Dilantin, Phenytek) is a widely used anti-seizure medicine (LaRoche, 2007). The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited, possibly by promoting sodium efflux from neurons. Phenytoin tends to stabilize the threshold against hyper-excitability caused by excessive stimulation. The current status of new (second generation) anti-epileptic drugs has been recently reviewed (Bialer et al., 2007). [Pg.262]

In general, barbiturates produce a generalized depression of synaptic function. The threshold for electrical stimulation in the motor cortex is increased by barbiturates, resulting in a decreased propensity for motor seizures. [Pg.30]

Secobarbital depresses the sensory cortex decreases motor activity depresses cerebral function and produces drowsiness, sedation, and hypnosis. In the motor cortex, secobarbital increases the threshold for electrical stimulation, which contributes to its anticonvulsant properties. [Pg.39]

Transcranial magnetic stimulation (TMS), whereby a pulsed magnetic field creates current flow in the brain and can temporarily excite or inhibit specific areas, is being developing as an analytically and therapeutically useful non-invasive tool for studying the human brain. Tlie application of TMS to the motor cortex can produce a muscle twitch or may... [Pg.95]

Fig. 25.3. Striatal dopaminergic stimulation of the direct and indirect pathways modulates the thalamus excitatory outflow to the motor cortex. Fig. 25.3. Striatal dopaminergic stimulation of the direct and indirect pathways modulates the thalamus excitatory outflow to the motor cortex.

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See also in sourсe #XX -- [ Pg.35 ]




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