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7 - Lesions of cortex and post-stroke ‘plastic’ reorganization
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- By Paolo M. Rossini, Clinica Neurologica Università Campus Bio-Medico, Rome, Italy; AFaR Dept. Neuroscience, Ospedale Fatebenefratelli, Isola Tiberina, Rome, Italy; IRCCS Centro S. Giovanni di Dio, Brescia, Italy, Joachim Liepert, Department of Neurology, University of Hamburg, Germany
- Edited by Simon Boniface, Ulf Ziemann, Johann Wolfgang Goethe-Universität Frankfurt
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- Book:
- Plasticity in the Human Nervous System
- Published online:
- 12 August 2009
- Print publication:
- 15 May 2003, pp 166-203
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Summary
General introduction
Stroke is still the third cause of death and the first cause of chronic, highly disabling disease because of the frequent neurological sequelae affecting sensorimotor integration, movement programming and execution, walking, language, balance, mood and sensory perception. It is a well-accepted notion that, following the acute ischemic block of blood perfusion, there is a central core of dead neurons circumscribed by a shell of so-called ischemic penumbra, where the neurons adjacent to the damaged core are functionally blocked but still alive, because of the suboptimal flow from arterioles and capillaries and collaterals from the bed of vessels in the lesional periphery. This situation is of relatively brief duration (from hours to few days) and is followed either by a full recovery of the non-functioning, but still living, neurons (with a rapid, partial or total restoration of the lost functions) or by a complete loss of the perilesional contingent of brain cells with consequent stabilization of the clinical picture, i.e. the presence of more or less severe deficits. Several mechanisms contribute to the final volume of the lesioned tissue; from what can be inferred from the ischemia/reperfusion animal model, they include: ‘inflammatory-like’ reactions in which cytokines (mainly interleukin-1 and tumour necrosis factor) attract polymorphonuclear leukocytes, which create mechanical obstruction to erythrocytes' circulation by adherence to corresponding endothelial cell ligands, as well as becoming a source of oxygen free radicals (including nitric oxide, superoxide and peroxynitrite; del Zoppo & Garcia, 1995); later, a platelet activating factor induces platelets aggregation in the damaged area of microcirculation; in the core of the ischemic area, neuronal death may be mediated by the effects of excitatory neurotransmitters, e.g. glutamate which promotes calcium influx in the injured cells, and the accumulation of lactic acid as the result of a metabolic switch to anaerobiosis (Garcia et al., 1994).
5 - Neuromagnetic methods and transcranial magnetic stimulation for testing sensorimotor cortex excitability
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- By Paolo M. Rossini, Department of Neurology, CRCCS AFaR Ospedale Fatebenefratelli, Rome, Italy, Alfredo Berardelli, Departimento Scienze Neurologiche, Università La Sapienza, Rome, Italy, Roberto Cantello, Clinica Neurologica, Università del Piemonte Orientale, Novara, Italy
- Edited by Renzo Guerrini, University of London, Jean Aicardi, Hôpital Robert-Debré, Paris, Frederick Andermann, Montreal Neurological Institute & Hospital, Mark Hallett, National Institutes of Health, Baltimore
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- Book:
- Epilepsy and Movement Disorders
- Published online:
- 03 May 2010
- Print publication:
- 13 December 2001, pp 59-76
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Summary
Magnetoencephalography (MEG): physiological background
Magnetoencephalography (MEG) is a non-invasive technique able to spatially identify the synchronous firing neurons in restricted cortical areas, either for spontaneous cerebral activity or in response to an external stimulus. MEG is unaffected by scalp and skull, and preferentially reflects the tangential component of dipoles in the depth of gyri and sulci.
The neuromagnetic technique consists of measurement of the magnetic field over the scalp, as generated by the bioelectrical currents in the brain. In order to achieve the sensitivity needed to measure these very weak magnetic fields (about 10 as compared to the earth magnetic field), the use of new superconducting magnetometers (superconducting quantum interferences devices or SQUID) and of devoted shielding is mandatory. Under the symmetry conditions, well approximated in the case of the head, it can be shown that the component of the magnetic field perpendicular to the skull is mostly sensitive to the tangential component of the primary current source, and negligibly to the field generated by the volume currents and to the distortions, smearing effects and filtering of frequency components, mainly in the faster rhythms caused by the intervening tissues (Romani & Rossini, 1988; Okada et al., 1999). This represents an advantage in respect to the purely electric measurement of neural activity, especially for the postsynaptic component at the level of the cortical mantle. The magnetic field is simultaneously measured over many scalp sites, with a rapid sampling in the time domain, and from these data the isofield contour maps are calculated and studied.