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Books on the topic 'Somatosensory nervous system'

Author: Grafiati

Published: 2 February 2023

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1

Baumgartner, Christoph. Clinical Electrophysiology of the Somatosensory Cortex: A Combined Study Using Electrocorticography, Scalp-EEG, and Magnetoencephalography. Vienna: Springer Vienna, 1993.

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2

Evoked potential primer: Visual, auditory, and somatosensory evoked potentials in clinical diagnosis. Boston: Butterworth, 1985.

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3

Spehlmann, Rainer. Evoked potential primer: Visual, auditory, and somatosensory evoked potentials in clinical diagnosis. Boston: Butterworth, 1985.

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4

Snow, Peter J., and Peter Wilson. Plasticity in the Somatosensory System of Developing and Mature Mammals — The Effects of Injury to the Central and Peripheral Nervous System. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75701-3.

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5

1931-, Spehlmann Rainer, ed. Spehlmann's evoked potential primer: Visual, auditory, and somatosensory evoked potentials in clinical diagnosis. 2nd ed. Boston: Butterworth-Heinemann, 1994.

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6

Kuhn, H., G. Breithardt, Peter J. Snow, U. Gleichmann, J. Schoenmackers, H. H. Dahm, H. Gillmann, R. M. Jungblut, W. Krelhaus, and F. Loogen. Plasticity in the Somatosensory System of Developing and Mature Mammals - The Effects of Injury to the Central and Peripheral Nervous System. Springer, 2011.

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7

Peter, Wilson, and Peter J. Snow. Plasticity in the Somatosensory System of Developing and Mature Mammals -- the Effects of Injury to the Central and Peripheral Nervous System. Springer, 2012.

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8

Mauguière, François, and Luis Garcia-Larrea. Somatosensory and Pain Evoked Potentials. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0043.

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This chapter discusses the use of somatosensory evoked potentials (SEPs) and pain evoked potentials for diagnostic purposes. The generators of SEPs following upper limb stimulation have been identified through intracranial recordings, permitting the analysis of somatosensory disorders caused by neurological diseases. Laser activation of fibers involved in thermal and pain sensation has extended the applications of evoked potentials to neuropathic pain disorders. Knowledge of the effects of motor programming, paired stimulations, and simultaneous stimulation of adjacent somatic territories has broadened SEP use in movement disorders. The recording of high-frequency cortical oscillations evoked by peripheral nerve stimulation gives access to the functioning of SI area neuronal circuitry. SEPs complement electro-neuro-myography in patients with neuropathies and radiculopathies, spinal cord and hemispheric lesions, and coma. Neuroimaging has overtaken SEPs in detecting and localizing central nervous system lesions, but SEPs still permit assessment of somatosensory and pain disorders that remain unexplained by anatomical investigations.

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9

(Foreword), Thomas Woolsey, ed. Barrel Cortex. Cambridge University Press, 2008.

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10

Fox, Kevin. Barrel Cortex. Cambridge University Press, 2008.

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11

Fox, Kevin, and Thomas Woolsey. Barrel Cortex. Cambridge University Press, 2008.

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12

Fox, Kevin. Barrel Cortex. Cambridge University Press, 2008.

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13

Fox, Kevin, and Thomas Woolsey. Barrel Cortex. Cambridge University Press, 2009.

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14

Fox, Kevin, and Thomas Woolsey. Barrel Cortex. Cambridge University Press, 2008.

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15

Colvin, Lesley A., and Marie T. Fallon. Pain physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0009.

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The International Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’. A good understanding of the physiology of pain processing is important, with recent advances in basic science, functional neuroimaging, and clinical pain syndromes contributing to our understanding. It is also important to differentiate between nociception, the process of detecting noxious stimuli, and pain perception, which is a much more complex process, integrating biological, psychological, and social factors. The somatosensory nervous system, from peripheral nociceptors, to sensory nerves and spinal cord synapses has many potential sites for modulation, with ascending pathways to the brain, balanced by ‘top-down’ control from higher centres. Under certain circumstances, for example, after tissue injury from trauma or surgery, there will be continued nociceptive input, with resultant changes in the whole somatosensory nervous system that lead to development of chronic pain syndromes. In such cases, even when the original injury has healed, the pathophysiological changes in the nervous system itself lead to ongoing pain, with peripheral or central sensitization, or both. Additionally, in some chronic pain syndromes, for example, chronic widespread pain, it has been postulated that abnormalities in central processing may be the initiating factor, with some evidence for this from neuroimaging studies. Further work is needed to fully understand pain neurobiology in order to advance our management.

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16

Scadding, John. Neuropathic pain. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0386.

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Pain signalled by a normal sensory system, nociceptive pain, serves a vital protective function. The peripheral and central nervous somatosensory systems permit rapid localization and identification of the nature of painful stimuli, prior to appropriate action to minimize or avoid potentially tissue damaging events. A reduction or absence of pain resulting from neurological disease emphasizes the importance of this normal protective function of pain. For example, tissue destruction occurs frequently in peripheral nerve diseases which cause severe sensory loss such as leprosy, and in central disorders such as syringomyelia. Neuropathic pain results from damage to somatosensory pathways and serves no protective function. This chapter provides an overview of neuropathic pain, considering its context, clinical features, pathophysiology, and treatment.In the peripheral nervous system, neuropathic pain is caused by conditions affecting small nerve fibres, and in the central nervous system by lesions of the spinothalamic tract and thalamus, and rarely by subcortical and cortical lesions. The clinical feature common to virtually all conditions leading to the development of neuropathic pain is the perception of pain in an area of sensory impairment, an apparently paradoxical situation. The exception is trigeminal neuralgia.Neuropathic pain is heterogeneous clinically, aetiologically, and pathophysiologically. Within a given diagnostic category, whether defined clinically or aetiologically, there are wide variations in reports of pain by patients. This heterogeneity poses one of the greatest challenges in understanding the mechanisms of neuropathic pain. Knowledge of the pathophysiology is an obvious pre-requisite to the development of effective treatments. The goal of a pathophysiologically based understanding of the symptoms and signs of neuropathic pain is, of course, just such a rational and specific approach to treatment. While this is not yet achievable, clinical-pathophysiological correlations have led to some recent advances in treatment.

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17

Buchner, Helmut. Evoked potentials. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0015.

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Evoked potentials (EPs) occur in the peripheral and the central nervous system. The low amplitude signals are extracted from noise by averaging multiple time epochs time-locked to a sensory stimulus. The mechanisms of generation, the techniques for stimulation and recording are established. Clinical applications provide robust information to various questions. The importance of EPs is to measure precisely the conduction times within the stimulated sensory system. Visual evoked potentials to a pattern reversal checker board stimulus are commonly used to evaluate the optic nerve. Auditory evoked potentials following ‘click’ stimuli delivered by a headset are most often used to test the auditory nerve and for prognostication in comatose patients. Somatosensory evoked potentials to electrical stimulation of distal nerves evaluate the peripheral nerve and the lemniscal system, and have various indications from demyelinating diseases to the monitoring of operations and prognosis of comatose patients.

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18

Finnerup, Nanna Brix, and Troels Staehelin Jensen. Management issues in neuropathic pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0133.

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Neuropathic pain is a common complication to cancer, cancer treatment, HIV, and other conditions that may affect the somatosensory nervous system. Neuropathic pain may be present in up to 40% of cancer patients and may persist independently of the cancer and affect the quality of life in disease-free cancer survivors. Particular surgical treatment and chemotherapy may cause chronic persistent neuropathic pain in cancer survivors. The diagnosis of neuropathic pain can be challenging and requires documentation of a nervous system lesion and pain in areas of sensory changes. The pharmacological treatment may include tricyclic antidepressants, selective serotonin noradrenaline reuptake inhibitors (duloxetine or venlafaxine), calcium channel α2↓ agonists (gabapentin or pregabalin), and opioids. Topical lidocaine and capsaicin, NMDA antagonists, carbamazepine, oxcarbazepine, and cannabinoids may be indicated. Due to limited efficacy or intolerable side effects at maximal doses, combination therapy is often required and careful monitoring of effect and adverse reactions is important.

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19

Legatt, Alan D., Marc R. Nuwer, and Ronald G. Emerson. Intraoperative Monitoring of Central Neurophysiology. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0034.

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This chapter covers neurophysiological intraoperative monitoring (NIOM). It describes the relevant neurophysiological signals, their anatomical sources, the techniques used to record them, the manner in which they are assessed, and possible causes of intraoperative signal changes. Techniques used include electroencephalography (EEG), electromyography, and auditory, somatosensory, and motor evoked potentials. Some of these techniques can be used to localize and identify areas of cerebral cortex or the corticospinal tract. Recording of the electromyogram generated by reflex activity can be used to evaluate central nervous system function in some circumstances. EEG can be used to assess depth of anesthesia. Signals can be affected by anesthesia, and the chapter discusses various anesthetic agents, their effects on signals, and considerations for anesthetic management during NIOM. Personnel performing NIOM must be knowledgeable about the anatomy and physiology underlying the signals, the technology used to record them, and the factors (including anesthesia) that can affect them.

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20

M, Pubols Lillian, Sessle Barry J. 1941-, and International Union of Physiological Sciences. Congress, eds. Effects of injury on trigeminal and spinal somatosensory systems: Proceedings of a satellite symposium of the XXX Congress of the International Union of Physiological Sciences held at Timberline Lodge, Oregon, July 20-23, 1986. New York: Liss, 1987.

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