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Books on the topic 'Dorsal horn of the spinal cord'

Author: Grafiati

Published: 31 August 2024

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1

Cervero, F., G. J. Bennett, and P. M. Headley, eds. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0825-6.

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2

Fernando, Cervero, Bennett G. J, Headley P. M, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Processing of sensory information in the superficial dorsal horn of the spinal cord. New York: Plenum Press, 1989.

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3

Pang, Dachling. Total Resection of Complex Dorsal Spinal Cord Lipoma and Reconstruction of the Neural Placode. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81267-6.

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4

E, Coggeshall Richard, ed. Sensory mechanisms of the spinal cord. 3rd ed. New York: Kluwer Academic/Plenum Publishers, 2004.

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5

Willis, William D. Sensory mechanisms of the spinal cord. 3rd ed. New York: Kluwer Academic/Plenum Publishers, 2004.

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6

1932-, Coggeshall Richard E., ed. Sensory mechanisms of the spinal cord. 2nd ed. New York: Plenum Press, 1991.

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7

Pak, Youngshill. Characterization of voltage-activated K+ currents in rat spinal dorsal horn neurons in culture and modulation by adenosine. Ottawa: National Library of Canada, 1994.

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8

Quinn, Sean David Philip. Enhanced neuronal regeneration, by retinoic acid, of murine dorsal root ganglia and of fetal murine and human spinal cord, in vitro. Ottawa: National Library of Canada, 1990.

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9

Bennett, G. J., F. Cervero, and P. M. Headley. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Springer, 2013.

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10

Bennett, G. J., F. Cervero, and P. M. Headley. Processing of Sensory Information in the Superficial Dorsal Horn of the Spinal Cord. Springer London, Limited, 2012.

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11

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1 Primary Afferent Neurons and the Spinal Dorsal Horn. Springer, 2012.

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12

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1 Primary Afferent Neurons and the Spinal Dorsal Horn. Springer London, Limited, 2012.

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13

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1: Primary Afferent Neurons and the Spinal Dorsal Horn. 3rd ed. Springer, 2004.

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14

Collantes, Enrique. The importance of descending modulatory pain systems. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0044.

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The landmark paper discussed in this chapter is ‘Descending control of pain’, published by M. J. Millan in 2002. The perception of pain is affected by a complex interaction between nociceptors in the dorsal horn of the spinal cord, systems that transfer messages to cerebral structures. The complex interaction between the CNS and the peripheral nervous system in a modifiable and plastic neural system makes the perception of pain unique for each individual. In this regard, the author outlines the neurobiology of pain, providing a detailed description of the descending pathways which modulate the activity of spinal nociceptors which are located in the dorsal horn and which transfer nociceptive messages to cerebellar structures.

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15

Black, Sheila. The original description of central sensitization. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0040.

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The landmark study discussed in this chapter is ‘The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue injury’, published by Coderre and Melzack in 1992. Previous studies in this field implicate a contribution of excitatory amino acids (EAAs), specifically l-glutamate and l-aspartate, to injury-induced sensitization of nociceptive responses in the dorsal horn of the spinal cord. Repetitive stimulation of primary afferent fibres demonstrated that l-glutamate and NMDA can produce ‘wind-up’ of neuronal dorsal horn activity, and this is blocked by application of NMDA antagonists. This study uses the formalin test as a behavioural model to investigate the mechanisms underlying central sensitization and the role of EAAs, NMDA, their receptors, and their antagonists in this process.

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16

Bromley, Lesley. The physiology of acute pain. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199234721.003.0001.

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Acute pain as a result of tissue damage is self-limiting. Impulses are generated in primary sensory nerves by chemical mediators released from the damaged tissues. The spinal cord receives these impulses in the dorsal horn. At the level of the spinal cord, the impulses can be amplified or reduced in amplitude by descending inputs. At the level of the spinal cord, the representation of the painful area and the sensitivity of other, surrounding areas can be modified. At the level of the brainstem and thalamus, further modification can take place. The final perception of the pain can be modified by other central phenomena such as anxiety and fear. New imaging techniques have allowed a greater understanding of cortical representation of pain. The role of the glia in maintaining painful states is evolving.

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17

Humble, Stephen R. Plasticity in somatic receptive fields after nerve injury. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0023.

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Devor and Wall, in a pioneering electrophysiological study, examined the change in somatic receptive fields in the dorsal horn of the spinal cord after nerve injury. Rather than the anticipated loss of an area of electrophysiological perception, the system demonstrated ‘plasticity’ whereby novel receptive fields, remote to the corresponding area of damage, were evident. The authors postulated that this neuroplasticity occurred via a hitherto undefined spinal mechanism, which lead to an explosion of interest and research to elucidate the mechanisms of central plasticity. In this truly landmark paper, the idea of the nervous system being an inherently ‘hard-wired’ structure was made redundant and the concept of neuroplasticity was given robust form.

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18

Trigo Blanco, Paula, Maricarmen Roche Rodriguez, and Nalini Vadivelu. Pathophysiology of Pain and Pain Pathways. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0001.

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Pain is a distressing experience and an important cause of suffering and disability. Pain usually signals the presence of injury or disease and generates a complex physiologic and emotional response. It has a protective function in order to restore homeostasis at the autonomic and psychological levels. This chapter reviews the physiology and mechanisms of pain, as well as the pathways in the central and peripheral nervous system that transmit nociceptive information. The chapter divides the pain anatomical pathways into the peripheral nervous system, the spinal cord with the medullary dorsal horn system, and the ascending and supraspinal system. The authors explain the pain pathways as a three-neuron pathway that carries noxious information from the periphery to the cerebral cortex. This chapter defines important concepts such as sensitization, hyperalgesia, and allodynia, as well as describes the modulation process of nociception.

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19

Neural patterning in the dorsal spinal cord. 1998.

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20

Mease, Philip. Neurobiology of pain in osteoarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0013.

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Significant advances in our understanding of the neurobiology of pain in osteoarthritis (OA) have occurred in the last decade and are herein summarized. Pain is the predominant symptom of OA and occurs at multiple levels from non-cartilage peripheral tissues to spinal cord, and brain and back. At each level, nerve function is regulated by complex ionic channels, neuropeptide expression, and cytokine and chemokine activity. Previously considered a non-inflammatory condition, it is now recognized that cell proliferation and inflammatory cytokine production occurs in OA synovium, contributing to peripheral sensitization. Genetic profile influences nociceptive neuropeptide expression and thus, pain perception. Both peripheral and central sensitizing factors, including increased neuropeptide and microglial activity, lead to pain augmentation and persistence. Pain processing in brain centres such as the somatosensory cortex and insula are influenced by affective areas such as the amygdala. Descending receptor pathways through the midbrain to the dorsal horn, such as norepinephrine, serotonin, opioid, and cannabinoid, normally provide pain inhibitory function but this function may be diminished in chronic pain states such as OA, leading to allodynia and hyperalgesia. Functional neuroimaging has contributed to our understanding of the complex interplay of peripheral and central mechanisms. Recent evidence that grey matter volume decrease in chronic pain states may be reversible (e.g. after pain relief post OA hip arthroplasty) illuminates the potential for central neuroplasticity. Greater understanding of the neurobiology of OA pain provides evidence for therapeutic approaches that address peripheral and/or central pain mechanisms and provides a guide for future targeted pain therapeutics.

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21

Jr, William D. Willis. Sensory Mechanisms of the Spinal Cord. Springer, 2013.

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22

Jr, William D. Willis. Sensory Mechanisms of the Spinal Cord. Springer London, Limited, 2013.

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23

Sensory Mechanisms of the Spinal Cord. 2nd ed. Springer, 2003.

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24

Shah, Chirag D., and Maunak V. Rana. Advances in Dorsal Column Stimulation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0017.

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Spinal cord stimulation (SCS) has been a long established therapy for various pain conditions including low back pain, failed back surgery syndrome, complex regional pain syndrome, and other neuropathic and nociceptive pain states. Since the first report of SCS in 1967 by Shealy, advances have occurred in the technology used to achieve clinical analgesia. Developments in both the hardware and software involved have led to significant improvements in functional specificity, as seen in dorsal root ganglion stimulation, along with increasing breadth and depth of the field of neuromodulation. The patient experience during the implantation of the systems, as well as post-procedurally has been enhanced with improvements in programming. These technological improvements have been validated in quality evidenced-based medicine: what was a static area now is a dynamic field, with neuromodulation poised to allow physicians and patients more viable options for better pain control for chronic painful conditions.

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25

Donaghy, Michael. The clinical approach. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0030.

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This chapter describes the appropriate clinical approach to take when presented with a patient reporting a neurological symptom. Just under 10 per cent of the population consult their general practitioner about a neurological symptom each year in the United Kingdom. About 10 per cent of these are referred for a specialist opinion, usually to a neurologist. Nine conditions account for roughly 75 per cent of general neurological referrals and are diagnosed initially on purely clinical grounds, with the other 25 per cent representing the full range of other, potentially very rare, neurological disorders.This chapter underlines the importance of a thorough and informative history to achieve successful diagnosis. Crucial facets for a good history include information on the time course of symptom development, whether symptoms are negative or positive, previous neurological history (both personal and familial), as well as other potentially contributory general medical disorders. The general neurological examination is also described, as are specific examination manoeuvres that may be added to the general neurological examination in specific clinical circumstances.Reflexes play an important role in diagnostic neurology because they reflect the integrity of, or alterations in, the neural structures responsible for their arc. Loss of a reflex may be due to interruption of the afferent path by a lesion involving the first sensory neurone in the peripheral nerves, plexuses, spinal nerves, or dorsal roots, by damage to the central paths of the arc in the brainstem or spinal cord, by lesions of the lower motor neurone at any point between the anterior horn cells and the muscles, of the muscles themselves, or by the neural depression produced by neural shock. In clinical practice, the most useful and oft-elicited reflexes are the tendon reflexes of the limbs, the jaw jerk, the plantar response, the superficial abdominal reflexes, the pupil-light response, and in infants, the Moro reflex. The place of these particular reflexes in the routine neurological examination is outlined, and the elicitation and significance of these reflexes and of a wide variety of others which are used occasionally are described.Examinations that allow localization lesions that are responsible for muscle weaknesses and the assessment of somatosensory abnormalities are described, as are neurological disorders that result in identifiable gait disorders. The clinical signs and examinations relevant to autonomic disorders are also discussed.Intensive care may be required for patients critically ill either as a result of primary neurological disease, or in those in whom a neurological disorder is a component of, or secondary to, a general medical disorder. Indications for admission to neurological intensive care have been defined (Howard et al. 2003): impaired consciousness, bulbar muscle failure, severe ventilatory respiratory failure, uncontrolled seizures, severely raised intracranial pressure, some monitoring and interventional treatments, and unforeseen general medical complications. Naturally specific treatments indicated for the particular diagnosis should be instituted along with general intensive care measures.Finally, the discussion of diagnoses of chronic or terminal conditions with patients is discussed, with particular focus on the best way to present the diagnosis to the patient.

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26

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 2: Ascending Sensory Tracts and their Descending Control. 3rd ed. Springer, 2004.

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27

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 2 Ascending Sensory Tracts and Their Descending Control. Springer London, Limited, 2013.

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28

Wong, Stacy N., and Line G. Jacques. Neuropathic Groin Pain. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0017.

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Chronic neuropathic groin pain may be iatrogenic or posttraumatic and can be disabling or even crippling in some individuals. Patients may have significant sleep disturbances and may experience psychosocial effects along with significant physical limitations. A combination of pharmacologic treatments with physical therapy and local infiltrations may be useful. Neurostimulation techniques, including spinal cord stimulation, peripheral nerve stimulation, and dorsal root ganglion stimulation, have shown promising results in the treatment of chronic neuropathic pain. In certain cases, surgical approaches, including selective neurectomy, can be effective; in other cases, the pain will remain chronic and intractable despite all interventional measures. In summary, patients with neuropathic groin pain can be treated after a thorough pretreatment investigation. Dorsal root ganglion stimulation is a viable option and should be considered when treating this challenging patient population.

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29

Mason, Peggy. Developmental Overview of Central Neuroanatomy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0003.

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The central nervous system develops from a proliferating tube of cells and retains a tubular organization in the adult spinal cord and brain, including the forebrain. Failure of the neural tube to close at the front is lethal, whereas failure to close the tube at the back end produces spina bifida, a serious neural tube defect. Swellings in the neural tube develop into the hindbrain, midbrain, diencephalon, and telencephalon. The diencephalon sends an outpouching out of the cranium to form the retina, providing an accessible window onto the brain. The dorsal telencephalon forms the cerebral cortex, which in humans is enormously expanded by growth in every direction. Running through the embryonic neural tube is an internal lumen that becomes the cerebrospinal fluid–containing ventricular system. The effects of damage to the spinal cord and forebrain are compared with respect to impact on self and potential for improvement.

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30

Chiravuri, Srinivas. Lateral Femoral Cutaneous Neuropathy—Meralgia Paresthetica. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0014.

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Meralgia paresthetica is characterized by anterolateral thigh pain, paresthesia, or dysesthesia without motor weakness. This is due to idiopathic or iatrogenic injury to the lateral femoral cutaneous nerve (LFCN, dorsal rami of L2-L3). Risk factors include obesity, diabetes, and external compression near the inguinal ligament’s attachment to the anterior superior iliac spine. Diagnosis is based on clinical presentation and electrodiagnostic studies. Initial management includes behavioral modification, physical therapy, and pharmacotherapy. More invasive treatment modalities include LFCN infiltration, pulsed radiofrequency, direct nerve stimulation, and spinal cord stimulation. Ultrasound-guided neurectomy is also an effective way to localize the nerve structure and ensure complete nerve transection.

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31

McClenahan, Maureen F., and William Beckman. Pain Management Techniques. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0011.

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This chapter provides a broad review of various interventional pain management procedures with a focus on indications, anatomy, and complications. Specific techniques reviewed include transforaminal epidural steroid injection, lumbar sympathetic block, stellate ganglion block, cervical and lumbar radiofrequency ablation, gasserian ganglion block, sacroiliac joint injection, celiac plexus block, lateral femoral cutaneous nerve block, ilioinguinal block, lumbar medial branch block, obturator nerve block, ankle block, occipital nerve block, superior hypogastric plexus block, spinal cord stimulation, and intrathecal drug delivery systems. The chapter reviews contrast agents, neurolytic agents, botulinum toxin use, corticosteroids, and ziconotide pharmacology and side effects in addition to diagnosis and management of local anesthetic toxicity syndrome. It also discusses indications for neurosurgical techniques including dorsal root entry zone lesioning. In addition, information on radiation safety and the use of anticoagulants with neuraxial blocks is covered.

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32

Guillery, Ray. The pathways for perception. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198806738.003.0002.

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Chapter 2 outlines some of the evidence on which the seemingly strong standard view has been based. The early discovery that ventral nerve roots of the spinal cord provide a motor output and dorsal nerve roots provide a sensory input supported the dichotomy of the standard view. Then as each sensory pathway was traced to the thalamus for relay to the cortex, the separate inputs from the sensory receptors—visual, auditory, gustatory, and so on—could be seen as providing the cortex with a ‘view’ of the world. The nature of this view became strikingly clear once investigators could understand (read) the messages that pass along the nerve fibres on the basis of very brief changes in membrane potentials, the action potentials. However, many branches given off by sensory fibres on their way to the thalamus remain unexplained on the standard view. These are important for the integrative sensorimotor view and their precise functional roles need to be defined.

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33

Hilton-Jones, David, and Martin R. Turner, eds. Oxford Textbook of Neuromuscular Disorders. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199698073.001.0001.

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Part of the Oxford Textbooks in Clinical Neurology series, the Oxford Textbook of Neuromuscular Disorders covers the scientific basis, clinical diagnosis, and treatment of neuromuscular disorders with a particular focus on the most clinically relevant disorders. The resource is organized into seven sections, starting with the general approach to the patient with neuromuscular disorders and then focusing on specific neuromuscular conditions affecting the peripheral nervous system from its origins at the spinal cord anterior horn on its outward course to their effector muscles and the inbound sensory pathways. Chapters on specific neuromuscular conditions are illustrated with typical case histories and their presenting features, allowing readers to put rarer conditions into their clinical context more easily.

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34

Crum, Brian A., Eduardo E. Benarroch, and Robert D. Brown. Neurologic Disorders Categorized by Anatomical Involvement. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0523.

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Neurological disorders of the brain, spine, and peripheral nervous system are examined. Symptoms and signs related to disorders of the cerebral cortex may lead to alterations in cognition and consciousness. Unilateral neurologic symptoms involving a single neurologic symptom commonly localize to the cerebral cortex. Abnormalities of speech and language are localized to the dominant cerebral hemisphere, whereas abnormalities of the nondominant hemisphere may lead to visuospatial deficits, confusion, or neglect of the contralateral side of the body. The hypothalamus is important in many functions that affect everyday steady-state conditions, including temperature regulation, hunger, water regulation, sleep, endocrine functions, cardiovascular functions, and regulation of the autonomic nervous system. Cortical and subcortical abnormalities may also lead to visual system deficits, usually homonymous visual defects of the contralateral visual field. Sensory levels, signs of anterior horn cell involvement, and long-tract signs in the posterior columns or corticospinal tract suggest a spinal cord lesion.

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