Chronic Pain Management and Arthritis
Deborah Fish Ragin in Health Psychology, 2017
The second category is neuropathic pain, best described as a malfunction of our nervous system. It is believed to result from lesions of or damage to the somatosensory system, a network of receptors and pathways that transmit sensory information about us and our environment—such as pain, temperature, and position and movement of our body—to our central nervous system. Common examples of neuropathic pain caused by lesions include spontaneous shooting or burning sensations, greater discomfort than normal in response to normally painful stimulus, and sensations of aching, throbbing, or soreness when encountering nonpainful stimuli (University of Bristol, 2012). Illnesses such as diabetes, certain types of cancer, or chronic alcohol use can trigger neuropathic pain because of the damage they can cause to the nervous system.
The Somatosensory System
Golara Honari, Rosa M. Andersen, Howard Maibach in Sensitive Skin Syndrome, 2017
The primary sensory modality subserving the body senses is collectively described as the somatosensory system and comprises all the peripheral afferent nerve fibers and specialized receptors subserving proprioceptive (joint, muscle) and cutaneous sensitivity. The former processes information about limb position and muscle forces, which the central nervous system (CNS) uses to monitor and control limb movements and, via elegant feedback and feedforward mechanisms, ensures that a planned action or movement is executed fluently. This chapter will focus on sensory inputs arising from the skin surface—cutaneous sensibility—and describe the neurobiological processes that enable the skin to be sensitive. Skin sensations are multimodal and are classically described as subserving the three submodalities of touch, temperature, and pain. We will also consider the growing evidence for a fourth submodality, present only in hairy skin, that is preferentially activated by slowly moving, low-force, mechanical stimuli.
Disorders of Sensation, Motion, and Body Schema
Rolland S. Parker in Concussive Brain Trauma, 2016
The final outcome reflects network-wide and local-circuit modifications. In the uninjured person practice improves sensory and motor representation, that is, performance. Training in one task may alter circuits so that a given neuron is less effective in another. By implication there is a “zero sum game,” indicating that training in one skill should not be hampered by practice in another. This has implications for TBI: New circuits have to be reformed through practice to be helpful and compensate for loss of input. After restricted motor cortex lesions, training on finger movement skills helps reform the cortex so that more neurons are devoted to finger movements. Adjacent cortical neurons extend themselves into cortical area deprived area deprived of sensory input. Reorganization of sensory representation occurs after a limited loss of sensory inputs. Postlesion reorganization manifests new cortical fields representing body parts that were not previously responsive to its stimulation, for example, sensory representation of the fingers (Kaas, 2002b; Stein & Hoffman, 2003). In the somatosensory system input change occurs in the parietal cortex and the somatosensory thalamus (ventroposterior N).
Hypnotic Automaticity in the Brain at Rest: An Arterial Spin Labelling Study
Published in International Journal of Clinical and Experimental Hypnosis, 2019
Pierre Rainville, Anouk Streff, Jen-I Chen, Bérengère Houzé, Carolane Desmarteaux, Mathieu Piché
The first brain imaging study examining more directly the brain correlates of hypnotic involuntariness showed robust parietal activity while subjects moved their arm in response to hypnotic suggestions that their arm would be moved passively (Blakemore, Oakley, & Frith, 2003). Importantly, the study included control passive and active movements in a nonhypnotic condition to allow comparing brain responses associated with normal sensory feedback alone (passive condition) and executive motor processes (active condition). In the normal passive condition, the afferent sensory signal conveyed through the somatosensory system activated the parietal cortex in the region of the inferior parietal lobule (parietal operculum/supramarginal gyrus). In the active condition, motor cortices were also activated to produce the motor command. In this condition, there was less parietal activity, consistent with the feedforward model of motor control (Wolpert & Ghahramani, 2000). Indeed, during voluntary actions, a motor command is sent to the motoneurons while a copy of this efferent signal is sent to sensory areas of the parietal cortex to monitor the correspondence between the sensory feedback and the expected effect of the action that was prescribed (i.e., prediction signal). Importantly, when the feedback matches the expectations, activity is reduced in the parietal cortex. However, when there is a mismatch (i.e., prediction error) or during passive movement (i.e., no prediction signal), the parietal cortex is strongly activated.
Surround inhibition in patients with juvenile myoclonic epilepsy
Published in Neurological Research, 2021
Bengi Gul Turk, Naz Yeni, Aysegul Gunduz, Ceren Alis, Meral Kiziltan
Certain physiological steps in the generation of SI are still unknown. In motor system, basal ganglia were suggested to be the origin of inhibitory output via thalamus to the cortex in order to choose the most accurate voluntary movement [18,20]. Deficient SI in the motor system in Parkinson’s disease also supports this hypothesis [21]. Tinazzi and colleagues showed a defect of somatosensory SI in dystonic patients and attributed it to a reduction in cortical inhibitory function in dystonia [3]. Actually, this is a subject of discussion whether there is a shared mechanism that disturbs SI in dystonia and bradykinesia of Parkinson’s disease. Similar to motor system, SI in the somatosensory system may enable to perform the desired movements by inhibiting the undesired ones [18]. The SI in the somatosensory system may be associated with the somatosensory and motor cortices, and with cuneate nucleus, locus ceruleus, thalamus and brainstem [22]. Tinazzi and colleagues [3] demonstrated the presence of SI at the spinal, brainstem and cortical levels of the lemniscal pathway.
Mechanisms of action of vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) in pain: a narrative review
Published in Nutritional Neuroscience, 2023
A. M. Paez-Hurtado, C. A. Calderon-Ospina, M. O. Nava-Mesa
Pain is a serious and widespread public health problem affecting around 10%–20% of adults worldwide [1–5]. There are three different types of pain subcategorized according to their pathophysiological mechanisms by the International Association for the Study of Pain. Nociceptive pain is a pain sensation caused by ‘an actual or threatened damage to non-neural tissue and is due to activation of nociceptors’ [6]. Pain initiated or caused by a lesion or a disease of the somatosensory system is referred to as neuropathic pain. Nociplastic pain is defined as ‘pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain’ [6]. Inflammatory pain is a type of nociceptive pain which results from hypersensibility of nociceptors by inflammatory mediators [7].
Related Knowledge Centers
- Auditory System
- Haptic Perception
- Nervous System
- Physiology
- Proprioception
- Thermoception
- Visual System
- Pain
- Sensory Nervous System
- Sense of Smell