Pain is a complex process that involves sensory and emotional components. People experience pain stimuli throughout life due to factors or activities that trigger people to pain. An injury to any part of the body causes inflammation which triggers pain receptors; hence the brain act on the pain and sends back a stimulus corresponding to the pain in one part of the body. The brain and the spinal cord perform critical functions in relieving pain after an injury. The spinal cord and the brain are made up of nerves comprising many axons that aid in spreading impulses to the rest of the body.
Central nervous system process of pain.
Pain processes typically begin when dysfunction in body tissues or the body comes into contact with an object. An injury triggers the inflammation process to take place. One of the components of the inflammation process is pain sensation. Peripheral sensitization is the primary response to pain. The inflammation process causes nerve changes, releasing endogenous inflammatory mediators such as histamine, serotonin, and adenosine triphosphate. This inflammation mediator thus activates and sensitizes nociceptors. Nociceptors primarily serve as pain receptors. The nociceptor’s pain receptors, however, fire pain signal through the axonal nerves to the spinal cord, which thus fires the pain signal to the brain. Axons with myelin sheath transmit the pain signal faster than axons without myelin sheath.
The pain signal is thus conducted along the axon of the movement of sodium and potassium ion-like series that generates a wave-like depolarization. The spinal transmit pain impulse to the brain through sensory neurons that enter the spinal cord via the dorsal route. The primary afferent fibres transmit the signal across a synapse to the secondary neurons, which will thus pass the signs to the brain stem. Once the brain receives the pain impulses, they will be relayed to the cortex. The brain acts on the pain signal and provides feedback to respond to the pain. The brain works as the central terminal change of the pain. Once the secondary neurons are activated by neurotransmitters released from the afferent fibre, it produces an electrical signal. It distributes the electrical signals along its axon to various brain areas. These brain parts include the hypothalamus, grey matter, basal ganglia, and the cerebral cortex. The cortex is consistently activated when noxious stimuli stimulate the nociceptors, and the activation of the central nervous system results from the pain’s subjection. The integrated combination of the thalamus, cortex and corticolimbic structures, which form the neuromeric, effectively processes pain perception.
The various parts of the brain misinterpret the pain perception by locating the pain and ruling out the intensity through the somatosensory cortex. The pain electrical signals to the brain allow an individual to perceive what to do. For instance, once hit by a stick, the individual will tend to withdraw the hand or rub the area to relieve pain (Lee et al., 2020). The anterior cortex responds to the pain by triggering an emotional response such as fear, thus creating attention drawn from the pain. The hypothalamus produces adrenaline hormone that prepares the individual for flight or runs when the pain is intense. However, the central nervous system triggers an inhibitory response in which hormones such as dopamine, adrenaline, endorphins and serotonin are released. Once the hormones are released in the central nervous system, the chemicals are moved to the spinal cord to inhibit any more perception of the pain signal by the nociceptors from releasing neurotransmitters from the primary afferent fibre. Prevention of the direct afferent fibre thus prevents the secondary neuron from reaching its threshold, stimulating an action potential.
The role of glial cells and positive feedback loop.
Glial cells are non-neuronal and set within the central nervous and peripheral nervous systems; glial cells offer metabolic and physical sustenance to the neurons. Glial cells include microglial, astrocytes, and Schwan cells; glia cells maintain homeostasis, form myelin sheath and clean debris. Glial cells do not participate e in synapse transfer. Instead, they control the levels of neurotransmitters surrounding the synapses. Glial cells can sense the neurotransmitters’ levels in the synapse and can respond by releasing molecules that directly influence the neuron’s activity. Astrocytes are significant in modifying synapses and however how the neurons communicate. Glial cells keep the viability of neurons. Glial cells clean the debris when a neuron dies (Donnelly et al., 2020). Myelin sheath wrapped in the glia cells allows electrical signals to travel faster down the axon. Electrical impulses will thus travel faster to the brain and relay back feedback. Microglial cells respond to an injury or disease in the central nervous system. Pain resulting from an injury triggers the migration of the glial cells to the place of the injury site to either clear out dead cells or remove harmful toxins. Glial cells also inhibit the growth of pathogens when an individual is injured.
The positive feedback loop is typical of an injury answer that helps create quick changes necessary to mount an emergency response. Increased response of nociceptors will typically sensitize the dorsal horn of the spinal cord, making it faster to report nociceptive signals to the brain (Yang, & Zhou, 2019). A positive feedback loop enhances deviate changes. It moves a system from its point of equilibrium state and makes it more unstable. Positive feedback loops drive away an individual from a negative stimulus. For instance, when a person hits a tree, he will tend to massage the affected area to relieve pain.
Donnelly, C. R., Andriessen, A. S., Chen, G., Wang, K., Jiang, C., Maixner, W., & Ji, R. R. (2020). Central Nervous System Targets: Glial Cell Mechanisms in Chronic Pain. Neurotherapeutics, 17(3), 846-860.
Lee, G. I., & Neumeister, M. W. (2020). Pain: Pathways and Physiology. Clinics in Plastic Surgery, 47(2), 173-180.
Yang, Q. Q., & Zhou, J. W. (2019). Neuroinflammation in the Central Nervous System: Symphony of Glial Cells. Glia, 67(6), 1017-1035.
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