Somatic Sensations PDF

Somatic sensations Mona A Hussain Assistant prof. in Physiology department- FOM- PSU  Somatic sensations The somatic senses are the nervous mechanisms that collect sensory information from all over the body. These senses are in contradistinction to the special senses, which mean...

Somatic sensations Mona A Hussain Assistant prof. in Physiology department- FOM- PSU  Somatic sensations The somatic senses are the nervous mechanisms that collect sensory information from all over the body. These senses are in contradistinction to the special senses, which mean specifically vision, hearing, smell, taste, and equilibrium. Classification of somatic sensations (1) the mechanoreceptive somatic senses, which include both tactile and position sensations that are stimulated by mechanical displacement of some tissue of the body; (The tactile senses include touch, pressure, vibration, and tickle senses, and the position senses include static position and rate of movement senses.) (2) the thermoreceptive senses, which detect heat and cold; and (3) the pain sense, which is activated by factors that damage the tissues. Skin receptors and Proprioceptors Proprioceptors: muscle spindle, Golgi tendon organ and Joint kinesthetic receptors.  Ascending tracts Conscious sensation: 1- Dorsal Column/Medial Lemniscal System in the Spinal Cord and Medulla 2- Spinothalamic Tract (Anterolateral System) Unconsciuos sensory information: 1- Dorsal spinocerebellar tract—carries proprioceptive input to the cerebellum from the lower extremities and lower trunk. 2- ventral cerebellar tract—carries proprioceptive input to the cerebellum from the upper extremities and upper trunk. Transmitted sensations  Pain Definition: “an unpleasant sensory and emotional experience associated with actual or potential tissue damage” Types: 1- physiologic or acute pain (fast Pain)and 2- pathologic or chronic pain, (slow pain) which includes inflammatory pain and neuropathic pain.  Pain receptors (Nociceptors) Nociceptors are classified by modality: 1- Mechanical nociceptors: respond to mechanical damage, such as cutting, crushing, or pinching. 2- Thermal nociceptors: respond to temperature extremes, especially heat. 3- Chemical nociceptors: respond equally to many kinds of irritating chemicals released from damaged tissue. The nociceptor free nerve endings are found in skin and deep tissue, joints, muscle, and bone. Because of their value to survival, nociceptors do not adapt to sustained or repetitive stimulation.  Pain Acute pain typically has a sudden onset and recedes during the healing process; it can be regarded as “good pain” as it serves an important protective mechanism. The withdrawal reflex is an example of the expression of this protective role of pain. Chronic pain can be considered “bad pain” because it persists long after recovery from an injury and is often refractory to common analgesic agents, including nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids.  Fast pain Slow pain Onset 0.1 second after 1 second after stimulation stimulation Duration fast slow Quality Sharp - pricking - localized burning, aching, throbbing and nauseous, and poorly localized Site Skin Skin and deep tissues Receptors Free nerve endings Free nerve endings Type of stimuli mechanical and thermal mechanical , thermal and chemical Transmission of pain signal small type Aδ fibers at type C fibers at velocities into CNS velocities between 6 and between 0.5 and 2 m/sec. 30 m/sec Dorsal horn lamina Lamina I (lamina SGR (Lamina II and III) marginalis) Second order neuron Neospinothalamic tract Paleospinothalamic tract  Fast Pain Slow Pain Termination Third order neuron is Brain stem (reticular nuclei, tectal area of ventral posterolateral midbrain and periaquedactal region. nucleus of thalamus then Multiple short-fiber neurons relay the pain fibers reach signals upward into the intralaminar and somatosnsory area ventrolateral nuclei of the thalamus and into certain portions of the hypothalamus and other basal regions of the brain. (strong arousal effect on nervous activity throughout the entire brain ) Neurotransmitter Glutamate Glutamate and Substance P  DEEP & VISCERAL PAIN The main difference between superficial and deep or visceral pain is the nature of the pain evoked by noxious stimuli. This is probably due to a relative deficiency of Aδ nerve fibers in deep structures, so there is little rapid, sharp pain. highly localized types of damage to the viscera seldom cause severe pain and diffuse stimulation of pain receptors may cause severe visceral pain. In addition, deep pain and visceral pain are poorly localized, nauseating, and frequently are accompanied by sweating and changes in blood pressure. Example: 1- the muscle spasm associated with injuries to bones, tendons, and joints. The steadily contracting muscles become ischemic, and ischemia stimulates the pain receptors in the muscles. The pain in turn initiates more spasm, setting up a vicious cycle. 2- Distention of hollow viscera visceral pain often radiates or is referred to other areas.  REFERRED PAIN Irritation of a visceral organ frequently produces pain that is felt not at that site but in a somatic structure that may be some distance away. When pain is referred, it is usually to a structure that developed from the same embryonic segment or dermatome as the structure in which the pain originates. For example, the heart and the arm have the same segmental origin. MECHANISM: CONVERGENCE – PROJECTION THEORY Referred Pain CONVERGENCE – PROJECTION THEORY  Insensitive Viscera A few visceral areas are almost completely insensitive to pain of any type. These areas include: 1- the parenchyma of the liver and 2- the alveoli of the lungs. *** the liver capsule is extremely sensitive to both direct trauma and stretch, and the bile ducts are also sensitive to pain. ***In the lungs both the bronchi and the parietal pleura are very sensitive to pain.  MODULATION OF PAIN TRANSMISSION: Gate theory Gate-control mechanism: (rubbing or shaking an injured area decreases the pain due to the injury ) Transmission in nociceptive pathways can be interrupted by actions within the dorsal horn of the spinal cord at the site of sensory afferent termination. the simultaneous activation of cutaneous mechanoreceptors whose afferents emit collaterals that terminate in the dorsal horn. The activity of these cutaneous mechanosensitive afferents may reduce the responsiveness of dorsal horn neurons to their input from nociceptive afferent terminals.  Actions of opioids to reduce sensory transmission in pain pathways at the level of the dorsal root ganglion (DRG) and spinal cord dorsal horn region  MODULATION OF PAIN TRANSMISSION: Opioid There are interneurons in the superficial regions of the dorsal horn that contain endogenous opioid peptides (enkephalin and dynorphin). These interneurons terminate in the region of the dorsal horn where nociceptive afferents terminate. Opioid receptors are located on the terminals of nociceptive fibers and on dendrites of dorsal horn neurons, allowing for both presynaptic and postsynaptic sites of actions for opioids. Activation of the postsynaptic opioid receptors hyperpolarizes the dorsal horn interneuron by causing an increase in K+ conductance. Activation of the presynaptic opioid receptors leads to a decrease in Ca2+ influx, resulting in a decrease in release of glutamate and substance P. MODULATION OF PAIN TRANSMISSION: descending pathway