STUDY - Technical - New Dacian's Medicine
About
Pain (1).
Translation Draft
At the moment I only provide you with the title, the material being in the works but, as you are convinced, I will post it (for those like me the debt is duty)...
And, to get off to the most academic start possible, the generally accepted definition of pain is: "Unpleasant sensory and emotional experience, determined or related to actual or potential tissue damage, or described in terms of such injuries" (at the "level" of the Dex, the pain being described simply as physical and/ or moral suffering borne by someone, grief, sorrow).
Pain is the one universally perceived as a signal of the disease, being also the most common "perceived" symptom. And, the first "purpose" of medicine being to preserve and restore health and to alleviate suffering, it is obvious why pain is one of the main milestones of medical activities. But the "defining" elements compel me to proceed to some "clarifications"...
Pain can be described on the basis of three components: 1. physiological (mode of transmission, receptors involved, biochemical processes, etc.), 2. behaviours that express pain and accompany it) and 3. (thoughts, feelings and representations related to pain).
And, pain has only a simple classification in: acute (which lasts between 6 weeks and 6 months, with anxiety as associated feeling, since pain has the significance of imminent danger for the individual - represented by forms: 1. superficial, short-lived, well-located and with a "sharp" character, in the skin, mucous membranes and 2. deeper, more persistent, more difficult to locate, with a burning character , in the muscles and membranes) and chronic (lasts more than 6 months and is localized in the internal organs, generally of a pressure character, producing an important discomfort, with subjective, familial, professional, etc. - represented by forms: 1. recurrent, benign, of increased intensity, repeated, with free interval, as in migraine, 2. intractable, constant, of variable intensity, as in back pain and 3. , as in rheumatic arthritis, cancer).
The "classic" function of the sensory system of pain is to detect, locate and identify tissue injury processes. Because different diseases produce different types, characteristic, of tissue damage, quality, duration over time and localization of pain, as well as localization of sensitivity, provide important diagnostic milestones and are used to assess the response to treatment.
It is often described as a process of tissue destruction or penetration (e.g. stabbing, burning, breaking, torsion, compression) and/ or as a physical or emotional reaction (example: frightening, emetic, disgusting). Moreover, any pain of moderate or high intensity is accompanied by anxiety and the impulse to remove or limit the sensation.
These properties illustrate the duality of pain: both sensation and emotion. When acute, pain is characteristically associated with a change in behaviour and a response to stress, consisting of increased blood pressure, increased heart rate, pupil diameter and elevated levels of plasma cortisol (hormone with regulating functions in other glands, secreted by the adrenals). In addition, local muscle contractions are common (example: limb flexion, abdominal wall stiffness, etc.).
As for the structures underlying the initiation of the sensation of pain, I will only tell you that they are called nociceptors (from the "comasing" of harmful terms with receptors) and are made up of primary receiving structures, motor neurons and sympathetic postganglionary neurons (cellular bodies of the primary aferants located in the spinal ganglia on the posterior roots of the spinal nerves, located in the vertebral holes) , the collection and transmission structures of the primary aferants, from here it comes to the central pathways of pain (from the spinal cord) etc. etc. etc. etc. (I am not mischievous when I assure you that at least 99% of doctors not involved in the "pharmaceutical" research of pain or something similar can not really describe much about this structure of pain, so I will not bore you with such details). It is important to note that nociceptors (the vast majority) can respond to several different types of harmful stimuli, such as burning, intentional mechanical stimuli such as a pinch, and the application of chemical irritants.
Important here, the level of "taking over" the future sensation of pain, is sensitization. When intentional stimuli are applied, repeat and prolong, if the tissue is damaged or if inflammation is present, the threshold for activating primary aferential nociceptors is lower and the trigger frequency is higher for all stimulus intensities.
Inflammation mediators such as bradychinin, some prostaglandins and leukotrienes contribute to this process called sensitization. In sensitized tissues, usually harmless stimuli end up producing pain, sensitization being an important clinical process that contributes to sensitization, inflammation and hyperalgesia (a striking example of sensitization is sunburnt skin, in which severe pain can be caused by a simple touch, or a slight slap on the back, or by a warm shower).
Compared to superficial structures (skin, cornea, etc.), viscera are relatively insensitive under normal conditions to nociceptive stimuli. In contrast, when affected by a pathological process with an inflammatory component, deep structures such as cavities or cavitational viscera become characteristically particularly sensitive to mechanical stimulation (here being "silent" nociceptors, their "activity" being the reason why, in pathological situations, relatively insensitive deep structures can become the source of severe and disabling pain and sensitivities).
That's how we got to the central pathways of pain. Note at this level is that the convergence of several sensory stimuli to a single spinal neuron transmitter of pain is of great importance because it underlies the phenomenon of irradiated pain.
All spinal neurons that receive stimuli from the viscera and deep musculoskeletal structures also receive stimuli from the skin. The convergence of the paths occurs in the spinal segment of the dorsal root that ensures the upward innervation of this structure.
For example, the adhesions in the central diaphragm are derived from the third and fourth cervical ganglia of the dorsal root. Primary differences with the cellular body in the same ganglion receive impulses from the skin of the shoulder and the lower part of the neck.
Thus, both the sensory impulses in the shoulder skin and those in the central diaphragm converge in the neurons that transmit pain in the third and fourth cervical spinal segments. Because of this convergence and the fact that spinal neurons are most often activated by stimuli from the skin, the activity triggered in the spinal neurons by stimuli in the deep structures is mislocated by the individual (the one who perceives this pain) in an area that is coarsely extended to the region of the skin innervated by the same spinal segment.
Thus, an inflammation near the central diaphragm is described as discomfort in the shoulder area. This spatial displacement of the pain sensation in the area of the lesion that causes it is known as irradiated pain.
There would follow some descriptions of the upward pathways of pain. But I will point out, for later, that the spinotalamic pathway is essential for the sensation of pain because interrupting these pathways produces permanent deficits in the perception of pain and temperatures.
Then, to be retained, the axons of the spinotalamic tract connect with the talamic neurons that are projected into the somatosensory cortex. This pathway from the spinal cord to the thalamus and somatosensory cortex seems to be extremely important for the sensory aspects of pain, i.e. location, intensity and quality.
The axons of the spinotalamic tract also connect with the thalamic and cortical regions related to the emotional response (such as the cingulate gyrus and the frontal lobe). This path is meant to contribute to the unpleasant affective or emotional dimension of pain.
And, what needs to be retained further is one of the relatively significant roles of the thalamus, that of "the selector factor of the important stimuli that are projected at the corresponding upper levels in the cortex area".
In other words, at this level of the thalamus, a selection of stimuli from all levels of perception of the body is made, leaving to pass further to the cortex (areas of interpretation and response) only those stimuli that are "accepted" a certain importance, the other stimuli being simply lost or become accessories to other processes.
Here's a first step in the modulation mechanism of pain. So the pain caused by similar injuries varies greatly in different situations and in different people. It is known that athletes can have severe fractures accompanied by small pain have, for example, in war, some wounds produced by soldiers were easily borne, although they produced (would have produced) unbearable pain to civilian patients. Moreover, even the suggestion of comfort (placebo) has a significant analgesic effect.
On the other hand, many patients even find minor lesions (venous puncture, for example) unbearable, and it has been shown that the anticipation of pain induces the appearance of painful sensation even in the absence of a harmful stimulus. And, the powerful effect of anticipation and other psychological variables on the perceived intensity of pain implies the existence of brain circuits, which can modulate the activity of the ways of transmission of pain.
That's because pain modulation is two-way. Pain modulation circuits not only cause analgesia, but are also capable of increasing pain. Both the pain-relieving and pain-inhibiting neurons in the brain bulb project themselves on/ and control the spinal pain-transmitting neurons. Because pain-transmitting neurons can be activated through modulating neurons, theoretically (or real???) it is possible to generate a painful signal without peripheral harmful stimulus. Such a mechanism could clarify that pain can be induced by self-suggestion and provide a framework for understanding how psychological factors can contribute to chronic pain.
We'll continue tomorrow...
At the moment I only provide you with the title, the material being in the works but, as you are convinced, I will post it (for those like me the debt is duty)...
And, to get off to the most academic start possible, the generally accepted definition of pain is: "Unpleasant sensory and emotional experience, determined or related to actual or potential tissue damage, or described in terms of such injuries" (at the "level" of the Dex, the pain being described simply as physical and/ or moral suffering borne by someone, grief, sorrow).
Pain is the one universally perceived as a signal of the disease, being also the most common "perceived" symptom. And, the first "purpose" of medicine being to preserve and restore health and to alleviate suffering, it is obvious why pain is one of the main milestones of medical activities. But the "defining" elements compel me to proceed to some "clarifications"...
Pain can be described on the basis of three components: 1. physiological (mode of transmission, receptors involved, biochemical processes, etc.), 2. behaviours that express pain and accompany it) and 3. (thoughts, feelings and representations related to pain).
And, pain has only a simple classification in: acute (which lasts between 6 weeks and 6 months, with anxiety as associated feeling, since pain has the significance of imminent danger for the individual - represented by forms: 1. superficial, short-lived, well-located and with a "sharp" character, in the skin, mucous membranes and 2. deeper, more persistent, more difficult to locate, with a burning character , in the muscles and membranes) and chronic (lasts more than 6 months and is localized in the internal organs, generally of a pressure character, producing an important discomfort, with subjective, familial, professional, etc. - represented by forms: 1. recurrent, benign, of increased intensity, repeated, with free interval, as in migraine, 2. intractable, constant, of variable intensity, as in back pain and 3. , as in rheumatic arthritis, cancer).
The "classic" function of the sensory system of pain is to detect, locate and identify tissue injury processes. Because different diseases produce different types, characteristic, of tissue damage, quality, duration over time and localization of pain, as well as localization of sensitivity, provide important diagnostic milestones and are used to assess the response to treatment.
It is often described as a process of tissue destruction or penetration (e.g. stabbing, burning, breaking, torsion, compression) and/ or as a physical or emotional reaction (example: frightening, emetic, disgusting). Moreover, any pain of moderate or high intensity is accompanied by anxiety and the impulse to remove or limit the sensation.
These properties illustrate the duality of pain: both sensation and emotion. When acute, pain is characteristically associated with a change in behaviour and a response to stress, consisting of increased blood pressure, increased heart rate, pupil diameter and elevated levels of plasma cortisol (hormone with regulating functions in other glands, secreted by the adrenals). In addition, local muscle contractions are common (example: limb flexion, abdominal wall stiffness, etc.).
As for the structures underlying the initiation of the sensation of pain, I will only tell you that they are called nociceptors (from the "comasing" of harmful terms with receptors) and are made up of primary receiving structures, motor neurons and sympathetic postganglionary neurons (cellular bodies of the primary aferants located in the spinal ganglia on the posterior roots of the spinal nerves, located in the vertebral holes) , the collection and transmission structures of the primary aferants, from here it comes to the central pathways of pain (from the spinal cord) etc. etc. etc. etc. (I am not mischievous when I assure you that at least 99% of doctors not involved in the "pharmaceutical" research of pain or something similar can not really describe much about this structure of pain, so I will not bore you with such details). It is important to note that nociceptors (the vast majority) can respond to several different types of harmful stimuli, such as burning, intentional mechanical stimuli such as a pinch, and the application of chemical irritants.
Important here, the level of "taking over" the future sensation of pain, is sensitization. When intentional stimuli are applied, repeat and prolong, if the tissue is damaged or if inflammation is present, the threshold for activating primary aferential nociceptors is lower and the trigger frequency is higher for all stimulus intensities.
Inflammation mediators such as bradychinin, some prostaglandins and leukotrienes contribute to this process called sensitization. In sensitized tissues, usually harmless stimuli end up producing pain, sensitization being an important clinical process that contributes to sensitization, inflammation and hyperalgesia (a striking example of sensitization is sunburnt skin, in which severe pain can be caused by a simple touch, or a slight slap on the back, or by a warm shower).
Compared to superficial structures (skin, cornea, etc.), viscera are relatively insensitive under normal conditions to nociceptive stimuli. In contrast, when affected by a pathological process with an inflammatory component, deep structures such as cavities or cavitational viscera become characteristically particularly sensitive to mechanical stimulation (here being "silent" nociceptors, their "activity" being the reason why, in pathological situations, relatively insensitive deep structures can become the source of severe and disabling pain and sensitivities).
That's how we got to the central pathways of pain. Note at this level is that the convergence of several sensory stimuli to a single spinal neuron transmitter of pain is of great importance because it underlies the phenomenon of irradiated pain.
All spinal neurons that receive stimuli from the viscera and deep musculoskeletal structures also receive stimuli from the skin. The convergence of the paths occurs in the spinal segment of the dorsal root that ensures the upward innervation of this structure.
For example, the adhesions in the central diaphragm are derived from the third and fourth cervical ganglia of the dorsal root. Primary differences with the cellular body in the same ganglion receive impulses from the skin of the shoulder and the lower part of the neck.
Thus, both the sensory impulses in the shoulder skin and those in the central diaphragm converge in the neurons that transmit pain in the third and fourth cervical spinal segments. Because of this convergence and the fact that spinal neurons are most often activated by stimuli from the skin, the activity triggered in the spinal neurons by stimuli in the deep structures is mislocated by the individual (the one who perceives this pain) in an area that is coarsely extended to the region of the skin innervated by the same spinal segment.
Thus, an inflammation near the central diaphragm is described as discomfort in the shoulder area. This spatial displacement of the pain sensation in the area of the lesion that causes it is known as irradiated pain.
There would follow some descriptions of the upward pathways of pain. But I will point out, for later, that the spinotalamic pathway is essential for the sensation of pain because interrupting these pathways produces permanent deficits in the perception of pain and temperatures.
Then, to be retained, the axons of the spinotalamic tract connect with the talamic neurons that are projected into the somatosensory cortex. This pathway from the spinal cord to the thalamus and somatosensory cortex seems to be extremely important for the sensory aspects of pain, i.e. location, intensity and quality.
The axons of the spinotalamic tract also connect with the thalamic and cortical regions related to the emotional response (such as the cingulate gyrus and the frontal lobe). This path is meant to contribute to the unpleasant affective or emotional dimension of pain.
And, what needs to be retained further is one of the relatively significant roles of the thalamus, that of "the selector factor of the important stimuli that are projected at the corresponding upper levels in the cortex area".
In other words, at this level of the thalamus, a selection of stimuli from all levels of perception of the body is made, leaving to pass further to the cortex (areas of interpretation and response) only those stimuli that are "accepted" a certain importance, the other stimuli being simply lost or become accessories to other processes.
Here's a first step in the modulation mechanism of pain. So the pain caused by similar injuries varies greatly in different situations and in different people. It is known that athletes can have severe fractures accompanied by small pain have, for example, in war, some wounds produced by soldiers were easily borne, although they produced (would have produced) unbearable pain to civilian patients. Moreover, even the suggestion of comfort (placebo) has a significant analgesic effect.
On the other hand, many patients even find minor lesions (venous puncture, for example) unbearable, and it has been shown that the anticipation of pain induces the appearance of painful sensation even in the absence of a harmful stimulus. And, the powerful effect of anticipation and other psychological variables on the perceived intensity of pain implies the existence of brain circuits, which can modulate the activity of the ways of transmission of pain.
That's because pain modulation is two-way. Pain modulation circuits not only cause analgesia, but are also capable of increasing pain. Both the pain-relieving and pain-inhibiting neurons in the brain bulb project themselves on/ and control the spinal pain-transmitting neurons. Because pain-transmitting neurons can be activated through modulating neurons, theoretically (or real???) it is possible to generate a painful signal without peripheral harmful stimulus. Such a mechanism could clarify that pain can be induced by self-suggestion and provide a framework for understanding how psychological factors can contribute to chronic pain.
We'll continue tomorrow...
Have
a good day and good health!
Dorin, Merticaru