This document summarizes the pain pathway in the human body. It begins with an introduction to pain and its characteristics. It then discusses the different types of pain sensations conducted by different nerve fibers. It explains Gate Control Theory and the differences between somatic and visceral sensory function. It provides details on pain receptors, the pathway of sensory impulses from receptors to the brain, and examples of tooth pulp pain and referred pain. It concludes with management strategies for pain.
Pain is defined as an “unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such”.
Free nerve endings – responsible for carrying noxious stimulus from both superficial as well as deep somatic and visceral pain sensations therefore reffered as nociceptors
According to type of impulses they carry second order neuron can be classified as –
LOW THRESHOLD MECHANOSENSORY( ligth touch, pressure and Proprioception)
NOCIOCEPTIVE SPECIFIC ( Noxious stimulation)
WIDE DYNAMIC RANGE ( wide range of stimulus intensities from nonnoxious to noxious.
SILENT NOCICEPTORS (It is an afferent neuron that appear to remain or silent to any mechanical stimulation .These neuron become active with tissue injury and add to the nociceptive input entering the CNS.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is defined as an “unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such”.
Free nerve endings – responsible for carrying noxious stimulus from both superficial as well as deep somatic and visceral pain sensations therefore reffered as nociceptors
According to type of impulses they carry second order neuron can be classified as –
LOW THRESHOLD MECHANOSENSORY( ligth touch, pressure and Proprioception)
NOCIOCEPTIVE SPECIFIC ( Noxious stimulation)
WIDE DYNAMIC RANGE ( wide range of stimulus intensities from nonnoxious to noxious.
SILENT NOCICEPTORS (It is an afferent neuron that appear to remain or silent to any mechanical stimulation .These neuron become active with tissue injury and add to the nociceptive input entering the CNS.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.
Pain pathway gate control theory
Pain management
An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to CNS where it is interpreted as such.
1. Exteroceptors: arising from receptors from skin & mucosa. sensed at conscious level
E.g. Merkel corpuscles : Tactile receptors.
Free Nerve ending :Perceive superficial pain.
2. Proprioceptors : From musculoskeletal structures.
The presence , positions & movement of body. below conscious levels.
E.g. 1) Muscle spindles : Skeletal muscle fibers. Mechanoreceptors.
2) Free nerve ending : Perceive deep somatic pain & other sensations.
3. Interoceptors : From viscera of body below conscious level.
E.g. Pacinian corpuscles : perception of touch-pressure.
Free nerve ending : Perceive visceral pain & other sensations.
this seminar consists of pain,components of pain,pain pathways - ascending and analgesic followed by management of dental pain and local anesthesia,composition,various techniques used and pediatric implications for the administration of the locan anesthetics and the newer agents wich are available in topical,injectable and intra osseous techniques
INTRODUCTION
HISTORY
EPIDEMIOLOGY
DEFINITIONS OF PAIN
BENEFITS OF PAIN
NOCICEPTION
PAIN RECEPTORS
THEORIES OF PAIN
CHARACTERISTICS OF PAIN
PAIN PATHWAY
MECHANISM OF PAIN
PAIN ASSESSMENT
APPLIED ASPECTS
CONCLUSION
REFERENCES
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Comparing Evolved Extractive Text Summary Scores of Bidirectional Encoder Rep...University of Maribor
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11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Track: Artificial Intelligence
https://www.etran.rs/2024/en/home-english/
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
What is greenhouse gasses and how many gasses are there to affect the Earth.moosaasad1975
What are greenhouse gasses how they affect the earth and its environment what is the future of the environment and earth how the weather and the climate effects.
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
This presentation explores a brief idea about the structural and functional attributes of nucleotides, the structure and function of genetic materials along with the impact of UV rays and pH upon them.
4. INTRODUCTION
Unpleasant sensory & emotional experience associated with actual or
potential tissue damage.
Its imp: , symptoms of many diseases & when pt experiences pain
he/she consults a physician.
5. Characteristics
• specific with specific receptors & afferent fibers.
•Less adaptation & continues as long as pain causing agent persists.
•Chronic pain- psychological effects.
•Tolerance level varies from individuals.
•Cerebral cortex – localization, discrimination & interpretation.
6. Types of pain sensation
1) Fast pain- short & sharp
conducted by Aδ fibers
localization of pain is better
2) Slow pain- more prolonged & severe
conducted by C fibers
dull, diffused & localization is poor
3) Deep pain- contraction of skeletal muscles
when pain is severe, causes sweating, nausea &
vomiting, fall in B.P
7. Aδ – fast, sensitive to mechanical noxious stimuli.
small, myelinated. High conductance speed
C – slow, sensitive to many noxious stimuli (chemical,
etc.) – small, unmyelinated. Slow conductance speed
8. Receptors
They are specialized afferent nerve endings designed to respond
appropriate & adequate stimulus.
Function
Converts various forms of energy into action potential in nerve fibers
Act as transducers
Situated at various parts of body- skin, eye, ear, nose, muscle etc
9. Properties
Excitability – specificity
receptive response
Adaptation
Effect of extend of stimulus
Localization & projection
Effect of strength of stimulus
Quality or modality of sensation
Intensity of sensation
Fatigue
10. Classification
•Exteroreceptors- responds to change in external enviornment
a) cutaneous receptors- touch, pain, temp:
b) chemical receptors- taste & smell
c) teleceptors- vision & hearing
11. •Interoceptors – exited by stimuli within the body
a) Stretch receptors- alvoeli of lungs
b) Chemoreceptors- aortic & carotid bodies
c) baroreceptors- carotid sinus & aortic arch
d) Osmoreceptors- hypothalamus
e) Volumereceptors- right atrium
f) Proprioreceptors- muscle spindle, tendon
g) Visceroreceptors- present in visera
12. Nociceptors
are special receptors that respond only to noxious stimuli
and generate nerve impulses which the brain interprets as
“pain”.
13. 1. Prevents serious damage.
2. Teaches one what to avoid
3. If pain is in joints, pain limits the activity, so no
permanent damage can occur.
but pain can become the problem, and cause people to
want to die.
Purpose of pain
14. Differences btw Somatic & Visceral sensory function.
Somatic :- seen on skin & subcutaneous tissues
subserve sensory function of touch, temp,sensation,
pressure & pain
Visceral:- have no proprioreceptors & sparesly distributed
subserve osmorecptors, barorecptors
15. PAIN STIMULI
3 types- thermal, mechanical & chemical.
Nociceptive stimuli- stimuli which threatens the welfare of tissues &
causes pain.
Chemical substances that can induce pain
intrinsic- bradykinin, histamine, prostaglandins
extrinsic- irritant acid, alkali, plant & animal stings & venoms
16. 1. gray matter
2. white matter
3. gray commissure
4. central canal
Dorsal and ventral nerve
roots
Internal Anatomy
19. Three major pathways carry sensory information
Posterior column pathway (gracile & cuneate fasciculi)
Anterolateral pathway (spinothalamic)
Spinocerebellar pathway
20. THREE neurons from the
receptor to the cerebral
cortex
First order neuron:
Cell body located in the
dorsal root ganglion. The
Axon passes to the spinal
cord through the dorsal root
of spinal nerve, runs
ipsilaterally and synapses
with second-order neurons
in the cord and medulla
oblongata
21. Second order neuron:
Has cell body in the
spinal cord or medulla
oblongata &
Terminate on 3rd order
neuron
Third order neuron:
Has cell body in
thalamus
Axon terminates on
cerebral cortex
ipsilaterally
25. Pain
Free nerve
ending
Posterior nerve
root ganglion
Fibers from lateral
spinothalamic tract
Ventral posterolateral nucleus of thalamus,
reticular formation & midbrain.
Sensory cortex
Receptor
First order neuron
Second order neuron
Third order neuron
center
26. Tissue ischemia
Blood flow is blocked for few min- pain
Results in anaerobic metabolism & release of bradykinin &
proteolytic enzymes- cell damage
27. Muscle spasm
Indirect effect muscle spasm to compress the blood vessels & cause
ischemia
Results – release of chemicals and increase in metabolism in muscle
tissue.
28. Visceral pain
They are dull & diffuse, poorly localized, and associated with
symptoms like nausea & referred to other areas
Stimuli for visceral pain
ischemia, obstruction, spasm, chemical stimuli.
29. REFERRED PAIN FROM VISCERAL ORGANS
Referred pain
Pain felt in a part of the body that is
fairly remote from tissue causing pain.
Pain at diaphragm is felt over tip of
shoulder
Pain at maxillary sinus felt at nearby
teeth.
A tooth abscess can cause jaw bone
pain.
30. Convergence theory
both somatic & visceral
afferent fibers converge upon 2nd
order neuron
Somatic fibers conduct
impulses more frequent.
Visceral pain is felt as somatic
pain because brain is familiar
with somatic regions.
31. Facilitation theory
Visceral & somatic fiber join at adjoining spinothalamic neurons( 2nd
order neurons)
When strong impulses conduct, activation of spinothalamic neurons,
resulting in impulses passing through spinothalamic pathway
This results in misinterpretation in location of pain.
32. Melzack & Waller- 1965
Pain impulses in spinal cord can
be modified by other afferent
impulses entering the spinal cord
with posterior horn acting as gate
Gate control hypothesis/ gate theory of pain
33. Gate open Gate closed
Physiological Aδ and C fibers
active, Overuse,
Fatigue , improper
mechanics, tired
Aδ or Aα active,
Relaxation, exercise,
strengthening/
conditioning
Medical Extent of
injury/pathological
condition
Medication,
cooling/heating
Congenitive Focusing on pain,
anxiety , fear,
depression, stress
Distraction,
relaxation,
happiness, positive
attitude
34. Tooth pulp pain
1) Exposure of dentinal tubules elicit
toothache & other non noxious
sensation.
2) Both Aδ & C fibers respond to
stimuli in dentine
3) Transmission of stimuli across
dentin, mediated by movement of
fluid through odontoblast tubules.
35. 4) Fibers terminate at medullary dorsal horn & synapse and also at
trigeminal sensory nucleus
5) From trigeminal nucleus send inf: thalamus & sensory cortex
6) Pulpal innervation are capable of regenerating & reinnervating
36. Determinants of painful experience during dental treatment
Pain occurs due to invasive procedures like extractions & surgeries or
non invasive procedures. With regard to children, studies have shown
that dentists do not believe in pain referred by children & tend not to
use available methods to control pain.
Conclusion: anxiety is determinant for pain during dental care & pain
is related to local anesthetic procedures. There are evidences that
dentists attitude are determinants for pain.
Ruth et al Rev.dor; 2012; 13(4)
39. The sensory functions are affected by lesions in sensory pathways or
other nervous disorders.
1) Anesthesia – loss of sensation
2) Hyperesthesia- increase sensitivity to sensory stimuli
3) Hypoesthesia- decrease sensitivity to sensory stimuli
4) Hemiesthesia – loss of sensation to one part of body
5) Paresthesia- abnormal sensation
40. 6) Dissociated anesthesia- loss of some sensation with loss of
consciousness produced by anesthetic agents
7) General anesthesia- loss of all sensation with loss of conciousness
produced by anesthetic agents
8) Local anesthesia- loss of sensation restricted area of body
9) Tactile anesthesia- loss of tactile sensation
41. 10) Hyperaglasia-increase in sensitivity to pain
11) Paraglesia- abnormal pain sensation
12) Thermic anesthesia- loss of thermal sensation
13) Pallanesthesia- loss of sensation of vibration
14) Analgesia- loss of pain sensation
42. Herpes zoster- viral infection affecting dorsal root ganglion. Results
in severe pain which facilitates the pain towards the ganglion.
43. Tic Doulourex
Pain felt at one side of the face
Felt like sudden electric shock, may last for secs or may be continous
Corrected by surgery at hypersensitive area
45. In a study by Pornachi et al- A case reported on a 63yr old woman with
Brown-Sequard Syndrome due to spontaneous C5-C6 cervical disc
herniation. Anterior discectomy was performed with favorable
outcome.
Neurology Asia .2007;12;65-67
47. Conclusion
Pain can induce physiological & anatomical changes within the
nervous system. The complexity of pain transmission means there
are many pharmological targets & multimodel therapy is required to
optimize pain control.
48. References
Essential of oral physiology- Robert M Bradley
Textbook of medical physiology- Guyton & Hall
Essential of medical physiology- K.Sembulingam & Prema
Sembulingam
Textbook of human physiology- S Chand
Articles
•Determinants of painful experience during dental treatment- Ruth
Suzanne et al Rev.Dor 2012;13(4)
•Case report study on Brown sequard syndrome- Ponachi et al
Neurology Asia 2007;12;65-67
•Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin
P.Rae anesthesia & intensive care medicine; 2010;12(1)