Chronic pelvic pain is defined as persistent pain lasting at least 6 months in the pelvis or lower abdomen that affects around 4-15% of women. It has no clear cause in 30% of cases. Neurogenic inflammation, where C-fibers release inflammatory substances, is thought to play a role in chronic pelvic pain by sensitizing nerves and sustaining pain even after initial tissue injury resolves. Pudendal neuralgia, where the pudendal nerve is damaged or inflamed, is a potential underlying cause. Diagnosis involves clinical exams and potentially pudendal nerve blocks, which provide diagnostic and therapeutic benefits. Guided nerve blocks provide over 60% success rates in relieving pain based on follow
An update on the epidemiology and treatment of neuropathic pain. The slides were developed for a presentation in a departmental seminar at the Curtin University, Australia.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
An update on the epidemiology and treatment of neuropathic pain. The slides were developed for a presentation in a departmental seminar at the Curtin University, Australia.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
Option of interventional pain therapy in multimodal treatment of chronic cancer and non-cancer pain
Established role when pharmacotherapy or surgery not suitable
Indications well accepted
Evidence for efficacy moderate to strong
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
Peripheral neuropathy is a common condition, encountered by physicians as well as neurologists. However, a large number of challenges remain. These include difficulty in diagnosing, delay in diagnosis, investigations and lack of effective treatments. This presentation discusses these unmet needs and provides suggestions to overcome them.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented to General Practitioners and Hospital Doctors in London
25th September 2007
Management oF Chronic Pain-- Seminar.pptxssusera931bd
The management of chronic pain involves a comprehensive approach aimed at reducing pain, improving functionality, and enhancing the quality of life for individuals living with persistent pain
Option of interventional pain therapy in multimodal treatment of chronic cancer and non-cancer pain
Established role when pharmacotherapy or surgery not suitable
Indications well accepted
Evidence for efficacy moderate to strong
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
Peripheral neuropathy is a common condition, encountered by physicians as well as neurologists. However, a large number of challenges remain. These include difficulty in diagnosing, delay in diagnosis, investigations and lack of effective treatments. This presentation discusses these unmet needs and provides suggestions to overcome them.
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented to General Practitioners and Hospital Doctors in London
25th September 2007
Management oF Chronic Pain-- Seminar.pptxssusera931bd
The management of chronic pain involves a comprehensive approach aimed at reducing pain, improving functionality, and enhancing the quality of life for individuals living with persistent pain
—Pain following Spinal Cord Injury (SCI) is very common. So this study was conducted to find out prevalence, associated factors and pattern of Neuropathic Pain (NP) among SCI patients, for which 494 consecutive eligible patients of Spinal Cord Injury (SCI) admitted in the Department were evaluated for NP. It was observed that 13.76% of SCI patients complained of neuropathic pain. In 21 to 30 years age group 23.13% and 61.76% cases of neuropathic pain had dorso-lumbar injury. 48.30% cases of neuropathic pain had onset in 2 nd and 3 rd week. Discomfort was more at night (36.76%), in below the knee area and dorsum of the foot. Hot burning type of sensation was the commonest descriptor of NP and range of movement (ROM) exercises and tepid cold water sponging were relieving factors.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Dolore pelvico cronico: epidemiologia ed eziopatogenesi
1. Dolore pelvico cronico:
epidemiologia ed
eziopatogenesi
F. Cappellano
Neurourology Dept
“Pain Team” Coordinator
Policlinico Multimedica IRCCS
Sesto San Giovanni ( Milano)
2. DEFINITION
ACUTE vs CHRONIC PAIN
ACUTE PAIN
occurs in conjunction with autonomic reflex
responses and associated with signs of
inflammation and infection
symptom of underlying tissue injury and disease
it is a protective mechanism.
CHRONIC PAIN
in contrast doesn’t have such physiologic role
it is itself not a symptom, but a disease
lasting 6 months or longer
is characterized by psychological, affective and
behavioral responses that differ from acute pain.
3. Chronic pelvic pain
Chronic pelvic pain is defined as a chronic or
persistent pain, continuous or recurrent for at least 6
months, perceived in structures related to the pelvis
or lower abdomen (Guidelines on Chronic Pelvic Pain – EAU,
2012)
Real incidence not known (about 4-15% of women),
Female to male ratio 9:1 ,
10% of gynecology referrals,
12% of hysterectomies, 40% of diagnostic
laparoscopies,
High impact on quality of life,
In 30% of cases no apparent cause is determined.
Consider :
pudendal neuralgia and neurogenic inflammation !
4. EPIDEMIOLOGY
• Follow up study 1 to 6 years (mean follow-up period 3.4y)
• From April 1998 to November 2002
• age >18 year-old
• 72/139 women (60%)
• Life Chart interview
• Demographic and clinical variables
• MPQ-DLV to assess self-reported pain + McGill VAS
• SCL-90 to assess psychological distress
Pain 132 (2007) S117–S123
5. EPIDEMIOLOGY
• After 6 years of follow up 75% women had not reach recovery
• No women reported malignancy or any newly diagnosed physical illness
• 25% recovery (improvement gain scores)89% clinical improvement
50% after 2 years
25% after 3 years
11 % no pain
• Recovery was not associated with any demographic, clinical or pain related
variable measures at baseline
Pain 132 (2007) S117–S123
8. Neural mechanisms of pain
Elbadawi and Light proposed
neurogenic inflammation as a
trigger taking place in this disease
When activated by noxious events
such as nociception, C-fibers not
only do they convey information to
the CNS (afferent function), but
they also can release substance P,
CGRP, tachykinins, somatostatin,
nitric oxide and other factors into
the local environment (efferent
function).
9. Neurogenic inflammation
NI is not necessarily a mechanism leading
to a disease but it’s part of the tissue
response to injury
It seems to be an adaptive response,
activating cells for local defence but
sometimes it can become maladaptive
Recently the involvement of NI has also
been suggested in the development of IC
Elbadawi, Steers, 1997
10. Neural mechanisms of pain
Once activated, C-fibers can
become sensitized, meaning
that they no longer remain
silent even after inflammation
resolves (Gebhart, 1999)
Efferent actions increase
local vascular permeability
and inflammation, a process
called ‘neurogenic
inflammation’ (Holzer, 1998 )
11. Wind–up phenomenon
Wind-up is a form of short-
term plasticity in spinal dorsal
horn that can be observed
during electrical stimulation of
C-fibers
The action potential firing of
some wide dynamic range
(WDR) neurons in deep dorsal
horn increases progressively.
Wind-up may facilitate
induction of LTP at C-fiber
synapses, as a progressive
postsynaptic depolarization
Central sensitization is
triggered by impulses in
nociceptive C-fibers.
3 Hz
13. Neurogenic inflammation and estrogen
Women have a higher incidence of inflammatory
disorders than men and also appear to perceive painful
stimuli differently
Estrogen have the capacity to modulate neurogenic
inflammation through interaction with a variety of
mediators of inflammation
Estrogen receptors may play a role in determining the
intensity of the response to neurogenic inflammation .
(Bjorling 2001)
14. Estradiol’s influence on CNS
function
The CNS can retain a
‘memory’ of central
neuronal changes
induced by neuronal
input that can be
‘recalled’ by estradiol
action on activity of
CNS neurons
15. Pudendal neuropathy
Pudendal neuralgia by a mechanical
and/or inflammatory damage to the
nerve may be the underlying condition of
CPP once other causes for the
symptoms may be excluded.
Usually a pudendal nerve entrapment
(PNE) is believed to be the cause of
pudendal neuralgia, but a neurogenic
inflammation can often sustain this
condition
18. Neurogenic inflammation
NI is not necessarily a mechanism leading
to a disease but it’s part of the tissue
response to injury
It seems to be an adaptive response,
activating cells for local defence but
sometimes it can become maladaptive
Recently the involvement of NI has also
been suggested in the development of IC
Elbadawi, Steers, 1997
19. NI and organs cross talk
In visceral pain
conditions NI not only
plays a role in pain and
inflammation at the site
of viscus, but also
appears to be an
important mechanism in
referred pain.
Malykhina 2007, Neuroscience
20. Diagnosis
Clinical examination is necessary
Sensory loss on perineum or genitals is suggestive of
sacral nerve root lesion, without pain but associated
with sphincters motor disorders
Unilateral pain elicited by compression of the area
near the ischial spine during rectal or vaginal
examination
CT scan, MRI and other radiological procedures are
not useful for diagnosis
Neurophysiology tests may serve as complementary
diagnostic measures
Psycological evaluation for depression is mandatory
22. Pudendal nerve block
Guided pudendal nerve blocks are the first
line of conservative treatment for pudendal
neuralgia, usually associated to oral drugs
and physical therapy.
They are performed for making a diagnosis
of pudendal neuralgia, for its prognostic
value and mainly for the therapeutic effect.
23. Pudendal nerve block
Responders have a complete relief of pain
for about 36-48 hours , a mild flare up of
pain for 2 to 3 days and then a relief up to
complete wellness for about 15 days.
The subsequent blocks are made at 3
weeks interval, after a clinical reassessment
of the patient and an evaluation of the VAS,
until a complete recovery or stabilization of
the pain at an acceptable level is obtained.