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
Pain is the common symptom in many chronic conditions such as cancers, neuropathies, and chronic disease. It is also experienced in trauma varying from mild to severe based on the location and degree of trauma. This presentation is a brief outline on types of pain, classification of pain, pain pathways and management of pain
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.
The presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes is called diabetic peripheral neuropathy.
The diagnosis is principally a clinical one. Patients with type 1 diabetes for 5 or more years and all patients with type 2 diabetes should be assessed annually.Treatment goals include
good glycemic control,symptomatic treatment and halt progressive nerve damage.
Pain is the common symptom in many chronic conditions such as cancers, neuropathies, and chronic disease. It is also experienced in trauma varying from mild to severe based on the location and degree of trauma. This presentation is a brief outline on types of pain, classification of pain, pain pathways and management of pain
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.
The presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes is called diabetic peripheral neuropathy.
The diagnosis is principally a clinical one. Patients with type 1 diabetes for 5 or more years and all patients with type 2 diabetes should be assessed annually.Treatment goals include
good glycemic control,symptomatic treatment and halt progressive nerve damage.
Medical management of neuropathic painSudhir Kumar
This presentation looks at medical therapies for the treatment of neuropathic pain. Neuropathic pain is commonly caused by diabetes, herpes zoster, trigeminal neuralgia, cancer, vitamin B12 deficiency, vasculitis, etc.
A comprehensive presentation on dependence on and abuse of pregablin and gabapentin and the context of the drugs in the pharmaceutical market - by a substance use nurse
Acute Transverse Myelitis
Blockage of the Spinal Cord’s Blood Supply
Cervical Spondylosis
Compression of the Spinal Cord
Hereditary Spastic Paraparesis
Subacute Combined Degeneration
Syrinx of the Spinal Cord and Brain Stem
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.
Definition n classification •Pathophysiologyof pain. •Physiological Effects of pain. •Pharmacological & non-pharmacological methods of analgesia. •Principles of pain management.METHODS OF CONTROLLING METHODS OF CONTROLLING
Non-pharmacological Preoperative counseling TENS Acupuncture
Pharmacological Opioids •Im •IV infusion •IV PCA Local anaesthetics: •Local Infiltration •Nerve Blocks •Epidural Blocks NSAIDS •IM •IV infusion •IV PCA
NON-PHARMACOLOGICAL METHODS PRE-OP COUNSELLING: Well informed patients about: •Nature of operation •Nature of post operative pain •Methods of analgesia available
Cope better with Post –op Pain
NON-PHARMACOLOGICAL METHODS TENS (Trans Cutaneous electric nerve stimulation)
Stimulates afferent myelinated (A-beta) nerve fibers at 70hz
Inhibitory circuits within sp cord activated
Nerve impulse transmission reduced
Maximum benefit in neurogenic pain
PHARMACOLOGICAL METHODS OPIODS •Activate opiodreceptors within the CNS •Reduce transmission of nerve impulses by modulation in the dorsal horn
PHARMACOLOGICAL METHODS
LOCAL ANAESTHETICS –Blocks the conduction of nerve impulses –Can be given with adrenaline because •Decreases absorption of L.A allowing larger doses •Also acts on alpha 2 receptors which potentiates analgesic effect
PHARMACOLOGICAL METHODS
NASIDS –Blocks synthesis of PG’s –Only suitable for miledto moderate pain
PRINCIPLE OF MANAGEMENT OF PAIN •Pre-emptive analgesia •Balanced or combination analgesia •Analgesia ladder
PHARMACOLOGICAL METHODS
Balanced Analgesia –NASID are used in conjunction with opioids. –Reduces amount of opioids –Reduces side affect of opioids,ASSESMENT OF PAIN •Observe the behaviour of the patient •Monitor analgesic requirement of the patient –Visual Analogue Score( VAS )
–Verbal Rating Score ( VRS ) •None •Mild •Moderate •severe
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
Parkinsonism is a clinical syndrome and, typically, when the condition
appears to be idiopathic and responsive to levodopa therapy, is referred
to as Parkinson’s disease1
• The four cardinal features of the parkinsonian syndrome are:2
– Bradykinesia
– Muscular rigidity
– Resting tremor
– Postural instability (and gait impairment)
• These features are not always observed in every patient, at any given
time
To make a diagnosis of PD, the physician must distinguish between
different forms of parkinsonism:1
– Parkinson’s disease
– Secondary parkinsonism
– Parkinsonism as part of another neurodegenerative disorder (e.g., multiple
system atrophy, progressive supranuclear palsy, corticobasal degeneration, or
Lewy body dementia)
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Sequencing in management of Multiple sclerosisAmr Hassan
Sequencing of DMTs for individual multiple sclerosis patients should be designed in such a way to maximize disease control and minimize risk based on the mechanism of action, pharmacokinetic and pharmacodynamic properties of each therapy. This includes the DMT patients are being switched from to those they are being switched to. The reversibility of immune system effects should be a key consideration for DMT sequence selection. This feature varies across DMTs and should factor more prominently in decision making as newer treatments become available for the prevention of disability accumulation in patients with progressive MS. In this short review, we discuss the landscape of existing therapies with an eye to the future when planning for optimal DMT sequencing. While no cure exists for MS, efforts are being directed toward research in neuroregeneration with the hope for positive outcomes.
A neuromuscular disorder that leads to weakness of skeletal muscles.
Symptoms
Causes
Prevention
Complications
Common tests & procedures
Neurological examination:
Repetitive nerve stimulation test:
Antibody test:
Pulmonary function tests (PFTs): To check any breathing difficulty.
CT scan: To rule out a presence of tumor in thymus.
Magnetic resonance imaging (MRI): MRI of the chest is performed to rule out a presence of tumor in thymus.
Edrophonium (Tensilon) test:
Medication
Procedures
Nutrition
Prediction of outcome of Multiple sclerosisAmr Hassan
Prediction of outcome of Multiple sclerosis
An understanding of the natural history of multiple sclerosis(MS) in a patient is important to begin proper treatment at the correct time, especially when there is a high risk for poor prognosis. Factors that predict unfavorable prognosis are a primary or secondary progressive course, older age at disease onset, short interval between first and second attacks, initial cerebellar or pyramidal symptoms, a large number of functional systems involved at onset, moderate to severe disability within the first 2 years, and the presence of typical plaques or greater lesion volume shown by magnetic resonance imaging results during the first 5 years. However, there are no established laboratory tests able to predict long-term prognosis.
Lifestyle modification in epilepsy
Lifestyle Modifications
Lifestyle modifications can include:
Adequate sleep: Fatigue is one of the most common seizure triggers, and disrupted sleep can make the brain more vulnerable to misfiring.
Avoiding drugs and alcohol: These can be triggers for seizures in patients with epilepsy. Even one or two drinks can provoke seizures.
Minimizing emotional stress: Although there is not definitive proof that stress causes seizures, those who maintain healthy stress levels have reported that they believe it reduces their risk.
Frequency of exercise: In addition to a range of health benefits, regular exercise can help reduce risk of seizure. However, you should consult your physician before starting a new exercise routine, as some exercise can, rarely, cause seizures.
Childhood demyelinating syndromes
In the past decade, the number of studies related to demyelinating diseases in children has exponentially increased. Demyelinating disease in children may be monophasic or chronic. Typical monophasic disorders in children are acute disseminated encephalomyelitis and clinically isolated syndromes, including optic neuritis and transverse myelitis. However, some cases of acute disseminated encephalomyelitis or clinically isolated syndrome progress to become chronic disorders, including multiple sclerosis and neuromyelitis optica. This review summarizes the current knowledge on monophasic and chronic demyelinating disorders in children, focusing on an approach to diagnosis and management.
Diabetic polyneuropathy
Diabetic polyneuropathy (DPN) is defined as peripheral nerve dysfunction. There are three main alterations involved in the pathologic changes of DPN: inflammation, oxidative stress, and mitochondrial dysfunction.
Excessive daytime sleepiness
The most common causes of excessive daytime sleepiness are sleep deprivation, obstructive sleep apnea, and sedating medications. Other potential causes of excessive daytime sleepiness include certain medical and psychiatric conditions and sleep disorders, such as narcolepsy.
Vagal Nerve stimulation
Vagus nerve stimulation (VNS) is a medical treatment that involves delivering electrical impulses to the vagus nerve. It is used as an add-on treatment for certain types of intractable epilepsy and treatment-resistant depression. Frequent side effects include coughing and shortness of breath. Serious side effects may include trouble talking and cardiac arrest.
Dystonia
Dystonia is a movement disorder in which your muscles contract involuntarily, causing repetitive or twisting movements.
The condition can affect one part of your body (focal dystonia), two or more adjacent parts (segmental dystonia) or all parts of your body (general dystonia). The muscle spasms can range from mild to severe. They may be painful, and they can interfere with your performance of day-to-day tasks.
Dystonia: Causes, Types, Symptoms, and Treatments
Trigeminal neuralgia is sudden, severe facial pain. It's often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums.
Trigeminal neuralgia
Contents
Overview
Symptoms
Causes
Diagnosis
Treatment
Nootropics and smart drugs are natural or synthetic substances that can be taken to improve mental performance in healthy people.
They have gained popularity in today’s highly competitive society and are most often used to boost memory, focus, creativity, intelligence and motivation.
Here’s a look at the ]best nootropics and how they enhance performance.
Nystagmus is a condition of involuntary (or voluntary, in some cases)eye movement, acquired in infancy or later in life, that in extremely rare cases may result in reduced or limited vision. Due to the involuntary movement of the eye, it has been called "dancing eyes"Contents
1 Causes
1.1 Early-onset nystagmus
1.2 Acquired nystagmus
1.3 Other causes
2 Diagnosis
2.1 Pathologic nystagmus
2.2 Physiological nystagmus
3 Treatment
4 Epidemiology
Basics of Neuroradiology
Neuroradiology is an essential tool in management of patients with neurological and neurosurgical disorders. The aim of this presentation will be to acquaint the reader to understand how images are formed on a computed tomography (CT) and magnetic resonance imaging (MRI) along with a review of the relevant neuroanatomy. This understanding will be helpful to the reader in interpretation of images and diagnosis of various neurological disorders.
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
3. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
5. What is pain?
“An unpleasant sensory
and emotional experience
associated with actual or
potential tissue damage,
or described in terms of
such damage.”
Amr Hasan El-Hasany M.D.
Merskey H et al, eds. In: Classification of Chronic Pain: Descriptions of Chronic Pain
Syndromes and Definitions of Pain Terms. 1994:209-212.
7. “Pain is a more terrible lord of
mankind than death itself.”
Albert Schweitzer
8. ALLODYNIA
Pain due to a stimulus which does not normally provoke pain.
ANALGESIA
Absence of pain in response to stimulation which would normally
be painful.
ANESTHESIA DOLORASA
Pain in an area or region which is anesthetic.
Amr Hasan El-Hasany M.D.
9. CAUSALGIA
A syndrome of sustained burning pain, allodynia, and hyperpathia
after a traumatic nerve lesion, often combined with vasomotor and
sudomotor dysfunction and later trophic changes.
CENTRAL PAIN
Pain initiated or caused by a primary lesion or dysfunction in the
central nervous system.
DYSESTHESIA
An unpleasant abnormal sensation, whether spontaneous or evoked.
Amr Hasan El-Hasany M.D.
10. HYPERALGESIA
An increased response to a stimulus which is normally painful.
HYPERESTHESIA
Increased sensitivity to stimulation, excluding the special senses.
HYPERPATHIA
A painful syndrome characterized by an abnormally painful
reaction to a stimulus, especially a repetitive stimulus, as well as
an increased threshold.
Amr Hasan El-Hasany M.D.
11. HYPOALGESIA
Diminished pain in response to a normally painful stimulus.
NEURALGIA
Pain in the distribution of a nerve or nerves.
Note: Common usage, especially in Europe, often implies a
paroxysmal quality, but neuralgia should not be reserved for
paroxysmal pains.
NEURITIS
Inflammation of a nerve or nerves.
Note: Not to be used unless inflammation is thought to be
present. Amr Hasan El-Hasany M.D.
12. NEUROPATHY
A disturbance of function or pathological change in a nerve: in
one nerve, mononeuropathy; in several nerves, mononeuropathy
multiplex; if diffuse and bilateral, polyneuropathy.
NEUROPATHIC PAIN
Pain initiated or caused by a primary lesion or dysfunction in the
nervous system.
PARESTHESIA
An abnormal sensation, whether spontaneous or evoked.
Amr Hasan El-Hasany M.D.
13. Sign/Symptom Description (example)
Spontaneous symptoms
• Spontaneous pain
Persistent burning, intermittent shock-like or
lancinating pain
• Dysesthesias
Abnormal unpleasant sensations
e.g. shooting, lancinating, burning
• Parasthesias Abnormal, not unpleasant sensations e.g. tingling
Stimulus-evoked
symptoms
• Allodynia
Painful response to a non-painful stimulus
e.g. warmth, pressure, stroking
• Hyperalgesia
Heightened response to painful stimulus e.g.
pinprick, cold, heat
• Hyperpathia Delayed, explosive response to any painful stimulus
14. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
15. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
18. Nociceptive Pain
An appropriate
physiologic response
to painful stimuli
Neuropathic Pain
An inappropriate
response caused by a
primary lesion or
dysfunction in the
nervous system
Merskey H et al, eds. In: Classification of Chronic Pain: Descriptions of Chronic Pain
Syndromes and Definitions of Pain Terms. 1994:209-212.
19. Neuropathic Pain Muscle/skeletal Pain
(nociceptive pain)
Chronic pain (months/years) Acute pain (hours or days)
Caused by injury or disease to
nerves
Caused by injury or inflammation that
affects both the muscles and joints
Mild to excruciating pain that can last
indefinitely
Moderate to severe pain that
disappears when the injury heals
Causes extreme sensitivity to touch –
simply wearing light clothing is
painful
Causes sore, achy muscles
Sufferers can become depressed or
socially withdrawn because they see
no relief in sight and may experience
sleep problems
Sufferers can become anxious and
distressed but optimistic about relief
from pain
Wall PD. Textbook of Pain. 4th ed; 1999; Jude EB. Clin in Pod Med and Surg.1999;16:81-97; Price SA. Pathophysiology: Clinical Concepts of
Disease Processes. 5th ed; 1997: Goldman L. Cecil Textbook of Medicine. 21st ed; 2000
20. Neuropathic Pain Muscle/Skeletal Pain
Price SA. Pathophysiology: Clinical Concepts of Disease Processes. 5th ed; 1997; Galer BS et al. Diabetes Res Clin Pract. 2000;47:123-
128
Classification of pain
21. versus
A time-based definition
Acute Pain
Time limited, <3
months
Results from injury to
tissue
Resolves with healing
Example: herpes zoster
Chronic Pain
Persistent, ≥3 to
6 months
Continues after initial
injury heals
Example: postherpetic
neuralgia
Merskey H et al, eds. In: Classification of Chronic Pain: Descriptions of Chronic Pain
Syndromes and Definitions of Pain Terms. 1994:209-212.
22. *Nociceptive; mixed nociceptive and neuropathic; or neuropathic.
Cole BE. Hosp Physician. 2002;38:23-30.
Insult Resolution
<1 month 1 month <6 month 6 months
Acute
Pain
Subacute
Pain
Chronic
Pain*
23. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
24. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
25. Transduction
1. Noxious stimuli (thermal, mechanical, and
chemical) - - - - - tissue damage
2. Traumatized tissues release inflam. mediators (PGs,
Bradykinin, 5HT, SP, Histamine.
3. Nociceptive free nerve endings sensitized by
opening Na + channels - - - - Depolarization
4. So; noxious stimuli are converted to impulse (in
milliseconds)
26. The 1st order neurone
Is the cell of the posterior root ganglion & its axon.
This axon is divided into a lateral & a medial branch.
The lat. branch forms the afferent sensory nerve.
The medial branch enters the spinal cord to ascend a few
segments forming Lissauer's tract, and relays in the cells of
Substantia Gelatinosa of Rolandi (S.G.R.) capping the post,
horn of the gray matter.
2/4/2016
26
27. The 2nd order neurone
Is the cell of S.G.R. & its axon.
This axon crosses to the OPPOSITE side & ascends in the
Lateral Spinothalamic Tract of the spinal cord then in the
lateral lemniscus of the brain stem, to relay in the thalamus.
2/4/2016
27
Pathway of Pain
28. The 3rd order neurone
Starts in the cell of the thalamus, its axon ascends to pass
through the posterior limb of the internal capsule conducting
the impulse to the cortical sensory area in the parietal lobe.
2/4/2016
28
Pathway of Pain
33. Ascending Pathways:
Spino-Reticulo-Diencephalic: connected to R.F
(connected to hypothalamus and Cingulate gyrus
“autonomic components”) and medial thalamus
Spinothalamic: VLNT
The Thalamus:
The central switching station of the brain.
The lateral nuclei deal with sensory / discriminative
aspects.
The medial ones with 'affective' pain.
34. Major cortical players are:
• Primary sensory cortex, S I
• Secondary sensory cortex, S II
• Anterior part of the insula
• Cingulate gyrus.
Cortical structures
Tangentially involved in the perception of pain !?!?!
36. Descending pathways originate from three main
areas:
• Cortex
• Thalamus
• Brainstem: Periaqueductal grey matter (PAG)
37. Descending pathways originate from three main
areas:
1. The somatosensory cortex
2. The periventricular nucleus of the hypothalamus
3. The pontine reticular formation
4. Raphe nuclei and adjacent medullary reticular formation
38. From PAG R.F of
medulla (raphe nucleus)
in ventromedian medulla
(5HT) Dorsolateral
funiculus of the spinal
cord, to end up in
Interneurones next to
SGR (lamina II)
(enkephalin) that inhibit
incoming pain impulses.
39.
40.
41. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
42. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
43. Pain initiated or caused by a primary lesion or
dysfunction in the nervous system.
Neuropathic pain is usually chronic, difficult to
treat, and often resistant to standard analgesic
management.
44. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
45. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
47. Peripheral Mechanisms
After a peripheral nerve lesion, neurons become more
sensitive and develop abnormal excitability and elevated
sensitivity to stimuli [peripheral sensitization] .
48. Central Mechanisms
As a consequence of ongoing spontaneous activity
arising in the periphery, STT neurons develop an
increased background activity, enlarged receptive field
and increased responses to afferent impulses, including
normal tactile stimuli [central sensitization].
49. Peripheral Sensitization
“ Healthy “
nociceptors
Abnormal
nociceptors
Central Sensitization
Normal
transmission
Central
reorganization
CNS
PNS
Neuropathic
Pain
Nociceptive Pain
Physiologic
state
Pathologic state
Peripheral
Nervous
System
Central
Nervous
System
50. Peripheral Mechanisms
Membrane
hyperexcitability
Ectopic discharges
Peripheral sensitization
Central Mechanisms
Wind up
Central sensitization
Central reorganization
of Ab fibers
Loss of inhibitory controls
Attal N et al. Acta Neurol Scand. 1999;100(suppl):12-24; Woolf CJ et al. Lancet.
1999;353:1959-1964.
51. NEUROPATHIC PAIN
Abnormal sensations
are transmitted along
myelinated Aβ or A
fibers or unmyelinated
C fibers
52. Na+ = sodium ion channels.
Injured nerves develop higher number of Na+ channels
55. Peripheral Mechanisms
Membrane
hyperexcitability
Ectopic discharges
Peripheral sensitization
Central Mechanisms
Wind up
Central sensitization
Central reorganization
of Ab fibers
Loss of inhibitory controls
Attal N et al. Acta Neurol Scand. 1999;100(suppl):12-24; Woolf CJ et al. Lancet.
1999;353:1959-1964.
56. •Sensitization of DHC resulting from high frequency stimulation
by nociceptive thus DHC continue to discharge despite
cessation of C fiber stimulation.
57. •Wind-up is a frequency-dependent increase in the excitability of
spinal cord neurones, evoked by electrical stimulation of afferent
C-fibres.
•Glutamate (NMDA) and tachykinin NK1 receptors are required to
generate wind-up and therefore a positive modulation between
these two receptor types has been suggested by some authors.
58.
59. Peripheral Mechanisms
Membrane
hyperexcitability
Ectopic discharges
Peripheral sensitization
Central Mechanisms
Wind up
Central sensitization
Central reorganization
of Ab fibers
Loss of inhibitory controls
Attal N et al. Acta Neurol Scand. 1999;100(suppl):12-24; Woolf CJ et al. Lancet.
1999;353:1959-1964.
60. 2-Central sensitization involves:
• Prolonged depolarization of dorsal horn neurons
and changes in postsynaptic membrane receptors
Changes in postsynaptic dorsal horn membrane
receptors manifest as:
• Reduced activation threshold
• Increased receptive field
• Increased response to suprathreshold stimulus
61.
62. Peripheral Mechanisms
Membrane
hyperexcitability
Ectopic discharges
Peripheral sensitization
Central Mechanisms
Wind up
Central sensitization
Central reorganization
of Ab fibers
Loss of inhibitory controls
Attal N et al. Acta Neurol Scand. 1999;100(suppl):12-24; Woolf CJ et al. Lancet.
1999;353:1959-1964.
63. Dorsal root ganglion
C
Ab
Midline
Normal terminations of primary afferents in the dorsal horn
After nerve injury
Woolf CJ et al. Curr Opin Neurobiol. 1994;4:525-534.
Touch
Pain
64. Baron, 2001
Under physiologic
circumstances: central
terminals of AB low
threshold mechanosensetive
afferent proeject to
dorsal horn laminae ventral
to substania gelatinosa (SG)
3-Central Organization
65. Baron, 2001
3-Central Reorganization
Partial degeneration of
nociceptive C- fibers:
central terminals of AB
low threshold
mechanosensetive
afferent sprout dorsally
into (SG)
Functional contact with
differentiated 2nd order
neurone
Pathogenesis of neuropathic pain
67. Peripheral Mechanisms
Membrane
hyperexcitability
Ectopic discharges
Peripheral sensitization
Central Mechanisms
Wind up
Central sensitization
Central reorganization
of Ab fibers
Loss of inhibitory controls
Attal N et al. Acta Neurol Scand. 1999;100(suppl):12-24; Woolf CJ et al. Lancet.
1999;353:1959-1964.
68. Baron, 2001
4- Loss of Inhibitory Controls
• Neurons in the dorsal horn can facilitate or inhibit transmission
of sensation
• Inhibition is mediated by GABA and glycine
• Experimental peripheral nerve injury in animals decreases
GABA and glycine levels and downregulates GABA and opioid
receptors
• Inhibition is lost and excitatory mechanisms dominate, resulting
in the propagation of pain impulses.
Pathogenesis of neuropathic pain
71. Dysesthesias
Paresthesias
Spontaneous pain*
Stimulus-evoked pain
Loss / impairment of
sensory quality
Numbness and reduced
sensation
Baron R. Clin J Pain. 2000;16:S12-S20.
Positive sensory signs
and symptoms
Negative sensory signs
and symptoms
Sensory changes and pain may coexist
*Also known as stimulus-independent pain
72.
73. ALLODYNIA
Pain due to a stimulus which does not normally provoke pain.
ANALGESIA
Absence of pain in response to stimulation which would normally
be painful.
ANESTHESIA DOLORASA
Pain in an area or region which is anesthetic.
Amr Hasan El-Hasany M.D.
75. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
76. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
77. Neuropathic pain
Pain initiated or caused by a primary
lesion or dysfunction in the nervous system
Peripheral neuropathic pain Central neuropathic pain
Merskey H et al. (Eds) In: Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes
and Definitions of Pain Terms. 1994:209-212.
78. Peripheral causes of neuropathic
pain
Trauma
– e.g. surgery, nerve entrapment, amputation
Metabolic disturbances
– e.g. diabetes mellitus
Infections
– e.g. herpes zoster (shingles), HIV
Toxins
– e.g. chemotherapeutic agents, alcohol
Vascular disorders
– e.g. polyarteritis nodosa
Nutritional deficiencies
– e.g. niacin, thyamine, pyridoxine
Direct effects of cancer
– e.g. metastasis, infiltrative
Central causes of neuropathic
pain
Stroke.
Spinal cord lesions.
Multiple sclerosis.
Tumors.
Wall PD, Melzack R (Eds).Textbook of pain. 4th Ed. 1999; Galer BS, Dworkin RH (Eds) A clinical guide to neuropathic pain.
2000:Woolf CJ et al. Lancet. 1999;353:1959-1964.
79. Painful Diabetic Neuropathy (PDN)
Low back pain Neuropathic pain affects up to 55% of patients with
chronic low back pain.
Postherpetic Neuralgia (PHN) Neuropathic pain affects 25 to 50% of
people over 50 who have had herpes zoster.
Cancer Neuropathic pain affects about 33% of cancer patients.
Spinal cord injury Neuropathic pain affects 75% of patients with
spinal cord injury.
Stroke Neuropathic pain affects 8% of post-stroke patients.
Multiple sclerosis Neuropathic pain affects approximately 55% of
patients with multiple sclerosis.
Neuropathic Pain is highly prevalent among
a number of different patients
82. Social Consequences
Marital/family
relations
Intimacy/sexual
activity
Social isolation
Socioeconomic
Consequences
Healthcare costs
Disability
Lost workdays
Quality of Life
Physical functioning
Ability to perform
activities of daily
living
Work
Recreation
Psychological Morbidity
Depression
Anxiety, anger
Sleep disturbances
Loss of self-esteem
1.U.S. News & World Report.Washington, DC: U.S. News & World Report L.P.; March 17, 1997:55-57, 60-62, 65, 67.
2.Becker N, Sjogren P, Bech P, Olsen AK, Eriksen J.Treatment outcome of chronic non-malignant pain patients managed in a
Danish multidisciplinary pain centre compared to general practice: a randomized controlled trial. Pain. 2000;84:203-211.
83. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
84. •Definitions and glossary
•Classification of pain
•Pathways of pain
•Neuropathic pain
Pathogenesis of neuropathic pain
Causes of neuropathic pain
Management of neuropathic pain
Amr Hasan El-Hasany M.D.
85. • Type, distribution and location
of pain
Character of complaints
e.g. burning, shock-like, pins
and needles etc.
Based on anatomic drawing
Dermatomal
Non-dermatomal
• Duration of complaints
• Average intensity of pain in the
last day/week (0-10)
• Extent of interference with
daily activity (0-10)
1. Jensen and Baron. Pain. 2003;102:1-8
Identify the following:1 Areas of further exploration
• Previous medical history
• Exposure to toxins or other
drug treatment
e.g. radiation
• Use of pain medications
• Associated psychological and
mood disturbance
86. EMG-NCV
To localise pain-
generator/nerve or root
lesion
To rule out :
- Axonal Vs focal segmental
demyelination
- Underlying small-fiber or
mixed polyneuropathy
87. Nerve ( eg, sural nerve ) : to diagnose
vasculitis, amyloidosis, sarcoidosis,
etc.
Skin : to evaluate density of
unmyelinated fibers within dermis
and epidermis
92. Level of Risk
Most invasive
Least invasive
Interventional
techniques
Oral
medications
Topical
medications
Psychologic/
physical
approaches
Injections
Treatment should begin at an appropriate
point along the risk continuum
100. Consider nonpharmacologic treatmentsFirst Step
Second Step Initiate first-line drug monotherapy
(Pregabalin or Gabapentin or TCA or SNRI)
Third Step Partial response: add
No response: Switch to alternate first-line
Forth Step Partial response: add
No response: Switch to tramadol/oxycodone
Fifth Step Ineffective/not-tolerated: pain specialty clinic
104. • Pregabalin modulates the hyperexcited neuron by:
-High affinity binding the α2-δ subunit of voltage-gated
calcium channels.
-Attenuating calcium influx into presynaptic terminals.
-Reducing excessive release of excitatory
neurotransmitters.
105.
106. • Pregabalin has linear pharmacokinetics
Pregabalin Pharmacokinetic
•Bockbrader H, Hunt T, Strand J, Posvar E, Sedman A. Pregabalin pharmacokinetics and safety in healthy volunteers:
results from two phase 1 studies. Neurology 2000; 54:A421
•Ben-Menachem E. Pregabalin pharmacology and its relevance to clinical practice. Epilepsia 2004; 45:13–8
• Pregabalin monograph.
Pregabalin Gabapentin
Time to the effective
dose
1 day 9 days
107. • Gabapentin monograph.
• Pregabalin monograph.
Indications Pregabalin Gabapentin
Neuropathic pain
associated with
diabetic peripheral
neuropathy
√
Neuropathic pain
associated with
postherpetic
neuralgia
√ √
Fibromyalgia √
FDA approved indications for Pregabalin and Gabapentin
108. • The recommended dosage scheme
Dosing should begin at 50 mg three times / day increased to
100 mg three times / day, based on efficacy and tolerability.
The recommended dosage in the treatment of Fibromyalgia
300 – 450 mg / day.
109. Since Pregabalin is predominantly excreted unchanged in the
urine, undergoes negligible metabolism in humans and does
not bind to plasma proteins, its pharmacokinetics are unlikely
to be affected by other agents through metabolic interactions
or protein binding displacement.
In vitro and in vivo studies showed that Pregabalin is unlikely
to be involved in significant pharmacokinetic drug interactions.