This document discusses several neuromodulation techniques for treating neurological conditions like depression. It describes transcranial magnetic stimulation (TMS), which uses magnetic fields to stimulate brain regions involved in mood control. Deep brain stimulation involves implanting electrodes in the brain to regulate abnormal impulses through electrical stimulation. Vagus nerve stimulation stimulates the vagus nerve with electrical impulses to treat epilepsy and depression. All three methods aim to improve symptoms but have risks like infection, side effects from stimulation, and require follow up surgeries as batteries need replacement over time.
Transcranial magnetic stimulation (TMS) is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain.
This video explains the physics of this method and how it can be used in daily practice.
More about magnetic simulators: http://www.neurosoft.ru/eng/product/neuro-msd/index.aspx
Transcranial magnetic stimulation (TMS) is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain.
This video explains the physics of this method and how it can be used in daily practice.
More about magnetic simulators: http://www.neurosoft.ru/eng/product/neuro-msd/index.aspx
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
This lecture is all about the recognition of an abnormal EEG, its characteristics, its appearance and all about how to differentiate the abnormal activity with normal EEG background.
EEG Maturation - Serial evolution of changes from Birth to Old AgeRahul Kumar
This presentation discusses in detail the evolution of the EEG patterns in the human brain, as the brain develops and matures. The sequence of changes as well as the shifting patterns coinciding with Myelination are discussed.
This presentation reviews the common artifacts in EEG, their identification and rectification. Examples of various artifacts are provided in the presentation.
Normal EEG patterns, frequencies, as well as patterns that may simulate diseaseRahul Kumar
This presentation discusses the vast range of traces that show the variations in normal EEG patterns, as well as discussing the frequency and amplitudes of various normal waveforms.
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.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
This lecture is all about the recognition of an abnormal EEG, its characteristics, its appearance and all about how to differentiate the abnormal activity with normal EEG background.
EEG Maturation - Serial evolution of changes from Birth to Old AgeRahul Kumar
This presentation discusses in detail the evolution of the EEG patterns in the human brain, as the brain develops and matures. The sequence of changes as well as the shifting patterns coinciding with Myelination are discussed.
This presentation reviews the common artifacts in EEG, their identification and rectification. Examples of various artifacts are provided in the presentation.
Normal EEG patterns, frequencies, as well as patterns that may simulate diseaseRahul Kumar
This presentation discusses the vast range of traces that show the variations in normal EEG patterns, as well as discussing the frequency and amplitudes of various normal waveforms.
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.
Magnets - Not Drugs: TMS IMMH San Antonio 2014Louis Cady, MD
In this talk, Dr. Cady covers a remarkable new treatment for depression: transcranial magnetic stimulation. The historical roots of this treatment are traced, followed by a review of the literature in terms of the proven efficacy of this treatment. A comparison with ECT shows that TMS has a very favorable profile, with remarkably fewer side effects and incredibly better tolerated side effects compared to ECT. Given that this was a "CME" talk, off-label uses of TMS were reviewed, including stepping stones for future avenues to explore
Trans-cranial Direct Current Stimulation (tDCS) has been found effective and easy way in Stroke Rehabilitation. This is a literature review of few articles that reported the results of clinical trials of such DC stimulation in patients with stroke during their rehabilitation.
This presentation gives an over view: of the depression, its symptoms, prevalence, and patho-physiology. It then reviews various treatment options for depression, first starting with medication, and then moving to neuro-modulation. Focus is then on the similarities and differences of ECT and TMS. And finally information is provided about PineWood TMS.
Repetitive Transcranial Magnetic Stimulation at Southeastern Psychiatric Asso...Miriam Isreb
Repetitive Transcranial Magnetic Stimulation is a noninvasive treatment that uses a magnetic field to stimulate nerve cells in the dorsolateral prefrontal cortex, to relieve symptoms of depression. For more information, please review the e-brochure.
If you have any questions or are interested in receiving this treatment, please email sepa.tms@gmail.com
Physiology of Neuromodulation and neuromodulators. Difference between neuromodulation and synapse. Recent advances in neuromodulation, clinical application of neuromodulation.
Transcranial Magnetic Stimulation ( TMS) for Chronic PainDr. Rafael Higashi
Aula sobre avanço no tratamento da dor crônica com o uso de Estimulação Magnética Transcraniana (EMT) ministrada por Dr. Rafael Higashi, médico neurologista, no departamento de tratamento da dor do Centro Médico da Universidade de Nova York, NYU, EUA.
www.estimulacaoneurologica.com.br
MAGNETS NOT DRUGS - 5 1 2012 - Deaconess Hospital Grand RoundsLouis Cady, MD
On May 1, 2012, Dr. Cady presented "Magnets, Not Drugs" to the medical staff at Deaconess Hospital, Evansville, IN, for their weekly Grand Rounds program. In this presentation, Dr. Cady reviews the "three things you could do in psychiatry before TMS," which he categorizes as "shrinking, shocking, and drugging." Using the Faraday principle of electromagnetic induction, and applying it to neurochemistry, this new development resulted in a breakthrough treatment for depression, FDA approved only three years ago. In this presentation Dr. Cady reviews TMS (transcranial magnetic stimulation) completely.
Future communication experts must be able to handle scientific methods in order to be effective. This presentation is a simple view on how it can be done
Epilepsy is a brain condition that causes repeated, sudden, brief changes in the brain's electrical activity. These changes cause various types of symptoms.
Headache is classified mainly into two categories: Primary and secondary.
Primary headache is usually benign and longstanding. Common primary headaches are migraine and tension type headache. They have typical features – Migraine, tends to be pulsating in character, affecting one side of the head, associated with nausea, disabling in severity and it usually lasts between 3 hours and 3 days.
Diagnostic presentation HeadacheUnited States UniversitLinaCovington707
Diagnostic presentation
Headache
United States University
Introduction
Headache is the most common pain in the united states.
Headache means pain or discomfort in the head, face, or neck.
Headache can be caused by inflammation or spasm related to cranial vessels, nerves, or muscles Headache can be primary or secondary. (Dlugasch & Story, 2021)
Classification of headache
Primary headache
Most common, not a symptom of underlying an underlying disease
Benign
Can be recurrent
It mainly occurs early in an individual
Decrease after ages 40 to 50
Migraine
Tension-type headache
Trigeminal autonomic cephalgia
Other primary headache disorders (Rizzoli & Mullally, 2018).
Secondary headache
Caused by an underlying condition
Trauma or injury to the head or neck
Cranial or cervical vascular disease
Nonvascular intracranial disorder
A substance or its withdrawal
Infection
Affliction of homeostasis
Illness of the skull, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure
Psychiatric disorder (Rizzoli & Mullally, 2018).
The red flag of headache
If an older patient complaint of New headache
Abnormal neurologic examination such as mental status changes and papilledema
If there is any New change in the headache pattern
Intensifying headache
New headache if in case of HIV risk factors, cancer, or an immunocompromised status
Systemic illness signs (e.g., fever, stiff neck, rash)
If precipitate by cough, exertion, Valsalva maneuver
If the Headache in pregnancy or postpartum period
If a patient says it is the First or worst headache of my life (Rizzoli & Mullally, 2018).
Pathophysiology of headache
Stimulation of primary nociceptors
Lesions in the pain-producing pathway of PNS and CNS
Pain producing structure
Scalp
Middle meningeal artery
Dural sinuses
Flax cerebri
Proximal segment of the large pial arteries (Dlugasch & Story, 2020)
Pathophysiology of headache continue
There are no nociceptors in the brain parenchyma
So the pain originates from surrounding structures, such as blood vessels, meninges, muscle fibers, facial structures, and cranial or spinal nerves.
Any stretching, dilatation, constriction, or any nociceptor when they stimulate stimulation structures can cause the perception of headache.
The secondary headache depends on the cause and diseases
( Rosenthal & Burchum, 2021)
migraine headache
Migraine headache is a headache associated with systemic complaints. The person feels a severe throbbing pain or a pulsing sensation, usually on one side of the head, along with nausea, vomiting, and extreme sensitivity to light and sound. The attacks can last for hours to days, and the pain can be severe that it interferes with daily activities (Dlugasch & Story, 2020).
Triggers to migraine headache
Emotional stress
Hormonal change during menstruation
Alcohol intake
Change in weather
Odors
Disturbance in sleep or not getting enough sleep
migraine heada ...
This is a slide presentation that provides informaton on taumatic brain injuries and the PREP program at the Shepherd Center. This is an edited version of a presentation and is NOT the full slide presented by deckto deal with specific issues our family is facing and is not an official Shepherd publication.
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. definition of TMS :
Transcranial magnetic stimulation (TMS) is a procedure that
uses magnetic fields to stimulate nerve cells in the brain to
improve symptoms of depression. Transcranial magnetic
stimulation may be tried when other depression treatments
haven't worked.
With TMS, a large electromagnetic coil is placed against your
scalp near your forehead. The electromagnet used in TMS
creates electric currents that stimulate nerve cells in the
region of your brain involved in mood control and depression
3.
4. Precautions :
Tell your doctor or mental health provider if:
You're pregnant or thinking of becoming pregnant.
You have any metal or implanted medical devices in your
body. Due to the strong magnetic field produced during TMS,
some people who have the following devices cannot have TMS:
Aneurysm clips or coils
Stents
Implanted stimulators
Electrodes for monitoring brain activity
Any magnetic implants
Bullet fragments
Any other metal device or object implanted in your body
5. Result :
If TMS works for you, your depression symptoms may
improve or go away completely. Symptom relief may take
a few weeks of treatment.
TMS may be less likely to work if:
1- Your mental illness causes detachment from reality
( (psychosis)
2- Your depression has lasted for several years
3-Electroconvulsive therapy (ECT) hasn't worked to
improve depression symptoms
It's not yet known if TMS can be used to treat depression
for the long term, or whether you can have periodic
maintenance treatments to prevent depression symptoms
from returning.
6. Deep brain stimulation :
Deep brain stimulation involves implanting electrodes within certain areas of
your brain. These electrodes produce electrical impulses that regulate
abnormal impulses. Or, the electrical impulses can affect certain cells and
chemicals within the brain. The amount of stimulation in deep brain
stimulation is controlled by a pacemaker-like device placed under the skin in
your upper chest. A wire that travels under your skin connects this device to
the electrodes in your brain.
Deep brain stimulation is used to treat a number of neurological conditions,
such as:
Essential tremor
Parkinson's disease
Dystonia
Deep brain stimulation is also being studied as a treatment for epilepsy,
cluster headaches, Tourette syndrome, chronic pain and major depression.
Many candidates for deep brain stimulation are participants in clinical trials.
7.
8. Surgery risks :
Deep brain stimulation involves boring small holes in the skull to implant the
electrodes, and surgery to implant the device that contains the batteries under
the skin in the chest. Complications of surgery may include:
Bleeding in the brain (hemorrhage)
Stroke
Infection
Breathing problems
Nausea
Heart problems
Incision scarring
With deep brain stimulation, surgery isn't a one-time procedure. The batteries
that are implanted in the chest have a limited life span, and when they run out,
your symptoms may quickly return. Replacing the batteries requires another
surgery. It's also possible for a wire connecting the batteries to an electrode to
break or for other malfunctions to occur.
9. Possible side effect after surgery :
Seizure
Infection
Headache
Insomnia
Memory problems
Temporary pain and swelling at the
implantation site
10. Possible side effects of stimulation
Numbness or tingling sensations
Muscle tightness of the face or arm
Speech problems
Balance problems
Lightheadedness
Unwanted mood changes, such as mania and
depression
11. Preparation :
Before surgery, you need to have medical
tests to make sure that deep brain stimulation
is safe for you and is a good option in your
case. You also need brain-imaging studies,
such as an MRI, before the surgery, to map
the areas of your brain where the electrodes
will be implanted.
12. Result :
Deep brain stimulation won't cure your
disease, but it may help lessen your
symptoms. If deep brain stimulation works,
your symptoms will improve significantly, but
they usually don't go away completely. In
some cases, medications may still be needed
for certain conditions. Deep brain stimulation
isn't successful for everyone
13. Vagus nerve stimulation
Vagus nerve stimulation is a procedure that stimulates the vagus nerve
with electrical impulses. Vagus nerve stimulation can be used to treat
epilepsy when other treatments haven't worked. Vagus nerve
stimulation is also a treatment for depression, and it's being studied for
conditions such as multiple sclerosis, migraine and Alzheimer's
disease.
There's one vagus nerve on each side of your body, running from your
brainstem through your neck to your chest and abdomen.
With vagus nerve stimulation, a device is surgically implanted under the
skin on your chest. A wire is threaded under your skin connecting the
device to the left vagus nerve. When activated, the device sends
electrical signals along the vagus nerve to your brainstem, which then
sends signals to certain areas in your brain
14.
15. Risks :
Pain where the cut (incision) is made to
implant the device
Infection
Incision scarring
Difficulty swallowing
Vocal cord paralysis, which is usually
temporary, but can be permanent
16. Side effects :
Voice changes
Hoarseness
Throat pain
Cough
Headache
Chest pain
Breathing problems, especially during exercise
Difficulty swallowing
Abdominal pain or nausea
Tingling or prickling of the skin
17. When vagus nerve stimulation may
be a good option :
The Food and Drug Administration (FDA) has approved vagus
nerve stimulation for people who:
Are 12 and older
Have focal (partial) epilepsy
Have seizures that aren't well controlled with medications
In addition, the FDA has approved vagus nerve stimulation for the
treatment of depression in adults who:
Have chronic, hard-to-treat depression (treatment-resistant
depression)
Haven't improved after trying four or more medications or
electroconvulsive therapy (ECT), or both
Continue standard depression treatments along with vagus nerve
stimulation
18. Result :
Vagus nerve stimulation isn't a cure for epilepsy. Most
people with epilepsy won't stop having seizures
altogether. But many people will have fewer seizures,
as many as 30 to 50 percent fewer. Seizure intensity
may lessen as well.
It can take as long as two years of vagus nerve
stimulation before you notice any significant reduction
in the number of seizures. Vagus nerve stimulation may
also shorten the recovery time after a seizure. People
who've had vagus nerve stimulation to treat epilepsy
generally have an improved quality of life.
Editor's Notes
In TMS therapy, an electromagnet is applied to the left side of the forehead. This induces currents in neurons in the left prefrontal cortex--where brain imaging studies have shown a deficit in activity in depressed patients. It is thought that this can induce activity and blood flow to this area, but also causes changes in areas deeper in the brain (responsible for mood regulation) to which neurons in the cortex connect. Side effects of TMS tend to be mild, especially compared to antidepressants, and the most common complaint is a mild headache
The deep brain stimulation system targets either the subthalamic nucleus or globus pallidus interna regions of the brain involved in muscle movement.
The vagus nerve is comprised of 90% afferent, i.e., sensory nerve fibers, and plays a central role in transmitting information about the functional status of various organs to the brain1. This role also entails the monitoring of the body’s inflammatory processes: When microbial infections occur, the immune cells release pro-inflammatory signals - an accumulation of which can result in systemic inflammation. The vagus nerve thus alerts the brain when there is an excess of molecules such as cytokines. The brain, now notified of a potent infection, reflexively triggers the release of anti-inflammatory substances to avert harmful inflammation2. A serendipitous electrical stimulation of the vagus nerve helped decipher that this attenuation occurs via the efferent fibers that make up the reminder of the vagus nerve. It was thus demonstrated for the first time that the brain can regulate the levels of the Tumor necrosis factor (TNF) via the vagus nerve – a mechanism termed cholinergic anti-inflammatory pathway3.
Electrically stimulating the vagus nerve using pacemaker-like devices to tackle seizures in epileptic patients has been in practice since the 1990’s, and so has been the treatment of depression with vagal nerve stimulation (VNS). These procedures have relied on the fact that the vagus nerve serves as a portal to the brain stem; thus, psychiatric diseases have been the prime target of VNS4.