Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.
Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.
Epilepsy Management: Key issues and challengesPramod Krishnan
This brief presentation summarises the key issues and challenges in Epilepsy management, including diagnosis, treatment, compliance, special populations, adverse effects, psychiatric comorbidities and ASM withdrawal.
This presentation focusses on the importance of diagnostic biomarkers for Alzheimer's disease. MRI, amyloid PET and CSF biomarkers are discussed in detail.
This presentation looks at the benign or non-epileptiform variants in EEG, their characteristics and identification. Examples of the common benign variants are provided in the presentation.
This presentation reviews the common artifacts in EEG, their identification and rectification. Examples of various artifacts are provided in the presentation.
This is a brief review of autoimmune epilepsies, especially autoimmune encephalitis, SREAT, NORSE, FIRES and Rasmussen's encephalitis. A brief overview of investigations and treatment is included.
This presentation looks at the role of Pregabalin in refractory trigeminal neuralgia and chemotherapy induced peripheral neuropathy through illustrative case studies.
This review focusses on the role of role of gut microbiota in health and disease, specifically multiple sclerosis. It looks at the interaction of gut microbiota, enteric nervous system, central nervous system, neuroendocrine system in the pathogenesis of multiple sclerosis
This presentation summarises the importance of genetics in epilepsy, whom to test, and the various tests available. It looks at the role of genetics in various forms of epilepsy and recent advances in precision medicine.
EEG in convulsive and non convulsive seizures in the intensive care unitPramod Krishnan
Case based discussion regarding the utility of EEG in the management of convulsive and non convulsive seizures, including status epilepticus in the intensive care unit
A review of epilepsy in the elderly, the etiopathogenesis, clinical challenges, diagnosis, use of antiseizure drugs and outcomes. Also the various special considerations in managing elderly patients with epilepsy.
A review of the common antiseizure drugs with broad spectrum action. We look at the major evidence in favour of valproate, topiramate, perampanel and brivaracetam.
Treatment of epilepsy polytherapy vs monotherapyPramod Krishnan
This presentation reviews the evidence regarding use of early polytherapy in patients with epilepsy with regards to seizure control and adverse effects. The advantages and disadvantages of polytherapy compared to monotherapy is addressed.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
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.
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
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
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
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.
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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.
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
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5. Levin KH. The Neurologist 2004;10: 61–74) Currently recognized forms of GB Syndrome AMSAN AMAN Axonal forms Miller Fischer syndrome Pure autonomic form Pure sensory form Facial diplegia with paresthesia Parapretic Pharyngo-cervico-brachial Regional presentations of AIDP Preserved reflexes Prominent sensory loss Pure motor Asymmetric Atypical forms of AIDP AIDP
9. Other Antecedent factors Haber P et al. JAMA 2004; 292: 2478–81. Souayah N et al. Vaccine 2007; 25: 5253–55. Pritchard J et al. J Neurol Neurosurg Psychiatry 2002; 73: 348–49. In a patient with h/o GB syndrome any future vaccination should be done with due deligence, for fear of relapse. Other physical stress SLE Surgery HIV seropositivity Thrombolysis Lymphoma Vaccines: Influenza, hepatitis, rabies (old type), tetanus
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25. AIDP AMAN Other axonal forms Schwann cell membrane Preterminal motor endings Axonal membrane Demyelination, Conduction block, Sec Axonal degen Degeneration of motor endings Axonal degeneration Slow Regeneration Rapid Regeneration Remyelination Rapid recovery Rapid recovery Slow Recovery
42. Diagnostic Criteria for GB Syndrome ºExcluding M. Fisher and other variant syndromes Modified from AK Asbury, DR Cornblath: Ann Neurol 1990; 27: S21, 1990. 6. Electrophysiologic evidence of demyelination 3. Facial or other cranial nerve involvement 5. Typical CSF profile (cytoalbumin dissociation) 2. Mild sensory involvement 4. Absence of fever 1. Relatively symmetrical weakness Supportive 4. Exclusion of other causes [e.g., vasculitis, toxins, botulism, diphtheria, porphyria, localized spinal cord or cauda equina syndrome] 3. Disease course < 4 weeks 2. Areflexia 1. Progressive weakness of 2 or more limbs due to neuropathyº Required
64. Recent trials Of IVIg No significant difference in the outcome. IVIg 0.4 g/kg/d X 5d vs PE total 200- 250ml/kg In upto 7 sessions over 4 Wks. N=47 Adults Nomura et al. 2000 Early relapse more in 2 d group. No other differences IVIg 1g/kg/day X 2 day Vs 0.4g/kg/day X 5 day. N=50. Children Able to walk without aid. Korinthenberg et al. 2005 No significant difference in the disability score. IVIg 0.5 g/kg/day X 2 days Vs supportive care. N=21. Children Able to walk without aid. Korinthenberg et al. 2005 Result Treatment Subjects Study
65. Recent trials Of IVIg IVIg and PE were more effective than steroids (Dexa). Steroids Vs Steroids + IVIg vs Steroids + PE N= 54 Children. Wang et al. 2001 6d group appeared to benefit, but not statistically significant. IVIg 0.4g/kg/day X 3 days Vs 6 days. N= 39. Adults with CI to PE. Raphael et al. 2001 IVIg and PE were equally effective. IVIg 0.4 g/kg/dX 5d vs PE 40-50ml/kg 5 times in 2 weeks vs immuno-absorption 5 times in 2 weeks. N= 67. Adults and children Diener et al. 2001 Result Treatment Subjects Study
66. Recent trials Of Steroids Steroids (oral, parenteral) alone are not beneficial in GBS. Hughes RA et al. Cochrane Database Syst Rev 2006; 2: CD001446. No difference in outcome. IVIg 0.4g/kg/d X 5d + IV Methylprednisolone 500mg/d for 5 day vs IVIg + placebo. N= 225 Van Koningsveld et al., 2004 No difference in outcome. Prednisone 60 mg/d X 4d, 45mg/d X 3d, 30 mg/d X 10d, then tapered and stopped Vs no treatment N= 20 Bansal et al. 2004 Result Treatment Subjects Study
82. Koeppen S et al. Neurocrit. Care 2006;05:235–242. 75% sensory 43% muscle weakness 13% orthostatic hypotension 48% residual neuropathy 1-14 40 de la Cour and Jakobsen, 2005 28% normal/ minor symptoms 24% unassisted gait 12% assisted gait 24% wheel chair/ bed bound 1 25 Cheng et al. 2004 31% residua 1 96 Cheng et al. 2003 48% muscle aches and cramps (38% in UL, 66% in LL) 69% sensory 3-6 yrs 122 Bernsen et al. 2001 4% moderate, 6% severe 42% mild residual symptoms 1 yr 53 Chang et al. 2000 Outcome Duration after onset No Author Long-term Neurological outcome in GB syndrome
83. GBS Disability Scale (modified) Most commonly used measure of levels of activity and participation. Plasma Exchange/Sandoglobulin GBS Trial Group, 1997 Death. 6 Requiring assisted ventilation ( for any part of the day or night). 5 Confined to bed or chair bound. 4 Able to walk with a stick, appliance or support (5m across an open space). 3 Able to walk without support of a stick (5m across an open space) but incapable of manual work/running. 2 Minor symptoms or signs of neuropathy but capable of manual work/capable of running. 1 Healthy. 0
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Editor's Notes
(B) Longitudinal section of the cauda equina. The nodes of Ranvier are stained selectively with protein G (arrowheads). (D) Wallerian-like degeneration of nerve fibers. Sciatic nerve cross section with toluidine blue stain. Myelin ovoids produced by Wallerian like degeneration of myelinated fibers are present. (B) Longitudinal section of the cauda equina. The nodes of Ranvier are stained selectively with protein G (arrowheads). (D) Wallerian-like degeneration of nerve fibers. Sciatic nerve cross section with toluidine blue stain. Myelin ovoids produced by Wallerian like degeneration of myelinated fibers are present.
(A) Longitudinal sections of rabbit ventral roots immunolabeled for voltage-gated Na (Nav) channels at nodes (red), contactin associated protein (Caspr) at paranodes (green), and the membrane attack complex (MAC) (blue). MAC staining appears at nodes in the acute phase. As MAC deposition spreads, Nav channels and Caspr become markedly disrupted, finally disappearing. (B) Nav channels located at the nodes form multiprotein complexes. Caspr forms axo-glial junctions at paranodes, which act as a diffusion barrier restricting the lateral mobility of nodal Nav channels. (C) Anti-GM1 IgG Ab cause complement-mediated attack with MAC at the nodal and paranodal axolemmas. Nav channel clusters are altered by the destruction of structures that mediate their stabilization.