This presentation looks at EEG signal generation, pyramidal cells, recording of EEG, source localisation, polarity, analysis of dipole, derivations, montages,
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 presentation looks at EEG signal generation, pyramidal cells, recording of EEG, source localisation, polarity, analysis of dipole, derivations, montages,
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.
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.
Epileptogenesis is the process by which a brain network that was previously normal is functionally altered toward increased seizure susceptibility, thus having an enhanced probability to generate spontaneous recurrent seizures (SRSs). The process of epileptogenesis occurs in 3 phases: the occurrence of a precipitating injury; a 'latent' period of epileptogenesis and chronic, established epilepsy. Structural and molecular changes associated with epileptogenesis include selective neuronal loss,axonal and dendritic reorganisation, neurogenesis, altered expression of neurotransmitters, and changes at glial architecture. Antiepileptogenesis can be complete or partial. Complete prevention aborts the development of epilepsy while partial prevention can delay the development of epilepsy or reduce its severity. Targeting signaling pathways that alter the expression of genes involved in epileptogenesis may provide novel therapeutic approaches for preventing epileptogenesis. The mTOR and REST pathways are exciting new potential targets for intervention in the epileptogenic process.
This presentation is about different diseases which presents or are associated with myotonia. Referrences were taken from Bashir Katirji Neuromuscular textbook, continuum, and seminar of neurology journal.
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.
Epileptogenesis is the process by which a brain network that was previously normal is functionally altered toward increased seizure susceptibility, thus having an enhanced probability to generate spontaneous recurrent seizures (SRSs). The process of epileptogenesis occurs in 3 phases: the occurrence of a precipitating injury; a 'latent' period of epileptogenesis and chronic, established epilepsy. Structural and molecular changes associated with epileptogenesis include selective neuronal loss,axonal and dendritic reorganisation, neurogenesis, altered expression of neurotransmitters, and changes at glial architecture. Antiepileptogenesis can be complete or partial. Complete prevention aborts the development of epilepsy while partial prevention can delay the development of epilepsy or reduce its severity. Targeting signaling pathways that alter the expression of genes involved in epileptogenesis may provide novel therapeutic approaches for preventing epileptogenesis. The mTOR and REST pathways are exciting new potential targets for intervention in the epileptogenic process.
This presentation is about different diseases which presents or are associated with myotonia. Referrences were taken from Bashir Katirji Neuromuscular textbook, continuum, and seminar of neurology journal.
This gives an overall idea and knowledge about epilepsy and epileptogenesis. This does not serve as a complete medical tool,but as a learning material for, health and allied health students.
Epilepsy is a fascinating disease and cannot be understood in a single ppt, this just gives out and outline on the definition, diagnostic tools, incidence, types, and a intro on treatment protocols medical and surgical
It is a great source of comprehensive knowledge on the topic and information on the treatment
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.
Electrophysiological assessment of neuromuscular transmissionRahul Kumar
The Presentation discusses the detailed aspects of the Electrophysiological Aspects of Neuromuscular transmission, as well as the diagnostic features of the various types of NMJ Disorders.
Spindles and transients - Sleep Phenomena, Mechanisms and SubstratesRahul Kumar
This presentation discusses in detail the transients that occur mainly in late stage 1 and stage 2 of sleep, and may be confused to be pathological. The prototype here are theK complexes and the Sleep Spindles.
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.
Artifacts in EEG - Recognition and differentiationRahul Kumar
This Presentation discusses the variously commonly seen artifacts in EEG, and how to recognize them. In EEG interpretation, it is often more important to identify an artifact than to identify true pathology. Once all the artifacts are ruled out, one is sure that what one is dealing with represents disease/abnormality
EEG in Neonates - Normal Variants and Pathological TracesRahul Kumar
This pattern discusses the various EEG patterns seen in term as well as pre term neonates. Normal Variations as well as pathological traces are discussed
This pattern discusses the various EEG patterns seen in term as well as pre term neonates. Normal Variations as well as pathological traces are discussed
EEG - Montages, Equipment and Basic PhysicsRahul Kumar
This presentation discusses the 10-20 system of electrode placement, with its modifications. Also discussed are the Equipment Specifications, basic Physics and sources of interference
This presentation discusses the basic principles governing EEG Rhythm Generation, and discusses the various circuits that generate and maintain cerebral oscillations.
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
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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
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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
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
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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
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.
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Epileptogenesis - Mechanisms and Clinical Implications
1. Förster et al. Nature Reviews Neuroscience advance online publication;
published online 16 March 2006 | doi:10.1038/nrn1882
2. Definition of Terms
• Epileptogenesis refers to the transformation of the brain
to a long-lasting state in which recurrent, spontaneous
seizures occur
• Seizure expression is the process which is concerned
with processes that trigger and generate seizures
• Epileptogenicity is the property of a tissue that is
capable of generating spontaneous behavioral and/or
electrographic seizures
– Clark, S. and Wilson, W. A., Adv. Neurol., 1999, 79, 607–630.
6. GENETIC
FACTORS
• Over 40 genes associated with
human epilepsy have been
identified
• at least 133 single gene
mutations in mice have been
linked to an epileptic
phenotype
• it had been assumed that
generalized rather than partial
epilepsies, and idiopathic
rather than symptomatic
epilepsies had a genetic basis.
ACQUIRED
PROCESSES
7. GENETIC
FACTORS
ACQUIRED
PROCESSES
• Acute or Chronic
• increased AMPA and
NMDA synaptic
transmission, acute
decrease in GABAergic
inhibitory synaptic
transmission, and an
increase in net excitatory
effects, leading to
increases in ectopic action
potentials or depolarizing
potentials.
8. GENETIC
FACTORS
ACQUIRED
PROCESSES
• Nonsynaptic mechanisms
such as changes in coupling
through gap junctions29,
iron-mediated changes in
Ca++ oscillations or
glutamate release and
generation of oxygen- free
radicals
• acute neuronal loss alone is
not necessary for the
generation of acute
epileptiform bursts in vitro
19. Excitotoxicity-Role of Glu and GluR
Excitotoxicity is thought to be a major mechanism contributing to neuronal
degeneration in many acute CNS diseases, including ischemia, trauma and epilepsy
Postsynaptic neuron
Presynaptic neuron
Glu Rc
Glutamate
vesicles
Glutamate
Opening of ion channelCa++ influx and release of
Ca++ from ER
Activation of lipases,
proteases, endonucleases
Direct cell damage Formation of ROS
Cell death
67. Paroxysmal Depolarization
Shifts
• Protracted bursts of action potentials typical of
neurons in an epileptic neuronal aggregate
• Produces local synchonization
• How might these shifts be produced?
70. Early-LTP induction
• Excitatory stimulus of the cell causes
excitatory post-synaptic potential (ESPS) (e.g.
glutamate binding to AMPA receptor)
• Stimulus may be either a large single stimulus
or many smaller rapid stimuli that summate
(post-tetanic potentiation)
• Sufficient stimulus leads to unblocking of
NMDA receptor and Ca influx into the cell
71. Early-LTP induction
• Ca influx leads to short-term
activation of protein kinases
• Phosphorylation increases
activity of AMPA receptor and
mediates its insertion into the
cell membrane
Calcium/calmodulin-dependent
protein kinase II (CaMKII)
75. Late-LTP: Expression
• Protein products are thought to lead to increase
in:
– Number and surface area of dendritic spines
– Postsynaptic sensitivity to neurotransmitter
perhaps by enhanced synthesis of AMPA receptors
76. Propagation in temporal lobe
epilepsy: kindling
• Mesial temporal
circuit can sustain
epileptic activity
• Repeated electrical
stimulation of the
amygdala gradually
leads to spontaneous
seizures due to
reorganization of
synaptic connections
in the dentate gyrus
79. • A primary epileptogenic area has a macroscopic abnormality
and can generate seizures independent of the presence of
surrounding or remote epileptogenic areas
• A secondary epileptogenic area becomes epileptogenic
because of the influence of epileptogenic activity in a primary
epileptogenic area, which is separated from it by at least one
synapse
• Morrell, F., Epilepsia, 1960, 1, 538–560
80. • A mirror focus is a type of secondary epileptogenesis in
which the secondary epileptogenic zone is located in a
contralateral homotopic area with regard to the primary
epileptogenic zone
• Morrell, F., in Basic Mechanisms of Epilepsies (eds Jasper, H. H., Ward, Jr A. A.
and Pope, A.), Little Brown, Boston, 1969, pp. 357–370
• Secondary epileptogenesis likely to be due to kindling
• Goddard, G. V., Nature, 1967, 214, 1020–1021
81. Phases of Secondary
Epileptogenesis
• dependent phase
• intermediate phase
• independent phase
– Depend on the interrelationship of primary and
secondary zones
– Morrell, F. and Tsuru, N., Biol. Bull., 1974, 147, 492,
Morrell, F. and Tsuru, N., electroencephalogr. Clin.
Neurophysiol., 1976, 60, 1–11
83. Definition of Terms
• Epileptogenesis refers to the transformation of the brain
to a long-lasting state in which recurrent, spontaneous
seizures occur
• Seizure expression is the process which is concerned
with processes that trigger and generate seizures
• Epileptogenicity is the property of a tissue that is
capable of generating spontaneous behavioral and/or
electrographic seizures
– Clark, S. and Wilson, W. A., Adv. Neurol., 1999, 79, 607–630.
84. Epilepsy Biomarkers/
Surrogate Markers
• Markers of epileptogenesis
• Development of an epileptic condition
• Monitoring of the condition once epilepsy is established
• Markers of epileptogenicity
• Localization of the epileptogenic lesion
• Measurement of severity
85. Use of biomarkers
• Predict who are likely to develop chronic
seizures
• Predict pharmacoresistance
• Delineate brain areas for resection
• Determine the efficacy of therapy
• Develop anti epileptogenic drugs…
86. Target Mechanisms
•
•
•
•
•
•
•
•
•
Cell Loss ( eg. Hippocampal atrophy)
Axonal sprouting
Synaptic reorganization
Altered neuronal function
Neurogenesis
Altered glial function and gliosis
Inflammation
Angiogenesis
Altered excitability and synchrony