Parkinson's disease is a progressive nervous system disorder that affects movement. Symptoms start gradually, sometimes starting with a barely noticeable tremor in just one hand. Tremors are common, but the disorder also commonly causes stiffness or slowing of movement
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, trouble talking, and trouble walking.
Parkinson's disease is a progressive nervous system disorder that affects movement. Symptoms start gradually, sometimes starting with a barely noticeable tremor in just one hand. Tremors are common, but the disorder also commonly causes stiffness or slowing of movement
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, trouble talking, and trouble walking.
Epilepsy is simply aberrant electrical activity spreading throughout an area of, or the whole of, the brain.
Antiepileptic medications limit the propagation of this spread and inhibit development of symptoms.
Drugs used to treat epilepsy are termed antiepileptics.
Aim of pharmacological treatment of epilepsy is to minimize seizure activity / frequency, without producing adverse drug effects.
All new antibacterial agents which have been approved after the year 2000 have been described along with their mechanism of action, development of resistance, spectrum of activity and the stage of developmental in case of yet to be approved drugs.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
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
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
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
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!
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.
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.
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
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2. What is EPILEPSY?
Epilepsy is a chronic CNS disorder characterized by brief episodes of
Seizure is a sudden time limited involuntary alteration of behavior
with or without loss of consciousness accompanied by an
2
3. Pathophysiology of EPLILEPSY
• Each individual neuron is linked with hundreds of other neuron via
synapses.
• Neurons discharge electrical current and neurotransmitters are
released at synaptic levels and permits inter-communication.
• There are two types of Neurotransmitters:
1. Inhibitory Neurotransmitters: GABA (Gamma amino butyric acid)
acts on ion channels and increases chloride outflow and decreases
chances of action potential.
2. Excitatory Neurotransmitters: Glutamate and Aspartate allows
sodium and calcium influx which paves way for action potential
formation.
4. • Seizures occur due to the imbalance between the inhibitory and
excitatory Neurotransmitters.
• A normal neuron discharges repetitively at low baseline frequencies.
If neurons are damaged, injured/ suffer a chemical/ metabolic insult,
the changes in discharge pattern develops.
• During epilepsy, regular low frequency discharges are replaced by
bursts of high frequency discharges followed by periods of inactivity.
• A single Neuron discharging in an abnormal manner is usually not
clinically significant. But when a whole population of neurons
discharge synchronously in an abnormal manner, epileptic seizure
occurs.
5. Causes of EPLILEPSY
• In 28% cases, cause can be determined, in rest 72% cases, cause is
idiopathic.
• Determined causes:
1) Inherited genetic
2) Acquired: Trauma, Metabolic infections, Tumour, Neuro surgery,
Drugs, etc.
of inhibitory neurotransmitter such as the
4) Increase excitatory neurotransmitter.
6. 5) Concentration of is reversed.
6) Abnormality in the potassium conductance.
7) Defect in the voltage sensitive channel
6
10. Types of
epilepsy
Generalized
seizures
Tonic – clonic
seizure (Gran
mal seizure)
Absence
seizure
(petit mal
seizure)
Atonic
seizure
Myoclonic
seizure
Localized (partial
or focal)
Simple partial
seizure
(jacksoninan)
Complex partial
(psychomotor)
seizure
10
11. Types of EPLILEPSY
• Generalized seizures
1.Tonic-clonic seizures(Major epilepsy,
Grand mal)
• Lasts 1-2 min
• Usual sequences is aura-cry-
unconsciousness-tonic of all
body muscles-clonic followed by
prolong sleep
• Stiffening of arms and legs followed by
rhythmic jerking.
12. Types of EPLILEPSY
2. Absence siezures (Minor epilepsy, Petit
mal)
• Lasts about 1-2 min
• Momentary loss of consciousness
• Little jerking
• Often subside prior to puberty.
13. Types of EPLILEPSY
3. Atonic seizures (Akinetic epilepsy)
• Unconsciousness with relaxation of all
muscles
• Due to excessive
• Patient may fall , after 10 seconds to a
minute, they recover and regain
consciousness and can stand and walk
again.
14. Types of EPLILEPSY
4. Myoclonic seizures
of
muscles of limb or the whole body
• Juvenile myoclonic epilepsy (JME) is
the most common form of this
condition.
15. Types of Epilepsy
• Simple partial seizure(Cortical focal epilepsy)
oLasts 1/ 1-2 min
oConvulsion are of muscles or localized sensory
disturbance depending on the area of cortex involved in seizure
oWithout loss of consciousness
oComplex partial seizure(Temporal lobe epilepsy, Psychomotor
epilepsy)
oAttack of bizarre and and purposeless movement
oEmotional changes lasting 1-2 min along with impairment of
consciousness.
oThe seizure focus is located in the temporal lobe.
15
18. CLASSIFICATION
• Group 1- Blockade of voltage-dependent Na+ or Ca channels
(generalised and partial seizures)
• Group 2- Enhance inhibitory events mediated by GABA (absence,
generalised, partial seizures)
• Group 3- Blocks T-type calcium channels (absence seizures).
• Group X- Reduce events mediated by excitatory amino acid glutamate
20. Group 1- Blockade of voltage-dependent Na+ or Ca
channels (generalised and partial seizures)
20
21. Carbamazepine
Clinical uses:
• Primary generalized tonic clonic seizures.
• Partial seizures with or without secondarily generalization.
• Bipolar disorders.
• Chronic pain syndromes: Trigeminal neuralgia.
Pharmacokinetics:
• Initial half-life is 20- 40 hrs but decreases to 20-40 hr on chronic
medication.
• Active metabolite: 10-11 epoxy carbamazepine.
22. Carbamazepine
Dose:
• Available only in oral form.
• Effective in children, in whom a dosage of 15-25 mg/kg/d is appropriate.
• In adults, daily doses of 1 g or even 2 g are tolerated.
Neurotoxic side effects :
• Blurred or double vision
• Lethargy, headache.
• Worsening of myoclonic, Atonic & absence seizures.
24. Phenytoin
Clinical uses :
• Partial & generalized tonic clonic seizures.
• 2nd line agent for patients with mixed seizures (myoclonic/tonic-
clonic).
• Status epilepticus.
Neurotoxic Side effects:
• Dose related : Diplopia & Ataxia.
• Peripheral neuropathy.
• Behavior changes.
25. Phenytoin
Systemic side effects :
• Skin rash
• Lymphadenopathy ( abnormally enlarged lymph nodes)
• Gingival hyperplasia
• Pulmonary fibrosis
• Hirsutism
• Teratogenic ( Fetal Hydantoin syndrome includes cleft lip and palate,
congenital heart disease)
• Megaloplastic anemia ( folate deficiency ).
NOTE – phenytoin is also an anti-arrthymetic drug treatment with
phenytoin should not be stopped abruptly.
26. Lamotrigine
Decreases the release of excitatory neurotransmitters
(glutamate/aspartate).
Clinical uses :
• Monotherapy in partial seizures
• Adjunctive therapy in generalized tonic clonic seizure
• Mixed seizures
Side effects :
• Dizziness, headache, Diplopia
• Nausea
• Hypersensitivity skin rash
not to be used in those < 16 years
27. Oxcarbazepine
It is a 10- keto analogue to carbamazepine.
Clinical uses:
• Partial seizures
• Generalized tonic clonic seizures
• Affective disorders
• Trigeminal neuralgia
Side effects :
• CNS : sedation, dizziness, ataxia, diplopia
• Hyponatremia but less less than carbamazepine
• Allergic skin reaction
28. Zonisamide
• Sulfonamide derivatives.
• Blocking of voltage dependent Na & T- type Ca channels.
• Partial & Generalized tonic clonic seizures.
• Useful against infantile spasm and certain types of myoclonias.
Side effects :
• CNS: confusion, ataxia, sedation, poor concentration
• Anorexia & weight loss
• Skin rash
• decreased sweating, hyperthermia
• Renal stones (rare)
C/I : Allergy to sulfonamides.
29. • Group 2- Enhance inhibitory
events mediated by GABA
(absence, generalised, partial
seizures)
29
30. Phenobarbital
M.O.A :
• Binds to GABA receptor improving its effect by extending GABA
mediated chloride channel opening.
Clinical uses:
• Partial seizures
• Generalized tonic clonic seizures
• Neonatal seizures
• Status epilepticus
Side effects:
• Sedation, ataxia, nystagmus ( rapid, rhythmic and involuntary eye
movements), vertigo
• Agitation & confusion, at high doses.
• Alteration of sleep cycles
31. Gabapentin
It is an amino acid, an analogue to GABA.
Clinical uses:
• Partial seizures
• Generalized tonic clonic seizures
• Neuropathic pain: post herpetic neuralgia
Side effects:
• CNS: sedation, ataxia, headache, tremor
• GI upset.
• Weight gain.
32. Tiagabine
Inhibition of GABA reuptake into presynaptic neurons.
Clinical uses:
• Adjunctive treatment for partial and generalized seizures
Side effects:
• CNS: sedation, tremor, depression, confusion
• Nausea, abdominal pain
• Not recommended in children under age of 12 years.
33. Vigabatrin
• Irreversible inhibitor of GABA transaminase.
Clinical uses:
• 2nd line treatment in patients with refractory partial seizures
• 1st line treatment in infantile spasm (west’s syndrome)
• May worsen myoclonic jerks and generalized absence and precipitate
status epilepticus
Side effects :
• CNS: sedation, dizziness, headache
• Change in mood, agitation
• Retinal toxicity… irreversible
• Weight gain
34. Clonazepam
Clinical uses
• Myoclonic seizures
• Generalized seizures (mainly absence)
• Status epilepticus
• Infantile spasm
Side effects:
• Sedation, ataxia, irritability.
• Cardiovascular & Respiratory depression .
• Hyper salivation in pediatric .
• Idiosyncratic reaction like blood dyscrasia is rare.
35. Group 3- Blocks T-type calcium channels (absence seizures).
35
36. Ethosuximide
• Reduces T- type calcium currents in thalamic neurons
• Effective against absence seizures
• May increase tonic- clonic seizures
Side effects :
• Nausea & Vomiting.
• Sleep disturbances.
• Drowsiness & Hyperactivity.
37. Drugs With Multiple Mechanisms Of
Actions
● Valproate
● Felbamate
● Topiramate
39. Valproate
Side effects:
• CNS: Tremor
• Dose related GI symptoms
• Increase appetite & weight gain
• Hair loss
• Hepatotoxicity esp. < 2 years.
• Thrombocytopenia
• Teratogenic, spina bifida ( major birth defect, type of neural tube defect
40. Felbamate
M.O.A:
• Inhibition of voltage – dependent sodium channels
• Potentiate GABA response at GABA receptors
• Inhibition of the excitatory N-methyl-D-aspartate (NMDA)
receptors
Clinical uses:
• Broad spectrum of action
• Effective in some patients with partial seizures
• 3rd line drug in refractory seizures- in lennox gastaut syndrome
Side effects:
• CNS: Insomnia, Diplopia, Ataxia
• Weight loss.
41. Topiramate
M.O.A:
• Blockage voltage – dependent sodium channels
• Enhances activity of GABA at non benzodiazepine
• Site on GABA (A) receptors
• Antagonizes NMDA receptors
• Weakly inhibits carbonic anhydrase enzyme
Clinical uses:
• Adjunctive therapy for partial & generalized seizures
• Adjunctive therapy for Lennox-Gastaut syndrome & infantile spasm
42. Topiramate
Side effects:
• CNS: confusion, ataxia, poor concentration
• Cognitive impairment
• Visual disorders: myopia, glaucoma (rare)
• Weight loss
• Parasthesia & renal stones due to inhibition of carbonic anhydrase
enzyme.
• Teratogenic in animals
43. Drugs With Unknown Mechanism Of
Actions
Levetiracetam:
• Broad spectrum
• Add- on therapy for refractory partial seizures
Side effects:
• CNS: Fatigue, dizziness, agitation, anxiety
• Increases susceptibility to infection, rhinitis or flu like symptoms
• Anemia, leukopenia
44. Pregabalin
Clinical uses:
• Adjunctive therapy for partial seizures
• Peripheral neuropathic pain.
Renally excreted and is not hepatically metabolized
Side effects :
• Dizziness, somnolence and ataxia
• Blurred or double vision
• Weight gain
• Peripheral edema
• May cause euphoria
• New onset myoclonus has been reported
45. ECT
45
• Electroconvulsive therapy (ECT), formerly known as electroshock
therapy, and often referred to as shock treatment, is
a psychiatric treatment in which seizures are electrically induced in
patients to provide relief from mental disorders.
46. KETOGENIC DIET
46
• Based on finding that starvation, which burns fat for energy has an
antiepileptic effect
• Used primarily to treat severe childhood epilepsy, has been effective in
some adults & adolescents
• High fat, low carbohydrate and protein intake
• Requires strong family commitment
47. VAGUS NERVE STIMULATION
47
• Device is implanted to control seizures by delivering
electrical stimulation to the vagus nerve in the neck, which
relays impulses to widespread areas of the brain.
• Used to treat partial seizures when medication does not
work.
48. COMMON CAUSES OF FAILURE OF
ANTIEPILEPTICS
1. Improper diagnosis of the type of seizures
2. Incorrect choice of drug
3. Inadequate or excessive dosage
4. Poor compliance
48
49. TREATMENT IN SPECIAL
SITUATIONS
ANTIEPILEPTIC AND PREGNANCY :
• Seizures are very harmful for pregnant women.
• Monotherapy usually better than drugs combination.
• Folic acid is recommended to be given for every pregnant
women with epilepsy.
• Phenytoin, sodium valproate are absolutely contraindicated and
oxcarbamazepine is better than carbamazepine.
49
50. EPILEPSY IN ADOLESCENTS AND YOUNG
ADULTS
Important points to remember are:
• Avoiding sleep deprivation,
• alcohol and substance abuse, driving, potentially risky leisure activities
like rock climbing, horse riding, etc.
• Prolonged television (TV) viewing, playing video games and dancing
in dark rooms with flickering/flashing lights (discotheques).
50
51. SURGERY IN EPILEPSY
• All patients with medically intractable epilepsy (MIE) should be
evaluated at a center performing epilepsy surgery.
• A patient having MIE with an identifiable lesion on imaging, correlated
with electrophysiology [Electroencephalogram (EEG)] is a potential
candidate for epilepsy surgery. Even if imaging is negative, patients
still can be surgical candidates on further investigation.
• Epilepsy surgery should be done only in specialized centers.
• Surgery has a high chance of achieving seizure freedom (in 60– 70% of
cases) and a reduction in seizure frequency in the remaining 30–40%
cases.
• When indicated it should be considered as early as feasible rather than
an option of last resort.
51
52. SURGERY IN EPILEPSY
• Epilepsy surgery may be resective or nonresective.
• Resective surgery includes lesionectomy (resection of the lesion and
the surrounding epileptogenic area), amygdalohippocampectomy with
or without temporal lobe resection, multilobar resection and
hemispherectomy.
• Nonresective surgery includes multiple subpial transections corpus
colostomy and vagus nerve stimulation (VNS).
52
54. Pathophysiology
Decrease in INT/Increase in ENT/Abnormalities in Ion channel
Rhythmic and repetitive hyper synchronous discharge of neuron
Seizures
Repetitive Seizures
Epilepsy
