This document provides an overview of seizures in childhood, including definitions, classifications, etiologies, approaches, and complications. It discusses the main types of seizures including focal, generalized tonic-clonic, absence, myoclonic and neonatal seizures. It also covers febrile seizures and status epilepticus. The management of seizures involves stabilizing the child, treating the underlying cause, and using anticonvulsant medications like phenobarbital, phenytoin or benzodiazepines. Outcomes depend mainly on the underlying etiology.
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.
Follow us on: Pinterest
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
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.
Follow us on: Pinterest
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
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
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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
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
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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
1. 1
DEBREBIRHAN UNIVERSITY
Asrat weldeyes health science campus
Approach of seizure in childhood
Prepared by: Yohannes Mamo
Shegaw Merkebu
Zelalem Mekonnen
Modulator: Dr.Yemisrach (Pediatrician)
January 2015 E.C
2. Outline
2
Definition of seizure
Etiology of seizure
Classification of seizure
Approach to children with seizure
Complication
3. Introduction
3
A seizure is a transient occurrence of signs and/or
symptoms resulting from abnormal excessive or
synchronous neuronal activity in the brain. this can
cause changes in awareness, behavior, and/or
abnormal movements.
4. 4
Acute symptomatic/ provoked seizures occur
secondary to an acute problem affecting brain
excitability
Electrolyte imbalance structural, inflammatory, or
metabolic disorders of the brain
An unprovoked seizure - without know or fixable
cause. it trigger by stress or sleep deprivation.
Reflex seizures - seizure precipitated by a
sensory stimulus. including visual (flickering lights,
patterns, reading, music)
5. 5
Epilepsy is considered when
1. Two or more unprovoked seizures occur in a time
frame of longer than 24 hr.
2. A known epilepsy syndrome.
Epileptic syndrome is one or more specific seizure
types and has a specific age of onset and a specific
prognosis
Epileptic encephalopathy is an epilepsy syndrome
in which there is a severe EEG abnormality that is
thought to result in cognitive and other impairments.
6. Epidemiology
6
4–10% of children experience at least one seizure
(febrile or afebrile) in the first 16 yr of life.
The cumulative lifetime incidence of epilepsy is 3%,
and more than half of the disorders start in childhood.
Febrile seizures occur in 2 % to 4 % of the pediatric
population.
Approximately 30% of patients who have a first
afebrile seizure later develop epilepsy
7. Cause of seizure
7
1. Idiopathic
2. CNS infections
Meningitis, Encephalitis,
Brain abscess,
Syphilis(tertiary)
3. Metabolic
Electrolyte imbalance
(calcium, sodium,
magnesium, phosphorus)
Hypoglycemia
4. Structural
Head trauma
Brain tumor
Stroke
5. Others
Sepsis
Drug abuse
Ingestion of toxins and
accidental
9. Mechanism of seizure
9
1.Decreased excitability in inhibitory GABAergic
interneurons,
leading to increased excitability (GLUTAMATE) and
epilepsy.
2. Activation of metabotropic and ionotropic glutamate
receptors, as well as the tropomyosin-related kinase
B receptor.
10. Classification of seizures
10
EEG + Clinical
EEG is an important adjunct in classification of seizures
Classifying the seizure type
Provides a clue to the cause of the seizure disorder
Allows a firm basis for making a prognosis
Helps in choosing the most appropriate treatment
12. 12
1.Focal seizures. initial activation of a system of
nervous limited to one part of hemisphere
2. Generalized seizures, indicate synchronous
involvement of all of both hemispheres
3. Unknown onset if there is not enough clinical
information available to determine if the seizure is
focal or generalized
4. Unclassified are unusual and a determination of
onset cannot be made despite an adequate workup
13. Focal seizure
13
Accounts 15 % of seizures in children
limited to only one part of cerebral hemisphere
Can progress to generalized seizure
May or may not have change in consciousness
14. 1.Focal seizures without impairment
of consciousness
14
Can be sensory or motor form
Lasts not longer than 10 – 20 seconds
May have jacksonian march from face to arm to
leg, head and eye movements to the contralateral
side or
postictal (Todd) paralysis that can last minutes or
hours
EEG: unilateral spikes/sharp waves on temporal
15. 2.Focal seizures with impairment of
consciousness
15
Usually lasts 1- 2 minute
Often preceded by an aura (crying, fear
,hallucination)
But <7 years old children are less likely to report
aura
Automatisms- confused, repetitive, purposeless
behaviour
Such as chewing, lip smacking, swallowing, or
“picking” movements of the hands
limited awareness of his actions and no memory of
16. 3. Generalized seizures that
evolve from focal seizure.
16
Can be tonic, clonic or tonic-clonic seizure lasts 1-2
min.
Head movement, tongue biting, urinary and stool
incontinence, vomiting with risk of aspiration,
cyanosis, fracture
EEG Shows focal or sharp waves lobe where the
seizure originates.
17. Generalized seizures
17
Discharges from both hemispheres
There is,
Always LOC
No warning
Symmetrical & Bilateral synchronous discharge
on EEG
18. Generalized tonic-clonic
seizure
18
The tonic phase appears as full body stiffening
Typically with the lower extremities extended &
upper extremities either flexed or extended with neck
extension.
Ictal cry, the sound of forced air expired against a
closed glottis due to contraction of the diaphragm and
chest muscles.
Tongue biting ,cyanosis ,apnoea ,falling drooling of
saliva, eye roll back associated with the tonic phase
19. Cont..
19
Generalized tonic-clonic seizures last 1–3 minutes
The tonic phase is followed by a clonic phase of
rhythmic jerking of the extremities
Often associated incontinence of urine or stool
They are always accompanied by loss of
consciousness
20. Cont..
20
Post-ictal period characterized by lethargy, decreased
arousal, confusion aphasia, fatigue, headaches, and
body aches.
Post-ictal periods can last from minutes up to a few
hours.
A prolonged post-ictal period or persistent altered
mental status after a seizure should raise concern for
an alternative etiology
such as a medication effect or non-convulsive status
21. Cont…
21
The EEG pattern during a GTC typically shows
diffuse voltage attenuation with low amplitude fast
generalized poly-spikes or
beta activity during the tonic phase evolving to
synchronous spike and wave during the clonic
phase
22. Tonic seizure
22
Continuous muscle contraction that can lead to
fixation of limbs and axial musculature in flexion or
extension
Frequently occur in sleep or when the child is
emerging from sleep.
They can last up to 1 minute, though most are often
<20 seconds
The EEG usually shows generalized, low-voltage, fast
polyspikes with diffuse voltage attenuation
23. Clonic seizures
23
Rhythmic, repetitive jerks fast muscle
contractions and slightly longer relaxations
The extremities are often flexed
They can be focal or generalized.
24. Atonic seizures
24
Atonic seizures are characterized by a brief loss
of tone & accompanied by impaired
consciousness,
though these seizures can be so brief that mental
status changes may not be detectable.
Loss of tone occurs primarily in the trunk, but
more subtle forms can manifest as jaw drops
Atonic seizures typically last 2–5 seconds
Atonic seizures often result in a fall if the patient
is standing can lead to signifcant injury
25. Myoclonic seizure
25
Characterized by a brief contraction of a muscle
The shock-like jerks that occur are very brief
<200 milliseconds
Appear most often in the upper arms & shoulders
or upper legs
Commonly no definite impairment in
consciousness
The EEG during a myoclonic seizure shows a
burst of generalized spike- or polyspike-waves
26. Absence seizures
26
Brief episodes characterized by behavioral
arrest and impaired conscious that externally
present as staring spells.
The spells are brief, typically lasting only 3–20
seconds
Sudden cessation of motor activity or speech
with a blank facial expression and flickering of
eyelids.
Children noted by their teachers or parents to
27. Typical absence seizures
27
Start and end abruptly, no postictal state &
resume pre seizure activity
Often associated subtle motor components such
as swallowing or chewing movements, lip
smacking, or repetitive blinking
Hyperventilation in the office can often induce a
typical absence seizure and is a useful diagnostic
maneuver
28. Atypical absence seizures
28
Marked by a loss of awareness
The onset and offset of impaired to
consciousness is more gradual.
Due to incomplete impairment in consciousness
,the patient may continue performing an activity
with less attention, coordination
There can be a gradual loss of truncal tone
resulting in slumping but not falls.
The spells are not provoked by hyperventilation
29. Febrile Seizure
29
seizure that occur at 38oc or higher, that are not
the result of CNS infection or any metabolic
imbalance, and in the absence of prior afebrile
seizures w/c occurs b/n 6-60 months
Pick age of onset 12 -18 months
Recur in approximately 30% in 1st episode, in
50% after 2nd or more episodes, & 50% of infants
onset of febrile seizure younger than 1 yrs.
30. 30
Simple febrile seizure
Primary generalized, usually tonic-clonic seizure
Attack associated with fever
Lasting for a maximum of 15 min
Not recurrent with in 24hrs
do not have an increased risk of mortality
31. 31
Complex febrile seizure
Focal seizure persisting for more than 15 minute
Repeated convulsions occur within 24 hr
Approximately 2-fold long-term increase in mortality
rates
32. Febrile infection–related (or
refractory) epilepsy (FIRES)
32
Predominantly in older >5 yr.
Male children and associated with an
encephalitis-like illness but without an identifiable
infectious agent
33. Risk factors for recurrence of febrile seizure
33
major
Age <1 yr
Duration of fever <24
hr
Fever 38 – 39⁰c
Having no risk factors
carries a recurrence risk
of approximately 12%; 1
risk factor, 25–50%; 2
risk factors, 50–59%; 3
or more risk factors, 73–
minor
Family history of febrile
seizure
Family history of
epilepsy
Complex febrile seizure
Daycare
Male gender
Lower serum sodium at
time of presentation
34. Risk Factors for Occurrence of
Subsequent Epilepsy After a Febrile
Seizure
34
35. Indication for LP in febrile
seizure
35
Indication
Children <06 month of age
Children 06-12 month of age
I. Immunization status unknown
II. Immunizations deficient in HIB & S.
pneumonia
Children at any age
I. Signs & symptoms of meningitis /ill
appearing
II. Child has received antibiotics prior to
36. Mgt of febrile seizure
36
Counseling & anti pyretic
Anti epileptic
Only acute treatment of seizure is necessary if seizure
lasts >5minutes.
Diazepam, 0.3 mg/kg orally TID for the duration of the
illness, usually 2–3 days
Otherwise long term antiepileptic treatment is not
recommended.
37. Neonatal seizure
37
Neonates are at particular risk for the
development of seizures because:
Metabolic, toxic , structural and; infectious
diseases are more likely than at any other period
of life.
Generalized tonic-clonic convulsions tend not to
occur in the 1st month of life
Because arborisation & myelination are
38. Neonatal seizure types
38
1. Focal Seizures
Rythmic twiching of muscle groups
Often associated with localized structural lesion,
infections & subarachnoid hemorrhage
2. Tonic Seizures
Characterized by rigid posturing of the extremities
& trunk
39. 39
3. Myoclonic Seizures
Brief focal or generalized jerks of extremities
4. Subtle seizures
More common in full-term infants.
Not associated with EEG seizures
Have poor response to conventional
anticonvulsants
Consist of chewing motion, excessive salivation
,apnea, pedaling movements
41. Investigation
41
Depend on history and physical examination
Blood glucose
Serum electrolytes
CBC
Blood culture
CSF analysis
Cranial USG and CT
Metabolic profile in cases of inborn error of
metabolism
42. Treatment
42
Stabilize vital signs, ABC of life
Correct transient metabolic disturbances
Hypoglycemia- 2ml/kg 10% dextrose IV over
1 min, followed by a continuous
Hypocalcaemia – IV 5% calcium gluconate 2
ml/kg under careful cardiac monitoring,repeat
every 6 hrs over the first 24 hrs.
Hypomagnesemia – 50% magnesium sulfate
IM at 0.2 ml/kg
43. 43
Phenobarbital – Loading 20mg/kg, additional dose of
10mg/kg can be given if seizure not controlled, then
maintenance of 5mg/kg/day divided twice daily OR
Phenytoin 20mg/kg loading, and maintenance of 4 –
6mg/kg/day
For immediate cessation of seizure,Diazepam 0.1 to
0.3 mg/kg slowly IV until seizures stop
Prognosis
Underlying etiology is the main determinant of
outcome
44. Status Epilepticus
44
Is a continuous convulsion lasting longer than 05
min, or
The occurrence of serial convulsions between which
there is not return of consciousness
45. Type of status epilepticus
45
Convulsive status epilepticus the most common in
older child
Non convulsive status
Febrile status epilepticus-
Most common in preschool child
Is a continuous convulsion lasting longer than 30 min
Neonatal status epilepticus
46. Managment of status epilepticus
46
General measures:
Check airway, breathing and circulation
Give oxygen (facemask)
Insert nasogastric tube
Open iv line & draw blood for CBC, electrolytes,
glucose & creatinine
If hypoglycemia - give glucose (5 ml/kg of 10 %
dextrose)
47. Cont…
47
Emergent antiseizure treatment should start with
a benzodiazepine.
If the patient has IV/IO access
Lorazepam IV 0.1 mg/kg/dose (max 4 mg) or
Diazepam IV 0.15–0.2 mg/kg/dose (max 10 mg)
If the patient does not have IV access
Diazepam PR
2–5 years: 0.5 mg/kg
6–11 years: 0.3 mg/kg
≥ 12 years: 0.2 mg/kg (max 20 mg)
48. Cont.…
48
If the seizure persists after 5 minutes following
the first treatment, a second benzodiazepine
dose (lorazepam or diazepam) should be
administered
If the seizure persists 2nd line treatment loading
dose of phenobarbital 20mg/kg/dose IV infusion
for 20 minute , or valproate 40 mg/kg/dose IV
infusion for 5 minute
If seizure doesn't stop with in 30 minutes repeat
loading dose of the second-line treatment
49. Cont..
49
For persistent seizure activity following repeat 2nd
line, treatment transitions to the initiation of
continuous infusion of anesthetic agents &
secured airway
Midzaolam initial loading dose of 0.1–0.2 mg/kg
and a continuous infusion rate of 0.1–0.2
mg/kg/hr or
Pentobarbital with a loading dose of 2–5 mg/kg
followed by a continuous infusion at a rate of 0.5–
1 mg/kg/hr
50. Approach to a children with
Seizure
50
Evaluation of the First Seizure
The initial evaluation of an infant or a child
during or shortly after a suspected seizure
should include:
Assessment of the adequacy of the airway,
ventilation, and circulation (ABC).
Positioning
Measure vital signs and glucose
concentration.
51. 51
History
Ensure whether seizure really occurred
Previous seizure
Seizure characteristics
Associated symptoms or signs, (hypoglycemia,
meningitis, cardiac arrhythmia, or acute pulmonary
embolism)
History of trauma
A past and current psychosocial history, including
potential stressors
56. 56
CNS
level of conscious: using modified GCS or Blantyre coma score
Posture: decorticate or decelerbrate
Focal neurological deficit: slow-growing glioma, as the cause
of the seizure disorder
Meningeal signs
57. Investigation
57
CBC, ESR
Serum glucose
Serum electrolytes (Na ,
Ca)
Blood culture
Serum level of
anticonvulsant
Toxicology screening
(urine and serum )
Blood film
LP
EEG: - help predict the
risk of seizure
recurrence and to
assess for focal
abnormalities.
CT or MRI: -for
structural underlying
58. Principle of Management
58
Assess airway ,breathing ,circulation(ABC of life)
Give oxygen
Don’t put anything in the mouth
Avoid sharp material around the pt.
Establish diagnosis
Arresting seizure by treating underling conditions
Principles of pharmacologic therapy
59. When to Initiate Ant seizure Drug
59
Should be started in any patient with recurrent
seizures of unknown aetiology
A known cause that cannot be reversed.
Initiate therapy in a patient with a single seizure
is controversial.
60. Cont..
60
Establish diagnosis
correctly determine seizure type , epileptic
syndrome , etiology and precipitating factors.
Principles of pharmacologic therapy
use a single drug till maximum dose or side
effect
Add additional drug with different site of
61. Type of seizure and drug of
choice
61
Seizure type Drug of choice
Focal seizure
Carbamazepine, phenytoin
phenobarbitone
Absence seizure Ethosuximide,
Valproite, clonazepam
Tonic-clonic seizure
Phenytoin ,phenobarbitone
Myoclonic
Valproate, Clonazepam
Infantile spasm Predinsolone
62. Management of acutely
convulsing child
62
Assess ABC of life
Give oxygen
Correct hypoglycemia
Arrest the seizure with:
Diazepam 0.2-0.5 mg/kg iv/rectal or
Lorazepam 0.05-0.1mg/kg iv
Position the child –recovery position
64. Cont…
64
If seizure persists –load with phenytoin or
phenobarbital
Initial screening history and physical examination
Obtain laboratory studies
65. Epilepsy surgery
65
Seizures must be medically intractable (a patient
has failed 3 drugs)
Seizures must be debilitating
properly defined epileptogenic zone
66. Causes of intractable epilepsy
66
Improper diagnosis of seizure type
Improper dose
Genetic syndromes and brain malformations
67. When to stop anticonvulsant
67
Two seizure free years are required for a patient with
no risk factors.
Drugs should be withdrawn slowly , weaning
process may take 2-3 months
Normal EEG finding
Risk factors for recurrence:
Age > 12 yrs at onset
Neurologic dysfunction
History of prior neonatal seizures
69. Prognosis
69
There is a high incidence of early death (24 -30 %)
associated
with neonatal seizures, and a high incidence of neurologic
impairment, developmental delay, and post neonatal
epilepsy
among survivors.