This document provides an overview of normal and sleep EEG patterns. It defines EEG and describes normal wakeful adult EEG patterns such as alpha rhythm and sleep stages. It also discusses EEG patterns in different age groups from premature infants to elderly adults. Descriptors of EEG activity and various activation procedures are explained. Common artifacts and benign variants are also summarized. The document aims to familiarize readers with the basic components of normal EEG for clinical interpretation and diagnosis.
EEG variants, are always to be recognized while interpreting the EEG one must be aware of these. Major and most common EEG is variants are discussed in the stated presentation.
Syed Irshad Murtaza.
EEG variants, are always to be recognized while interpreting the EEG one must be aware of these. Major and most common EEG is variants are discussed in the stated presentation.
Syed Irshad Murtaza.
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.
This presentation looks at abnormal EEG patterns with examples for each. Benign variants, artifacts and focal ictal patterns are not part of this presentation.
This presentation reviews the common artifacts in EEG, their identification and rectification. Examples of various artifacts are provided in the presentation.
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.
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.
This presentation looks at abnormal EEG patterns with examples for each. Benign variants, artifacts and focal ictal patterns are not part of this presentation.
This presentation reviews the common artifacts in EEG, their identification and rectification. Examples of various artifacts are provided in the presentation.
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.
This presentation discusses the basic principles governing EEG Rhythm Generation, and discusses the various circuits that generate and maintain cerebral oscillations.
Electroencephalography is the technique used to acquire electrical signals of brain through electrodes which are placed by certain montage. Different wave patterns can be observed which is useful in detecting any abnormal conditions or neurological brain disorders in human beings. There is broad future scope for medical research and creating EEG based equipments for real time applications.
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.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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- 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
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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.
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
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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...
EEG dr archana
1. Normal and
Sleep EEG
Dr Archana Kushwah
Choithram Hospital & Research Centre ,Indore
Guide Dr Vinod Rai
Choithram Hospital & Research Centre ,Indore
2. Normal & Sleep EEG
Introduction
Definition
Descriptors of EEG activity
Normal EEG (Wakeful adult)
Normal Sleep EEG
Normal EEG (Extremes of age)
Activation procedures
Artifacts
Benign or normal EEG variants
3. Hans Berger (1873–1941) recorded the first human
EEG in 1924
Brief History
● Vladimirovich (1912)
● first animal EEG study (dog)
● Cybulski (1914)
● first EEG recordings of induced seizures
● Berger (1924)
● first human EEG recordings
● 'invented' the term electroencephalogram
(EEG)
● American EEG Society formed in
1947
● Aserinsky & Kleitman (1953)
● first EEG recordings of REM sleep
4. INTRODUCTION (What, Where, How)
What
Electrical potential generated by summation
of cortical nerve cell(Pyramidal cell) EPSP &
IPSP: Not AP
5. INTRODUCTION (What, Where, How)
Where
Thalamic pacemaker cells in nucleus reticularis
Thalamocortical neurons stimulated
excitatory impulses to cortex.
6. INTRODUCTION (What, Where, How)
How
EEG is difference in voltage between 2
recording electrodes plotted over time.
7.
8. Definition of normal EEG
Normal EEG
Absence of abnormal components
No criteria for normal patterns
Requires recognition of normal patterns at
different ages and level of alertness
Normal EEG does not always mean normal brain function.
Abnormal EEG does not always mean abnormal brain
function.
9. Descriptors of EEG
Morphology
Repetition
Frequency
Amplitude
Distribution
Phase relation
Timing
Persistence
Reactivity
10. Descriptors : 1.Morphology
Wave : difference of electrical potential between two recording electrodes
Wave form : describes the shape of wave.
Transient &/or paroxysm: stands out against the background
11. Descriptors : 2.Repitition
Rhythmic
Semi rhythmic
Irregular
polymorphic
Descriptors : 3.Frequency
Number of times a wave recurs in 1 sec.
Slow waves < 8 Hz. Fast waves > 13 Hz.
12. Total vertical distance of a wave.
Measured in 𝜇𝑉 not in mm.
Low< 20𝜇𝑉 :medium 20-50𝜇𝑉 :high >50𝜇𝑉
Changing the montage changes the voltage.
Amplitude assymetry ~ confirmed by montage
change.
Descriptors : 4.Amplitude
13. Wide spread/ diffuse/ generalised.
Lateralized.
Focal / localized.
Multifocal epileptiform pattern
3 or more anatomically distinct areas generating
epileptiform activity.
In describing location electrode names should
be used.(not head regions / brain areas)
Descriptors : 5.Distribution
14. Descriptors : 6.Phase relation
Timing and polarity of components of waves
in 1 or more channels.
In phase (Troughs and peaks occur at same time in different
channels)
Out of phase (Troughs and peaks donot coincide)
Phase reversal (peaks pointing in oppposite direction)
15. Descriptors :
7.Timing
• Synchronous(same
time)
• Asynchronous
• Independent
• 5millisec and <time
can be appreciated
by digital
instruments.
8.Persistence
• How often a wave or
pattern occurs
during the recording.
• Persistence index
• High /moderate/ low
• Sporadic / periodic
9.Reactivity
• Changes produced
by various
maneuvers.
• Opening or closing
eyes
• Hyperventilation
• Photic stimulus
• Sensory stimulus
• Changes in level of
alertness.
• Movement
17. Alpha rhythm
Frequency
≥ 8 Hz & ≤ 13 Hz
Distribution
posterior head region
Reactivity
Blocked by eye
opening and other
alerting maneuver.
Disappears in
drowsiness and sleep
18. Alpha rhythm(frequency)
8-13 Hz
Nearly constant in a given individual throughout
life(decline of 1 or more Hz is abnormal)
Frequency in two hemisphere should be same
difference of over 1 Hz is abnormal
Hemisphere with lower frequency is abnormal.
Squeak phenomenon
Brief increase in frequency after eye closure
followed by rapid deceleration to baseline frequency.
19. Alpha rhythm (distribution)
Greatest amplitude and most persistent in
occipital, posterior temporal and parietal
areas.
Alpha frequency activity restricted to FP1and FP2
is eye movement artifact until proven otherwise.
20. Alpha rhythm (reactivity)
Blocked by eye opening, sudden alerting,
attention to visual and other stimuli, mental
concentration.
Bancaud phenomenon
Unilateral blocking of alpha rhythm indicates
presence of abnormality of non reactive hemisphere.
Paradoxical alpha rhythm
Alpha rhythm appears on eye opening and
disappears on eye closure in drowsy patient.
Partial alerting response
21. Alpha rhythm
Phase relation
Often not in phase
Amplitude
Commonly more on right side
Left side should be at least 50% of right.
Asymmetry depends on occipital bone thickness.(not
on handedness)
Alpha variants
Slow alpha variant ~3.5-6.5 Hz: admixture with
normal alpha: blocks as alpha.
Fast alpha variant ~ 16-20Hz: blocks as alpha.
Physiological purpose
Possibly integrated with visual system function.
22. Beta rhythm
Frequency
Over 13 Hz
Upper beta range ~ gamma
range
Distribution and reactivity
Frontal
MC
Blocked by movement / intention
to move/tactile stimulus (opposite
hemisphere)
Widespread
Not blocked by any stimulus
Posterior (fast alpha)
Accentuates in
Drowsiness and stage 1 sleep.
Excess medication (BDZ &
Barbiturate)
23. Beta rhythm
Amplitude
Assymetry ~> 35% is
abnormal
Breach rhythm
Localised increase in
beta activity in skull
defect areas.
Physiological
significance
Possibly integrated with
S/M function of the brain.
Almost always a good
prognostic sign.
24. Mu rhythm
Wicket/comb/arceau rhythm
<5% EEG: young adults
7-11Hz
For few seconds in central or
centroparietal area(difference
from alpha by blocking)
At different times on both
sides
Intermittent & asymmetrical :
persistent asymmetry on same
side is abnormal
Facilitated when scanning
visual images.
Blocked by ~ voluntary/
reflex/passive
movement/intention to move
/tactile stimuli.
Physiological significance
Somatosensory process
associated with movement.
25. Lambda rhythm
Saw tooth shaped
Positive polarity
Occipital
Appears on looking at
images containing
visual details.
100-250 millisecond
duration,< 50microvolt
Resembles POST in
shape and distribution.
Accompanied by eye
movement & eye blink
artifact.
Neither presence nor absence is abnormal
Asymmetry is abnormal
26. Vertex sharp transients (V waves)
Single, negative polarity
Maximal over vertex extends
to F,P,T area.
Common in normal sleep
Wakeful adults
Sudden loud
noise/startle/percussions of
hands or feet.
>2 times /sec, bilateral
synchronous
27. Kappa
rhythm
Bursts of very
low amplitude
of alpha or
theta
frequency
In temporal
lobe engaged
in mental
activity.
Normal
posterior
theta rhythm
Slow alpha
variant
Rhythmic slow
waves of 4-5
Hz
Blocking &
distribution
same as alpha.
Low voltage
EEG
No activity over 20
microV
More common in
advancing age /
tense subjects.
< 10microV abnormal
<2 microV
electrocerebral
inactivity(brain dead)
28. Normal sleep EEG (adults)
Elements of normal sleep activity
Slow waves
Positive occipital sharp transients
Vertex sharp transients
Sleep spindles
K complexes
Sleep stages
Sleep cycle
29. Slow waves
More prominent posteriorly.
Less persistent, more asynchronous, low
amplitude, fast frequency in light sleep than
deep.
30. POSTS
Triangular
waves in
occipital area
4-6Hz.
Mono /bi
phasic
Lambdoid
waves (Shape
& distribution)
Prominent lambda waves are
associted with more POSTS &
photic driving responses.
31. Sleep spindles
12-14Hz
Duration >0.5 sec
Maximum over
central
After 2 years
simultaneous and
symmetrical
K COMPLEX
Resembles v wave in
distribution , reactivity
and polarity
>0.5 sec
Less sharply contoured
32. Stages of sleep
Stage W
• Slowing
• Predominance of alpha
• Prominent beta in drug
induced
• SEM (first EEG sign of
drowsiness)
Stage 1
• Disappearance of alpha(30
sec Epoch ~ < 50% alpha)
• Paradoxical alpha
• Slow waves
33. Sleep stage 2
Sleep spindles
K complexes
Slow waves continue
POSTS often
persists
V wave often persist
34. Sleep stage 3 & 4
Stage 3
• 20-50% of 30 sec Epoch
contains
• Waves of 2Hz or <
• Waves of <75 microV
• In C3-A1 or C4-A2
• K complexes / sleep
spindles/POSTs
Stage 4
• >50%
• K complexes blend with slow
waves
• Spindles & POSTs rare
• After 55 yr~ St 3& 4 rare(only
amplitude criteria apllied)
35. REM sleep
> 50% of a 30 sec
Epoch contains
Low voltage EEG
Prominent theta
wave
Rapid eye movt.
Reduced muscle
tone
Resemble stage 1
but no v wave
Saw tooth wave
Alpha frequency ~1-
2 Hz
Appearance of REM
in routine EEG is
pathological.
36. Sleep cycle
Each cycle~ all stages NREM & REM: 4-7 cycles /sleep
1st cycle shortest: later 80-120 min. :REM sleep ~ appears 70-90 min after onset of sleep.
Young adults: 30-50% stage 2; 20-40% stage 3&4: 5-10% stage 1
REM sleep: 25% in young adults & 20% in 5th decade.
37. EEG of elderly(>60years)
Alpha rhythm
Frequency, persistence, reactivity &voltage ↓
Beta activity
More prominent : incidence & amplitude↑
Sporadic general slow waves
More common than young adults.
Intermittent temporal slow waves
Especially on lt. side
< 1% of waking record should be delta range
< 10% in theta range(Arrena et al)
Sleep
Fairly prominent slow waves
Sleep depth and consolidation reduced(St 3,4↓ 𝑡𝑜 <
10% )
REM sleep ↓ to < 20%
38. EEG of premature age to 19
years
Maturation of EEG parallels anatomical &
physiological development of brain
EEG of neonate is a function of actual age of brain
Conception age (CA)= gestational age + legal age
Always try to record normal active newborns
immediately after feeding(quiet wakefulness)
40. EEG of premature age to 19
years CA~ 29-32 wks
Lowest Interhemispheric synchrony
Temporal theta burst(temporal saw tooth wave)
Highly useful for estimating CA
41. EEG of premature age to 19
years
CA~ 32-34 wks
Multifocal sharp transients ; abundant delta
brush
EEG reactivity starts.
42. EEG of premature age to 19
years
CA ~ 34-37 wks
Frontal sharp transients/ mono
rhythmic frontal slowing
Trace alternans(delta brush &
multifocal sharp transietns ↓)
Inter hemisheric synchrony ↓
Activity Moyene.
CA ~ 38 -42 wks
Similar to full term
4 basic pattern
Low voltage irregular (wakeful &
active sleep)
Mixed vol (wakeful & transitional
sleep)
High vol. slow
Trace alternans
43. EEG of premature age to 19
years
Full term to 3 month
Precursor of alpha rhythm~
3-4 Hz
Sleep spindles appear
Asymmetry up to 8 months
; beyond 2 yr asyym. Is
abnormal.
Trace alternans / multifocal
sharp transient disppear.
Interhemispheric
synchrony 100%
Reaction to tactile and
auditory +
Lamba waves
44. EEG of premature age to 19
years
3 months – 1 year
Wakefulness~ BGA –
theta & delta range
Occipital rhythm
Drowsiness
Hypnogogic
hypersynchrony
Sleep
Starts to resemble
adult
Cone / O waves
Sleep spindles
appears at 3-6 mnt;
assym. up to 8 mnt.
V waves & k complex
~ 3-6 mnt.
45. EEG of premature age to 19
years
1-19 YEARS
Gradually becomes same as adult
Alpha frequency gradually increases.
Slow waves more prominent up to 4 years.
Posterior slow waves of youth
Most common at 8-14 years
Hypnogogic hypersynchrony rare after 12 years
SEM appears at 10 years.
14-6 Hz burst more common than adults.
POST begin to appear.
46. Activation procedures
Hyperventilation
Sleep deprivation
Photic stimulation
Others
Pattern or video game sensitivity
Auditory stimuli
Reading
Eye opening /closing and mental concentration
Tactile stimulation
Drugs
47.
48.
49. Artifacts
Physiological
Blinking and eye movements
Muscle artifact
Movement artifact
ECG
Pulse wave artifact
Skin potential
Movements of tongue and
oropharyngeal structures
Dental restoration
Non
physiological
External electrical interference
Internal electrical
malfunctioning of recording
system
50.
51.
52.
53.
54.
55.
56.
57.
58. Benign or normal EEG variants
Rhythmical
patterns
RMTD/RTTD
Alpha variants
SREDA
Midline theta rhythm
Frontal arousal rhythm
Benign patterns
with epileptiform
morphology
14 & 6 Hz positive
burst(Ctenoids)
Small sharp spikes(SSS)
6 Hz spike and wave
bursts(Phantom)
Wicket spikes
Breach rhythm.
