The document provides a historical overview of convulsive therapies including ECT. It discusses key developments such as the first reported use of inducing seizures with camphor in the 1500s and the accidental discovery by Sakel in the 1920s that insulin-induced seizures were effective for psychosis. The modern technique of ECT was developed in 1938 by Cerletti and Bini using electricity to induce seizures. The document then covers indications, contraindications, adverse effects, the ECT procedure and stimulus, and mechanisms of action and effectiveness of ECT.
Impulse-control disorders (ICDs) are psychological disorders characterized by the repeated inability to refrain from performing a particular action that is harmful either to oneself or others.
The individual fails to resist performing a potentially harmful act and it is usually accompanied by a sense of tension or arousal before committing the act and a sense of relief or pleasure when it is committed.
The hallmark in describing any of the ICDs is a tendency to gratify an immediate desire or impulse regardless of the consequences to one's self or to others.
Impulse-control disorders (ICDs) are psychological disorders characterized by the repeated inability to refrain from performing a particular action that is harmful either to oneself or others.
The individual fails to resist performing a potentially harmful act and it is usually accompanied by a sense of tension or arousal before committing the act and a sense of relief or pleasure when it is committed.
The hallmark in describing any of the ICDs is a tendency to gratify an immediate desire or impulse regardless of the consequences to one's self or to others.
This presentation is about geriatric Psychiatry awareness. it contains basic information about what is geriatric psychiatry, which are the main psychiatry disorder found in elderly and how to manage them?. it contains some detailed information about late life depression, delirium and dementia in geriatric population.
SCHIZOPHRENIA:
slide 1: A long-term mental disorder of a type involving a breakdown in the relation between thought, emotion, and behavior, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation.
slide 14: Types:
• Paranoid-type schizophrenia is characterized by delusions and auditory hallucinations (hearing voices that don't exist) but relatively normal intellectual functioning and expression of emotions. People with paranoid-type schizophrenia can exhibit anger, aloofness, anxiety, and can be argumentative.
• Disorganized-type schizophrenia is characterized by speech and behavior that are disorganized or difficult to understand, and flattening or inappropriate emotions. People with disorganized-type schizophrenia may laugh inappropriately for no apparent reason, make illogical statements, or seem preoccupied with their own thoughts or perceptions. Their disorganized behavior may disrupt normal activities, such as showering, dressing, and preparing meals.
• Undifferentiated-type schizophrenia is characterized by some symptoms seen in all of the above types, but not enough of any one of them to define it as another particular type of schizophrenia.
• Residual-type schizophrenia is characterized by a past history of at least one episode of schizophrenia, but the person currently has no "positive" symptoms (such as delusions, hallucinations, disorganized speech, or behavior). It may represent a transition between a full-blown episode and complete remission, or it may continue for years without any further psychotic episodes.
Catatonic Schizophrenia
This type of schizophrenia includes extremes of behavior, including:
Catatonic excitement - overexcitement or hyperactivity, in which the patient may mimic sounds (echolalia) or movements (achopraxia) around them.
Catatonic stupor - a dramatic reduction in activity in which the patient cannot speak, move or respond. Virtually all movements stops.
Conclusion
It is clear now, through the use of genetic linkage studies and microbiology, that schizophrenia does indeed have a biological explanation. However, the biological explanation is only part of the story. A yet unknown combination of intense stress, sociocultural situations, and cognitive processes may lead to the actual onset of schizophrenia aided by natural precursors. The most compelling explanation seems to be that a genetically inherited biological abnormality gives rise to hallucinations/delusions as a result of intense stress and eventually leads to other negative symptoms in reaction to the hallucinations/ delusions. At any rate, the current understanding of schizophrenia explains that the symptoms, however easily identifiable, are the result of a complex interaction between nature and nurture that can be treated adequately through the use of atypical anti psychotic drugs and psychotherapy.
This presentation is about geriatric Psychiatry awareness. it contains basic information about what is geriatric psychiatry, which are the main psychiatry disorder found in elderly and how to manage them?. it contains some detailed information about late life depression, delirium and dementia in geriatric population.
SCHIZOPHRENIA:
slide 1: A long-term mental disorder of a type involving a breakdown in the relation between thought, emotion, and behavior, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation.
slide 14: Types:
• Paranoid-type schizophrenia is characterized by delusions and auditory hallucinations (hearing voices that don't exist) but relatively normal intellectual functioning and expression of emotions. People with paranoid-type schizophrenia can exhibit anger, aloofness, anxiety, and can be argumentative.
• Disorganized-type schizophrenia is characterized by speech and behavior that are disorganized or difficult to understand, and flattening or inappropriate emotions. People with disorganized-type schizophrenia may laugh inappropriately for no apparent reason, make illogical statements, or seem preoccupied with their own thoughts or perceptions. Their disorganized behavior may disrupt normal activities, such as showering, dressing, and preparing meals.
• Undifferentiated-type schizophrenia is characterized by some symptoms seen in all of the above types, but not enough of any one of them to define it as another particular type of schizophrenia.
• Residual-type schizophrenia is characterized by a past history of at least one episode of schizophrenia, but the person currently has no "positive" symptoms (such as delusions, hallucinations, disorganized speech, or behavior). It may represent a transition between a full-blown episode and complete remission, or it may continue for years without any further psychotic episodes.
Catatonic Schizophrenia
This type of schizophrenia includes extremes of behavior, including:
Catatonic excitement - overexcitement or hyperactivity, in which the patient may mimic sounds (echolalia) or movements (achopraxia) around them.
Catatonic stupor - a dramatic reduction in activity in which the patient cannot speak, move or respond. Virtually all movements stops.
Conclusion
It is clear now, through the use of genetic linkage studies and microbiology, that schizophrenia does indeed have a biological explanation. However, the biological explanation is only part of the story. A yet unknown combination of intense stress, sociocultural situations, and cognitive processes may lead to the actual onset of schizophrenia aided by natural precursors. The most compelling explanation seems to be that a genetically inherited biological abnormality gives rise to hallucinations/delusions as a result of intense stress and eventually leads to other negative symptoms in reaction to the hallucinations/ delusions. At any rate, the current understanding of schizophrenia explains that the symptoms, however easily identifiable, are the result of a complex interaction between nature and nurture that can be treated adequately through the use of atypical anti psychotic drugs and psychotherapy.
Electroconvulsive therapy (ECT) is a procedure, done under general anesthesia, in which small electric currents are passed through the brain, intentionally triggering a brief seizure. ECT seems to cause changes in brain chemistry that can quickly reverse symptoms of certain mental health conditions.
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.
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
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.
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
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
- 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
3. Historical overview of convulsive therapies
The roots of Convulsive therapy can be
found in 1500s when Paracelsus gave
Camphor to patients by mouth to induce
seizures and cure psychiatric ailments.
In 1758, the first report was published
which mentioned the use of camphor for
the treatment of mania by inducing
seizures.
4. Another breakthrough was achieved in 1927 by a young
Polish neurophysiologist and neuropsychiatrist named
Manfred J. Sakel.
• Sakel discovered accidentally, by
causing convulsions with an overdose
of insulin, that the treatment was
efficient with patients afflicted with
psychosis, particularly schizophrenia
5. In 1930 he began to perfect, what was to become
the "Sakel's Technique" for treating schizophrenics.
According to his findings, more than 70 % of his patients
improved after Insulin shock therapy.
6. In 1934, Hungarian Neuropsychiatrist,
Ladislas Meduna treated a patient of
catatonic schizophrenia by inducing
seizure with intra-muscular injection of
Camphor oil.
He observed greater glial cells in
epileptics & schizophrenics have lesser
glial cells, hence he tried to increase glial
cell concentration with induced seizures
7. Later camphor was replaced by
Pentamethylenetetrazol (Metrazol)
In 1937, the Italian neuropsychiatrists
Ugo Cerletti and Lucio Bini began to
induce seizures experimentally with
electricity
8. They found that seizures could be more
easily induced and regulated with
electricity than with pharmacological
agents, thereby decreasing the number of
missed or recurrent seizures
On May 15, 1938, a seizure was
successfully elicited with electricity in a
39-year-old delirious manic man.
9. After 10 to 20 ECT shocks in alternate days, the
improvement in most of the patients were startling.
Significant improvements in the technique of ECT have
been made since then, including the use of muscle
relaxants, such as succinylcholine, the anesthesia of
patients with short-acting agents, pre-oxygenation of the
brain, the use of EEG seizure monitoring and better
devices and shock waveforms.
10. Despite these advances, the popularity of ECT greatly
decreased in the 1960s and 1970s, due to the use of more
effective neuroleptics and as a result of a strong anti-ECT
movement.
However, ECT gained evidence again in the last 15 years,
due to it's efficacy.
It is the only somatic therapy from the 30's that remains in
widespread use today.
12. Indications of ECT
1. Major depression, both unipolar and bipolar and
Psychotic depression
2. Mania
3. Schizophrenia with acute exacerbation; Catatonic
subtype, particularly
4. Schizoaffective disorder
5. High suicidal risk
6. Others: Parkinson disease, Neuroleptic malignant
disorder, Intractable Seizures
13. Primary Use
Rapid definitive response required on medical or
psychiatric grounds
Risks of alternative treatments outweighs benefits
Past history of poor response to psychotropics or good
response to ECT
Patient preference
14. Secondary Use
Failure to respond to pharmacotherapy in the current
episode
Intolerance of pharmacotherapy in the current episode
Rapid definitive response necessitated by deterioration of
patient’s condition
15. Contraindications
ECT has no absolute contraindications.
Medical conditions associated with increased risk:
Space-occupying intracerebral lesion (tumor, hematoma,
etc.)
Other condition causing increased intracranial pressure
Recent myocardial infarction
Recent intracerebral hemorrhage
16. Unstable vascular aneurysm or malformation
Pheochromocytoma
High anesthesia risk (American Society of
Anesthesiologists [ASA] class 4 or 5)
Mortality Rate
Extremely low, estimated at 2–10 per 100,000 patients
(0.0001%) - same ratio as for the induction of brief
general anesthesia
17. Cognitive Changes
Cognitive changes are often the most notable and most
distressing side effects
Factors that may increase cognitive side effects
18. Postictal Disorientation:
All patients experience some transient postictal
disorientation, lasting from a few minutes to a few hours,
following awakening from the ECT treatment.
Having received general anesthesia likely contributes to
this disorientation
19. Interictal Confusion:
Occasionally, postictal confusion may not fully disappear
and, when severe, may develop into an interictal
confusional state or delirium.
Uncommon
Rapidly disappears over a period of days following the
conclusion of treatments
20. The ECT team at NIMHANS has developed and validated
a short and sensitive battery (Battery For ECT Related
Cognitive Deficits – B4ECT-ReCoDe) for a quick
assessment of cognitive deficits associated with ECT in
the Indian setting
21. Cardiovascular Complications
They are the main cause of mortality and serious
morbidity with ECT, although most such complications
are minor.
During the seizure and acute postictal period, both the
sympathetic and parasympathetic autonomic systems are
sequentially stimulated.
Activation of the parasympathetic system causes a
transient reduction in cardiac rate
22. Activation of the sympathetic system increases heart rate,
blood pressure, and myocardial oxygen consumption.
These changes occasionally giving rise to transient
arrhythmias and, in susceptible individuals, transient
ischemic changes.
During parasympathetic stimulation, cardiac arrhythmias,
such as bradycardia, premature ventricular contractions, or
sinus arrest, may be seen.
23. The risks of cardiac arrhythmias, ischemia, and
hypertension are greatly diminished by the use of
oxygenation before and during the seizure, and these risks
can be lowered further in susceptible patients by
pretreatment with appropriate medications.
Stress on the heart during ECT equivalent to
climbing up about 2 floors.
24. Other Adverse Effects
General somatic complaints (e.g., headaches, nausea,
muscle soreness) are usually minor but are frequent
side effects of ECT.
Lasting up to several hours, but occasionally longer.
A soft bite block or other such device is used to
prevent injury to the tongue or teeth
25. ECT Stimulus
Generation & behaviour of
electrical stimulus has been
conceptualized by Ohm’s law:
V (voltage) = I (current) × R
(resistance)
26. 1. Waveform of the stimulus:
Earlier ECT machines delivered current in the form of
sine waves.
The slow rising and trailing edges of the sine wave do not
produce efficient cerebral stimulation.
This delivers substantial amounts of electrical stimulation
below seizure threshold and continues stimulation even
while the neuronal tissue is in post-depolarization
refractory period.
27. This may increase the cognitive adverse effects without
enhancing the benefits.
Hence, the sine wave has been modified to eliminate the
rising and trailing edges, retaining only the peaks in the
form of ‘rectangular’ pulses
28. Stimulus is given in the form of brief pulses (0.5ms) with
no stimulus in between the pulses.
Intermittent stimulation using pulses is more efficient as it
allows the tissue to recover from post-depolarization
refractory period.
Brief pulse ECT is able to induce seizures with
substantially less charge and energy compared to sine
wave.
29. Pulse width – 0.5-2ms: brief pulse
<0.5ms: ultra-brief
Stimulus duration - total period for which the stimulus
train is applied
Sine wave – less than 1s
Pulse wave – 0.5 – 8s
In the brief pulse ECT, the actual duration of stimulus will
be even lesser if the inter-train interval (where stimulus
is not provided) is excluded.
30. Frequency - number of cycles per second (Hz)
In the transformer-based sine wave stimuli, this is always
the line frequency (50Hz or 60 Hz)
Brief pulse – pulses per second (PPS)
Directionality & Polarity : Stimulus in ECT is
bidirectional, alternating current
31. Pulse amplitude:
The amplitude of the delivered current is an important
determinant of the volume of nervous tissue that is
directly stimulated by the ECT.
Modern ECT uses a constant current of around 800-
900mA
32. Charge:
Total amount of electrons traversing the inter-electrode
tissue
It is the product of current and actual duration of stimulus
in milli-Coulomb (mC)
Charge = current (in Amperes) × pulse width (in
milliseconds) × pulse frequency × length of train (in
seconds)
33. 2. STIMULUS INTENSITY
Determines treatment efficacy & cognitive adverse
effects; measured as charge in mC
Stimulus threshold should be supra-threshold to be
efficacious
Bilateral ECT – 1.5 to 2.5 times threshold
Unilateral ECT – 2.5 to 6 times threshold
34. 3. ELECTRODE PLACEMENT
Unilateral ECT
Stimulus is provided to only one hemisphere (usually
right) to minimize cognitive dysfunction
Electrode 1: Fronto-temporal site i.e., 1 inch above the
midpoint of an imaginary line linking the outer canthus
and the external auditory meatus
Electrode 2: 1 inch lateral to the vertex position, on the
same side (usually right)
35. Bilateral ECT
Bifrontal placement - electrodes are placed 5 cm vertically
above the outer canthus of each eye along an imaginary
vertical line perpendicular to a line connecting the pupils
Bitemporal placement - electrodes are placed on the
frontotemporal sites, one on each side
37. Selective Preferences Of Electrode Placement
Unilateral ECT
• Concern about potential cognitive side-effects (children,
elderly, brain damaged)
• Instrument limitations (e.g., sine wave stimulus)
Bilateral ECT
• Mania or schizo-affective disorder
• Patient has not satisfactorily responded to UL ECT
(usually after 6 ECTs)
• When more urgent response is essential (suicidal, starving
etc)
38. 4. FREQUENCY OF TREATMENTS
ECT is generally administered twice or thrice a week
However, it is recommended that the patient be evaluated
both for therapeutic and adverse effects
5. NUMBER OF SESSIONS
Decided based on the degree and rate of clinical
improvement and adverse effects
A typical course of ECT for depression consists of 6 to 12
sessions
39. Continuation ECT - begins after the index course, lasts
up to 6 months, and is designed to prevent relapse of the
episode
Maintenance ECT - to prevent further episodes for
longer periods
Frequency of ECT is slowly tapered off to once a month
40. ECT Procedure
Administration of ECT without a muscle relaxant is
known as unmodified ECT.
In modified ECT, anesthesia, muscle relaxant, and the
seizure-eliciting electrical stimulus are administered in the
same order.
Use of a muscle relaxant prevents musculoskeletal injuries
resulting from peripheral seizures
41. Preparation of patient:
Avoid solid food for at least 6 hours before treatment.
Moderate amounts of clear fluids can be taken till 2 hours
Oral medications should be taken 2 hours before treatment
Pass urine to prevent bladder rupture during ECT.
Dentures, jewellery, hair clips, contact lenses and hearing
aids should be removed.
Hair should be dry and clean.
42. Modification Procedures:
Short acting barbiturates are commonly used as induction
agents. E.g: Thiopentone (3-5 mg/kg)
Succinylcholine (0.5-1 mg/kg) is the preferred muscle
relaxant due to its rapid onset, short duration of action,
and rapid recovery.
Patient is allowed to breathe 100% oxygen through face
mask for 3 minutes at 15 -20 breaths per minute
43. Atropine (0.6 mg) given along with intravenous anesthetic
helps in preventing vagal effects of electrical stimulation
on heart
Seizure Monitoring:
1. Cuff method
2. EEG monitoring
44. Cuff method:
Technique
Place the BP cuff (preferably between knee and ankle). If
unilateral ECT is used cuff should be attached to the right
side (ipsilateral) to confirm generalization of seizures.
Just prior to the injection of succinylcholine inflate the
cuff to a pressure 50 - 80 mm Hg above systolic blood
pressure.
45. Observe that fasciculation after succinylcholine injection,
which appear in other parts of the body do not appear in
the isolated limb.
Apply the stimulus and note the time.
At the start of tonic phase of seizure release the cuff.
Record the total duration of tonic and clonic phases till the
last clonic movement
46. EEG monitoring:
Although not mandatory, it has distinct advantages and is
recommended where possible as it is the most direct
measure of cerebral activity available.
The length of the convulsions measured by direct
visualization is approximately 70% that of EEG seizures
48. Motor and EEG ictal responses during ECT
Stage Motor response EEG response
Onset- epileptic recruiting
rhythm
- 10 Hz waves with increasing
amplitude
Tonic phase- polyspikes Tonic muscular
contractions
Bursts of high amplitude
spike discharges lasting 10-
15 seconds
Tonic –clonic phase –
polyspike and slow wave
complexes
Regular myoclonic
contractions
Polyspikes intermixed with
slow waves
Post- ictal cortical extinction Post-ictal sleep Isoelectric or flat EEG
Recovery Gradual regaining of
consciousness
Resumption of delta, then
theta & then alpha activity
49. Determination of Seizure Adequacy
Achievement of an adequate seizure duration has been
assumed to be both necessary and sufficient to ensure
therapeutic adequacy of ECT treatment
20- second motor response and/or
25-second EEG response
50. Other Physiological Monitoring:
Vital signs such as Blood pressure and Pulse should be
recorded before and after ECT.
ECG monitoring is considered mandatory during ECT
procedure.
Pulse oximetry
51. Missed seizure, inadequate and prolonged seizures are
known phenomena during ECT.
These are dependent on the seizure threshold.
The threshold is lower in a) young subjects, b) manic
patients, and c) during the first ECT session.
Conversely, benzodiazepines, carbamazepine and
thiopentone elevate the threshold.
52. Missed seizures:
When electrical stimulation is not followed by any motor
or EEG seizure activity, it is termed a missed seizure.
Wait for 20 seconds before restimulation to allow for
delayed onset of seizures.
Restimulation should occur only after 45 seconds with
higher dosage.
53. Methods of managing missed seizure :
Change of anesthetic agent to Etomidate or Ketamine
Vigorous hyperventilation
Use of EEG monitoring
Change to bilateral ECT, as the seizure threshold is high
with unilateral ECT
Reducing the frequency of sessions
54. Reducing the frequency of sessions (from 3/wk to 2/wk)
can facilitate adequate seizures
Lower change rate by shortening pulse width or increasing
interpulse intervals by decreasing frequency of stimulus
Avoiding / reducing the dosage of Anti-epileptics and
Benzodiazepines.
55. Prolonged seizure:
In most situations, the seizure terminates within 100
seconds.
The American Psychiatric Association task force defines a
prolonged seizure if seizure duration is beyond 180
seconds.
Prolonged seizures can be terminated by intravenous
diazepam 10 mg. or thiopentone 100-200mg
56. Mechanisms of action of ECT
Mechanisms of action of ECT have been studied in five
important domains:
1. Neuroplasticity
2. Contribution of EEG correlates
3. Neurophysiology
4. Neurotransmitters
5. Neuroendocrinology
57. Neuroplasticity:
This happens through remodelling of synapses, generation
of new neurons, proliferation of glial cells, and
improvement in blood supply in specific brain areas.
Animal studies have more robust findings favouring the
role of ECT in promoting neuroplasticity, particularly in
hippocampus, and recently in the prefrontal cortex and
amygdala also
58. Serum levels of BDNF, an important neurotrophin
regulating synaptogenesis and neuronal cell growth, have
been found to be increased following ECT.
One study demonstrated increases in volumes of amygdala
and prefrontal cortex.
59. Contribution of EEG correlates :
Anticonvulsant theory:
Gradual increase in seizure threshold occurs over the
course of successive ECT sessions.
The plasma levels of inhibitory neurotransmitter GABA
has been noted to increase following ECT
Hence, it has been postulated that the clinical
improvements following ECT are not due to seizure per
se, but due to the brain’s efforts to reduce the probability
of occurrence of subsequent seizures
60. Connectivity Resetting :
This is supported by the finding that ECT leads to
frequency specific modification of theta activity and
reduced blood flow in the Subgenual, ACC, Medial frontal
cortex, and increased blood flow to the Thalamus
Thus, it is postulated that ECT rectifies the aberrant
modulatory activity of alpha and theta oscillations by the
thalamus.
61. It stimulates the thalamo-cortical loop, takes over the
thalamic pacemaker function, resets it, and restores the
functional connectivity and control between various brain
areas.
62. Neurophysiology:
The related hypothesis is called “Reducing
Hyperconnectivity”.
ECT produces post-ictal states of diffuse slowing of
EEG with high amplitude delta and theta activity.
This is followed by a period of post-ictal suppression,
which initially lasts for few hours after each ECT
session.
63. This slowing gradually prolongs over many sessions of
ECT into an inter-ictal suppression
PET and SPECT studies have also shown decreased blood
flow and glucose metabolism in the frontal lobe, following
ECT.
Functional MRI studies are few, but they have
corroborated the reduced functional connectivity in frontal
cortex post-ECT.
64. Overall, it can be assumed that ECT reduces the
“hyperconnectivity” secondary to depression in the frontal
cortex, particularly in the VMPFC, DMPFC, and some
parts of ACC.
65. Neurotransmitters :
ECT has been found to affect 5-HT, DA, and adrenergic
system. More pronounced on DA than on 5-HT and
adrenaline.
Increased dopamine release consistently in the striatum,
and inconsistently in the frontal and occipital regions.
It also causes up-regulation of DRD1 and DRD3 receptors
66. There is evidence of inhibition of adrenergic α2 auto
receptors by ECT, resulting in increased secretion of
catecholamines.
ECT increases concentrations of glutamine, (a metabolite
of glutamate) and N-acetyl aspartate, a neuronal marker in
the ACC, PFC, and amygdala. This supports the
neuroplastic hypothesis of ECT.
ECT also increases GABA levels, particularly in ACC,
PFC, and occipital cortex, thus reinforcing the
anticonvulsant hypothesis.
67. Neuroendocrinology:
Neuroendocrine-diencephalic theory of depression
hypothesized that the HPA axis is disturbed producing a
state of hypercortisolemia and abnormal DST
ACTH, cortisol and prolactin levels increased soon after a
session of ECT and came down to normal level within few
hours.
Normalisation of DST has been correlated with clinical
response
68. Major depressive disorder
ECT was found to be 20 to 40% more effective than
medications
Response to ECT in antidepressant non-responders is
around 50 to 70 %
Effectiveness of ECT
69. Comparison of ECT versus antidepressants (MAOI &
TCA) - a significant superior effect of ECT noted
- Gangadhar BN et al (1982), Pagnin D et al
An RCT found ECT to be superior to paroxetine in
medication-resistant major depression, in terms of both
degree and speed of response
- Folkerts HW et al
Equal efficacy in unipolar & bipolar depression –
- Narayanaswamy JC et al
70. ECT is an effective short-term treatment for depression,
and is probably more effective than drug therapy. Bilateral
ECT is moderately more effective than unilateral ECT,
and high dose ECT is more effective than low dose
- UK ECT Review Group.
71. Mania:
Second-line treatment (CANMAT, APA), third-line
(NICE)
Response rates 75-80%; Increased responsiveness in rapid
cyclers & mixed affective states
Controlled retrospective comparisons have found ECT to
be equivalent to lithium, & at least as efficacious as
typical neuroleptics
72. Schizophrenia:
Indicated in treatment-resistant patients and those who
relapse on monotherapy
Combination treatment is more effective than ECT alone,
& more effective than medications alone
Equivalent to pharmacotherapy in management of NMS;
superior in that it treats underlying condition where
neuroleptics cannot be used
73. Response to ECT among a group of adolescents was
around 76%. The main diagnosis was schizophrenia &
MDD
- Grover et al, 2013
Another study on children with a predominant diagnosis
of catatonia showed ECT was efficacious in 77.3%
patients
– Jacob et al, 2014
74. Delirium tremens:
ECT is an effective method of suppressing the symptoms
of delirium associated with alcohol withdrawal
In all cases, one treatment produced a period of sedation
followed by a clearing of the sensorium and termination of
hallucinations within 24 hours.
-William H. C. Dudley, Jr. and J. G. Williams
75. ECT in Special Populations
Elderly population:
ECT is particularly useful in the elderly
Medication intolerance is common
Drug interactions are common
Cognitive side effects are more common
Response to ECT is better in the elderly
Seizure threshold is greater ⇒ It may be difficult to get
adequate seizures
76. Pregnancy:
Use of psychotropics is associated with problems in first
and last trimester
Untreated psychiatric disorders may have adverse effect
on the baby
ECT is effective
Many guidelines on mood disorders advocate use of ECT
as first line treatment for major depression and mania in
first trimester
77. APA Taskforce on ECT: “low risk and high efficacy in
the management of specific disorders in all three
trimesters of pregnancy”
78. Children and adolescents:
ECT should be used with extreme caution (and very rarely
as a first-line treatment) in young people because of the
lack of evidence from randomised controlled trials
Seizure threshold is low
Propensity for prolonged seizures
Two consultants need to independently opinion about the
need for ECT
79. Relapse after ECT
51.1% of patients (depression) relapsed by 12 months
following successful initial treatment with ECT, with the
majority (37.7%) relapsing within the first 6 months
-Ana Jelovac et al
C-ECT and continuation pharmacotherapy may be more
effective than either alone for preventing relapse.
-Nagy A. Youssef et al
80. References:
Gangadhar BN, Sundar AS, Thirthalli J, Varambally S, Muralidharan J,
Kumar CN et al. ECT Administration manual. 2nd ed. Bangalore:
NIMHANS; 2013
Max Fink. Convulsive therapy: a review of the first 55 years. Journal of
Affective Disorders 63 (2001) 1–15
UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in
depressive disorders: a systematic review and meta-analysis. Lancet. 2003
Mar 8;361(9360):799-808
Gangadhar BN, Viswanath B, Keshavan M, Sundar AS. Hnadbook of
Electroconvulsive therapy. Bangalore: NIMHANS; 2015.
81. Ziad Nahas, Jeffrey P. Lorberbaum, Frank A. Kozel, Mark S. George.
Somatic Treatments In Psychiatry. Textbook of Biological Psychiatry.
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Mankad MV, Beyer JL, Weiner RD, Krystal AD. Clinical Manual of
Electroconvulsive Therapy. First Edition. . Washington DC. American
Psychiatric Publishing; 2010
Jelovac A, Kolshus E, McLoughlin DM. Relapse following successful
electroconvulsive therapy for major depression: a meta-analysis.
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Youssef NA, McCall WV. Relapse prevention after index electroconvulsive
therapy in treatment-resistant depression. Ann Clin Psychiatry.
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82. Pagnin D, de Queiroz V, Pini S, Cassano GB. Efficacy of ECT in
depression: a meta-analytic review. J ECT 2004 Mar;20(1):13-20.
Gangadhar BN, Kapur RL, Kalyanasundaram S. Comparison of
electroconvulsive therapy with imipramine in endogenous depression: a
double blind study. Br J Psychiatry 1982 Oct; 141():367-71.
Folkerts HW, Michael N, Tölle R, Schonauer K, Mücke S, Schulze-
Mönking H. Electroconvulsive therapy vs. paroxetine in treatment-resistant
depression -- a randomized study. Acta Psychiatr Scand 1997
Nov;96(5):334-42.
Grover S, Malhotra S, Varma S, Chakrabarti S, Avasthi A, Mattoo SK.
Electroconvulsive therapy in adolescents: A retrospective study from north
India. J ECT 2013;29:122-6.
83. Narayanaswamy JC, Viswanath B, Reddy PV, Kumar KR, Thirthalli J,
Gangadhar BN. Efficacy of ECT in bipolar and unipolar depression in a real
life hospital setting. Asian J Psychiatry 2104;8:43-6.
William H. C. Dudley, J. G. Williams. Electroconvulsive Therapy in
Delirium Tremens. Comprehensive Psychiatry, Vol.13, No.4
(July/August),1972
Jacob P, Gogi PK, Srinath S, Thirthalli J, Girimaji S, Seshadri S, et al.
Review of electroconvulsive therapy practice from a tertiary child and
adolescent psychiatry centre. Asian J Psychiatr 2014;12:95-9.