This document provides an overview of the neuropsychiatric aspects of epilepsy. It defines key terms like seizure and epilepsy and discusses classifications of seizures and epilepsies. It covers the prevalence, etiology, investigations, and various neuropsychiatric aspects of epilepsy like disorders related to seizure occurrence such as preictal, ictal, peri-ictal, and postictal. It also discusses management approaches aimed at adequate seizure control and patient safety.
The association of neuropsychiatric disorders with cerebrovascular disease has been recognized by clinicians for over 100 years. Disease of the vascular system contribute greatly to the sum total of psychiatric disability, chiefly in the elderly population, mainly as a result of stroke, cerebrovascular accidents & subarachnoid haemorrhage.
The association of neuropsychiatric disorders with cerebrovascular disease has been recognized by clinicians for over 100 years. Disease of the vascular system contribute greatly to the sum total of psychiatric disability, chiefly in the elderly population, mainly as a result of stroke, cerebrovascular accidents & subarachnoid haemorrhage.
Certainly, let's expand on th
"Exploring the Enigma of Epilepsy: Navigating the Seizure Spectrum. Join us on a compelling visual voyage as we unravel the intricacies of epilepsy, a condition that affects millions worldwide. In this presentation, we embark on a journey through the diverse facets of epilepsy, from its neurological underpinnings to its profound impact on individuals, families, and communities.
This comprehensive presentation will guide you through the seizure spectrum, shedding light on various seizure types, triggers, and diagnosis techniques. We'll also delve into the emotional and social aspects of living with epilepsy, providing insights into the challenges faced and the resilience displayed by those who confront this condition daily.
Furthermore, we'll explore the cutting-edge advancements in epilepsy research and treatment, offering hope for improved quality of life and a better understanding of this complex neurological disorder.
By the end of this visual odyssey, you'll not only gain a deep understanding of epilepsy but also the tools to support and empower those affected by it. Together, we strive for a world where epilepsy is demystified, stigma is erased, and those living with it can lead fulfilling lives.
Certainly, here are some relevant tags for your SlideShare presentation on epilepsy:
1. # Epilepsy
2. # Neurological Disorders
3. # Seizures
4. # Epilepsy Awareness
5. # Epilepsy Education
6. #Medical Research
7. # Epilepsy Support
8. # Seizure Types
9. # Neurology
10. # Epilepsy Treatment
11. # Epilepsy Community
12. # Epilepsy Research
13. # Living With Epilepsy
14. # Epilepsy Awareness Month
15. # Epilepsy Care
16. # Understanding Epilepsy
17. # Epilepsy Advocacy
18. # Epilepsy Resources
19. # Epilepsy Prevention
20. # Epilepsy Presentation
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
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
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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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
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.
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Neuropsychiatric aspects of epilepsy
1. NEUROPSYCHIATRIC
ASPECTS OF EPILEPSY
Presented by : Dr Swati ( junior resident)
Coordinated by :Dr Sneha( senior resident)
Faculty Incharge : Dr Dinesh Kataria( HOD)
2. CONTENTS:
Definitions
Earlier classification
Latest classification of ILAE 2017
Prevalence
Etiology
Investigations
importance of neuropsychiatric aspect of epilepsy
Different Neuropsychiatric aspects of epilepsy
Management
3. Seizure is defined as:
Intermittent, stereotyped disturbance of consciousness,
behaviour , emotion, motor function or sensation
Mechanism-abnormal cortical discharge
Diagnosis depends primarily on clinical judgement (1)
Epileptic seizures are sudden, involuntary behavioral
events associated with excessive or hyper
synchronous electrical discharges in the brain (2)
1.LISHMAN’S 4th EDITION
2.CTP
5. The task force proposed that epilepsy be considered to be a
disease of the brain defined by any of the following
conditions: (1)
(1) At least two unprovoked (or reflex) seizures occurring >24 h
apart
(2) one unprovoked (or reflex) seizure and a probability of
further seizures similar to the general recurrence risk (at least
60%) after two unprovoked seizures, occurring over the next
10 years
(3) diagnosis of an epilepsy syndrome
One seizure does not signify epilepsy (up to 10% of people
worldwide have one seizure during their lifetime) (2)
(1) ILAE official report: a practical clinical definition of epilepsy. Fisher RS, et al. Epilepsia. 2014
(2) Megiddo I, Colson A, Chisholm D, DuaT, NandiA, and Laxminarayan R (2016). Health and economic
benefits of public financing of epilepsy treatment in India:An agent-based simulation model. Epilepsia
Official Journal of the International LeagueAgainst Epilepsy doi: 10.1111/epi.13294
6. CLASSIFICATION OF EPILEPSY
(Commission on Classification and Terminology of the
International League Against Epilepsy 1981, 1989)
Classifying seizures based on
1. Semiology
clinical signs and symptoms )
2. Epileptic syndromes
Its derived from the classification of seizures
7. INTERNATIONAL CLASSIFICATION OF EPILEPTIC SEIZURES
(I) PARTIAL SEIZURES (II)GENERALISED SEIZURES
A Simple partial seizures
B Complex partial seizures
C Partial seizures evolving
to secondarily generalised
seizures
(III) UNCLASSSIFIED
EPILEPTIC SEIZURES
A1 Absence seizures
A2 Atypical absence
seizures
B Myoclonic seizures
C Clonic seizures
DTonic seizures
ETonic–clonic seizures
F Atonic seizures
(Adapted from Commission on Classification andTerminology of the
International LeagueAgainst Epilepsy 1981 with permission.)
8. INTERNATIONAL CLASSIFICATION OF EPILEPSIES AND
EPILEPTIC SYNDROMES
(1) Localisation-related (local, focal, partial) epilepsies
and syndromes
1.1 IDIOPATHIC
Benign childhood epilepsy with centrotemporal spikes
Childhood epilepsy with occipital paroxysms
Primary reading epilepsy
1.2 SYMPTOMATIC
Chronic epilepsia partialis continua of childhood (Kojewnikoff’s
syndrome)
Syndromes characterised by seizures with specific modes of
precipitation
Temporal lobe epilepsy
Frontal lobe epilepsy
Parietal lobe epilepsy
Occipital lobe epilepsy
1.3 CRYPTOGENIC
9. (2)Generalised epilepsies and syndromes
2.1 Idiopathic (with age-related onset)
• Benign neonatal familial convulsions*
• Benign neonatal convulsions*
• Benign myoclonic epilepsy in infancy*
• Juvenile absence epilepsy (pyknoepilepsy)
• Childhood absence epilepsy
• Juvenile myoclonic epilepsy (impulsive petit mal)
• Epilepsy with grand mal seizures on awakening
• Other generalised idiopathic epilepsies
• Epilepsies with seizures precipitated by specific modes of activation
2.2 Cryptogenic or symptomatic
West syndrome
Lennox–Gastaut syndrome
Epilepsy with myoclonic–astatic seizures
Epilepsy with myoclonic absences
10. 2.3 Symptomatic
• 2.3.1 Non-specific etiology
Early myoclonic encephalopathy*
Early infantile epileptic encephalopathy with suppression-burst*
Other symptomatic generalised epilepsies not defined above
• 2.3.2 Specific syndromes
Epileptic seizures complicating other disease states
3 Epilepsies and syndromes undetermined, whether
focal or generalised
4 Special syndromes
4.1 Situation-related seizures
• Febrile convulsions
• Isolated seizures or isolated status epilepticus
• Seizures occurring only when there is an acute metabolic or toxic event
due to factors such as alcohol, drugs, eclampsia, non-ketotic
hyperglycaemia
12. PREVALENCE OF EPILEPSY
70 million persons with epilepsy (PWE)worldwide
nearly 12 million PWE are expected to reside in
India, contributes nearly 1/6 global burden
overall prevalence (3.0-11.9 per 1,000 population)
incidence (0.2-0.6 per 1,000 population per year)
higher rates in male gender, rural population, and
low socioeconomic status
1.department of Epidemiology, Centre for Public Health, National Institute of Mental Health and
Neurosciences, Bangalore, Karnataka, India.
2.Director/Vice-chancellor and Professor of Neurology, National Institute of Mental Health and
Neurosciences, Bangalore, Karnataka, India.
13. Approximately 50 million people worldwide-one
of the m/c neurological diseases globally
estimated 2.4 million people diagnosed with
epilepsy each year
In high-income countries annual new cases are
between 30 and 50 per 100 000 people in the
general population
In low- and middle-income countries, this figure
can be up to two times higher
http://www.who.int/mediacentre/factsheets/fs999/en/ updated on feb 21017
14. DALYs due to epilepsy in
Southeast Asia (GBD 2010).
SEARO = South-East Asia
Regional Office
15. AETIOLOGY
Globally,TRAUMA- most frequently reported
Central nervous system infections -including abscesses,
encephalitis with all aetiologies, and bacterial meningitis
Antenatal(60.4%,) and perinatal(57.7% )risk factors and
cerebrovascular disorders(55%) -most frequently reported
by responding countries
Idiopathic epilepsy (including the genetic causes) 54.4%
17. Proposed Relationships of Psychiatric
Disturbances to Epilepsy
Common neuropathology, genetics, or developmental
disturbance
1. Ictal or subictal discharges potentiate abnormal behavior
2. Kindling or facilitation of a distributed neuronal matrix
3. Changes in spike frequency or inhibitory–excitatory balance
4. Altered receptor sensitivity, e.g., dopamine receptors
5. Secondary epileptogenesis
Absence of function at the seizure focus
1. Inhibition and hypometabolism surrounding the focus
2. Release or abnormal activity of remaining neurons
3. Dysfunction or downregulation of associated areas
18. Neurochemical
1. Dopamine and other neurotransmitters
2. Endorphins
Gonadotropins and other endocrine hormones
Psychodynamic and psychosocial effects of living with
epilepsy
1. Dependence, learned helplessness, low self-esteem, weak defense
mechanisms
2. Disruption of reality testing
Neurobiological and psychodynamic factors potentiate
each other
Sleep disturbance
Antiepileptic drug related
19. INVESTIGATIONS:
1. Electroencephalography
Obtained interictally when the patient is asymptomatic
Interictal EEG abnormal-support for a diagnosis of epilepsy
interictal EEG- never relied to exclude diagnosis of epilepsy
or indeed to prove it
ictal EEG accompanied by video
recording (video-EEG ) of clinical semiology-gold standard
for diagnosis
Scalp EEG -most widely used confirmatory test, sensitivity
ranges from 29 to 55 percent
20. 2. Neuroimaging
MRI is the structural imaging method of choice in epilepsy
CT- lower sensitivity
Used when MRI is contraindicated or in acute settings where
CT allows better access to a medically unstable patient during
scanning
If patient planned for epilepsy surgery -other tests aid in
localizing the seizure focus include invasive EEG, SPECT
scans, and PET scans
3.CARDIOLOGICAL INVESTIGATIONS:
routine ECG and a 24-hour ECG recording -first steps.
21. 3.Blood investigations
Cbc
Liver function test
Kindey function test
Blood sugar
4. SERUM PROLACTIN
rises after tonic–clonic epileptic seizures
peaking 10–20 mins after seizure,returning to
baseline after about 6 hours
less reliable following complex partial seizures
22. Importance of NPA
Bidirectional relationship between psychiatric
disorders and epilepsy (CTP)
Psychiatric disorders are over-represented in
people with chronic intractable epilepsy
Studies estimated that up to 50% of patients with
epilepsy develop psychiatric disorders, the most
common being depression, anxiety and psychotic
disturbances(1)
Important implications in diagnosis and
management of psychiatric disorders
MARSH L, RAOV. Psychiatric complications in patients with epilepsy: a review. Epilepsy Res 2002; 49: 11-33.
LISHMAN’S 4th EDITION
23. 20 to 60 percent prevalence of psychiatric problems
among epilepsy patients (CTP)
Among patients attending epilepsy clinics,
approximately 30% had a prior psychiatric
hospitalization, and 10 to 20% were on at least 1
psychotropic drug
Need to adjust mood-stabilizing and other
psychotropic effects of antiepileptic drugs-seizure
threshold lowering effects
Need to monitor the potential interaction of
antiepileptic and psychotropic drugs (CTP)
24. Disorders related in time to
seizure occurrence
seizure itself is known as the ictus.
interictal - period between the postictal
abnormalities and the next ictus
peri-ictal - period just before or after the ictus
applied when there is insufficient
information to know when the ictus ends or
begins.
25. Subjective symptoms
begin at least 30 minutes before seizure onset,
last 10 minutes to 3 days (CTP)
Different from aura- with gradual onset and
prolonged duration
Reported in 7–20% of patients
Ill-defined feelings of malaise with headache,
tiredness, and dysphoria
Prodromal mood changes-irritability, lability,
depression, anxiety or aggression and are
relieved by the seizure
PREICTAL DISORDERS:
26. ICTAL DISORDERS:
Mood and behavioural changes - occur as direct
manifestation of the seizures, including anxiety,
depression, hallucinations
episodes - brief (<1-3 minutes)
stereotyped, begin and end abruptly
associated with other ictal phenomena (oral,
motor automatisms)
usually occur with partial seizures ,can also occur
in generalised seizures
27. Epileptic Aura
brief, paroxysmal and highly stereotyped
They are not psychiatric disorders –importance
occasionally be mistaken for the paroxysmal
symptoms of functional psychiatric illness
Hallucinations and odd abberrations of thought, such
as forced thinking or crowding of thoughts, may raise
the possibility of psychosis
Epileptic automatisms
Behavioural concomitants of ictal or postictal delirium
Brief, lasting few sec to several mins
EG: Oro-alimentary lip-smacking, lip-pursing,
chewing, licking, tooth grinding or swallowing
Mimetic -facial expression suggesting an emotional
state, often fear
28. ICTAL ANXIETY:
Very Common
up to 1/3 patients with partial seizures reports
fear as part of their aura
Confused with panic attacks
Eg. Right temporal foci
ICTAL DEPRESSION:
less frequently than ictal anxiety
symptoms are guilt,hopelessness, worthlessness,
and suicidal ideation
29. ICTAL PSYCHOTIC SYMPTOMS:
manifest as visual, gustatory or auditory
hallucinations
usually not well defined
mainly associated with partial seizures
ICTAL AGGRESSION:
very rare
mostly involves undirected or unintentional
violence
30. TREATMENT:
aimed at adequate seizure control
maintaining the patient’s safety is the
primary concern
Educating their families about the psychiatric
manifestations is also important
31. POSTICTAL DISORDERS:
more likely to occur following clusters of
seizures ,generalised seizures or status
epilepticus
DELIRIUM
epileptic seizures begin abruptly, recovery of
normal function is usually gradual
In a complex partial seizure-transition occer
over minutes.
32. Prolonged recovery - in temporal lobe
seizures
abrupt recovery - frontal lobe seizures
Consciousness-profoundly impaired in GTCS
and recovery more protracted
in the elderly and/or patients with learning
difficulties- prolonged recovery
Aggressive behavior-usually undirected or
resistive
patient is likely to be amnesic for the event
diffuse EEG slowing without ictal discharges
33. POST ICTAL PSYCHOSIS:
Brief self-limiting episodes of psychosis that
are of abrupt onset and follow seizures
M/c psychotic disorder seen in epilepsy
Prevelance-6-10% (common inTLE)
Epilepsy present for over 10yrs before 1ST
episode
Precipitating event - exacerbation of seizures
(cluster of complex partial seizures or a
secondarily generalised seizure)
followed by a lucid interval (12-72 hours)
34. Sudden onset of psychotic symptoms
marked agitation and behavioural
disturbance
pleomorphic - mixed picture
paranoid, grandiose and religious delusions
auditory, visual and somatic hallucinations
prominent variable affective changes
Duration:16 hours to 18 days (mean 3.5 days)
35. PSYCHOSIS CHARACTERISTICS
Atypical paranoid psychosis–paranoia with sudden
onset
Psychosis alternating with seizures
Preserved affective warmth
Failure of personality deterioration
Less social withdrawal than schizophrenia
Less systematized delusions than schizophrenia
More hallucinations and affective symptoms than
schizophrenia
More religiosity than schizophrenia
More positive, as opposed to negative, symptoms
Few schneiderian first-rank symptoms
36. Logsdail andToone’s Diagnostic Criteria for
Postictal Psychosis
1. Episode of psychosis (often with confusion and
delirium),developing within 1 week of a seizure or
cluster of seizures
2. Psychosis lasting at least 15 hours and less than 2
months
3. Mental state characterized by delirium or delusions
(e.g.paranoid, non paranoid, delusional,
misidentifications) or hallucinations (e.g., auditory,
visual, somatosensory, olfactory) in clear
consciousness
37. 4. No evidence of:
a) a history of treatment with antipsychotic
medications
or psychosis within the past 3 months,
b) antiepileptic drug toxicity,
c) an EEG demonstrating non convulsive status,
d) a recent history of head trauma or
alcohol/drug intoxication or withdrawal (other
than benzodiazepines used for epilepsy)
38. Treatment of acute post-ictal psychosis
self-limiting
treatment with antipsychotic-not indicated
short courses of benzodiazepines
main focus of treatment -improved seizure
control.
14% and 20% of patients develop chronic
interictal psychoses, after several years and
recurrent episodes
39. POST-ICTAL MOOD DISTURBANCES:
include depression, anxiety or mania
Post-ictal depression - last longer (up to two
weeks) than other post-ictal states
Symptoms range-mild to severe
may involve suicidal behaviour (Common in
right sided temporal or frontal foci)
Post-ictal anxiety symptoms are less common
post-ictal mania - overactivity, irritability, and
disorganised or disinhibited behaviour ,brief in
duration.
40. INTERICTAL DISORDERS
Depressive disorder is the most prevalent
neuropsychiatric disorder in epilepsy
1.DEPRESSION
The prevalence of major depression in such settings
has been estimated as 17–21%
majority - having medically refractoryTLE
clinical picture-of chronic dysthymia,interrupted at
frequent intervals with brief periods of normal mood
Affective symptoms -pleomorphic, with prominent
irritability and endogenous somatic symptoms.
41. Can manifest as:
MDD, dysthymic disorder,adjustment disorder,
and depressive episode of bipolar disorder
Most patients have dysthymia- chronic interictal
depression (interictal dysphoric disorder of
epilepsy)
increased seizure control or a decrease in seizures
before the onset of interictal depressive
symptoms
Patients with this “alternating depression”
experience relief with a seizure or ECT
42. clinical features of major depression
persistent low mood, anhedonia,loss of interest
and biological symptoms of sleep or appetite
disturbance
can present with atypical depressive
symptoms-inter-ictal dysphoric disorder.
characterised by chronic intermittent
dysthymia, irritability and anxiety symptoms
good therapeutic response to antidepressant
medications
Suicide-risk higher than general population.
43. INTER-ICTAL ANXIETY DISORDERS:
incidence greater than in the general
population
Panic disorder, generalised anxiety,
agoraphobia, social phobia and obsessive
compulsive disorder (rare) can occur
common in patients with temporal lobe
epilepsy, especially left-sided foci
44. INTER-ICTAL BIPOLAR DISORDER
prevalence low (<5%)
characterised by periods of depressed mood
and episodes of mania.
preponderance of patients with complex
partial epilepsy, particularly with right-sided
foci.
45. INTER-ICTAL PSYCHOSIS
Prevalence- 4-10% in patients with epilepsy
Mainly in temporal lobe epilepsy
chronic disorder and clinically resembles chronic
schizophrenia
symptoms of delusions, hallucinations, thought
disorder
personality is preserved
risk factors-epilepsy (more than ten years),early
age of onset of epilepsy, bilateral temporal foci
spontaneous resolution - not common
46. Psychotic episodes are of relatively long duration-
vary greatly from days to years
Usually last longer than 1 month
No known direct relationship to seizure events or
ictal discharge
Worsening psychotic symptoms-with increase in
seizure frequency or with antiepileptic drug
withdrawal
Few others have worsening psychotic symptoms
on control of the seizures (alternating psychosis)
47. Proposed Predisposing Factors for the
Interictal Psychosis of Epilepsy:
EPILEPSY CHARACTERISTICS
Focal dyscognitive seizures with secondary generalized
tonic-clonic seizures
More auras and automatisms than nonpsychotic epilepsy
patients
Epilepsy present for 11 to 15 years before psychosis
Long interval of poorly controlled seizures
Recently diminished seizure frequency, especially
generalized tonic–clonic seizures
Left temporal focus
Mediobasal temporal lesions, especially tumors
48. PSYCHOSIS CHARACTERISTICS
Atypical paranoid psychosis–paranoia with sudden
onset
Psychosis alternating with seizures
Preserved affective warmth
Failure of personality deterioration
Less social withdrawal than schizophrenia
Less systematized delusions than schizophrenia
More hallucinations and affective symptoms than
schizophrenia
More religiosity than schizophrenia
More positive, as opposed to negative, symptoms
Few schneiderian first-rank symptoms
49. Risk factors-
early age of onset of seizures
A decade or more of poorly controlled partial
complex seizures with secondary generalized
tonic–clonic seizures
history of status
A family history of psychosis
Seizure control with drugs or removal of
seizure focus does not prevent its development
50. Treatment:
require treatment with neuroleptic drugs
Drugs with low risk of seizure exacerbation
include sulpiride, haloperidol,risperidone and
trifluoperazine.
Amisulpiride, olanzapine and quetiapine - a
higher risk
Depot neuroleptics –avoided
A ‘start low, go slow’ approach is again sensible
treatment of refractory psychosis poses a difficult
problem – clozapine can be started
51. PERSONALITY DISORDERS
High prevalence
Including borderline, atypical or mixed, histrionic, and
dependent disorders.
Patients tend to show dependent and avoidant
personality traits.
Most common-borderline personality
Pt’s frequently lack stable character,can be immature
and impulsive
Psychosocial difficulties,with associated mental
retardation, leads to dependency, low self-esteem,
overall borderline personality traits
52. SEXUALITY:
Men and women experience disturbances of
sexual arousal and a lower sexual drive
loss of erotic fantasies or dreams experience
impotence or frigidity
comorbid depression and anxiety may affect
sexual behavior
2-3 fold increased risk of erectile dysfunction
53. possibility of a subclinical hypongonadotropic
hypongonadism
antiepileptic medication- may cause erectile
dysfunction, decreased sexual desire, retrograde
ejaculation, and altered semen quality
Hormone replacement therapy may normalize
sexual drive and sexual performance
54. DISSOCIATIVE SEIZURES
In ICD-10, the term ‘dissociative convulsions’ refer to-
paroxysmal episodes of behaviour that resemble
epileptic seizures
due to unconscious psychological processes
functional neurological symptoms disorder in DSM-5
may imitate any form of epilepsy
convulsions are often not present
wilful, conscious attempt to simulate illness for
reasons that are understandable in terms of the
individual’s psychological state
55. Factitious disorder is in turn differentiated from
malingering-simulated to achieve some practical
gain
Video EEG monitoring is the gold standard
diagnosis of nonepileptic seizures does not rule
out epileptic seizures
Approximately 10 to 15% of nonepileptic seizure
patients have trueseizure disorder
56. Cognitive function in epilepsy
most people function within normal range of
cognitive ability
comparisons with appropriate control groups
demonstrate deficits
Potential causes are: possible cumulative effects
of neuronal damage due to repeated seizures,
brain injury-secondary to trauma
status epilepticus
effects of drug treatment-Adverse cognitive
effects are likely in patients taking two or more
antiepileptic drugs
57. Psychotropic medication in epilepsy
Most psychotropic drugs have the potential to
exacerbate seizures
the incidence of seizures with antidepressants and
antipsychotics is very low, well below 1%
Clozapine associated with a significant risk of seizures
seizures may be expected in 2–3% of patients with
doses 300–600 mg daily
Two studies have described improvement in seizure
control, one with fluoxetine and one with citalopram
Lithium -proconvulsant in overdose
probably not associated with any change in seizure
control at therapeutic doses.
58. Overdose & intoxication of TCA and tetracyclic anti
depressants ,SSRI, and SNRI- potential causes of seizure
High potential:
Antipsychotic Antidepressant
Chlorpromazine Bupropion
Clozapine Imipramine
Thioridazine Maprotiline
Perphenazine Amitriptyline
Olanzapine Amoxapine
Quetiapine Nortriptyline
SSRI and SNRI can be given as first-line antidepressants- due to
better tolerability profile
TCA andTeCA require higher dose for achieving their
antidepressant property-considered when patients failed to
respond with the first-line agents
59. TREATMENT-RELATED PSYCHIATRIC PROBLEMS
Antiepileptic drugs - can cause psychiatric problems,
most commonly-depression, anxiety, behavioural or cognitive
problems and psychosis(rare)
Improved seizure control - associated with the emergence of
psychiatric symptoms
forced normalisation- dramatic reduction in epileptiform
activity on EEG being associated with the emergence of
psychosis or sometimes behavioural /mood disturbances
Its common with most AEDs and therefore any new drug should
be started at low doses and increased slowly
.
61. Carbamazepine and valproate- antimanic and antidepressant
properties
Carbamazepine and valproate -dyscontrolled, aggressive
behavior in brain-injured patients
Lamotrigine -only antiepileptic well-established efficacy
preventing recurrence of depressive episode in bipolar
disorder
Clonazepam- anxiolytic properties, antimanic therapies
Gabapentin and pregabalin decrease anxiety,improve
general well-being in some epilepsy patients
62. EPILEPSY SURGERY:
Transient mood disturbances
(emotional lability, depression and anxiety)
reported following temporal lobe surgery
about 25% in the first 6-12 weeks
some patients (10%)-depression may persist
inter-ictal psychosis arising after surgery
Psychiatric disorders in epilepsy JACQUELINE FOONG
(Department of Neuropsychiatry, National Hospital for Neurology and Neurosurgery, QueenSquare, London)
63. PSYCHOLOGICAL TREATMENT OF EPILEPSY
Psychological approaches to seizure control are
helpful
stress is an aggravating factor
helping people deal with stress-reduction in
seizures
Cognitive–behaviour therapy target -anxiety and
coping skills
specific interventions -variety of cognitive and
relaxation techniques
patients can engage when they experience an aura
or prodromal symptoms