Neuropsychiatric aspects of Epilepsy

1. Presenter: Kaushik Nandi
Chairperson: Prof. Th. Bihari Singh

2. OVERVIEW:
 History
 Definitions
 Classification Of Epilepsy
 Epidemiology
 Psychiatric Disorders In Epilepsy
 localisation- related epilepsy
 Suicide In Epilepsy
 Personality Changes In Epilepsy
 Functional Non-epileptic Attacks
 Aggression In Epilepsy
 Epilepsy And Sexual Dysfunction
 Cognitive Function In Epilepsy
 Treatment Of Epilepsy

3. HISTORY:
 The oldest detailed account of epilepsy is on a
Babylonian tablet dating as far back as at least
2000 BC. It emphasizes the supernatural nature of
epilepsy, with each seizure type associated with
the name of a spirit or god - usually evil.
 Greek concept (5th century BC) describes it as
"The Sacred Disease"

4. HISTORY:
 The word "epilepsy" is derived from the Greek
"epilepsia" which means "to take hold of" or "to
seize.”
 Hippocrates viewed epilepsy as a brain disorder,
but his view did not begin to take root until the
18th and 19th centuries.

5. HISTORY:
 People with epilepsy were viewed with fear,
suspicion and misunderstanding, and were
subjected to enormous social stigma. They were
treated as outcasts and punished.
 However, some of them succeeded and, in fact,
became famous the world over. Among them were
Julius Caesar, Czar Peter the Great of Russia, Pope
Pius IX, the poet Lord Byron and others.

6. HISTORY:
 The foundation of our modern understanding was
laid in the 19th century with the proposal by
Hughlings Jackson (1873), a London neurologist,
that seizures were the result of sudden brief
electro-chemical discharges of energy in the brain
- the character of the seizures depending on the
location and function of the seat of the discharges.
 In 1920s, Hans Berger, a psychiatrist, developed
the human electroencephalograph (EEG )

7. HISTORY:
 Emil Kraepelin emphasized that epileptic patients
possessed personality changes & a predisposition
to psychosis
 Psychiatric disorders were thought to result from
psychosocial difficulties in epilepsy
 Defining temporal lobe epilepsy opened up
research into disturbances in limbic or emotional
brain

8. DEFINITIONS:
 Seizure is "a transient occurrence of signs and/or
symptoms due to an abnormal, excessive or
synchronous neuronal activity in the brain"
 However, a(single) seizure can occur in an
otherwise healthy individual. Such individuals are
generally not considered to have epilepsy.
 Epilepsy is a neurological condition characterised
by a tendency to unprovoked and recurrent
seizures

9. DEFINITIONS:
 Epileptogenesis: Epileptogenesis is the process
by which the previously normal brain is
functionally altered and biased towards the
generation of the abnormal electrical activity that
subserves chronic seizures.
 The concept of a ‘mechanism of epilepsy’ refers to
any biological feature of the brain that drives or
supports recurrent, unprovoked seizures.

10.  Examples of these biological features include
molecular, anatomical or circuit level alterations,
such as cell death or dysregulation of an ion
channel or neurotransmitter receptor.

11. DEFINITIONS:
 Aura: Simple partial seizures, which may or may
not progress into another seizure type.
 They are often mistakenly considered as a
prodrome for a seizure.
 Fit: The physical manifestation of a seizure.

12. DEFINITIONS:
 Prodrome: A pre-ictal phenomenon characterised
by subjective or objective awareness of a clinical
change that heralds the onset of a seizure, but that
does not form part of it.

13. CLASSIFICATION OF EPILEPSY
Generalised seizures (bilaterally symmetrical
and without local onset)
 Tonic, clonic or tonic–clonic ( grand mal)
 Absence ( petit mal):
 with loss of consciousness only
 complex – with brief tonic, clonic or automatic
movements

14. CLASSIFICATION OF EPILEPSY
Generalised seizures contd…
 Lennox–Gastaut syndrome
 Juvenile myoclonic epilepsy
 Infantile spasms (West syndrome)
 Atonic (astatic, akinetic) seizures (sometimes with
myoclonic jerks)

15. CLASSIFICATION OF EPILEPSY
Partial or focal seizures (seizures that begin
locally)
 Simple (without loss of consciousness or alteration
in psychic function):
 motor
 somatosensory
 autonomic
 pure psychic
 Complex (with impaired consciousness)

16. CLASSIFICATION OF EPILEPSY
Special epileptic syndromes
 Myoclonus and myoclonic seizures
 Reflex epilepsy
 Acquired aphasia with convulsive disorder
(Landau Kleffner Syndrome)
 Febrile and other seizures of infancy and
childhood
 Functional non-epileptic attacks

17. CLASSIFICATION OF SEIZURES
 The International League Against Epilepsy
(ILAE) 2017 describes seizures according to these
criteria
i. where seizures begin
ii. awareness in focal seizures
iii. motor and other symptoms in focal seizures

18. Classification of seizures
FOCAL ONSET UNKNOWN
ONSET
GENERALISED
ONSET
Aware /
Impaired
awareness
o Motor
o Non-motor
onset
o Focal to B/L
tonic-clonic
o Motor onset
o Non-motor
onset
(absence)
o Motor onset
o Non-motor
onset
o Unclassified

20. EPIDEMIOLOGY:
 Seizure disorders are common and usually have an
early onset.
 Epilepsy affects 20 to 40 million people worldwide
and has a prevalence of at least 0.63 percent and an
annual incidence of approximately 0.05 percent.
 The overall incidence is high in the first year, drops
to a minimum in the third and fourth decades of
life, then increases again in later life.

21. EPIDEMIOLOGY:
 More than 75 percent of patients have their first
seizure before 18 years of age, and 12 to 20 percent
have a familial incidence of seizures.
 Among adults, the most common seizures are
complex partial and generalized tonic-clonic
seizures.

22. EPIDEMIOLOGY:
 It is estimated that there are more than 10 million
persons with epilepsy in India.
 Its prevalence is about 1% in our population.
 The prevalence is higher in the rural (1.9%)
compared to urban population (0.6%)
 NMHS (2015-2016): Prevalence of epilepsy (GTCS
only) is 0.3%

23. EPIDEMIOLOGY:
 Psychiatric comorbidity occurs in 20-40% of
people with epilepsy.
 More psychopathology in people with epilepsy
than in other chronic neurological conditions.

24. Psychopathology in epilepsy
 Epilepsy patients are prone to psychosis,
depression, personality disorders, hypo-sexuality,
& other behavioural disorders
 Psychiatric disturbances are common in patients
with complex partial seizures than GTCS

25. Risk factors for psychopathology in epilepsy
CLINICAL
FACTORS
o Age at onset
o Duration
o Type &
frequency of
seizure
o Site of brain
affected
o Inter-ictal &
ictal EEG
abnormalities
PSYCHOSOCIAL
FACTORS
o Chronicity
o Low
socioeconomic
status
o Low education
o Stigma
o Legal
limitations
o Learned
helplessness
o Overprotection
by family
BIOLOGICAL
FACTORS
o Damage to brain
areas of psychic
functioning
o Kindling effect
o Secondary
epileptogenesis
o Altered receptor
sensitivity
o Antiepileptic drug
side effects

26. Psychiatric disorders in Epilepsy
Disorders clearly attributable to brain
disorder causing epilepsy
 Learning disability
 Specific epileptic syndromes
i. West syndrome
ii. Lennox - Gastaut syndrome
iii. Progressive myoclonic epilepsies
iv. Epilepsy with continuous spike-and-wave during
slow-wave sleep
 Cognitive & behavioural manifestations of other
acquired causes of epilepsy

27. Disorders strictly related in time to seizure
occurrence
PRE -
ICTAL
ICTAL POST-ICTAL INTER-ICTAL
Prodrome i. Aura
ii. Automatisms
iii. Non-
convulsive
status
epilepticus
i. Delirium
ii. Psychosis
i. Affective disorder
ii. Schizophrenia-like
psychosis
iii. Personality disorder
iv. Dementia
v. Dissociative seizures

28. PRE-ICTAL DISORDERS
PRODROME
 Subjective symptoms occurring in the hours or
even days leading up to a seizure seen in 7-20%
patients
 Gradual onset; prolonged duration; affective
symptoms
 Ill-defined, non-specific feelings – malaise,
headache, tiredness, irritability, dysphoria

29. ICTAL DISORDERS
EPILEPTIC AURA
 In simple partial seizure, ictal psychiatric
phenomena may be the only manifestation of
seizure
 In complex partial seizures aura precedes
clouding of consciousness & loss of awareness

30.  Ictal aura is brief, paroxysmal & highly
stereotyped
 Hallucinations, forced thinking or crowding of
thoughts can mimic psychosis
 Ictal anxiety can mimic panic disorder
 Clouding of consciousness with amnesia for the
episode can be present

31. EPILEPTIC AUTOMATISMS
 More or less coordinated, repetitive motor
activity usually occurring when cognition is
impaired & for which subject is usually amnesic
afterwards
 Automatic fumbling behaviour, such as lip-
smacking, hand-rubbing, picking at objects,
walking in circles, repeating meaningless
phrases, or undressing may be seen

32. Terms describing automatisms
 Oro-alimentary: Lip-smacking, lip-pursing,
chewing, licking, tooth grinding or swallowing
 Mimetic: Facial expression suggesting an
emotional state, often fear
 Manual or pedal: Indicates principally distal
components, bilateral or unilateral Fumbling,
tapping, manipulating movements

33. Terms describing automatisms
 Gestural (often unilateral): Fumbling or
exploratory movements with the hand, directed
toward self or environment.
 Hyperkinetic: Involves predominantly proximal
limb and axial muscles. Increase in rate of ongoing
movements or inappropriately rapid performance
of a movement.
 Hypokinetic: Decrease in amplitude and/or rate
or arrest of ongoing motor activity

34. Terms describing automatisms
 Dysphasic: Impairment of language without
dysfunction of relevant primary motor or sensory
pathways, manifested as impaired comprehension,
anomia, paraphasic errors or a combination of
these.
 Gelastic: Bursts of laughter or giggling, usually
without an appropriate affective tone
 Dyscrastic: Bursts of crying

35. Terms describing automatisms
 Vocal: Single or repetitive utterances consisting of
sounds such as grunts or shrieks
 Verbal: Single or repetitive utterances consisting
of words, phrases or brief sentences
 Spontaneous: Stereotyped, involve only self,
virtually independent of environmental influences
 Interactive: Not stereotyped, involve more than
self, environmentally influenced

36. NON-CONVULSIVE STATUS EPILEPTICUS
 Prolonged electrographic seizure activity results
in non-convulsive seizure symptoms
 Most common forms are complex partial status
& absence status
 Mental state abnormalities & behavioural
disturbance that results may be mistaken as
psychiatric disorder

37. Partial non-convulsive status epilepticus
 Complex partial status is the most common form
of non-convulsive status
 Classical picture is one of fluctuating delirium
with motor automatisms
 Psychomotor agitation or retardation, affective
disturbances, hallucinations, paranoid ideation,
or catatonic picture may be seen

38.  Simple partial status commonly involves focal
motor seizures
 Subjective experiential phenomena in absence of
impaired consciousness (aura continua) are the
most likely to be confused with psychiatric
disorder
 Absence status: prolonged state of impaired
consciousness associated with continuous 3-Hz
spike-wave EEG abnormality

39. POST – ICTAL DISORDERS
DELIRIUM
 Epileptic seizures begin abruptly but recovery
occurs gradually
 Typically, patients are alert and responsive within
15 minutes
 On occasions, full recovery of consciousness may
take much longer, especially in the elderly or in
patients with learning difficulties

40. POST-ICTAL PSYCHOSIS
 Brief self-limiting episodes of psychosis that are of
abrupt onset and follow seizures
 Accounts for about 25% of epileptic psychoses
 Prevalence is around 6%
 Epilepsy has usually been present for over 10 years
before the first episode

41.  Risk factors for development of post-ictal
psychosis include:
i. bilateral seizure foci
ii. processes associated with bilateral limbic
lesions (e.g. encephalitis, head injury)
iii.relative increase in seizure frequency preceding
the psychotic symptoms

42.  Precipitating event can be an exacerbation of
seizures followed by a lucid interval lasting 2 -
72 hrs (mean-1 day) where patient appears
normal
 Onset of psychotic symptoms is sudden &
dramatic accompanied by marked agitation &
behavioural disturbance
 Affective symptoms with grandiose & religious
delusions & simple auditory hallucinations are
common

43.  Duration of postictal psychosis is generally short
(Mean – 3.5 days) with a range from 16 hours to
18 days
 EEG may show diffuse background slowing or
an increase in inter-ictal epileptiform
abnormalities
 Episodes are self-limiting hence treatment with
antipsychotics is usually not indicated

44.  Severe agitation warrants hospitalisation and
treatment with benzodiazepines or low dose
antipsychotics
 14 - 20% of patients with recurrent postictal
psychosis will develop chronic inter-ictal
psychoses after several years
 There is no prophylactic role for antipsychotics
to prevent chronic psychosis

45.  Psychotic symptoms often worsen with increasing
seizure activity
 Rarely, psychotic symptoms alternate with
seizures & when patients are seizure free they
manifest mainly paranoid psychotic symptoms
 EEG normalizes during a psychotic episode is
called forced or paradoxical normalization
Alternating psychosis or forced
normalization

46. INTER – ICTAL DISORDERS
DEPRESSION
 Depression and anxiety are the most frequently
encountered inter-ictal psychiatric disorders in
epilepsy
 Estimated prevalence is 20-70%

47.  The clinical picture is one of chronic dysthymia
which is interrupted at frequent intervals by
brief periods of normal mood
 Other symptoms include atypical pain, phases
of euphoric/dysphoric affect, anxiety and phobic
symptoms
 Antiepileptic drugs can lower serum folate levels
and manifest with depressive symptoms

48.  Escitalopram & Sertraline are preferred first-
line medications
 MAO inhibitors have lower effect on seizure
threshold and TCA have higher effect
 Antidepressant dose should be increased
slowly in small increments

49. ANXIETY
 The most frequent diagnoses are agoraphobia,
generalised anxiety disorder & social phobia
 Fears (phobic anxiety), often relate to the
perceived risk of personal injury & brain
damage, & having seizures in unfamiliar
situations

50. INTER-ICTAL PSYCHOSIS
 Prevalence is between 3 & 7%
 Psychotic symptoms not temporally related to
seizure activity & mental state characterised by
delusions & hallucinations in clear consciousness
 Bizarre or disorganised behaviour, thought
disorder, personality change, negative symptoms
of schizophrenia or affective changes are not
commonly seen

51.  Mean age of onset is 30; after a mean duration of
epilepsy of 10-15 years
 Risk factors include:
i. early age of onset of seizures
ii. poorly controlled partial complex seizures
(usually with secondary generalization)
iii. Temporal lobe or left sided lesions

52. TEMPORAL LOBE EPILEPSY
 Temporal lobe epilepsy (TLE) is the most common
of the anatomically defined syndromes,
accounting for around 60% of all patients with
localisation-related epilepsy.
 Temporal lobe seizures produce the most varied
and complex auras of all.
 The most frequent cause of TLE is hippocampal
sclerosis, also known as mesial temporal sclerosis

53.  Other causes of TLE include dysembryoplastic
neuroepithelial tumours, cavernous angiomas,
gliomas, cortical dysplasia and gliosis secondary to
encephalitis or meningitis.
 Temporal lobe seizures may take the form of
simple and complex partial seizures, with both
occurring in some 70% of patients.
 A variety of autonomic features and visceral
sensations figure prominently in temporal lobe
auras.

54.  The epigastric aura is the most common, being
reported by up to 50% of patients.
 Other autonomic effects include changes in skin
colour, blood pressure, heart rate, perspiration,
salivation and piloerection. Subjective dizziness is
common.
 Affective experiences are a feature of
approximately 25% of temporal lobe auras. The
most common is anxiety, which is often intense
(ictal fear)

55.  Vocalisation is seen in approximately 50% of
temporal lobe seizures.
 The essential quality of recognition may change,
with strong feelings of familiarity or unfamiliarity
leading to déjà vu and jamais vu.
 Altered perceptual experiences include both
distortions of real perceptions (illusions) and
spontaneous hallucinations.

56.  Hallucinations of taste (gustatory) and smell
(olfactory) derive from medial temporal lobe
structures, particularly the amygdala, and are of
considerable significance for the diagnosis of TLE.
 The most frequent automatisms are oro-
alimentary (lip smacking, chewing, swallowing)
and gestural (fumbling, picking, rubbing
movements)

57. FRONTAL LOBE EPILEPSY
 20–30% of localization-related epilepsy
 Post-traumatic aetiology is common, although
tumours and cortical dysplasia are also frequent.
 Frontal lobe seizures tend to begin and end
abruptly, are brief (usually less than 1 minute),
often frequent, and show a tendency to occur at
night and in clusters.

58.  Motor phenomena, which may include complex
posturing and behavioural automatisms, are
usually present.
 Focal motor seizures may occur as a special form of
status epilepticus (Epilepsia partialis continua)
 Speech arrest is a feature of dominant hemisphere
frontal seizures but speech automatisms
accompanying hypermotor seizures arising from
the non-dominant hemisphere may also be
dramatic, with screaming and swearing.

59. PARIETAL LOBE EPILEPSY
 Rare, less than 5% of localisation-related epilepsy
 Tumors are the most common aetiology.
 Somatosensory auras are reported by some 80% of
patients, with elementary paraesthesia by far the
most common feature like tingling, numbness,
prickling, crawling or electrical sensations

60. OCCIPITAL LOBE EPILEPSY
 5–7% of localisation- related epilepsy but is probably
under-recognised.
 Childhood syndrome are frequently misdiagnosed as
migraine and in adults occipital lobe seizures
notoriously mimic other partial seizures because of
rapid propagation to temporal and frontal lobes.
 Elementary visual hallucinations are the
hallmark of occipital seizures but are not seen in all
cases

61.  The hallucinations consist mainly of bright, coloured
spots, circles, balls or blobs. They typically appear in
the contralateral hemifield and move, flash or twinkle.
 Negative phenomena, such as scotoma, ‘black or white
outs’, and ictal amaurosis are less common.
 Complex visual illusions and hallucinations are
associated with temporal lobe seizures but may be
seen with occipito-temporal foci.
 Common causes of occipital lobe epilepsy include
tumours, trauma and developmental malformations.

62. EPILEPSY AND SUICIDE
 Risk of suicide is 2.4 times higher in patients with
epilepsy
 11–12 times higher in those with epilepsy and
anxiety or psychosis
 32 times higher in those with epilepsy and
depression

63.  Death by suicide occurs in 3 to 7 percent of
epilepsy patients
 Higher risk of suicide is associated with early age
at onset of epilepsy, particularly during
adolescence
 Contributors to successful suicides include
paranoid hallucinations, agitated guilt to kill
themselves, & occasional ictal command
hallucinations to commit suicide

64. Personality changes associated
with epilepsy
 Extent of personality disorders in association
with epilepsy is 0.7–2.0% (most commonly
borderline)
 In partial epilepsy (particularly TLE), rates of
personality disorder range from 13 to 35%
 Treatment-refractory epilepsy commonly
associated with dependent & avoidant
personality disorders

65. Organic personality disorder: some people with
epilepsy (complex partial seizures; particularly TLE)
develop behavioural changes like:
 Viscosity – a tendency for prolonged interpersonal
contact, with pedantry & lack of socially
appropriate ending of conversations
 Hyposexuality – decreased libido & impotence

66.  Religiosity – very strong preoccupation with
religion and philosophy
 Hypergraphia – compulsive writing
 Aggression – increased incidence of inter-ictal
violence & hostility
 Combination of these traits is sometimes
referred to as Gastaut–Geschwind syndrome

67. FUNCTIONAL NON-EPILEPTIC ATTACKS
 These are a diverse group of disorders in which
paroxysmal events may be mistaken for epilepsy,
but are not caused by epilepsy
 Origin: physiological (10–20%)
psychogenic (80–90%)

68.  5–20% of patients in epilepsy clinics have only
non-epileptic fits
 About 80% of patients with psychogenic non-
epileptic seizures are women & are aged between
15 - 35 years
 Non-epileptic seizures may occur in people with
epilepsy (about 33%)

69. Common clinical presentation of non-
epileptic fits:
 Panic attack – may resemble an epileptic
seizure and loss of consciousness may occur
 Avoidance attack – typically this occurs when
the individual is unable to cope with a stressful
situation; the person may fall to the floor and
remain inert, with reduced muscle tone

70.  Abreactive attack – occurs as a delayed
response to highly stressful experiences, and
often happens towards the end of the day;
hyperventilation may precede increased body
tone and thrashing of the limbs
 Simulated attack – conscious or unconscious
simulation of an epileptic seizure, usually
involving some kind of gain

71. CAUSES OF FUNCTIONAL NON-EPILEPTIC ATTACKS
Psychogenic causes Physiological causes
 Depersonalisation
disorder
 Hypochondriasis
 Somatisation disorder
 Dissociative disorders
 Conversion disorders
 Panic disorders
 Factitious disorders
 Syncope
 Transient ischaemic
attacks
 Paroxysmal movement
disorders
 Narcolepsy
 Non-epileptic myoclonus

72. Comparative semiology of dissociative and epileptic
seizures
DISSOCIATIVE
SEIZURES
EPILEPTIC
SEIZURES
Duration > 2 min Common Rare
Motor features
• Gradual onset Common Rare
• Fluctuating course Common Very rare
• Eyes closed Common Rare
• Thrashing, violent movements Common Rare
• Side-to-side head movements Common Rare
• Asynchronous clonic movements Common Very rare
• Pelvic thrusting Occasional Rare
• Opisthotonous Occasional Very rare
• Automatisms Rare Common

73. Comparative semiology of dissociative and epileptic
seizures
DISSOCIATIVE
SEIZURES
EPILEPTIC
SEIZURES
Weeping Occasional Very rare
Recall for period of
unresponsiveness
Common Very rare

74. Observational features suggestive of non-
epileptic fits:
 Undulating motor activity
 Convulsion lasting >2 minutes
 Resisted lid opening
 Rapid postictal re-orientation
 Asynchronous limb movements
 Lack of cyanosis
 Retained awareness of surroundings in apparent
generalised fits

75. Common investigations in functional non-
epileptic attacks:
 EEG: single inter-ictal EEG may not be helpful in
diagnosis
 Provocation procedures: commonly used are
hyperventilation, photic stimulation or sleep
deprivation
 Serum prolactin: may not be very helpful due to
low sensitivity & specificity
 Home videos can be a very helpful
 Gold standard is video-EEG telemetry

76. Paroxysmal neurological disorders that
may be mistaken for Epilepsy:
 Transient ischaemic attacks
 Migraine
 Vertigo
 Hyperekplexia
 Paroxysmal movement disorders
 Sleep disorders
 Narcolepsy
 Non-REM disorders
 REM sleep behaviour disorder

77. AGGRESSION IN EPILEPSY
 Most aggression among epilepsy patients is not
related to epileptiform activity
 It is usually associated with psychosis or with
intermittent explosive disorder & correlates with
subnormal intelligence, lower socioeconomic
status, childhood behaviour problems, prior head
injuries, & possible orbital frontal damage

78.  Simple violent automatisms, such as spitting or
flailing the arms, can occur at the onset of
complex partial seizures
 Non-directed violent movements, aimless
destructive behaviour, or angry verbal outbursts
occur during postictal delirium

79. EPILEPSY AND SEXUAL DYSFUNCTION
 Men with epilepsy report less sexual interest. A
history of erectile dysfunction is found in up to
57%
 In women, hyposexuality is common with
abnormalities of arousal and orgasmic dysfunction
 Can be explained by biological factors (low
testosterone), medication related, or psychosocial
factors

80. COGNITIVE FUNCTION IN EPILEPSY
 Cognitive deficits are present at the time epilepsy
is first diagnosed & may even precede the onset of
seizures
 10–20% children with epilepsy have impaired
intellectual development manifest as persistent or
progressive cognitive deficit
 Progressive decline of memory seen in 50 %
patients with uncontrolled TLE

81.  Antiepileptic drugs are an important cause of
cognitive problems & is likely in patients taking
two or more antiepileptic drugs
 Cognitive deficits are possible cumulative effects
of neuronal damage incurred through repeated
seizures, brain injury secondary to trauma or
status epilepticus & psychosocial impact of
disorder

82. TREATMENT OF EPILEPSY
 Anti-epileptic medications
 Epilepsy surgery
 Vagal nerve stimulation

83. Effectiveness of antiepileptic drugs against
different seizure types.
Partial-onset
seizures
Generalised
onset:
tonic–clonic
seizures
Generalised
onset:
absence
seizures
First line Carbamazepine
Lamotrigine
Valproate Ethosuxamide
Alternatives
First generation
Valproate
Phenobarbital
Phenytoin
Benzodiazepines
Carbamazepine
Phenobarbital
Phenytoin
Benzodiazepines
Valproate
Second
generation
Gabapentin
Levetiracetam
Oxcarbazepine
Tiagabine
Topiramate
Zonisamide
Pregabalin
Lamotrigine
Topiramate
Levetiracetam
Lamotrigine

84. Neuropsychiatric aspects of
epilepsy surgery
 Patients with epilepsy who have not responded
to two or more anti-epileptic drugs could be
considered for epilepsy surgery
 Surgery involves removal of epileptogenic focus
 Most common surgery done is anterior temporal
lobectomy. Others are hippocampectomy,
lesionectomy & multiple subpial transection

85.  Seizure-free or near seizure-free rates as high as
80–90% have been achieved using surgery
 About a third of patients can present with
anxiety & depression 6–12 weeks after the surgery
irrespective of surgery outcome
 De novo psychosis is rarely seen post-epilepsy
surgery (0.5–1%)

86. Vagal nerve stimulation
 The procedure involves intermittent electrical
stimulation of the vagus nerve via a stimulator
inserted surgically over the anterior chest wall.
 The mechanism of action is unknown.
 VNS is usually considered for patients who prove
unsuitable for epilepsy surgery.

87.  Overall, a 50% reduction in seizure frequency is
seen in approximately 30% of patients.
 VNS is generally well tolerated: the main side
effects are intermittent hoarseness of the voice and
throat discomfort during stimulation but patients
usually habituate to this.

88. REFERENCES
 David AS, Fleminger S, et al. Lishman’s Organic
Psychiatry. 4th edition. John Wiley & Sons Ltd.
Publication; 2009.
 Sadock BJ, Sadock VA, Ruiz P. Kaplan and
Sadock’s Comprehensive textbook of Psychiatry.
9th edition. Philadelphia: Lippincott Williams
and Wilkins; 2009.
 Epilepsy and neuropsychiatric comorbidities.
Agrawal N, Govender S. Advances in psychiatric
treatment 2011;17:44–53.

89.  Operational Classification of Seizure Types by the
International League Against Epilepsy. Fisher RS,
Cross H et al.
 Epilepsy: Indian perspective. Santhosh NS, Sinha S.
Ann Indian Acad Neurol. 2014 Mar; 17(1): 3-11.
 Mechanisms of epileptogenesis: a convergence on
neural circuit dysfunction. Goldberg EM, Coulter DA.
Nat Rev Neurosci 2013;14(5): 337–49.
 Psychiatric Aspects of Epilepsy. Marcangelo MJ,
Ovsiew F, et al. Psychiatr Clin N Am 2007 :781–802
 Muthy RS. National Mental Health Survey of India
2015-2016. Indian J Psychiatry 2017;59(1):117.

90. THANK YOU