The document discusses neuropsychiatric aspects of epilepsy. It begins with definitions of key terms like seizure, epilepsy, and convulsion. It then provides epidemiological data on epilepsy prevalence and incidence globally. It describes different types of seizures including primary generalized seizures, partial seizures, and epilepsy syndromes. Causes of epilepsy including genetic, acquired, congenital, and withdrawal factors are outlined. Risk factors for developing epilepsy and common seizure triggers are mentioned. The pathophysiology involving glutamate and GABA neurotransmitters is explained. Finally, clinical presentations of different seizure types and differential diagnosis considerations are covered.

1. Neuropsychiatric Aspects of Epilepsy

2. DEFINITIONS
Seizure /ictus/ fits
 From a Latin word which means ‘to take possession of’
 Paroxysmal event due to abnormal excessive, hyper
synchronous discharges from an aggregate of CNS neurons.
Epilepsy
 Clinical phenomenon rather than a single identity.
 Recurrent seizures due to chronic underlying process.

3.  A convulsion is a medical condition where
body muscles contract and relax rapidly and repeatedly,
resulting in an uncontrolled shaking of the body.
Because a convulsion is often a symptom of
an epileptic seizures, the term convulsion is sometimes
used as a synonym for seizure. However, not all epileptic
seizures lead to convulsions, and not all convulsions are
caused by epileptic seizures.

4. Epidemiology of Epilepsy
 Epilepsy knows no geographical, racial or social boundaries.
About 50 million people in World have Epilepsy.
 It occurs in men and women and can begin at any age, but is
most frequently diagnosed in infancy, childhood, adolescence
and old age.
 Prevalence:
Developed countries- 0.5% (0.4% - 1%)
Developing countries- five times higher
 Incidence:
After infancy annual incidence- 20-70/100000 in developed
countries.
Developing countries- Incidence is double. (100/100000)
 The life time risk of having a single seizure:
About 5%.

5. CLASSIFICATION
Primary generalized seizure
 Absence(petit mal)
 Tonic Clonic
 Tonic
 Clonic
 Atonic
 Myoclonic
Partial seizures
 Simple partial
 Complex partial
 Partial with secondary generalization
Unclassified seizures
 Neonatal seizures
 Infantile spasms / West’s syndrome

6. EPILEPSY SYNDROMES AND OTHER SPECIAL FORMS
Epilepsy syndromes are disorders in which epilepsy is a predominant
feature, and there is sufficient evidence (e.g., through clinical, EEG,
radiologic, or genetic observations) to suggest a common underlying
mechanism.
Epilepsy syndromes
 Juvenile Myoclonic epilepsy
 Lennox Gastaut syndrome
 Mesial Temporal Lobe epilepsy
 Infantile spasms / West’s syndrome
 Landau-Kleffner syndrome (infantile acquired aphasia)
Other special forms
 catamenial epilepsy
 Reflex epilepsy eg : eating epilepsy , hot water epilepsy
 Gelastic epilepsy
 Diencephalic or autonomic

7. Etiology

8. What Causes Epilepsy?
 In about 70% of people with epilepsy, the cause is not known
 In 30%, most common causes are:
 Inherited genetic
 Acquired : Trauma, Neuro surgery,
Inflammatory, Metabolic,
Infections, Tumor, Toxic disorders, drugs,
 Congenital: inborn error of metabolism.
Withdrawal of drugs
Alcohol, Benzodiazepine,
Barbiturates, Other Anti-Epileptics

9. Psychiatric drugs
 ANTI DEPRESSANTS
 highest risk of seizures(0.5%)
– clomipramine 0.5%(tertiary amine
TCA )
– bupropion (0.4%, up to 2.2% with
doses higher than 450 mg per day)
– maprotiline (0.4%) (tetracyclic)
– Other TCAs: imipramine
 Intermediate in risk
– SSRI :- fluoxetine, sertraline,
fluvoxamine, citalopram, and
paroxetine
– NSRI :- venlafaxine,.
 Least risk
– monoamine oxidase inhibitors
(MAOIs)
 http://www.epilepsy.com/information/professionals/diagno
sis-treatment/drugs-their-contribution-
seizures/antidepressants
 Anti psychotics
– Highest risk:-
 clozapine
 loxapine
 chlorpromazine
– Intermediate ( less than 1.0–1.2%)
 fluphenazine
 thioridazine
 perphenazine
 Trifluoperazine
– Least seizure-induction
 haloperidol
 molindone
 pimozide
 The antipsychotics of choice on the basis
both of epileptogenesis and of the side effect
profiles are atypical agents:
 Risperidone, olanzapine, quetiapine
 http://www.epilepsy.com/information/professionals/diagnosis-treatment/psychotropic-
drugs-developmental-disabilities/comorb-3

10. Seizure Triggers
 Missed medication (#1 reason)
 Stress, anxiety
 Hormonal changes, Menses
 Dehydration
 Lack of sleep, extreme fatigue
 Photosensitivity
 Illicit Drug, alcohol use
 Certain Medications
 Fever in Some Children

11. Groups at Increased Risk for Epilepsy
 About 1% of the general population develops epilepsy
 The risk is higher in people with certain medical conditions:
 Mental retardation
 Cerebral palsy
 Alzheimer’s disease
 Stroke
 Autism

12. Pathophysiology

13. Glutamate and GABA (gamma-aminobutyric acid): the brain's
major "workhorse" neurotransmitters that regulate action potential
traffic.
GABA is an inhibitory neurotransmitter
which stops action potentials.
Glutamate, an excitatory neurotransmitter,
starts action potentials or keeps them going.
Both work together to control many processes,
including the brain's overall level of excitation.
What is going on inside the skull?

14. GABA
Glutamate
So then, what is a SEIZURE?
An unpredictable, uncontrolled,
abnormal and excessive
paroxysmal synchronization
imbalance of the excitatory
and inhibitory forces within
the CNS network of cortical
neurons in the cerebral
cortex.

15. Pathophysiology of Epilepsy contd
Repeated sub-threshhold of a neuron
generates an action potentials 
seizures
It has been suggested that chronic
epileptic discharges may lead to
secondary epileptogenesis.

16. Clinical presentations

17. Partial Seizures
Simple Partial Seizures:
 Consciousness is fully preserved
 Motor symptoms Involves motor strip, Manifested by
abnormal movement of an extremity,
– Jacksonian motor seizure: progression to adjacent muscle groups
– Todds palsy: transient paralysis
– Adversive seizure: Forced deviation of the eyes and turning head
to the opposite side.
 Somatosensory symptoms Involves sensory strip,
temporal(hearing and smell) or occipital(visual) lobe
 Autonomic symptoms involves temporal lobe
(tachycardia, pallor, flushing, sweating, Piloerection.

19. Simple Partial Seizures (continued)
  Psychic manifestation:
– Dysphasic- when cortical speech area affected (left preisylvian),
– Dysmnestic- disturbance of memory (mesobasal temporal right),
– Cognitive symptoms- dreamy state (mesobasal temporal and
temporal neocortex),
– Affective symptoms- fear, depression, anger, irritability, elation,
erotic thoughts (mesobasal temporal and temporal neocortex),
– Illusion of size, structured hallucination (mesobasal temporal and
temporal neocortex).

20. Copmplex Partial seizures
 Complex partial seizures (= psychomotor seizures)
Initial subjective feeling (aura), loss of consciousness, abnormal behavior
(perioral and hand automatisms)
Majority originate in Temporal lobe (60%); but also originate another lobe –
particularly Frontal(30%).

21. Complex Partial Seizures
Discriminating features
Consciousness is altered
Stereotyped
Focal spikes in interictal EEG
Consistent Features
Approximately 60-180 second duration
Paroxysmal
Post-ictal confusion
Variable Features
Presence of aura
Automatisms
May secondarily generalize to a tonic-clonic seizure
Associated with focal structural lesion
May elevate prolactin level
 May be confused with:
Drunkenness or drug use,
willful belligerence, aggressiveness

22. Partial seizures and 20 GTCS
 Partial seizures evolving to tonic/clonic convulsions –
secondary generalised tonic/clonic seizures (sGTCS)

23. Generalized seizures
(convulsive or non-convulsive)
 Gtcs
 Absences
 Myoclonic seizures
 Clonic seizures
 Tonic seizures
 Atonic seizures

24. Generalized tonic-clonic seizures
Discriminating features
Initial tonic phase followed by clonic activity involving all
extremities
Consistent Features
Loss of consciousness
Typically 60 second duration
Post-ictal period associated with confusion and drowsiness
Variable Features
Tongue biting or injury
Urinary incontinence
Nonspecific prodrome
post-ictal paralysis

25. Absense seizures
 Discriminating features
 Very brief duration (5-15 seconds) and 100 – 200 time/day mat
 Family H/O of typical absence seizures
 Response to ethosuximide and valproate
 Consistent Features
 EEG-3 cycles/ sec of generalized spike and wave(typical)
 No aura
 Impaired consciousness
 No post-ictal state
 Variable Features
 Automatisms
 Change in body tone
 Precipitation by hyper ventilation
Atypical absenceseizures
 Longer duration of loss of consciousness,
 Less abrupt onset and cessation
 More obvious focal signs
 Less responsive to drugs

26. Reflex epilepsy
 Hot water epilepsy : person gets a seizure whenever he/she pours hot
water on the head. Initially it is reported more from South India
especially from Bangalore.
 Eating epilepsy: Seizures are usually precipitated while a person starts
eating food. The masticatory and oro- mandibular movements might
trigger the seizure.
 Watching TV can precipitate seizures in a vulnerable individual. This is
akin to photo stimulation procedure seen in EEG recording.
 Hyperventilation can also precipitate seizures

27. Differential Diagnosis

28. Differential Diagnosis
 Syncope
– Vasovagal syncope
– Cardiac arrhythmia
– Valvular heart disease
– Cardiac failure
– Orthostatic hypotension
 Psychological disorders
– Psychogenic seizure
– Hyperventilation
– Panic attack
 Metabolic disturbances
– Alcoholic blackouts
– Delirium tremens
– Hypoglycemia
– Hypoxia
 Psychoactive drugs
(e.g., hallucinogens)
 Migraine
– Confusional migraine
– Basilar migraine
 Transient ischemic attack (TIA)
– Basilar artery TIA
 Sleep disorders
– Narcolepsy/cataplexy
– Benign sleep myoclonus
 Movement disorders
– Tics
– Nonepileptic myoclonus
– Paroxysmal choreoathetosis
 Special considerations in children
– Breath-holding spells
– Migraine with recurrent
abdominalpain and cyclic vomiting
– Benign paroxysmal vertigo
– Apnea
– Night terrors
– Sleepwalking

29. Non Epileptic Seizures Epileptic Seizures
Preceding ictus
1 Absence of explanatory disease or
signs
Frequent evidence of neurological
disease
2 Anxiety auras: palpitations, choking
etc.
Wide range of epileptic auras
3 Seizures may be induced or provoked Rarely induced except for reactive
seizures
DURING ICTERUS
1 Inconsistencies in clinical
presentation
Fit specific seizures types
2 Seizure may differ from attack to
attack
Stereotypical seizure pattern
3 Only occurs when others are present Often occurs without witnesses or at
night
4 Gradual onset, pronged
duration(>2min)
Abrupt onset, short duration(<2min)
5 Asymmetrical, out of phase
movements, pelvic thrusts, and
hyperarching
Decrescendo, symmetrical clonic activity
in GTC seizure

30. Non Epileptic Seizures Epileptic Seizures
DURING ICTERUS(continued)
6 Rare whole body rigidity Tonic rigidity at onset of GTC seizure
7 Rare incontinence, tongue biting, self
injury.
incontinence, tongue biting if generalised
8 Normal autonomic reactivity, corneal
reflexes, and pupillary response
Distrubed autonomic reactivity, corneal
reflexes, and pupillary response
9 Avoids noxious stimuli or eye opening Cannot avoid noxious stimuli
10 Vocalization may occur throughout
ictus
Single Vocalization, if present at onset
11 Normal ictal EEG Abnormal ictal EEG
AFTER ICTUS
1 No post ictal delirium Typical post ictal delirium
2 No increase prolactin Prolactin >1000IU/L,10 to 20 min post
ictally
3 Normal post ictal EEG Post ictal slowing on EEG
4 Subsequent recall of events during
ictus
No or fragmentary recall of ictal events
5. No relationship of ictal frequency to
anti epileptic medication
Diminished seizure frequency with anti
epileptic medication

31. Differential Diagnosis
Malingered Seizure Non Malingered NonEpileptic Seizure
PRECEDING ICTUS
1 More common in men Female
2 Abuse history less likely Physical or sexual abuse
3 Prior psychiatry history: less likely
to obtain
present
4 Evident secondary gain No clear 20 gain
5 Emotional precipitants: not clear Frequent
6 Seizures are not suggestible suggestible
DURING ICTUS
1 Seizures under volitional control not
2 Conscious awareness of seizures Subconscious awareness of seizures only
3 Cannot maintain deficits overtime Able to maintain
4 Errors in seizures behaviour are
likely to be major distortions
Errors in seizures behaviour are likely
to be omissions, perseverations, near
misses
Malingered Seizure Vs Non Malingered NonEpileptic Seizure

32. Malingered Seizure Non Malingered NonEpileptic Seizure
AFTER ICTUS
Angry anxious on confrontation, with
lack of evidence for epileptic seizures
Indifferent , detched
Uncooperative, including circumstantial
and evasive answers, may leave against
medical advice
Cooperative with the workup, but
answers may be devoid of content
Malingered Seizure Vs Non Malingered NonEpileptic Seizure

33. Features that Distinguish Generalized Tonic-
Clonic Seizure from Syncope
Features Seizure Syncope
Immediate precipitating factors Usually none Emotional stress, Valsalva,
orthostatic hypotension, cardiac
etiologies
Premonitory symptoms None or aura (e.g., odd
odor)
Tiredness, nausea, diaphoresis,
tunneling of vision
Posture at onset Variable Usually erect
Transition to unconsciousness Often immediate Gradual over secondsa
Duration of unconsciousness Minutes Seconds
Duration of tonic or clonic
movements
30–60 s Never more than 15 s
Facial appearance during event Cyanosis, frothing at
mouth
Pallor
Disorientation and sleepiness
after event
Many minutes to hours <5 min
Aching of muscles after event Often Sometimes
Biting of tongue Sometimes Rarely
Incontinence Sometimes Sometimes
Headache Sometimes Rarely

34. Investigations

35. Epilepsy – Investigation
 The concern of the clinician is that epilepsy may be symptomatic of a
treatable cerebral lesion.
 Routine investigation: Haematology, biochemistry (electrolytes, urea
and calcium), chest X-ray, electroencephalogram (EEG).
Neuroimaging (CT/MRI) should be performed in all persons aged 25 or
more presenting with first seizure and in those pts. with focal epilepsy
irrespective of age.
 Specialised neurophysiological investigations: Sleep deprived
EEG, video-EEG monitoring.
 Advanced investigations (in pts. with intractable focal epilepsy
where surgery is considered): Neuropsychology, Semiinvasive or
invasive EEG recordings, MR Spectroscopy, Positron emission
tomography (PET) and ictal Single photon emission computed
tomography (SPECT)

36. Tools to Confirm the Diagnosis of Epilepsy
EEG Imaging Scans
(Abnormal electricity) (Lesions)

37. EEG in epilepsy
 A normal single EEG does not exclude the diagnosis of epilepsy.
 If a normal awake EEG is obtained in an individual with the clinical
suspicion of seizures, one should repeat the EEG capturing sleep
because many epileptic abnormalities appear only in sleep
 Interictal findings in the EEG are invaluable aids for classifying
seizures and epilepsy syndromes

38. Management

39. Treatment Goals in Epilepsy
 Help person with epilepsy lead full and productive life
 Eliminate seizures without producing side effects
 Tailor treatment to needs of individuals/special populations :
Women, Children, Elderly, Hepatic or renal failure and other
diseases

40. What if not treated?
 Seizures can be potentially life threatening with brain failure,
heart and lung failure, trauma, accidents
 Sudden Unexpected Death in Epilepsy (SUDEP)
 Even subtle seizures can cause small damage in brain
 Long Term problems: fall in IQ, depression, suicide, Social
Problems, Quality of Life

41. Types of Treatment
 Medication
 Surgery
 Non-pharmacologic treatment
 Ketogenic diet
 Vagus nerve stimulation
 Life style modifications

42. Single Unprovoked Seizures
 Common affecting 4% of the population by age 80
 30%-40% of patients with a first seizure will have a second
unprovoked seizure ( epilepsy)

43. Single Unprovoked Seizures
 Risk factors for seizure recurrence include a history of
neurologic insult, focal lesions on MRI, epileptiform EEG,
and family history of epilepsy
 Adult patients with these risk factors have a 60%-70% of
recurrence

44.  Stay calm and track time
 Protect head, remove glasses, loosen
tight neckwear
 Move anything hard or sharp out of
the way
 Turn person on one side, position
mouth to ground
 Check for epilepsy or seizure disorder
ID
 Understand that verbal instructions
may not be obeyed
 Stay until person is fully aware and
help reorient them
 Call ambulance if seizure lasts more
than 5 minutes or if it is unknown
whether the person has had prior
seizures

45. Potentially Dangerous Responses to
Seizure
 Don’t restrain person

 Don’t put anything in the person’s mouth
 Don’t try to hold down or restrain the person
 Don’t attempt to give oral anti-seizure medication
 Don’t keep the person on their back face up

46. Safety Issues for Patients with
Epilepsy
 Cant Drive for about a year after the last seizure
 Climbing altitudes
 Swimming/ Bathing alone
 Operating heavy machinery or weapons that can be dangerous
 Cooking, hot water
 Taking care of babies
 Bone Health

47. Antiepileptic Drug Therapy
 AED therapy is not necessary if a first seizure provoked by
factors that resolve
 AED therapy may be indicated if there is a permanent
injury to the brain (stroke , tumor)
 In general AED therapy is started if there is a high risk of
recurrent seizures

48. Guidelines for Anticonvulsant Therapy
Start with one of the first line drugs
Start with low dose: Gradually increase to effective dose or
until side effects.
Check compliance
If first drug fails due to side effects or continue seizures,
start second line drugs whilst gradually withdrawing first.

49. Guidelines for Anticonvulsant Therapy
Try Three AED singly before using combinations
Beware about drug interactions
Do not use more than two drugs in combination at any one time
If above fails consider occult structural or metabolic lesion and
whether seizures are truly epileptic.

51. Second Generation AED’S
 Topiramate (Topomax – 1996)
 Oxcarbazepine (Trileptal – 2000)
 Lamotrigine (Lamictal – 1994)
 Gabapentin (Neurotin – 1993)
 Levetiracetam (Keppra – 1999)
 Tiagabine (Gabitril – 1997)
 Zonisamide (Zonegran – 2000)
 Pregabalin (Lyrica - 2005)
 Felbamate (Felbatol-1993)
 Vigabatrin (Sabril 2005-2006 Available in Canada and
Europe)

52. Second Generation AED’S
 With the exception of Felbamate second generation AED’S
have advantages over first generation agents.
 Generally lower side effect rates
 Little or no need for serum monitoring
 Once or twice daily dosing
 Fewer drug interactions
 There is no significant difference in efficacy with the second
generation agents
 Higher cost associated with the new agents
 Monotherapy is well established for Lamotrigine and
Oxcarbazepine
 The other agents are undergoing and many have completed
monotherapy trials

53. AED’S In General
 The most important factor in determining success of drug
therapy is the duration of the epilepsy
 The patient needs to know that AED treatment is a
commitment and non-compliance can be dangerous

54. Pregnancy Considerations
 Consider withdraw of AED’S if patient is a good candidate
 Use monotherapy where appropriate
 Folate 1-4 mg per day in all women on AED’S
 The risk of fetal malformations are increased in pregnant
women on AED’S
 Seizures during pregnancy can induce miscarriage
 Seizures during pregnancy can be deleterious to the mother
or fetus
 The possibility of prenatal diagnosis of malformations can
be considered with AFP levels and ultrasonography

55. AED: Side Effects
AED  Sodium
Valporate
Carbamazepine Phenobarbital Topiramate Phenytoin
Side Effects 
Neurological Ataxia,
Nystagmus,
Diplopia,
Tremor
Ataxia,
Nystagmus,
Diplopia
Ataxia,
Nystagmus,
Diplopia
Neuropathy
Ataxia Ataxia,
Nystagmus,
Diplopia,
Tremor,
Dystonia,
Asterixis
Neuropathy
Cognitive &
behavioral
Drowsiness Drowsiness Drowsiness Confusion
Drowsiness
Drowsiness
Dermatological Rashes,
Alopecia
Rashes, SJS, Rashes ---- Rashes,
Hirsutism,
Gum
Hypertrophy,
Hematological Blood
dyscrasias
Blood
Dyscrasias,
Thrombo-
-cytopenia
Megalobastic Anaemia,
Osteomalacia
---- Blood
dyscrasias
Osteomalacia
Endocrine Pancreatitis ---- ---- ---- ----
Hepatology &
Kidney
Liver
damage
---- ---- Nephro-
-lithiasis
Liver damage
Others Nausea,
Weight Gain
Hyponatremia Foliate deficiency,
Depression (adults),
Excitement (Children),
SLE
Nausea,
depression,
Taste
alteration,
Weight loss
SLE
Facial
Dysmorphism
Foliate
deficiency
Drug Interactions Other AEDs,
Antimalarials
Other AEDs,
OCP,
Antimalarials,
Corticosteroids
Other AEDs,
CCB,OCP,
Digoxin,
Antidepressant,
Antimalarials
Other AEDs,
OCP
Other AEDs,
OCP, Anti
Arrythmic,
Antimalarials,
Corticosteroids
Thyroxine

56. Withdrawal of AED
 After complete control of seizures for 3-5 years, withdrawal of Anti
Epileptic drugs may be considered. But in case of special professional
group (car driver, machine man etc) withdraw the AED after keen
follow-up.
 20% of pts will suffer a further sz within 2 yrs.
 AED should be tapered during the stopping of medications.
 Slow reduction by increments over at least 6 months.
 If the patient is taking two AEDs one drug should be slowly withdrawn
before the second is tapered.
 The risk of teratogenicity is well known (~5%), especially with
valproates, but withdrawing drug therapy in pregnancy is more risky
than continuation.
 Epileptic females must be aware of this problem and thorough family
planning should be recommended.

 Over 90% of pregnant women with epilepsy will deliver a normal child.

57. Epilepsy Surgery
Factors influencing decision
 Likelihood seizures are due to epilepsy
 Likelihood surgery will help
 Ability to identify focus of seizures
 Other treatments attempted, and seizures couldn’t be treated with 2-3
medications
 Benefits vs risks
Surgical treatment:
Removal of epileptic focus (eg:mesial temporal sclerosis)
Anterior Temporal Lobectomy
Corpus callostomy
Subpial transection

58. Vagus Nerve Stimulation
 Device is implanted to control seizures
 by delivering electrical stimulation to the
vagus nerve in the neck, which relays
impulses to widespread areas of the brain
 Used to treat partial seizures when
medication does not work


59. Ketogenic Diet
 Based on finding that starvation -- which burns fat for energy -- has
an antiepileptic effect
 Used primarily to treat severe childhood epilepsy, has been effective
in some adults & adolescents
 High fat, low carbohydrate
 and protein intake
 Usually started in hospital
 Requires strong family commitment

60. Other Treatment Approaches
 Behavioral therapy
 Biofeedback
 Relaxation
 Positive reinforcement
 Cognitive therapy
 Aromatherapy

61. Neuropsychiatric Aspects of
Epilepsy

62. PSYCHIATRY AND EPILEPSY
 Epilepsy associated with a range of psychiatric disorders.
 Increased prevalence of psychiatric problems among
epileptic patients.
 May have auras with psychic content
 One-fourth or more have schizophreniform psychoses,
depression, personality changes, or hyposexuality.

63. Why it is important to know Neuropsychiatry of Epilepsy
 Approximately 30 to 50% of patients with epilepsy suffer at
some time from a psychiatric disorder
 Important implications in diagnosis
 Important implications for the management
 Good opportunity to study organic basis of psychiatric
disorders.

64. Classification of psychiatric presentations and
disorders in Epilepsy
• Ictal psychic symptoms
• Nonconvulsive status: simple partial seizures, complex
partial seizures, and periodic lateralizing epileptiform
discharges
Ictal
• Prodromal symptoms: irritability, depression, headache,
• Postictal symptoms: Postictal psychoses, delirium
• Peri-ictal psychoses
Peri-ictal
(includes
preictal, post
ictal, mixed ictal)
• Schizophreniform psychosis
• Personality disorders
• Gastaut-Geschwind syndrome
Interictal
psychosis and
personality
disturbances

65. Classification of psychiatric presentations
and disorders in Epilepsy
•Mood disorders (depression
and mania)
•Anxiety disorders
including panic and
posttraumatic stress
disorder
•Aggression and violence
•Hyposexuality
•Suicide
•Dementia
Behavioral
disrubances
variobly related
to ICTUS

66. Phases Of Epilepsy
 Ictal period refers to events that take place during seizure
 Post ictal events shortly after seizures
 Inter ictal period is time between seizures in epilepsy
 Peri ictal disturbances include pre ictal dysphorias , ictal
and post ictal syndromes.
 Psychiatric phenomena can be associated with the seizure
itself, as well as the peri ictal and interictal phases of
epilepsy.

67. Phases of Epilepsy (continued)
 Different phases are not always readily distinguished,
 Affective auras, ictal automatisms, post ictal confusion,
and mood lability can confound psychiatric assessment
 Model for understanding basic mechanism underlying
various psychiatric disorder.
 Once identified , are best treated by optimizing treatment
accordingly.

68. Psychopathology of the
neuropsychiatric
presentation

69. Psychopathology
 The relationship of seizures, psychiatric syndromes, and
the mediobasal temporal lobes implies that many
behavioral changes are more than psychological reactions
to the psychosocial stressors of epilepsy

70. Proposed Relationships of Psychiatric
Disturbances to Epilepsy
1. Common neuropathology, genetics, or
developmental disturbance
a) The pathology itself could be the source of seizures and
behavioral changes. Ex: Left hemisphere and temporal lobe
lesions may be associated with a schizophreniform
psychosis, and depression with mesial temporal sclerosis
2. Ictal or subictal discharges potentiate abnormal
behaviour
a) Kindling or facilitation of a distributed neuronal matrix
b) Changes in spike frequency or inhibitory–excitatory
balance
c) Altered receptor sensitivity, for example, dopamine
receptors
d) Secondary epileptogenesis.
e) This may occur in temporal lobe seizures and the frontal
lobe seizures.

71. Proposed Relationships of
Psychiatric Disturbances to Epilepsy
3. Absence of function at the seizure focus
a) Inhibition and hypometabolism surrounding the focus
b) Release or abnormal activity of remaining neurons
c) Dysfunction or downregulation of associated areas
d) Ex:the interictal hypometabolism observed on PET scans may
lead to depression or other interictal behavioral changes
e) In schizophreniform psychosis SPECT scans have shown
reductions in cerebral blood flow in the left medial temporal
region.
4. Neurochemical
a) Dopamine and other neurotransmitters
b) Endorphins
c) Gonadotrophins and other endocrine hormones
(Increased dopaminergic or inhibitory transmitters, decreased prolactin, increased
testosterone, or increased endogenous opioids, all of which can affect behavior)

72. Proposed Relationships of
Psychiatric Disturbances to Epilepsy
5.Psychodynamic and psychosocial effects of living with
epilepsy
a) Dependence, learned helplessness, low self-esteem, weak
defense mechanisms
b) Disruption of reality testing
6.Neurobiological and psychodynamic factors potentiate
each other
7. Sleep disturbance
8. Antiepileptic drug relate

73. PSYCHIATRIC
PHENOMENA IN
EPILEPSY
Psychiatric phenomena can be associated with the seizure
itself, as well as the peri ictal and interictal phases of epilepsy.

74. Prodrome:-
The term ‘prodrome’ refers to a variety of subjective symptoms
occurring in the hours or even days leading up to a seizure.
Prodromal symptoms are distinguished from the aura of partial seizures by
their gradual onset and prolonged duration.
Non-specific, ill-defined feelings of malaise with headache, tiredness,
irritability and dysphoria are typical but there may be more pronounced
affective symptoms, in particular depression.
Prodromal symptoms are reported by 7–20% of patients and are more common
among patients with localisation-related epilepsy.
Also Described by patients with generalised epilepsy syndromes and they
should not be interpreted as evidence of focal brain disorder.
The pathophysiological basis for these symptoms is not understood
PSYCHIATRIC PHENOMENA IN EPILEPSY

75. PSYCHIATRIC PHENOMENA IN EPILEPSY
Auras of epilepsy
 Portion of the seizure which occurs before consciousness is lost.
 Range from simple discrete sensation to complex abnormalities
of emotion and ideation
 Appear abruptly, rarely occupy more than a few seconds.
 Must be distinguished from a prodromata which by their
gradual onset and prolonged duration.
 Specially important in TLE

76. Psychic Auras
Type Symptoms Probable Source
Dysphasic Nonfluent
Impaired comprehension
Left perisylvian language
areas
Dysmnesic Déjà vu, déjà vécu, déjà pensé, déjà
entendu, jamais vu, etc.,
prescience, illusion of memory
Mesobasal temporal,
especially on right
Cognitive Dreamy state, altered time sense,
derealization, depersonalization
Mesobasal temporal and
temporal neocortex
Forced thinking, forced actions, and
altered or obscure thoughts
Frontal association cortex
Affective Fear, anxiety, apprehension,
depression, pleasure, displeasure
Mesobasal temporal and
temporal neocortex
Illusions Macropsia, micropsia, teleopsia,
metamorphopsia, increased color
intensity, increased stereopsis
intensity
Lateral superior temporal
neocortex, especially on
right for visual illusions
Hallucination
s
Structured, hallucinatory
remembrances, autoscopy
Mesobasal temporal and
temporal neocortex

77. Epileptic Automatism
 Defined as state of clouding of consciousness
 Occurs during or immediately after seizure
 Individual retains control of posture
 Performs simple or complex movements
 Commonly preceded by aura
 Frequently terminates with a Grand Mal convulsions
 Lasts for a few seconds to hours

78. Epileptic Automatism (continued)
Chiefly in the form of:
 epigastric sensation
 confusion , difficulty with memory, diziness
 feeling of strangeness
 masticatory movements,
 dazed expressions,
 pulling at clothes and passing hand over face
 walking around , searching or moving objects, removing
clothes etc.

79. Automatisms
Term Description
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
Gestural
(often
unilateral)
Fumbling or exploratory movements with the hand directed
toward self or environment
Movements resembling those intended to lend emotional tone to
speech
Hyperkinetic Involves predominantly proximal limb and axial muscles
producing irregular sequential ballistic movements such
as pedalling, pelvic thrusting, thrashing, rocking movements
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

80. Automatisms
Term Description
Dysphasic Impairment of language without dysfunction of relevant primary
motor or sensory pathways, manifested as impaired
comprehension, anomia, paraphasic errors
Gelastic Bursts of laughter or giggling, usually without an appropriate
affective tone
Dyscrastic Bursts of crying
Vocal Single or repetitive utterances consisting of sounds such as grunts
or shrieks
Verbal Single or repetitive utterances consisting of words, phrases or brief
sentencses
spontaneo
us
Stereotyped, involve only self, virtually independent of
environmental influences
interactive Not stereotyped, involve more than self, environmentally
influenced

81. Epileptic Fugues
 Consists of longer lasting disturbances of behavior with
tendency to wander away.
 Actions are usually erratic, may appear to be drowsy or
intoxicated.
 Consciousness is said to be less severely impaired
 Abnormal behavior more complex, extended and
integrated.
 Lasts for many hours to days.
 Upon recovery amnesia is typically complete.

82. Twilight States
 “Twilight states” result from a protracted period of
intermixed ictal and postictal changes
 Range from automatisms and fugues to schizophrenia like
disorders.
 It lasts from one to several hours.
 May show as:
dream like absent minded behavior
muddling of comprehension
complete unawareness of environment
 Psychomotor retardation is common
 Marked perseveration in speech and action

83. Twilight States(continued)
 Abnormal affective states prominently panic , terror , anger
, ecstasy
 Hallucinations may form a large part
 Usually ends spontaneously
 May also terminate in Grand Mal Convulsions
 Memory for the content is usually incomplete

84. DEPRESSION
AND
EPILEPSY

85. DEPRESSION AND EPILEPSY
 Depressive disorder is the most prevalent neuropsychiatric
disorder in epilepsy, occurring in 7.5 to 25 % of epileptic patients
 A family history of depression has been reported in some
studies.
 Some studies found association between depression and early
onset and late onset epilepsy.
 More common in patients with CPS,TLE
 Tebartz van Elst et al found a positive correlation between left
amygdala volumes and depression
 They suggested that increased processing of negative emotional
information might increase blood flow.

86. DEPRESSION AND EPILEPSY
(CONTINUED)
LOCATION OF THE SEIZURE FOCUS
 Studies report a higher prevalence of mood disorders in TLE
 Supporting a specific role for temporal–limbic disorder.
 Left-sided foci and with an increased risk of depression
 Right-sided foci and with an increased risk of mania

87. DEPRESSION AND EPILEPSY
 Divided in to
 Interictal depression or dysthymia aka Interictal
dysphoric disorder of epilepsy.
 Postictal depression
 Ictal depression
 Peri ictal depression
Ictal depression
Rare and may lead to suicide
Peri ictal depression
Episodic mood disturbances, with agitation, suicidal behavior,
and psychotic symptoms,
Associated with increasing seizure activity.
Postictal depression
Associated CPS

88. Interictal dysphoric disorder of epilepsy.
 Also known as inter ictal depression/dysthymia
 Associated with paroxysmal irritability or agitation,
accompanying paranoia and hallucinations.
 Patients with interictal dysphoria tend to have frequent
complex partial seizures, with greater left-sided temporal foci
 Experience of certain psychic auras, especially those with
cognitive content, may predispose to interictal depression.

89. DEPRESSION AND EPILEPSY
(CONTINUED)
SEIZURE FREQUENCY/SEVERITY AND CONTROL;
THE ROLE OF FORCED NORMALIZATION
 Refers to an EEG phenomenon
 In which better seizure control and a reduction in interictal
epileptiform abnormalities are associated with emergence of
depressive symptoms, called as alternating depression.

90. DEPRESSION AND EPILEPSY
(CONTINUED)
IATROGENIC
 Poly pharmacy in epilepsy has been shown to be associated with
depression
 The anticonvulsants most associated with depression are
barbiturates(phenobarbital, primidone, phenytoin and
vigabatrin)
 Anticonvulsants least associated are Valproate, Gabapentin,
Lamotrigine.
 Decrease in folate levels associated with mainly depression

91. SUICIDE AND EPILEPSY
 Rates higher among epileptics
 20% deaths were due to suicides in mentally abnormal epileptics

 Complete Suicide risks is 4-5 fold among epileptics and those with CPS
of temporal lobe origin, as much as 25 times greater
 Suicidal behaviour is not directly related to reaction to the psychosocial
stressors of having seizure disorder
 Epileptic patients are likely to attempt suicide in conjunction with
borderline personality behaviour and contributors to successful suicides
include paranoid hallucination, agitated compunction and ictal command
hallucination

92. CHOICE OF ANTI DEPRESSANTS(AD) IN EPILEPSY
DEPENDS ON VARIOUS FACTORS
Efficacy
 No significant difference in newer ADs and TCAs
Interactions
 Fluoxetine or Fluvoxamine can cause toxic anticonvulsants
levels
 Sertraline, Paroxetine, and Citalopram have little effect
Safety
 Incidence of seizures with therapeutic doses of ADs varies
from 0.1 to 4%
 Not higher than incidence in general population

93. RISK FACTORS FOR ANTIDEPRESSANTS INDUCED SEIZURES
Patient related
 h/o seizures
 Family h/o seizure disorder
 Abnormal pretreatment EEG
 brain damage
 Dementia
 Learning disability
 Previous ECT
 Substance abuse
 Reduced renal/hepatic drug elimination capacity

94. Drug Related
 High dose/high plasma level
 Overdose
 Rapid dose escalation
 Concurrent use of drugs that lower seizure threshold
 Concurrent use of drugs that inhibit metabolism

95. BPAD AND EPILEPSY
 No sufficient data regarding incidence
 Maniacal episodes described in range of 1.5 to 4.8%
 Reported in patients with orbitofrontal and basotemporal
cortical lesions of the right side.
 Mania mostly related to peri-ictal state, improved seizure
control
 Hypomania has been described as occurring denovo after
temporal lobe surgery with right sided emphasis.

96. BPAD Treatment in Epilepsy
 Several studies have noted seizures in treatment with
Lithium at therapeutic levels.
 The use of anticonvulsants as Carbamazepine and Valproic
acid are known to be effective in t/t of BPAD in epilepsy

97. ANXIETY DISORDERS
AND
EPILEPSY

98. ANXIETY DISORDERS AND EPILEPSY
 Generalized anxiety , phobic and panic disorders are most
common.
 Studies implicates disease processes involving limbic
system.
 Anxiety and panic disorders occur among epileptic patients
and must be distinguished from simple partial seizures
manifesting as anxiety or panic.
 Conversely, anxiety symptoms during seizures need to be
distinguished from interictal anxiety.
 Ictal anxiety or fear is usually stereotyped, with rapid
onset and shorter duration than panic attacks.

99. ANXIETY DISORDERS AND EPILEPSY(CONTINUED)
 Anxiety can be reaction to acquiring the diagnosis of epilepsy.
 Some patients with epilepsy clearly have posttraumatic stress
disorder (PTSD) from the psychological trauma of their
recurrent seizures.
 Treatment of anxiety in epilepsy consists of relaxation
techniques, counseling, behavior therapy mainly.

100. OCD AND EPILEPSY
 Abnormal EEG in some patients of OCD
 Consisting of temporal sharp waves activity
 One case report described inverse relationship b/w seizures
and OCD
 Higher obsessionality scores a/w hyperperfusion in
ipsilateral temporal, thalamic and basal ganglia
 Treatment- Serotonergics may be given.
 Carbamazepine may be an effective and safer alternative
 Behavioral therapy and psychosurgery are effective

101. PSYCHOSES
AND
EPILEPSY

102. PSYCHOSES AND EPILEPSY
 Range from transient self limiting episodes to chronic illnesses
 Various population based studies found a prevalence of 2 to 7 %
 Divided into:
1) Psychoses in which confusion and impairment of consciousness
are outstanding features while affective or schizophreniform
elements are absent.
2) Psychoses with admixture of ‘organic’ and ‘functional’
manifestations.
3) Psychoses which occur in setting of clear consciousness and
take a form characteristic of schizophrenia or affective disorder

103. Clinical characteristics of psychosis in relation to
seizure activity
Ictal
psychosis
Post ictal
psychosis
Peri ictal
psychosis
Inter ictal
psychosis
Consciousnes
s
impaired Impaired or
normal
Impaired normal
Duration Hours to
days
Days to
weeks
Days to
weeks
months
EEG Status
epilepticus
Increased
epileptic and
Slow activity
Increased
epileptic and
Slow activity
unchanged
Treatment Anticonvulsa
nts (i/v)
Spontaneous
recovery in
many cases
Improved
seizure
control
Neuroleptic
drugs

104. POST ICTAL PSYCHOSIS(PIP)
Risk factors
 Bilateral cerebral dysfunction
 Ictal fear
 Clusters of seizures
 Absence of H/O febrile convulsions or mesial temporal sclerosis
 Less hippocampal sclerosis, anterior preservation of hippocampus
 Family H/O psychotic disorder

105. Clinical features and phenomenology of
post ictal psychosis.
 PIP develops in patients with CPS mostly
 Duration of PIP ranges from 1 to 90 days
 There can be
Delirium
Delusions, (paranoid, grandiose and religious delusions )
Hallucinations (auditory, visual and somatic)
Mood disorders
Aggressive behavior
Sexual disorders

106. The operational criteria for post ictal psychosis
1. characteristically followed by a lucid interval lasting up to 24 hours,
during which the patient appears to recover fully from the after-
effects of seizures.
2. The onset of psychotic symptoms is then often sudden and dramatic,
accompanied by marked agitation and behavioural disturbance.
3. Duration between one day and three months.
4. A mental state characterized by
a) clouding of consciousness, disorientation or delirium
b) delusions, hallucinations in clear consciousness
c) a mixture of a and b.
5. No evidence of factors which may have contributed to the abnormal
mental state
a) anticonvulsant toxicity
b) previous history of interictal psychosis
c) EEG evidence of status epilepticus
d) recent head injury or alcohol or drugs

107. PERI ICTAL PSYCHOSIS
 A wide range of phenomena including affective, behavioral ,
and perceptual experiences may occur
 Often accompanied by automatisms
 Consciousness is usually impaired
 Tends to be maintained
 Amnesia will often follow
 Diagnosis is made by EEG

108. INTER ICTAL PSYCHOSIS
 It tends to last days to weeks.
 Many patients, develop worsening psychotic symptoms
when an increase in seizure frequency or with antiepileptic
drug withdrawal,Few others have worsening psychotic
symptoms on control of the seizures (alternating psychosis).
 The terms alternating psychosis and forced or paradoxical
normalization refer to this demonstrable antagonism
between the psychosis and the seizures or EEG discharges

109. SCHIZOPHRENIA LIKE PSYCHOSIS OF EPILEPSY(SLPE)
 Develops in 7 -9 % cases of epilepsy
 TLE is the most common form of epilepsy
 Most patients have delusions without any changes in level of
consciousness
 Delusions are mainly paranoid
 Vivid hallucinations of all kinds may occur

110. Risk factors for SLPE
 Age of onset before or around puberty
 H/O intractable status epilepticus
 Epilepsy syndrome, TLE
 Seizure frequency is diminished
 Gender F>M
 No family history
 EEG- mesio basal focus L> R , or B/L
 SPECT- left temporal hyper perfusion
 Pathology- Ganglioglioma/ Hamartoma

111. Clinical features of SLPE
 Paranoid psychosis
 Religious delusions
 Preservation of affect and lack of negative symptoms
 Rarely catatonic symptoms
 Patients with frontal lobe epilepsy show marked emotional
withdrawal and blunted affect
 Psychosis Characteristics:
 - paranoia with sudden onset
 - psychosis alternating with seizure
 - preserved affective warmth
 - failure of personality deterioration
 - less social withdrawal
 - less systematized delusions
 - more hallucinations and affective symptoms
 - more religiosity
 - few schneidreian first-rank symptoms
 - no family history of schizophrenia

112.  Flor-Henry felt that there is a relationship between the
lateralization of the epileptic focus in patients with
temporal lobe epilepsy and psychosis. He postulated that
left- and right-sided seizure foci are more likely to be
associated with a schizophrenia-like and manic-depressive
presentation, respectively. Empirical support has been
mixed.

113. Treatment
 First line management of patients who only have episodes of
psychosis after seizures should be attaining seizure control
 All neuroleptics reduce seizure threshold, Rates of seizure range
from 0.5 to 1.2
 Avoid Clozapine (seizure induction 1%-4.4%) , Loxapine,
Chlorpromazine
 Of conventional Haloperidol is relatively safe
 Sulpiride , Quetiapine, Olanzipine and Risperidine are safe in
long term treatment
 When possible give only one drug
 Monitor seizure frequency

114. Forced Normalization
 Brief episodes of abnormal behavior recorded after dramatic
reduction in seizures using AEDs
 This phenomenon Is called alternative psychosis or forced
normalization when supportive EEG e% is available
 Landolt was the first to report improvement in EEG activity during
periods of abnormal behavior

115. Forced normalization: mechanism
 Not fully understood
 Possible mechanisms proposed are:
 The kindling phenomenon of long-term potentiation
 Channel disorder potentiation
 Epileptiform discharges may mimic ECT in a focal area and
this seizure suppression may lead to psychopathology

116. Forced Normalization: krishnamoorthy & Trimble criteria
 Primary (essential)criteria:
1.Esatblished diagnosis of epilepsy based on H%, EEG, &
imaging
2.Presence of behavioral disturbance of acute/ sub acute onset
characterized by one of the following
– Psychosis with thought disorder , delusion ,
hallucination
– Significant mood change, mania/hypomania or
depression
– Anxiety with depersonalization/ derealization
– Hysteria : motor, sensory , abasia
3A .Reduction in total no of spikes counted in a 60 mt awake EEG
recording by over 50% compared with a similar recording
performed during a normal state of behavior
Or
3B.Report of complete cessation of seizures for at least one wk ,
corroborated by a relative or a care giver

117. Krishnamoorthy&Trimble criteria
 Supplementary criteria
1.Recent change(with in 30 days) of pharmacotherapeutic regimen
2.Report of similar episodes of seizure cessation and behavioral
disturbance in the past
The diagnosis is made in the presence of
Primary criteria 1,2,and 3A
One primary criteria 1,2& 3B & one supportive criteri0n

118. Drugs implicit in forced normalization
 Ethosuximide
 Lamotrigene
 Vigabatrin
 Levetiracetam
 Topiramate

119. PERSONALITY DISORDER
AND
EPILEPSY
1. Overview
2. Type of seizures and personality
3. Etiology
4. Gastaut-Geschwind Syndrome

120. PERSONALITY DISORDER AND EPILEPSY
 Twenty-one percent of patients met threshold criteria for
an Axis II disorder.
 Borderline, atypical or mixed, histrionic, and dependent
disorders
 The most common personality disorder in epilepsy is a
borderline personality
 Epileptic aura was positively correlated
 It has been associated with poorer response to treatment,
lower compliance, and increased risk of suicide attempts
 Most commonly associated with TLE

121. Personality traits a/w Epilepsy
 Aggression, Anger
 Circumstantiality
 Dependence
 Passivity
 Depression, sadness, elation
 Emotionality
 Increased philosophical
interest
 hyposexuality
 Guilt
 Humourlessness
 Hyper graphia
 Hyper moralism
 Hyper religiosity
 Obsessionalism
 Paranoia
 viscosity

122. PD in association with type of epilepsy
 TLE > Grand mal > Petit mal
 In Petit mal patients are generally passive and ‘nice
mannered’
 They are referred for neurotic symptoms mainly
 In TLE children are more aggressive and less neurotic
 Brain injured epileptic patients are often aggressive,
explosive and unpredictable.

123. Etiology of PD in Epilepsy
MULTIFACTORIAL
Psychosocial Effects
 Behavioral disturbances closely related to adverse factors in
family
 Patient is liable to be object of anxious concern and
overprotection
 Attitude of dependency, egocentricity or hypochondriasis in
personality.
 Psychosocial difficulties stigmatized, feared, and subject to
difficulties in obtaining a job, driving an automobile, and
maintaining a marriage
 along with any associated mental retardation, contribute to the
dependency, low self-esteem, and overall borderline personality
traits present in many such patients

124. Etiology of PD in Epilepsy(continued)
Effects of brain damage
 Many problems seen are similar to those in brain damage
 Association claimed b/w TLE and PD is likely d/t brain
damage in limbic system
 Nothing specific to epilepsy about mental slowing,
perseveration, stickiness or viscosity of thoughts and
emotions.

125. Etiology of PD in Epilepsy(continued)
Effect of seizures and abnormal electrical activity
 Disorganization of cerebral functioning by epileptic
discharge also contribute
 Shown by :
Increased disturbance in some prior to fit
Traits may improve when fit frequency is low
Effect of temporal lobectomy postoperatively

126. Gastaut-Geschwind Syndrome
 A group of personality traits termed the Gastaut-Geschwind
syndrome.
 Mostly seen complex partial seizures, at temporal limbic focus.
 These patients are serious, humorless, and overinclusive and have
an intense interest in philosophical, moral, or religious issues.
 Experience multiple religious conversions or experiences.
 In interpersonal encounters, they demonstrate viscosity, (the
tendency to talk repetitively and circumstantially about a restricted range of topics)
 Viscosity may particularly occur in patients with left-sided or
bilateral temporal foci.
 left-sided focus had a more reflective ideational style and
maximized their problems, whereas those with a right-sided focus
had emotional tendencies and minimized their problems.

127. SEXUALITY AND EPILEPSY

128. Sexual Function in Epilepsy
 Decrease of sexual interest, a decrease in activity and impaired
performance are common
 Decreased libido and ED are reported in men receiving AEDs
 Decreased Testosterone, sperm count and morphological
abnormalities and reduced sperm mobility were reported
 Menstrual irregularities are increased in women with increased
seizure frequency, pts using Sod.Valproate, polytherapy.
 Infertility , PCOD occur more frequently.
 Hypo sexuality may be more pronounced in partial seizures
 More vaginismus in women, more ED in men with physiologic
origin

129. SEXUAL DISORDERS
 Especially reported with TLE, resolves with cessation of attacks
 Prevalence varies from 22-67%
 Most common sexual dysfunction is inter ictal disorder of
hyposexuality
 Self mutilation, homosexuality,transvestism , masochism,
exhibitionism and fetishism have been reported
 A woman with nymphomania proved to have incidental sexuality
from sensory simple partial seizures caused by a tumor in the
sensory cortex representing her genital region.
 Endocrine changes have been reported on t/t with liver enzyme
inducing antiepileptics

130. EPILEPTIC DEMENTIA

131. EPILEPTIC DEMENTIA
 Many undergo a decline in intellectual ability
 Progressive impairment of memory, concentration and
judgment
 Usually coupled with severe personality deterioration and
behavioral disorders
 Neuro imaging may demonstrate cerebral atrophy
 Common when epilepsy is secondary to a known brain
lesion.

132. EPILEPTIC DEMENTIA(continued)
In children a/w
 prolonged febrile status
 west syndrome
 Lennox – Gastaut syndrome
In adults
 Etiology differs from case to case
 Epileptic with brain damage dement earlier
 It may represent chronic end state of SLPE

133. Aggression,Violence and Crime
 Lay people have accredited to epilepsy aggressive and violent acts
and have even used this epilepsy defense in criminal proceedings.
This belief peaked in the 19th century.
 High violence rating scores are associated with abnormal temporal
electrical discharges on EEG and temporal lobe abnormalities on CT
 Male epileptics are 3 times more likely to receive a criminal
conviction.
 Aggression in epilepsy is usually associated with psychosis or with
intermittent explosive disorder and correlates with subnormal
intelligence, lower socioeconomic status (SES), childhood behaviour
problems, prior head injuries, and possible orbital frontal damage.
 Prevalence of epilepsy among prison inmates has been two to four
times that among the general population, studies from the United
Kingdom and the United States have not found more violent crimes
among prisoners with epilepsy than among prisoners without
epilepsy.

134. Can violence itself be a seizure?
 After the 1976 case of a New York City policeman who had never had
seizures and successfully claimed the epilepsy defense, criteria for ictal
violence were proposed that included video-EEG telemetry.
 Since then, epilepsy has rarely, if ever, been proved to directly result in
premeditated violence.
 More commonly, nondirected violent movements, aimless destructive
behavior, or angry verbal outbursts occur during postictal delirium,
postictal psychosis and subacute postictal aggression.

135. Criteria for the Assessment of Ictal
Violence in Epilepsy
 The diagnosis of epilepsy is established by at least one
specialist in epilepsy.
 The presence of epileptic automatisms are documented by
history and by closed circuit television EEG telemetry.
 The presence of violence during epileptic automatisms is
verified in a videotape-recorded seizure in which ictal
epileptiform patterns are also recorded on the EEG.
 The aggressive act is characteristic of the patient's habitual
seizures, as elicited by history.
 A clinical judgment is made by the epilepsy specialist
attesting to the possibility that the aggressive act was part
of a seizure.

136. Mechanisms of Aggression among Epilepsy Patients
Period Cause
Interictal Impulse-control disorder
Mental retardation or cognitive impairments
Personality disorders
Schizophrenia like psychosis of epilepsy
Medication related
Prodromal Mounting tension, irritability
Ictal Direct manifestation of the seizure
Violent automatism
Reaction to a negative aura
Subtle seizure equivalents
Post Ictal Resistive
Postictal psychosis
Subacute postictal aggression
Poriomania and somnambulism
In epilepsy, prolonged periods of compulsive wandering with amnesia have resulted from an admixture of ictal and
postictal changes and have been termed poriomania.

137. SUMMARY
 Psychiatric syndromes often occur in patients with epilepsy
at rates that seem to exceed the normal population.
 A lack of good prevalence studies makes it difficult to know
whether or not prevalence rates of these syndromes exceeds
that of other patient groups experiencing CNS dysfunction.
 Symptoms sometimes occur in association with seizures
episodes (either ictally or peri-ictally), and such
symptomatology tends to be brief and context-free.
 Classic psychiatric syndromes tend to occur inter-ictally.
 Depression appears to be the most common psychiatric
feature in patients with epilepsy.
 Multiple factors likely contribute to depression in epilepsy
(including psychosocial, neurologic, and treatment related
variables)

138. REFERENCES
 Harrison’s principles of internal medicine , 17th edition
 Organic psychiatry William Alwyn Lishman, 3rd edition.
 Ictal and postictalpsychiatric disturbances, Michael R.
Trimble Institute of Neurology, University College, London.
 CTP 9TH EDITION

139. Thank you