This document defines epilepsy as a chronic neurological disorder characterized by recurrent seizures resulting from abnormal neuronal activity in the brain. Seizures can vary in severity from brief periods of lack of awareness to major motor convulsions. Epilepsy is classified based on whether seizures originate in one area of the brain (focal) or engage both hemispheres (generalized). Common causes include trauma, tumors, infections, genetic factors, and metabolic imbalances. Diagnostic workup may include EEG, CT/MRI, and genetic testing. Treatment primarily involves anti-seizure medications, while refractory cases may be treated with surgery to remove the seizure focus.

1. Epilepsy
“On the sacred disease”
“Apasmara”
Dr.Sanjay kumar.H
SSIMS, Davanagere

2. Definition
 A chronic neurologic disorder manifesting by
repeated epileptic seizures (attacks or fits) which
result from paroxysmal uncontrolled discharges
of neurons within the central nervous system (grey
matter disease).
 The clinical manifestations range from a major
motor convulsion to a brief period of lack of
awareness.
 stereotyped and uncontrollable nature of the attacks
is characteristic of epilepsy.

3.  A seizure (from the Latin sacire , “to take
possession of ”) is a paroxysmal event due to
abnormal excessive or synchronous neuronal
activity in the brain.
 The meaning of the term seizure needs to be
carefully distinguished from that of epilepsy.
 Epilepsy describes a condition in which a
person has recurrent seizures due to a
chronic, underlying process.

4. Classification of Seizures:
ILAE-2010
 1. Focal seizures
(Can be further described as having motor, sensory, autonomic,
cognitive, or other features)
 2. Generalized seizures
a. Absence: Typical, Atypical
b. Tonic clonic
c. Clonic
d. Tonic
e. Atonic
f. Myoclonic
 3. May be focal, generalized, or unclear
Epileptic spasms

5. Pathogenesis
 The 19th century neurologist Hughlings Jackson
suggested “a sudden excessive disorderly
discharge of cerebral neurons“ as the causation
of epileptic seizures.
 Recent studies in animal models of focal epilepsy
suggest a central role for the excitatory
neurotransmiter glutamate (increased in epi) and
inhibitory gamma amino butyric acid (GABA)
(decreased)

6. Epidemiology and course
 Epilepsy usually presents in childhood or
adolescence but may occur for the first time at any
age.
Newborns
Early school age
Adolescents
Seniors

7. Epidemiology and course
 5% of the population suffer a single sz at some
time
 0.5-1% of the population have recurrent sz =
EPILEPSY
 70% = well controlled with drugs (prolonged
remissions)
 30% epilepsy at least partially resistant to drug
treatments = INTRACTABLE
(PHARMACORESISTANT) EPILEPSY.

8. Epilepsy versus epileptic
syndromes
Epilepsy is not a nosological entity – not one
disease! Not unique aetiology...
Might be a symptom of numerous disorders –
symptomatic epilepsy (TBI, tumours,
inflammation, stroke, neurodegeneration, ...)
Sometimes the cause remains unclear despite
careful history taking,examination and
investigation!

9. Focal seizures
 arise from a neuronal network either discretely
localized within one cerebral hemisphere or
more broadly distributed but still within the
hemisphere.
 Typically consciousness is preserved

10.  Three additional features of focal motor
seizures are worth noting
1. Jacksonian march
2. Todd’s paralysis
3. Epilepsia partialis continua

11. Focal seizures
EEG: epileptiform spikes or sharp waves, Since focal
seizures can arise from the medial temporal lobe or
inferior frontal lobe (i.e., regions distant from the
scalp), the EEG recorded during the seizure may be
nonlocalizing.
Can be detected?

12. Focal seizures with
dyscognitive features
 accompanied by automatisms , which are
involuntary, automaticbehaviors that have a
wide range of manifestations.
 consist of very basic behaviors such as
chewing, lip smacking,swallowing, or
“picking” movements of the hands, or display
of emotion or running.
 may show an anterograde amnesia or, in
cases involving the dominant hemisphere, a
postictal aphasia.

13. Focal seizures without
dyscognitive features
 motor, sensory, autonomic, or psychic
symptoms without impairment of cognition.
 For example, a patient movements are
typically clonic (i.e., repetitive,
flexion/extension movements) at a frequency
of 2–3 Hz; pure tonic posturing may be seen∼

14. Focal seizures
 Also psychomotor seizures
Initial subjective feeling (aura), loss of
consciousness, abnormal behavior (perioral and
hand automatisms)
Usually originates in TL

15. Focal (partial) seizures
 Partial seizures evolving to tonic/clonic convulsions
– secondary generalised tonic/clonic seizures
(sGTCS)

16. Generalized seizures
 are thought to arise at some point in the brain
but immediately and rapidly engage neuronal
networks in both cerebral hemispheres.

17. Generalized seizures
(convulsive or non-convulsive)
 Absence
 Myoclonic seizures
 Clonic seizures
 Tonic seizures
 Atonic seizures
 Clonic tonic

18. Causes
 Young adults (18–35 years)
 Trauma
 Alcohol withdrawal
 Illicit drug use
 Brain tumor
 Idiopathic
 Older adults (>35 years)
 Cerebrovascular disease
 Brain tumor
 Alcohol withdrawal
 Metabolic disorders (uremia,
hepatic failure,electrolyte
abnormalities, hypoglycemia,
hyperglycemia)
 Alzheimer’s disease and other
degenerative
 CNS diseases
 Idiopathic

19. Epilepsy
Differential Diagnosis
The following should be considered in the diff. dg. of epilepsy:
 Syncope attacks (when pt. is standing; results from global
reduction of cerebral blood flow; prodromal pallor, nausea,
sweating; jerks!)
 Cardiac arrythmias (e.g. Adams-Stokes attacks). Prolonged arrest
of cardiac rate will progressively lead to loss of consciousness –
jerks!
 Migraine (the slow evolution of focal hemisensory or hemimotor
symptomas in complicated migraine contrasts with more rapid
“spread“ of such manifestation in SPS. Basilar migraine may lead to
loss of consciousness!
 Hypoglycemia – seizures or intermittent behavioral disturbances
may occur.
 Narcolepsy – inappropriate sudden sleep episodes
 Panic attacks
 PSEUDOSEIZURES – psychosomatic and personality disorders

20. 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.

21.  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)

22. Epilepsy - Treatment
 drug therapy (anticonvulsants).
 In intractable cases surgery may be necessary
 treatment target is seizure-freedom and improvement in
quality of life!
 The commonest drugs used in clinical practice are:
Carbamazepine, Sodium valproate, Lamotrigine (first line drugs)
Levetiracetam, Topiramate, Pregabaline (second line drugs)
Zonisamide, Eslicarbazepine, Retigabine (new AEDs)
 Basic rules for drug treatment: Drug treatment should be
simple, preferably using one anticonvulsant
(monotherapy). “Start low, increase slow“.
Add-on therapy is necessary in some patients…

23. Epilepsy – Treatment (cont.)
 If pt is seizure-free for three years, withdrawal of
pharmacotherapy should be considered.
 It should be performed very carefully and slowly! 20%
of pts will suffer a further sz within 2 yrs.
 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.

24. Epilepsy – Surgical Treatment
 intractable epilepsy will benefit from surgery.
 Epilepsy surgery procedures:
 Curative (removal of epileptic focus) and palliative
(seizure-related risk decrease and improvement of
the QOL)
 Curative (resective) procedures:
 Anteromesial temporal resection,
 selective amygdalohippocampectomy,
 extensive lesionectomy,
 cortical resection,
 hemispherectomy.
 Palliative procedures: Corpus callosotomy and

25. Status Epilepticus
 A condition when consciousness does not return
between seizures for more than 30 min
 (practically 5min)
 state may be life-threatening with the development
of pyrexia, deepening coma and circullatory
collapse.
 Death occurs in 5-10%.

26. causes
 frontal lobe lesions (incl. strokes)
 following head injury,
 on reducing drug therapy,
 with alcohol withdrawal,
 drug intoxication,
 metabolic disturbances or
 pregnancy.

27. Treatment: AEDs intravenously ASAP