2. • Temporal lobe epilepsy
• Describe personality changes that take place in
long standing or poorly controlled epilepsy
• Define epilepsy;classify the epileptic syndrome
• a)Define epilepsy b)list 4 drugs used in treatment
of epilepsy,their doses for adult and side effects
c)How would u recognize a named complex
partial seizure?
• Dicuss the management of a 27 year old man
presenting with two episodes of generalised
seizures in the last one month.
3. QUESTION 1
• Primarily generalised seizure includes:
• A. complex partial seizures
• B. Grand mal
• C. Absence seizure
• D. Atonic seizure
• E. Tics
4. QUESTION 2
• Causes of seizure include:
• A. Tumours
• B.Hypoglycemia
• C. Drugs
• D. Head injury
• E. sleep deprivation
5. QUESTION 3
• The following are generalised epilepsies
• A. Jacksonian epilepsy
• B. Grand mal epilepsy preceded by aura
• C. grand mal epilepsy without aura
• D. petit mal epilepsy
• E. psychomotor epilepsy (temporal lobe)
6. QUESTION 4
• The following features may differentiate
between a syncopal attack and a seizure
• A. Upright posture at onset
• B convulsive movements of the limbs
• C. A bitten tongue
• D. Urinary incontinence
• e. confusion after the episode
7. QUESTION 5
• The following statements are true of epilepsy:
• A.Epilepsy should not be diagnosed on the basis of a
single fit
• B.Most cases of epilepsy appearing in adult life are
partial (focal)
• C.complex partial seizures always cause impairment of
consciousness
• D. Any abnormal neurological signs present more than
4 hours after a grand mal fit suggests a structural brain
lesion
• E petit mal seizures usually become more common as
patient gets older
8. OUTLINE
• Definition
• Epidemiology
• - causes of seizures in adulthood
• Classification of seizures
• Classification of epilepsy syndromes
• Aetiology of seizures and epilepsy
• Differential diagnosis
• Evaluation of a patient with seizures
• Management of epilepsy
-Drugs
- surgery
9. DEFINITIONS
• A seizure is a paroxysmal event due to
abnormal, excessive, hypersynchronous
discharges from an aggregate of central
nervous system (CNS) neurons
• Epilepsy describes a condition in which a
person has recurrent seizures due to a
chronic, underlying process
• A seizure can be evoked by any pathology
affecting the brain, transient or permanent
10. CLASSIFICATION OF SEIZURES
• Partial seizures are those in which the seizure
activity is restricted to discrete areas of the
cerebral cortex: usually associated with
structural abnormalities of the brain
• Generalized seizures involve diffuse regions of
the brain simultaneously: may result from
cellular, biochemical, or structural
abnormalities
• .Unclassified epileptic seizures:
13. Partial Seizures
• simple partial seizure: consciousness is fully
preserved during the seizure
• Complex partial seizure :consciousness is
impaired.
• partial seizures with secondary generalization:
Begin as partial seizures then spread diffusely
through out the cortex
16. Simple Partial Seizures
• cause motor, sensory, autonomic, or psychic
symptoms without an obvious alteration in
consciousness
• Motor seizures: arise from the contralateral
motor cortex
• Jacksonian march: movements arise from a
restricted region and progresses over seconds
to minutes to a larger portion of the extremity
17. Motor seizures
• : arise from the contralateral motor cortex
• Jacksonian march: movements arise from a
restricted region and progresses over seconds
to minutes to a larger portion of the extremity
• Todd’s paresis: localized paresis for minutes to
hours following a seizure
• Epilepsia partialis continua: simple motor
seizure that continue for hours or days
18. Sensory seizures
-Somatosensory seizures:
paraesthesias or numbness
epigastric sensation that rises from the stomach or chest
to the head
- Special sensory seizures:
Visual: flashing lights, hallucination
Auditory: crude sounds to music
Gustatory: taste hallucinations, crude or complex
Olfactory: unusual odours (burning rubber,kerosene)
Vertiginous: falling in space or floating
19. AUTONOMIC SEIZURES
• vomiting, pallor, flushing, sweating,
• piloerection, pupil dilatation, boborygmi,
• and incontinence
These usually arise from the frontal or temporal
region.
• Aura: simple partial seizures preceding
complex partial seizure or secondarily
generalized seizure.
20. PSYCHIC SYMPTOMS
• These are disturbances of higher cortical
function. Usually occur in complex partial
seizures
• Dysmnesic symptoms : déjà vu: a naive
experience had been experienced before.
jamais-vu:a previously experienced sensation
had not been experienced,
deja-entendu or jamais-entendu.
21. PSYCHIC SYMPTOMS
• Cognitive: dreamy states; distortions of the
time sense; sensations of unreality,
detachment, or depersonalization.
• Affective: fear, intense depression, Anger or
rage, Fear or terror,
• Illusions: macropsia or micropsia,
Depersonalization,
22. Complex Partial Seizures
• patient is unable to respond appropriately to
visual or verbal commands during the seizure
• impaired recollection or awareness of the ictal
phase
• aura is stereotypic for patient
• sudden behavioral arrest or motionless stare
• patient is typically confused following the seizure,
and the transition to full recovery of
consciousness may range from seconds up to an
hour
24. COMPLEX PARTIAL SEIZURES
Clinical features
Psychomotor triad :motor changes, automatism,
psychic changes
• Aura (focal symptoms and signs as in simple
partial seizures)
Absence (altered consciousness)
Automatism eg mimicry ( gelastic, lacrimic)
ambulatory, verbal, oro-alimentary, responsive
sudden onset and gradual recovery
Complex partial seizures arise from temporal
lobe (60%), or frontal lobe (30%). MTLS
Mayowa O Owolabi
25. Interictal personality disorders
• Very common in complex partial seizures
-humorlessnes, religiosity, obsessionalism,
hypersexuality
-Violent behaviour
-Memory loss
-Psychosis – paranoid schizophrenia
Automatisms :walk repetitively in small circles
(volvular epilepsy), run (epilepsia procursiva), or
simply wander aimlessly, either as an ictal or
postictal phenomenon (poriomania
26. Automatisms
• consist of very basic behaviors such as
chewing, lip smacking, swallowing, or
"picking" movements of the hands, or more
elaborate behaviors such as a display of
emotion or running
27. Partial Seizures with Secondary
Generalization
• Secondary generalization is observed frequently
following simple partial seizures
• Eye witnesses may overlook the subtle onset of
partial seizures
• History of an aura may be suggestive
• EEG analysis may be helpful in uncovering a focal
onset
• Distinguishing between partial and generalized
seizures has important implications in treatment
29. Generalized seizures
• Seizure that begin over the entire surface of the
brain are called generalized seizure.
• Convulsion start in generalized seizure because of
the involvement of motor system.
30. Generalised tonic clonic
seizures(Grand mal)
• Most common seizure type encountered in
clinical settings
• seizure usually begins abruptly without
warning
• Some patients may have vague premonitory
symptoms(prodrome) hours before the
seizure
• Tonic phase:
32. Tonic phase
• : tonic contraction of muscles throughout the
body. lasts 10–20 s
• muscles of expiration and the larynx at the
onset : ictal cry
• Respirations impaired, cyanosis,
• Jaw muscle contraction: tongue biting
• Increaed sympathetic tone leads to increases
in heart rate, blood pressure, and pupillary
size
33. CLONIC & POSTICTAL PHASE
• periods of muscle relaxation on the tonic muscle
contraction
• postictal phase is characterized by unresponsiveness,
muscular flaccidity, and excessive salivation that can
cause stridorous breathing and partial airway
obstruction
• Bladder or bowel incontinence may occur at this point
• Patients gradually regain consciousness over minutes
to hours, and during this transition there is typically a
period of postictal confusion
• headache, fatigue, and muscle ache may last hours
34. Absence Seizures (Petit Mal)
• sudden, brief lapses of consciousness without loss of
postural control
• The seizure typically lasts for only seconds
• no postictal confusion
• subtle, bilateral motor signs such as rapid blinking of the
eyelids, chewing movements, or small-amplitude, clonic
movements of the hands
• Absence seizures usually begin in childhood or early
adolescence,
• Most patients (60-70% have spontaneous remission in
adolescence)
• Precipitated by drowsiness, relaxation, hyperventilation,
photic stimulation
35. Atypical Absence Seizures
• the lapse of consciousness is usually of longer
duration, less abrupt in onset and cessation
• Accompanying motor signs
• EEG shows a generalized, slow spike-and-wave
pattern with a frequency of 2.5/s,
• EEG in typical absence seizures Typical 3-Hz
spike.
36. Myoclonic Seizures
• Myoclonus is a sudden and brief muscle
contraction that may involve one part of the
body or the entire body
• EEG may show bilaterally synchronous spike-
and-wave discharges
• May be seen in association with juvenile
myoclonic epilepsy
37. Atonic Seizures
• sudden loss of postural muscle tone lasting 1–2 s
• Consciousness is briefly impaired, but there is
usually no postictal confusion
• Also known as “drop attacks”
• EEG shows brief, generalized spike-and-wave
discharges followed immediately by diffuse slow
waves
• usually seen in association with known epileptic
syndromes
38. Epilepsy Syndromes
• An epileptic syndrome is an epileptic disorder
characterized by a cluster of signs and
symptoms customarily occurring together;
these include such items as type of seizure,
etiology, anatomy, precipitating factors, age of
onset, severity, chronicity, diurnal and circadian
cycling, and sometimes prognosis.
39. CLASSIFICATION OF EPILEPSY
Two divisions of the classification:
• Idiopathic or genetic- No underlying cause other than a possible
hereditary predisposition
• Symptomatic or structural/ metabolic :a known or suspected
disorder of the central nervous system (CNS).
• Cryptogenic or unknown
• Generalized epilepsies : epilepsies with generalised seizures
• localization-related, partial or focal epilepsies: Epilepsies with focal
or partial seizures
41. Genetics
• Risk of a non-provoked seizure
in offsprings of a parent with
epilepsy: 6%
– Idiopathic generalised
epilepsies: 9-12%
• Over 140 single gene diseases
are accompanied by epilepsy
– Inborn metabolic, storage
diseases
– Mitochondrial diseases
– Neurocutaneous diseases
• Chromosomal diseases
Tuberous sclerosis
42. Common causes of symptomatic epilepsies
• Head injury
• Tumors
• Infarcts, hemorrhages
• Blood vessel malformations
• Infections
• Cortical dysgenesis
Cause of newly diagnosed
epilepsies is unknown in 60-
65% (cryptogenic).
43. Some types of focal epilepsy
Temporal lobe epilepsy
http://www.wiredtowninthemovie.com/mindtrip-xml.html
Frontal lobe epilepsy
http://www.wiredtowninthemovie.com/mindtrip-xml.html
44. TEMPORAL LOBE EPILEPSY
• History of febrile seizures
• Aura
• Behavioral arrest/stare
• Complex automatisms
• Postictal disorientation, memory loss
• MRI- hippocampal sclerosis
• Often refractory to therapy
• Treatment- surgical resection
45. Temporal lobe epilepsy
Symptoms:
Often aura, experience feelings,
emotions, sensation rising up from stomach,
hear voices, odd smell or taste
Lip smacking, hand rubbing, shouting, laughing or
fiddling with buttons on clothes
Seizures usually last 1-2 minutes
47. Lennox- Gastaut Syndrome
• Onset between 1 -7 years
• Severe, with multiple seizure types (myoclonic,
atypical absence, tonic, tonic-clonic)
• Precipitated by drowsiness, or understimulation, not
hyperventilation
• Progressive mental retardation
• EEG 1-2.5Hz spike and wave
• Many causes (cryptogenic, symptomatic, cerebral
palsy, West syndrome, tuberous sclerosis)
• Poor prognosis
Mayowa O Owolabi
48. West Syndrome
• Infantile spasm described by DJ West in 1841
• Rare syndrome
• Family hx in 7-17%
• Usu develop between 4-8 mo
• Salaam attacks
• Hypsarrhythmia on EEG
• Response to cortocosteroids, ACTH
• Usu remit on therapy or spont.
• Poor long term prognosis, mental retardation and
continuing seizures are common sequalae
Mayowa O Owolabi
56. Diagnosis / differential diagnosis
Is it an epileptic
seizure? ?
Yes No
1. Seizure type?
2. Acute symptomatic
seizure or epilepsy?
Epilepsy
Idiopathic or
symptomatic?
Acute symptomatic seizure
Cause?
Symptomatic epilepsy
Cause?
Syncope?
TIA?
Psychogenic?
57. Epileptic seizure versus syncope
Syncope Tonic-clonic seizure
Position Upright Any
Facial colour Paleness Cyanosis
Onset Gradual; introduced by
dizziness, blurring of vision
Sudden; can start by ‘aura’
(simplex partial seizure)
Twitchings Rarely (‘convulsive syncope’) Always
Enuresis Rarely Often
Tongue bite No Often
Duration 10-20 seconds Few minutes
Postictal confusion No Yes
Perspiration Pronounced Not typical
58. EVALUATION
• A complete history is the cornerstone for
establishing a diagnosis of epilepsy
• Eye witness accounts essential
• symptoms before, during, and after the
episode
• Hx of early childhood events, such as perinatal
encephalopathy, febrile seizures, brain
infections, or head injurie
59. MANAGEMENT OF EPILEPSY
• EVALUATION: This is to establish that patient has epilepsy and to determine the
type of seizures and epilepsy.
• HISTORY: from patient or eyewitness. Line of questioning include:
• Tell me about the attacks or spells (patient may deny epilepsy)
• Is there a warning sign? If so, what is the warning sign
• Is there loss of consciousness, convulsions, biting of the tongue, injury,
incontinence of urine etc.?
• Is it associated with abnormal behaviour?
• What does the patient do after the seizure?
• When did the attack begin. How often do they occur
• Are the attacks related to time of the day, food intake, position, sleep, emotional
upset, fever, and fatigue, drugs or alcohol?
60. MANAGEMENT OF EPILEPSY
• What other factors precipitate the attacks?
• Any past history of febrile convulsions, head injury, brain infections?
• Any family history of epileptic seizures of febrile convulsions?
• What is the occupation of the patient, his social habits, income and
education?
• Physical examination: This is done to identify any focal neurological signs.
Complete neurological examination. Mental status and other higher
cerebral function, visual field, motor, sensory, coordination and reflexes.
61. EXAMINATION
• Careful examination of the skin may reveal
signs of neuro-cutaneous disorders, such as
tuberous sclerosis or neurofibromatosis,
• complete neurological examination : focal
signs may indicate brain lesion
62. INVESTIGATIONS
Investigations of epilepsy may be grouped into
those that are structural (MRI and CT),
functional (EEG, psychological, PET, SPECT) and
biochemical (blood tests, CSF examination).
63. EEG
• For diagnosis of epilepsy by providing findings of
epileptiform changes
• To determine whether the seizure disorder is
partial onset or generalised.
• To check for evidence of background
encephalopathy
All patients with a suspected seizure disorder
should have an EEG done
A normal Interical EEG does not rule out a seizure
disorder.
66. MRI
• Indications for MRI in evaluation of seizure
disorders
• . Partial seizures, on history and/or EEG.
• 2. Fixed or progressive neurological or
psychological deficit.
• 3. Onset of generalized seizures before the age
of 1 year and after 20 years.
• 4. Difficulty obtaining seizure control with AEDs.
• 5. Unexplained loss of seizure control or status
Epilepticus.
67. OTHER TESTS
• Functional imaging procedures such as positron
emission tomography (PET) and single photon emission
computed tomography (SPECT) are used to evaluate
patients with medically refractory seizures being
considered for surgery
• Routine blood tests and lumbar puncture are not
usually indicated in evaluation of patients but in
context of acute illnesses and also to provide a
baseline(in the case of biochemical tests) prior to
commencement of AEDS.
• Measurement of serum prolactin can be done to rule
out psychogenic seizures
68. TREATMENT
• Drug therapy is the mainstay of treatment
• Seizure classification is important for
determining treatment
• Patients with recurrent seizures of unknown
should be treated
69. TREATMENT
• Single seizures should be treated in the
following situations:
• 1) an abnormal neurologic examination,
• (2) seizures presenting as status epilepticus,
(3) postictal Todd's paralysis,
• (4) a strong family history of seizures,
• (5) an abnormal EEG
72. PHENYTOIN Adverse effects
• Ataxia and nystagmus.
• Cognitive impairment.
• Hirsutism
• Gingival hyperplasia, Coarsening of facial features.
• folate dependent megaloblastic anaemia,
• Osteomalacia,
• Inhibition of ADH,
• inhibition of insulin secretion→hyperglycemia and
glycosuria
• Hypoprothrominemia—coagulopathy
• Exacerbates absence seizures.
73. SODIUM VALPROATE
inhibits P450 system
Adverse effects:
– Elevated liver enzymes including own.
– Tremor, hair loss, changes in hair growth
– increased appetite Weight gain.
– coagulopathy (inhibition of platelet aggregation),
– Idiosyncratic hepatotoxicity.
– Negative interactions with other antiepileptics.
– Teratogen: spina bifida
74. CARBAMAZEPINE Adverse effects
• Stupor, coma,
• respiratory depression,
• drowsiness, dizziness,
• vertigo, ataxia,
• blurred vision, diplopia,
• bradycardia,
• skin rashes,
• GI upsets.
• Hyponatremia in elderly
• The 10,11-epoxide metabolite →blood dyscrasias
(leukopenia and aplastic anaemia), and serious liver
toxicity.
75. LEVETIRACETAM (Keppra)
• Adjunct Rx of refractory Partial Seizure
• Unknown mechanism of action but binds to presynaptic
vesicle protein
ADVERSE EFFECT
Dizziness, sleep disturbances, headache, and asthenia (LACK OF
ENERGY)
76. DISCONTINUATION OF TREATMENT
• Withdrawal of anti epileptic drug treatment
may be attempted in patients who have been
seizure free for 3 years and who have a
normal EEG at time of consideration.
• Antiepileptic drug therapy should be tapered
off and not stopped abruptly
78. MANAGEMENT OF STATUS
EPILEPTICUS
• Status epilepticus refers to repeated seizures
with no intervening recovery of consciousness
OR a single seizure that lasts up to 30 mins.
• However, for practical purposes it is advised to
treat any seizure that lasts more than 5 mins.
79. CAUSES OF STATUS EPILEPTICUS
• anticonvulsant withdrawal or noncompliance,
• metabolic disturbances,
• drug toxicity,
• CNS infection,
• CNS tumors,
• refractory epilepsy,
• head trauma
81. Status Epilepticus Treatment
Time post
onset Treatment
Onset Ensure adequate ventilation/O2
2-3 min. IV line with NS, rapid assessment, blood
draw
4-5 min. Lorazepam 4 mg (0.1 mg/kg) or diazepam 10
mg (0.2 mg/kg) over 2 minutes via
second IV line or rectal diazepam
7-8 min. Thiamine 100 mg, 50% glucose 25 mg IV
Phenytoin or fosphenytoin 20 mg/kg IV
(phenytoin PE) at 50 mg/per minute
phenytoin or 150 mg per minute fosphenytoin
( 0.75 mg/kg/min) Pyridoxine 100-200 mg IV in
children under 18 mo.
82. Status Epilepticus Treatment (cont.)
Time post
onset Treatment
10 min. Can repeat lorazepam or diazepam if
seizures ongoing
30-60 min. EEG monitoring unless status ended
and patient waking up
40 min. Phenobarbital 20 mg/kg at 5 mg per
minute (0.75 mg/kg per minute)
continued
Reference: Lowenstein DH, Alldredge BK, Status Epilepticus. NEJM 1998; 338: 970-976.
83. Status Epilepticus Treatment (cont.)
Time post
onset Treatment
70 min. Pentobarbital 3-5 mg/kg load, 1 mg/kg
per hour infusion, increase to burst-
suppression
OR
Propofol 3-5 mg/kg load, 5-10 mg/kg/hr
initial infusion then 103 mg/kg/hr
OR
Midazolam 0.2 mg/kg load, .25-2 mg/kg
infusion
Reference: Lowenstein DH, Alldredge BK, Status Epilepticus. NEJM 1998; 338: 970-976.
84. First Aid
Stay calm
Do not insert anything into the person's mouth
Keep person safe, remove dangerous objects
Do not restrain
85. OTHER MANAGEMENT ISSUES
• Restrictions on Driving, Climbing heights,
Working with heavy machinery, Swimming
alone
• Seizures in Pregnancy/Catamenia
• Social stigma
• Trauma
• Job limitation/medication expenses
• Medication side effects