epilepsy and status epilepticus (undergraduate)

1. Epilepsy
Dr Mohamed rizk khodair
Lecturer of neurology
October 6 university
Mohamedrizk.med@o6u.edu.eg

2. Agenda
A. Definiton
B. Causes
C. Classification
D. Diagnosis and Differential diagnosis
E. Management
F. Status epileptic and its management

3. Definition
Disorder of the brain characterized by recurrent seizures.
(One seizure does not signify epilepsy, Epilepsy is defined as having two or more unprovoked seizures).
Seizure: It is a transient event of abnormal excessive hypersynchronous neuronal activity of the brain variety
of symptoms.
Epilepsy:
Epilepsy is characterized by the following:
 ≥ 2 unprovoked (or reflex) seizures occurring more than 1 day apart.
Or
 1 unprovoked (or reflex) seizures with a high recurrence risk
(Positive family history, EEG finding)
Or
 Diagnosis of an epilepsy syndrome.

4. Epileptic seizures:
Clinically described as: (Stereotyped Attacks, Sudden Onset, Short Duration, Sudden
Offset)
Epileptic syndrome
 It is characteristic cluster of clinical and EEG features, often supported by specific
etiological findings (structural, genetic, metabolic, immune, and infectious).
 The diagnosis of a syndrome in an individual with epilepsy frequently carries prognostic
and treatment implications.
 Syndromes often have age-dependent presentations and a range of specific comorbidities.

5. Pathogenesis
 GABA is the main inhibitory neurotransmitter, while
Aspartate and Glutamate are the main excitatory
neurotransmitters.
 Excitatory and inhibitory pathways in the normal
brain constantly interact to regulate cerebral
synchronous discharge.
 Seizures are caused by rhythmic and recurrent
hypersynchronous discharge of excitatory neurons
when GABA receptors are inhibited.
 Seizures may be caused by ion channel abnormalities
(Na+, K+, Ca-), which prolong the depolarization
state.
 The shift in the balance between the inhibitory (γ-
aminobutyric acid (GABA)) and the excitatory
(glutamate) neurotransmission drive at the synaptic
level that can result in seizure activity.

6. Causes
A. Primary (idiopathic)
B. Secondary (symptomatic)
1) Local Causes: (remote)
 Neoplastic: Brain Tumor
 Vascular: ischemic stroke, ICH, SAH
&Arteriovenous malformation
 Trauma (birth injury, depressed fracture, penetrating
wound)
 CNS infections: meningitis & encephalitis.
2) General causes: (acute)
 Metabolic disturbances:
-Hyper ammonia
-Glucose transporter1 (GLUT1) deficiency.
-Mitochondrial disorders
-Cerebral folate deficiency.
 electrolyte disturbances:
-Hyponatremia
-Hypocalcemia
-Hypomagnesemia
 Endocrinal disturbances:
-Hypoparathyroidism (due to hypocalcemia)
-Primary adrenal insufficiency (due to hyponatremia)
 Drug abuse and withdrawal:
-Cocaine
-Amphetamine
-Opioids
-Marijuana
 Anoxia as asphyxia, CO poisoning

7. classification
Classified by 5 ways:
1. Etiology.
2. Observable manifestations of the seizures
"semiology."
3. Location in the brain where the seizures
originate as frontal lobe, temporal lobe
seizures.
4. Triggering event the seizures (primary reading
epilepsy).
5. As a part of discrete, identifiable medical
syndromes as epileptic encephalopathy.

8. Classification
Seizures occur from sudden excessive
rapid discharge of grey matter, due to
hypersynchronization of electrical
activity.
classification of epilepsy based on
electrical activity is either:
1. Generalized seizure: They begin
simultaneously in both cerebral
hemispheres.
2- Partial seizures begin focally in a
single area of the brain

9. Generalized Seizures
a. Grandmal epilepsy
b. Absence seizures
c. Myoclonic
d. Atonic (Astatic) seizures

10. A- GRAND MAL epilepsy:
Preictal Stage:
1-Prodroma (not essentially followed by the fit)
2-Aura (has localizing value, followed by the fit)
Ictal Stage
Sudden loss of consciousness. Patient collapses to the ground
while making a high-pitched cry (due to forcible expiration
against contracted laryngeal muscles)
1- Tonic stage: around 30 seconds
-generalized tonic contractions throughout the entire body. -
body stiffening
- Adducted at the shoulder, flexed at the wrists and elbows.
- Legs extended; feet inverted.
- persistent respiratory muscle contraction leading to cyanosis
and pallor.
2- Clonic stage:
-lasts for 30–50 sec. The four limbs flex quickly and jerkily
(may be Asymmetrical)
-tongue biting, incontinence, increased salivation, and mouth
frothing
Post-ictal stage: many hours or longer
disorientation, drowsiness, and tiredness along with gradual
return to consciousness

11. b- Absence seizure (petit mal):
 Begin early in childhood, brief attacks of transient impairment
of consciousness only, no aura.
 It may also be associated with bilateral motor signs as eyelid
flickering or chewing movement.
 abrupt onset with variable frequency can be over one
hundred times per day, each attack lasting for 5-15 seconds.
 Attack: the child stops anything they were doing and stares
blankly into space. When the attack is over, he resumes his
previous activity without any post-ictal disorientation.
 3 per second generalized spikes and waves are an EEG
characteristic.

12. c-Myoclonic seizures:
Which can affect either all or part of the body,
are rapid, jerky, short muscular contractions.
Polyspikes and slow wave complexes in the
EEG

13. d-Atonic seizures:
 sudden loss of postural tone and consciousness. no post-ictal confusion.
 It could be mistaken with TIA, syncope, or narcolepsy may be misconstrued

14. Partial seizures
A) Simple partial seizure:
(awareness)
1-Partial motor seizures:
2- Partial seizures with autonomic
symptoms.
3- Partial somatosensory attack.
4-Special sensory seizures.
B) Complex partial seizure
(impaired awareness)

15. A) Simple partial seizure: (awareness)
1. Partial motor seizures: (discharge from precentral gyrus -area4)
- Clonic movements can be focal limited to one part of the body or with sequential pattern
spread (march) called Jacksonian i.e., start in thumb, big toe or angle of the mouth then
spread.
- Todd's paralysis, a temporary paralysis or weakening, may occur and last for minutes to
hours.
2- Partial seizures with autonomic symptoms:
- Vomiting and nausea
- Epigastric discomfort and sweating
- Incontinence and flushing

16. 3- Partial somatosensory attacks: (discharge from postcentral gyrus)
Numbness or tingling sensations a rarely distressing.
may be jacksonian or focal.
4-Special sensory seizures:
a-Visual: flashes of light
b-Auditory: ringing sounds
c-Olfactory: unpleasant odor (uncinate seizures)

17. B) Complex partial seizures: (psychomotor fit)
1-Temporal Complex Partial Seizures (CPS):
Classic Sequence of:
-AURA: that of the temporal lobe i.e., special sensory unpleasant odor
-Arrest of activity (confusion) (impairment of consciousness).
-Automatism: lip smacking, chewing, swallowing.
-Amnesia of the fit except for aura.
- EEG: unilateral or bilateral temporal spikes or sharp waves.

18. 2-Frontal CPS:
-Characterized by frequent and brief
attacks.
-less common followed by postictal
confusion.
-No(aura) with immediate onset of
automatism.
-Automatism are: Bilateral, include
thrashing, rolling, kicking, or bicycling.
-EEG: unremarkable; show
generalized or focal frontal epileptiform
abnormalities.

19. Diagnosis
1- History: The crucial first step in making a diagnosis is taking a clinical history from the patient as well as
any witnesses to the clinical event(s).
2- EEG:
 This investigation is necessary for the identification and classification of epileptic disorders and seizures.
 According to studies, 12% to 50% of adults and 18% to 56% of children who present with new-onset
seizures have an epileptiform abnormality identified on a standard EEG.
 In both children and adults with an apparent first unprovoked seizure, an EEG is recommended as a part of
the neurodiagnostic evaluation since it may affect the management decision.
Remember:
-An abnormal EEG does not necessarily indicate epilepsy, as about 3% of people without epilepsy may exhibit
epileptiform discharges.
-normal EEG does not exclude epilepsy if the history is significant.

20. 3- Neuroimaging:
 To detect the cause (symptomatic or cryptogenic syndromes).
 Types: MRI brain (standard), ± CT brain, SPECT, PET, MRS, may be needed.
 Common abnormalities include:
1. contusions and lacerations.
2. infarction, hemorrhage, subdural hematoma, angiomatous malformations.
3. encephalitis, tuberculoma.
4. brain tumors.
5. mesial temporal sclerosis, focal cortical dysplasia.
6. Neurocutaneous diseases: Sturge Weber Syndrome, tuberous sclerosis.
4- Laboratory Studies:
To rule out induced seizures, patients with new-onset seizures frequently undergo routine laboratory testing that includes a complete blood
count, glucose, electrolytes including calcium and magnesium, blood urea nitrogen, and creatinine.
5- Toxicology:
Toxicology screening is not mandated in all cases but should be strongly considered if toxin exposure or substance abuse is a concern or if the
clinical findings are suggestive of a possible exposure.
6- CSF:
Lumbar puncture should be considered if the clinical picture is suggestive of possible meningitis, encephalitis, or subarachnoid hemorrhage
but is of limited value otherwise.

21. Differential Diagnosis
conditions that should be considered include the following:
 Syncope (e.g., cardiac arrhythmia, vasovagal syncope, dysautonomia)
 Metabolic conditions (e.g., hypoglycemia, hyponatremia)
 Migraine (e.g., migrainous aura, migraine equivalent)
 Vascular conditions (e.g., transient ischemic attacks)
 Sleep disorders (e.g., cataplexy, narcolepsy, night terror)
 Movement disorders (e.g., paroxysmal dyskinesia)
 Gastrointestinal conditions (e.g., esophageal reflux in neonates and infants)
 Psychiatric conditions (e.g., conversion, panic attacks, breath-holding spells,
malingering, secondary gain).

22. PSEUDO NON-EPILEPTIC SEIZURES TRUE EPILEPTIC SEIZURES
ONSET Gradual Usually, abrupt
DURATION 10-15 minutes Usually no more than 2-3 minutes
RECOVERY Abrupt Frequent post-ictal sleep
OCCURANCE In the presence of others Unpredictable
CONSCIOUSNESS Preserved but fluctuating in some cases From different degree of consciousness impairment to loss
of consciousness
POST-ICTALAMNESIA No Frequent
MOVEMENTS Non-synchronous movements of the entire body
(opisthotonic position, prolonged rigidity, out of phase limb
movements, side to side head movements, forward pelvic
thrusting, jaw clenching in the tonic phase of ictal event,
closed eyes at any stage of seizures)
Variable for each epilepsy type: in most cases, generalized
tonic-clonic movements starting with fast, small amplitude
movements to slower, larger movements of brief rigidity
BEHAVIOUR Highly variable Stereotyped
CRY Ictal weeping associated with moaning and screaming Monotonous epileptic cry
VOCALIZATION Rich in emotive contents Monotonous
INJURY No because of self-protection before fall Frequent (tongue biting, head, and limb injuries)
EMOTIONAL STRESS Patients deny a connection between their events and the
subjective experience of emotional stress
More seizures when patients are angry or anxious
OCCURRENCE IN SLEEP No Possible
EEG No association of abnormal brain discharge, maintenance of
alpha rhythm with only discontinuous muscle activity
Abnormal brain discharge
RESPONSE TO STIMULATIONS (HV,
IPS)
No Frequent
TREATMENT No response Frequent

23. Seizure vs syncope

24. First Aid for Seizures
•Record the time and duration of the seizure.
•Protect the head with a pillow or jacket.
•Remove objects that could cause injury.
•Do not try to stop the jerking or put anything in their
mouth.
•Roll the person onto their side when possible.
•Talk to the person, assessing their return to full
consciousness.
•Stay with and reassure the person until they have
recovered.

25. Management
A. General Measures:
1) Treat reversible conditions: e.g., hyponatremia, hypertensive encephalopathy,
withdrawal of drugs, and hypoglycemia.
2) Avoid precipitating factors as:
 Excess fatigue.
 Sleep deprivation.
 TV, photic stimuli.
 Heavy metals.
 Avoid dangerous places, activities to avoid accident.

26. B-Drug treatment:
1)Choose the proper antiepileptic drugs (AED) for the type of the fit.
2)Start by only one drug (monotherapy}, with gradual titration.
3)Use least effective dose -7 push 1st drug -7 add on another drug.
4)Check blood levels of the drug.
5)Duration: at least 2-4 years after last fit {fit free).
6)Stoppage: gradual after doing EEG.

27. Antiepileptic drugs and their mechanism of action:
Partial seizures Generalized seizures
Tonic-clonic absence myoclonic atonic/clonic
First choice
drugs
Carbamazepine
Phenytoin
Carbamazepine
Phenytoin
Valproate
Ethosuximide
Valproate
Valproate
Clonazepam
Valproate
Second choice
drugs
Valproate
Phenobarbital
Topiramate
Lamotrigine
Vigabatrin
Gabapentin
Phenobarbital
Lamotrigine
Topiramate
Clonazepam
Lamotrigine
Topiramate
Phenobarbital
Lamotrigine
Topiramate
Clonazepam
Nitrazepam
Topiramate
Lamotrigine

29. WHEN TO START ANTISEIZURE DRUG THERAPY?
The decision of starting antiseizure drug therapy at the time of a first unprovoked seizure in an adult should be
individualized.
The main factors to consider in making the decision are:
 The risk for recurrent seizures
 The approximate benefit that can be expected from immediate antiseizure drug therapy on the risk of
recurrent seizure.
 The side effect profiles of various antiseizure drug options.
 Regard to the social consequences of a recurrent seizure (e.g., implications for driving or employment)

30. Risk for seizure recurrence after a first unprovoked seizure include:
 Epileptiform abnormalities on EEG
 Remote symptomatic cause, as identified by clinical history or neuroimaging (e.g., brain tumor, brain
malformation, head injury with loss of consciousness, prior central nervous system infection)
 Abnormal neurologic examination, including focal findings and intellectual disability.
 A first seizure that occurs during sleep (i.e., a nocturnal seizure.

31. C- Surgical management:
Temporal lobectomy, corpus callosotomy &
hemispherectomy are indicated only in
medically intractable, seizures affecting
quality of life & localized focus.
D-Vagal nerve stimulation: the programmed
generator requires surgical placement in the
left chest region with wires wrapped around
the left vagus nerve intermittent stimulation
of the afferent fibers of the vagus nerve
causes desynchronization of cortical electrical
activity.

32. E. Ketogenic diet:
 High proportions of fat & small amounts of carbohydrates and proteins (3-
4:1).
 Mechanism: deprivation of brain from glucose depends on ketone bodies
ketosis  increased cerebral energy reserves increased GABA shunt
activity

33. Status Epilepticus
A single epileptic seizure of >30 minutes duration or a series of epileptic seizures during which
function is not regained between ictal events in a 30-minute period.
In 2015, the ILAE proposed a new definition of SE that reduced the time limits to 5 minutes of
ongoing seizure activity to diagnose convulsive SE (CSE), and 10 minutes for focal and absence SE
Etiology
A)Low blood concentration of AED
B)Remote symptomatic causes
C)CVS
D)Anoxia or hypoxia
E)Metabolic causes
F)Alcohol and drug withdrawal

34. Classification
 Status epilepticus, like seizures, is categorized electroclinically according to
whether seizure activity is focal or generalized.
 Both focal and generalized status epilepticus can be further classified
according to whether clinical seizure activity is convulsive or nonconvulsive

35. Diagnosis
1) Careful history of epilepsy, anticonvulsant use, focal onset, and rule out imitators.
2) Careful examination for signs of trauma, CNS infection, drug toxicity.
3) Lab tests: glucose·, Ca, Na, Mg, P04, drug toxicity, and CSF analysis.
4) Neuroimaging: as CT or MRI brain for unknown cause.

36. Complications of status epilepticus
1. Cerebral: brain damage (hypoxic, metabolic), cerebral hemorrhage, or
venous thrombosis
2. Cardiovascular: increased or decreased blood pressure, shock, HF,
myocardial infraction, arrhythmias.
3. Respiratory: respiratory failure, aspiration pneumonia & pulmonary edema.
4. Metabolic: dehydration, acute renal failure, electrolyte disturbance
(hyponatremia, hypoglycemia & acidosis)
5. Others: DIC, fracture, infection.
6. Death.

38. THANK YOU
Mohamedrizk.med@edu.o6u.eg