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Seizures and Epilepsy

Lets begin by discussing general points about Seizures and Epilepsy:

Incidence of epilepsy: 40 /100,000 children / yr

About 1 % of children will have at least one afebrile seizure by age 14 yrs

0.4 %-0.8 % (4/1000- 8/1000) will have epilepsy by age 11 yrs

Epilepsy is the most common neurologic problem in childhood

Now how can we differentiate between seizures and epilepsy?

A seizure is a sudden, involuntary, time-limited alteration in neurologic function

(movement, behavior) secondary to abnormal discharge of neurons in the CNS

Epilepsy is a chronic condition characterized by 2 or more unprovoked seizures.

Therefore we have recurrent seizures. In some textbooks it is stated as 2 attacks of
unprovoked seizures and in others it is stated as 3 or more attacks of unprovoked
Epilepsy is considered as a clinical diagnosis. Therefore when someone has 2-3
attacks of unprovoked seizures (not precipitated by fever, hypocalcaemia,
hypoglycemia, etc) this person is diagnosed as having epilepsy. Seizures provoked by
the above factors are simply called secondary seizures and NOT epilepsy. Thus
epilepsy is now said to be idiopathic or gene-related.

As you all know, the brain has an electrical discharge which consists of 4 brain waves:


Of course these electrical frequencies vary according to level of alertness, whether one is
asleep, etc. They can be recorded by an EEG (Electroencephalograph) or a video EEG. The
video EEG is a very important and reliable modality for diagnosis because there can be
conditions which mimic seizures. For example, the video EEG is connected to a little boy. If
he moved his arm suddenly and there was no change in the EEG then this is not considered
a seizure.

Neonatal Seizures
As you know the neonatal period limited to :
- First 28 days for term infants
- 44 weeks gestational age for pre-term infants.
A stereotypic, paroxysmal spell of altered neurologic function (behavior, motor, and/or
autonomic function) occuring during this period is called a neonatal seizure.
The incidence 1-5: 1000 live births
Neonatal seizures differ from seizures that occur in older children and from epilepsy.
What is the cause of this difference?
It is due to their immature CNS which cannot sustain a synchronized, well orchestrated
generalized seizure. This is because the CNS requires 2 to 3 years to obtain complete
myelination thus many nerve fibers are still uncovered.
What is the anatomical difference in neonates?
1. Dendritic and axonal ramifications are still in process
2. Synaptogenesis is not complete
3. Deficient myelination in cortical efferent systems
What is the physiological difference in neonates?
1. In limbic and neocortical regionsexcitatory synapses develop before inhibitory
synapses (therefore any stimulation of neurons could cause abnormal electrical
2. Immature hippocampal and cortical neurons more susceptible to seizure activity
than mature neurons
3. Deficient development of substantia nigra system for inhibition of seizures
4. Impaired propagation of electrical seizures, whether synchronous or asynchronous,
as recorded by EEG.
Probable Mechanisms of Some Neonatal Seizures
Probable Mechanism
-Failure of Na + -K + pump secondary to
 adenosine triphosphate
-Excess of excitatory neurotransmitter
-Excess of excitatory neurotransmitter
Deficit of inhibitory neurotransmitter

Hypoxemia, ischemia, and hypoglycemia

Hypoxemia, ischemia and hypoglycemia

Pyridoxine dependency
Pyridoxine dependency

(i.e., relative excess of excitatory

Membrane alteration  Na +

Hypocalcemia and hypomagnesemia

Neonatal Seizures









Now lets talk about each one separately:

Subtle Seizure:

More in preterm than in term

Eye deviation

Blinking, fixed stare

Repetitive mouth and tongue movements


Pedaling and tonic posturing of limbs


Primarily in Preterm

May be focal or generalized

Sustained extension of the upper an

d lower limbs (mimics decerebrate posturing)

Sustained flexion of upper with extension of lower limbs (mimics decorticate


Signals severe ICH (intracranial hemorrhage) in preterm infants


Primarily in term

Focal or multifocal

Clonic limb movements(synchronous or asynchronous, localized or often with no

anatomic order of progression)

Consciousness may be preserved

Signals focal cerebral injury

Myoclonic :


Focal, multifocal or generalized

Lightning-like jerks of extremities (upper limbs > lower limbs)

Note: It is very important to differentiate between jitterness and seizures:




Abnormality of gaze or eye


Movements are stimulus

sensitive (if you irritate the
child or put him under stress,
jitterness will increase but
seizure will not)

Predominant movement
4 times)


Clonic jerking <unequal>

(extends arm once, flexes 3-

Movements cease with passive

flexion (stops shaking when you
touch the limb)

Autonomic changes

Etiology of Neonatal Seizures:

Importance of knowing the etiology:

It is critical to recognize neonatal seizures, and to determine their etiology, as

sometimes the underlying cause is treatable and at others it can be due to a brain
insult, and of course the prognosis depends on the underlying cause.
For example, a baby has hypoglycemia as he was born to a diabetic mother, this
patient will have a good prognosis if discovered early before acquiring a brain insult.
However, if the seizure was due to infection, hemorrhage or malformation, the
prognosis will be bad. Thus we can recognize the importance of knowing the
Seizures are usually related to significant illness, sometimes requiring specific
Neonatal seizures may interfere with important supportive measures, such as
alimentation and assisted respirations for associated disorders. For example, a
neonate may have apnea as the presenting symptom of a seizure (subtle seizure). If
you do not deal with the apnea the neonate may develop anoxia hence brain anoxia
hence brain damage.
Experimental data give some reason for concern that under certain circumstances
the seizure per se may be a cause of brain injury.

What helps us in determining the etiology?

Clinical history provides important clue

Family history may suggest genetic syndrome

In the absence of other etiologies, family history of seizures may suggest poor
prognosis. (the doctor said poor but in the slides its good)

Pregnancy history is important

Search for history that supports TORCH infections TORCH infections may cause
meningitis, encephalitis, etc which could result in a brain insult.

History of fetal distress, preeclampsia or maternal infections

Delivery history

Type of delivery and antecedent events

Apgar scores are extremely important, especially the 5 minute and 10 minute scores
(which are important for the neonate).
The 1 minute score is important for the physician not the neonate. This is because if
an infant has a 1 minute APGAR score below 3, this means that the baby is severely
distressed, thus the physician must perform CPR, intubation, etc. However, the 1
minute score does NOT reflect the prognosis.
The 5 and 10 minute score however, if they are below 7, we will be worried that the
child may develop HIE (hypoxic ischemic encephalopathy) if it is associated with
abnormal manifestations of the CNS. However sometimes the APGAR score can be
misleading. If the baby has a low APGAR score yet was not in need of resuscitation,
then we must look for other causes of the seizure besides HIE.

HIE is a terminology used in the term infant to describe the clinical manifestation of
brain injury starting immediately or up to 48 hours after asphyxia(critical reduction in
oxygen delivery to the fetus antenatally, during labour or delivery)

Postnatal history (metabolic disturbances, sepsis)

Neonatal seizures in infants without uneventful antenatal history and delivery may
result from postnatal cause
Tremors may be secondary to drug withdrawal or hypocalcemia
Temperature and blood pressure instability may suggest infection (sepsis)

Comparison of prominent etiologic diagnoses of seizures in the newborn period. (Data

modified from Mizrahi and Kellaway, 1987; Rose and Lombroso, 1970)



Incidence (%)



As we can see from observing the chart above, the largest number of cases is due to
Hypoxia-ischemia (approximately half of all cases).
The second is metabolic, specifically hypocalcaemia
Then we have infection, trauma, hemorrhage, etc
Now if an infant is suspected or found to have neonatal seizure, what laboratory tests must
be done to rule out the above causes one by one, bringing us closer to the correct etiology?

Complete blood count, differential, platelet count

Blood glucose , Ca, Mg
Blood oxygen and acid-base analysis (pH)
Blood, CSF and other bacterial cultures
CSF analysis (to rule out meningitis)
Ultrasound (this can be performed on any infant with open fontanelles to see if
there is Ivh Intraventricular hemorrhage)
Serum immunoglobulins, TORCH antibody titers, and viral cultures (if we suspect any
Blood and urine metabolic studies (bilirubin, ammonia, lactate, FeCl, reducing
substance.) if we suspect a metabolic cause like hypoglycemia, hypocalcemia
Blood and urine toxic screen
Blood and urine amino and organic acid screen (as urea cycle defects as well as
organic acidemia may present with convulsions)

Identify the underlying cause and treat accordingly:
Hypoglycemia - D10 solution
Hypocalcemia - Calcium gluconate
Hypomagnesemia- Magnesium sulfate
Meningitis- initiation of antibiotics
Pyridoxine deficiency- Pyridoxine (if you give the baby whatever was deficient, and you treat
him with phenobarbitone, and there was no improvement, this should give you a hint that
this seizure could be caused by pyridoxine deficiency. When you start giving this baby

pyridoxine, you will notice on the EEG that the icteric activity will disappear and the seizures
will cease. )

Why do we treat patients with neonatal seizures?

To minimize brain damage

Some controversy exists about when to start anticonvulsants
If seizure is prolonged (longer than 3 minutes), frequent or associated with
cardiorespiratory disturbance, we must give anticonvulsants.

Drug Therapy for Neonatal Seizures

Standard Therapy

Initial Dose


Phenobarbital 20mg/kg

lV, lM, PO


20 mg/kg

lV, PO


20 mg/kg

lV, lM


0.05 to 0.1 mg/kg



0.25 mg/kg


AED= antiepileptic drug; IV= intravenous; IM= intramuscular; PO= oral

Regarding the doses, just know that the initial dose for the first three medications is 20
mg/kg which is different from the maintenance dose.
Notes about the table:

Fosphenytoin is just a newer version of Phenytoin

Lorazepam preferred over diazepam, however it is not available in Jordan.
Since Phenobarbital is given IV, IM and orally it can be used for the acute phase and
for maintenance; however Lorazepam and Diazepam can only be used for the acute
So for a baby with neonatal seizures not caused by metabolic disturbances, it is
preferable to give only these two medications Diazepam and Phenobarbital.

Acute therapy of neonatal seizures:

When an infant is seizing, the first thing you do is take a dipstick and the samples you
need then:

If with hypoglycemia give glucose

If no hypoglycemia- Phenobarbital:20mg/kg IV loading dose

If necessary : additional phenobarbital: 5 mg/kg IV to a max of 20 mg/kg (consider
omission of this additional Phenobarbital if the baby is asphyxiated)

Phenytoin: not given nowadays due to extensive side effects


What are the determinants of the duration of the anticonvulsant therapy for neonatal

Neonatal neurological examination

Cause of neonatal seizure

If a baby in the neonatal period is on Phenobarbital and the seizures stop, we evaluate

If neonatal neurological examination becomes normal discontinue therapy

If neonatal neurological examination is persistently abnormal, consider etiology
and obtain EEG
In most such cases- Continue phenobarbital
- Discontinue phenytoin
- Reevaluate in 1 month

One month after discharge

If neurological examination has become normal, discontinue phenobarbital

If neurological examination is persistently abnormal, obtain EEG

If there is seizure activity on EEG we continue Phenobarbital for another month

If there is no seizure activity on EEG, discontinue phenobarbital

This usually goes on for 6 months.

Complications of Neonatal Seizures:

Cerebral palsy



Spasticity (severe)

Feeding difficulties

By this we finish the first half of this lecture, and now we will begin with the second half:

Epilepsy in Childhood

Review the international classification of seizures.

Review some epilepsy syndromes that occur during infancy and childhood

Discuss the evaluation process of seizures in children

Discuss the medications used to treat pediatric seizures

Discuss alternative therapies for intractable epilepsy

What are the steps in evaluation of pediatric epilepsy?

Steps in evaluation:

1. Is the spell a seizure event?

2. What is the differential diagnosis?
3. Is it epilepsy (does it fit the clinical diagnosis of epilepsy)?
4. Is it part of an epilepsy syndrome?
5. What tests are needed?
6. What is the therapy?

International Classification of Seizure Types:

Seizure Classification





No change in

Consciousness is
impaired or lost

Diffuse onset

Partial Seizures: arise from specific foci (an area in part of one hemisphere is affected).
Partial seizures can become generalized.
Generalized Seizure: from the beginning both hemispheres are affected thus it has a diffuse
Partial Seizures:

Simple Partial Seizures

With motor signs

with somatosensory or special sensory symptoms

With autonomic symptoms

With psychic symptoms

Complex Partial sz (CPS)

Simple partial + iimpaired consciousness

Consciousness impaired at onset

CPS evolving to secondary generalized

Generalized Seizures:

Myoclonic seizures

Tonic seizures

Absence seizures

Tonic-clonic seizures

Atonic seizures

Conditions that mimic childhood epilepsy:


Breath-holding spells


Behavioral staring

Movement disorders ( e.g. tics)

Parasomnias( night terrors, sleep walking,..)

Migraine (hemiplegic migraine)

Familial hemiplegic migraine (FHM) is an autosomal dominant classical migraine
subtype that typically includes hemiparesis (weakness of half the body) during the
aura phase. It can be accompanied by other symptoms, such as ataxia, coma and
epileptic seizures. - Wikipedia

Benign myoclonus (movement without any abnormalities in the EEG)

Gastro esophageal reflux disease (if it is accompanied by vomiting, the infant can
develop torticollis while vomiting which can be confused with a seizure)

Epileptic Syndrome

An epileptic syndrome consists of a complex of signs and symptoms that occur

together in a child with epilepsy more often than would be expected by chance

An epileptic syndrome is defined by:

Seizure type(s)

Natural history

EEG(ictal and inter ictal)

Response to AEDs


Now lets talk about a few Epileptic Syndromes:

Infantile Spasms

Peak onset : 4-6 mo ( 90 % before 12 mo)

Clinically characterized by spasms, which are mostly a mix between flexion and
extension (it is sometimes called salam attack as it mimics the Indian salute/salam.
When putting arms together like the Indian salute, your forearm will be flexed and
your hand will be extended)

Spasms occur in clusters (can occur up to 20-30 times)

West syndrome = infantile spasms +mental retardation + hypsarhythmia

Hypsarhythmia abnormal EEG with characteristic wave patterns as if each limb has
its own electrical impulse.
Hypsarrhythmia is abnormal interictal high amplitude waves and a background of
irregular spikes seen in electroencephalogram, mostly in infant diagnosed with
infantile spasms. - Wikipedia

- Hormonal- ACTH, corticosteroids (if ACTH is not available) ,
- Anticonvulsants (the most effective for infantile spasms are the new AED
<Hormones and AED are used to treat idiopathic infantile spasm>
- Surgery (in symptomatic infantile spasm which has an underlying cause- we
perform surgery to remove the cause)

Prognosis: overall poor

Lennox- Gastaut Syndrome:

Age of onset:1-8 yrs ( 3-6 more common)

Clinically, A Triad:

1. Multiple seizure types (tonic most common)

2. Cognitive/ motor impairment
3. Slow spike and wave on EEG

Etiology: Usually symptomatic (surgery), could be idiopathic (medications)

30 % of patients with infantile spasms develop LGS.

LGS is one of the worst syndromes that could occur in adults and one of the most difficult to


AED (Valproate, benzodiazepines, lamotrigine. Topamax, Felbamate)

Nonpharmacologic (Ketogenic diet, Vagus nerve stimulator)


Prognosis: Very poor

Less than 15 % are seizure free

Impaired cognition and cerebral palsy are common

Notice the burst activity on EEG which is characteristic of LGS

Benign Partial Epilepsy of Childhood with centro-temporal

spike (BECTS)

Also called Benign Rolandic Epilepsy

The most common focal epilepsy in childhood

Represents 15 % of childhood epilepsy

Onset: 3-13 years( peak 6-8 yrs)

Typical seizures are nocturnal, partial with secondary generalization in a

neurologically and cognitively normal child (therefore called Benign)

The typical partial seizure involves:

Unilateral parasthesias of the tongue, lips, gums and cheeks

Unilateral clonic or tonic activity of above

Speech arrest and salivation

EEG: Central-temporal spikes.

Treatment: Almost every AED is effective

Gabapentin and Carbamazepine are preferred


Has the best prognosis of all epilepsies!

By mid teens the disorder resolves in almost all patients

Childhood Absence Epilepsy: (CAE)

Onset: 4-10 years

More common in females

Normal neurologic and developmental status

Multiple seizures daily (can reach 30-40)

Seizures last 5-15 second

EEG: Classical 3 Hz diffuse spike and wave discharges with normal background.

The seizures and the discharges are activated by hyperventilation and flickering
lights. (can be used for diagnosis)

Treatment: Ethosuximide, valproate, lamotrigine

Notice how there are 3 spikes in 1 second (3 Hz).

Juvenile Myoclonic Epilepsy: (JME)

Onset: commonly 12-18 yrs (8-26 yrs)

Seizures: 3 types:
1. Myoclonic
2. GTC (Generalized Tonic-Clonic)
3. Absence (in 15-40 %)

Seizures frequently occur upon awakening

Precipitating Factors:

Lack of sleep

Emotional stress

Alcohol consumption

Genetics: multiple loci: in the short and long arm in several locations 6p, 15q14,
8p,1p (the doctor did not read these locations)

EEG : Background is normal. Generalized 4-6 Hz polyspike and slow wave complexes;
Some have 3-4 Hz spike and slow wave complexes. (therefore it can mimic the
absence seizure on the EEG)

Treatment : Valproate, Lamotrigine,Topiramate


Seizures are controlled in the majority of patients.

JME is one form of epilepsy in which discontinuation of pharmacotherapy

cannot be recommended. In most books the recommendation for treatment
in general is 2-4 years but this cannot be applied to this syndrome because
when therapy is stopped, the seizures will return.

90 % relapse after discontinuation of AED

Etiology of Epilepsy in Childhood: (Secondary Epilepsy)


CNS malformations, neurocutaneous disorders (eg. Neurofibromatosis)

Hippocampal sclerosis (we talked about this when discussing febrile seizures)

Vascular disease(AV malformation, Berry Aneurysm)

CNS infection (meningitis, encephalitis, brain abscess)

Toxic disorders

Metabolic disorders

CNS neoplasm(less than 1 %)

Prenatal/perinatal injury


Miscellaneous: demyelinating disorders, vasculitis

Epilepsy not due to the above causes is termed idiopathic or caused by genetic factors.
To diagnose epilepsy we need to do the following:

Detailed History

Physical Examination

Supportive Investigations:

EEG/ Video EEG (as we mentioned earlier the video EEG is better than the
EEG because the EEG records for 20-30 minutes and there wont necessarily
be an abnormal electrical discharge within this time period. The video EEG is
especially useful if the history is not very informative and you are not sure
about the diagnosis, so you attach the video EEG which keeps recording for
24-48 hours and then you can analyze this EEG to make a diagnosis)

Neuroimaging (CT scan, MRI)

Metabolic work up (if we suspect infection)

Lumbar puncture


1. Anticonvulsant medications

2. Nonpharmacologic treatments

Ketogenic diet (we increase the fat in the diet so that more ketones are
formed and studies showed that this decreased the frequency of seizures)

Vagus nerve stimulator (similar to the pacemaker which is put in the heart.
This device is attached to the vagus nerve sheath. Now any abnormal
impulses in the brain will be transferred to the cranial nerves. When an
abnormal impulse reaches the vagus nerve, the vagus nerve through various
mechanisms, will stop the impulse therefore aborting the seizure. This device
has been FDA approved and shown to decrease the frequency of seizures,
and it has even been done on several cases in Jordan.

<The Ketogenic diet and the Vagus nerve stimulator are only done under certain
indications Cases which are resistant to Anticonvulsant Treatment (3 or more
drugs were used to control the seizure and there was no control)>

3. Epilepsy Surgery if there is a clear focus we can remove it.

Also in certain extremely severe cases where the seizure manifests itself all the time,

we can do palliative surgery, for example temporal lobectomy. We could also cut the
corpus callosum in half so the right and left side will work independently therefore
we decrease the generalization of the seizure.
Let us talk briefly about the history of AED Therapy in the US:
Theyve been present for around a century and a half so we have old preparations
(conventional) and newer (since the 1990s) preparations.
Some examples of the new preparations:

Levetiracetam (trade name Keppra)

Topiramate (Topamax)
Lamotrigine (Lamictal)

Now we will talk briefly about some important medications:


Maintenance dose(mg/kg/day) 2-5(neonate); 3-7(child)


IV formulation

Can quickly load and bolus

Once daily dosing if needed (because it has a long half life - 96 hours)

Widely available and inexpensive

Disadvantages (these are the most significant):

Hyperactivity in younger children

Cognitive concerns


Maintenance dose mg/kg/day 5-15 neonate/infant ; 3-7 child


IV formulation

Can quickly load and bolus

Once daily dosing if needed

Widely available and inexpensive

Disadvantages (rarely used in pediatrics due to its severe side effects, mostly given
by neurological surgeons after brain surgery)

Gum Hyperplasia



Hepatic failure


Possible hypersensitivity reaction

Bone marrow suppression


Maintenance dose mg/kg/day 10-40


Improved tolerability over phenobarbital and phenytoin

Possible mood stabilization

Sustained-release formulation (thus can be given once daily)

Relatively inexpensive


Rare idiosyncratic leukopenia and aplastic anemia (idiosyncratic can be

induced by any dose not dose related)

Bone marrow suppression

Double vision

Skin rash and hypersensitivity reactions(could cause Steven-Johnson


One of AED which could INCREASE the frequency of seizures

Valproate: (most common AED in use, not to be given below 2 years)

Maintenance dose mg/kg/day 15-60


Broad spectrum (can be used to treat any convulsion)




Weight gain

Bone marrow suppression

VALPROATE IS THE ONLY HEPATIC ENZYME INHIBITOR therefore when you give any other
medication you must be careful because its toxicity will increase.


Maintenance dose mg/kg/day 30-90


Well tolerated

Rapid escalation if needed

Used for neuropathic pain

Can be used to treat any type of convulsions.


Skin rash (Steven-Johnson syndrome) which is the most worrisome side


It is also one of the AED which could INCREASE the frequency of seizures


Maintenance dose mg/kg/day 20-80


Rapid titration if needed


Less data in children (not to be used before 4 years of age)


Maintenance dose mg/kg/day 20-50


Maintenance dose mg/kg/day 2-20 (infants); 2-10 (children)


Broad spectrum (can be used for any type of seizure)

Migraine prevention


Weight loss

Renal stones

It has limited use in pediatrics and not available here in Jordan.
Treatment of Pediatric Epilepsy:

Goal: Seizure control without side effects

Appropriate therapy requires accurate diagnosis:

Seizure type

Epilepsy syndrome

Treatment of Seizure Types: Traditional AED

Primary Generalized


Partial Onset



Simple Complex



Ethosuximide Benzodiazepines Carbamazepine, Phenytoin, Phenobarbital, Primidone


Treatment of Seizure Types: 2005, New AED

Primary Generalized


Partial Onset



Simple Complex



Ethosuximide Benzodiazepines Carbamazepine, Phenytoin, Phenobarbital, Primidone,

Gabapentin, Oxcarbazepine, Tiagabine, Pregabalin

Valproate, Felbamate, Lamotrigine, Levetiracetam, Zonisamide, Topiramate

Why have we added these preparations in addition to Valproate? Because they have fewer
side effects and they are less toxic on the liver (recall that valproate is an enzyme inhibitor)
What are the factors that affect our choice of AED?

Side effect profile (if a drug stopped the seizures yet caused idiosyncratic liver
failure, what did we gain?)

Titration schedule (any AED should never be given as a full dose immediately)
For example, if the maximum dose of valproate is 60 mg we should never start with
this amount. We start with 5 mg, and every 4-5 days we increase another 5 mg until

the seizures become controlled. Then we follow up the patient to observe the
frequency of seizures and the side effects experienced due to the given medication.
<some newer preparations do not need such a slow increase in the dose as in the
conventional way>

Other medications the patient is already on, we should know

Drug-drug interaction

Mechanism of action (we should not combine 2 medications that have the
same or similar mechanism of action. For example, if the drug the patient is
on is a Na inhibitor, we should look for a medication that acts on GABA or Ca
to increase efficacy)

Overall clinical experience

Physicians personal experience


Alternatives to Anticonvulsant treatment:

Medically intractable seizures (pharmacoresistant epilepsy)
It is estimated that 20-30 % of patients with epilepsy have medically intractable seizures
(which is actually a large percentage)
We have already mentioned the alternatives to anticonvulsant treatment earlier.
Done By:
Zeina Yanbeiy
If it is not truthful and not helpful, don't say it.
If it is truthful and not helpful, don't say it.
If it is not truthful and helpful, don't say it.
If it is truthful and helpful, wait for the right time. - Buddha
Do not believe in anything simply because you have heard it. Do not believe in anything simply because it
is spoken and rumored by many. Do not believe in anything merely on the authority of your teachers and
elders. Do not believe in traditions because they have been handed down for many generations. But after
observation and analysis, when you find that anything agrees with reason and is conducive to the good
and benefit of one and all, then accept it and live up to it. Buddha
Wu hay a7la ta7iye la a7la C 10 wu shuraka2na C 9 wu be3tezir innu il mo7adara 25 saf7a!