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Neonate Seizures PDF
Neonate Seizures PDF
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Provoked or acute symptomatic seizures are seizures
eizure occurring during the course of an acute illness, e.g.
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A seizure is the clinical manifestation of an abnormal meningitis or head injury.
excessive paroxysmal electrical discharge from the brain.
pileptogenesis
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This electrical discharge is conducted to the body and
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produces a seizure. It could manifest in many different ways Epileptogenesis is the sequence of events that converts
(Table 6.5.1). normal neuronal networks into hyperexcitable epileptogenic
The type of seizure depends on the following: networks.
• The area of the brain producing the discharge
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• The type of discharge pidemiology
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• The age of the patient In India, prevalence rates for epilepsy are 5.59 per 1,000
Thus there are many different kinds of seizures: populations. Males and females are equally affected and
these rates are the same in different geographical areas.
pilepsy
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Epilepsy is recurrent seizure for which there is no immediate tiology
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precipitating cause. Etiology is multifactorial, and almost any insult to the brain
can result in seizures. Epilepsy can result from brain injury
pileptic yndrome due to infections, infestations, hypoxic damage, birth injury,
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Epileptic syndrome is a syndrome where epilepsy is a malformations of the brain, genetic or metabolic causes
prominent feature. (Table 6.5.2).
diopathic pilepsies
Pathophysiology
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Idiopathic epilepsies (now known as genetic epilepsies)
The exact pathophysiology of epileptogenesis is still not
are epilepsies, which have no underlying cause except a
well understood. However, it is known that seizures are
genetic predisposition to epilepsy.
produced when there is an abnormality in the:
ymptomatic pilepsies • Neurotransmitters levels
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Symptomatic epilepsies are epilepsies where the cause is • Ion channels or
known, e.g. structural malformations, postmeningitic sequelae • Receptors.
and posthypoxic ischemic encephalopathy. In India and In many of the genetic epilepsies, there are abnormalities
countries where cysticercosis is endemic, neurocysticercosis of the ion channels or receptors due to mutations, resulting in
is the most common cause of focal seizures in children. epilepsies. These abnormalities can result in hyperexcitability
of neurons, which thus have a tendency to seizures.
Cryptogenic pilepsies The other epilepsies result from neuronal damage because
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Cryptogenic epilepsies are epilepsies, which are expected to of various insults like infections, trauma and vascular events.
have a cause, but despite investigations, no cause is found.
nvestigations
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Table 6.5.1 Clinical manifestations during seizures nvestigation of eizure
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• Abnormal motor activity, which may be a tonic contraction or single The plan of investigations depends on suspected cause (see
or repetitive jerks
“management of acute seizures and status epilepticus”).
• Impairment or loss of consciousness or awareness
• Abnormal behavior
lectroencephalogram
• Abnormal sensory phenomena, e.g. abnormal sensation in one part of
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the body, visual phenomena, smell, taste An EEG is the most important test for investigating epilepsy.
• Abnormal experience: Fear anger illusions or hallucination. Children It is a graphic recording of the electric activity of the brain.
often run to the parent when this occurs An EEG is normal not due to normal patterns, but because it
• Autonomic symptoms has no abnormal patterns. 339
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Table 6.5.2 Etiology of seizures and epilepsy Table 6.5.3 Electroencephalogram: information and limitations
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Causes of seizures Causes of epilepsy Information
Infections Sequelae of any of the acute causes Epileptic versus nonepileptic attacks
Viral encephalitis of seizures Seizure type and epilepsy syndrome (Figs 6.5.1 to 6.5.3)
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Pyogenic meningitis Cerebral malformations Photosensitivity
Tubercular meningitis Metabolic diseases Partial seizures: To identify the focus (Fig. 6.5.4)
Neurocysticercosis Degenerative brain diseases Identify etiology, e.g. SSPE (Fig. 6.5.5)
Metabolic events Neoplasms Monitor progress: Only in some epilepsies, e.g. typical absence seizures,
Hypoglycemia Genetic disorders West syndrome. In most cases clinical response should be the criterion
Hypocalcemia for judging response to treatment. Routine EEGs during treatment are
Hypomagnesemia not required
Dyselectrolytemia Withdrawal of drugs: EEG is not required. Only clinical seizure control
(hypernatremia/hyponatremia) should decide whether drug is to be stopped
Vascular events
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Limitations
Cerebrovascular accidents
Normal EEG does not exclude epilepsy
Drug intoxication/side effects
Must always be interpreted in the clinical context
Vascular events
With the exception of 3Hz spike wave discharges and hypsarrhythmia
Thrombosis
EEG is a poor guide to seizure control
Embolism
Hemorrhage Abbreviations: SSPE, Subacute sclerosing panencephalitis; EEG, Electroen
Neoplasms cephalogram
Hypoxia/anoxia especially during
delivery
Head trauma ther nvestigations
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Febrile seizures Other investigations depend on suspected etiology in case
of symptomatic epilepsies. These include metabolic and
genetic tests.
It is important to remember that EEG can be normal in
cases of epilepsy, while abnormal EEG does not necessarily
mean an epileptic disorder. Fifteen percent of cases of
atural History
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epilepsy have a normal EEG, while 10% of the normal In any given population with epilepsy, 30% may undergo
population has an abnormal EEG. Thus the EEG must be remission without treatment. This emerges from studies of
interpreted in the clinical context (Table 6.5.3 and Figs 6.5.1 epilepsy in poor countries where no treatment has been
to 6.5.5). given for epilepsy because of financial constraints. Of those
Ictal recordings are preferable over interictal ones. who are treated, 60–70% undergoes remission, while the
Special provocation procedures like sleep deprivation, remaining has intractable seizures.
hyperventilation and photic stimulation can be used to
increase the yield of EEG. Classification of eizures and
Video EEG is an EEG recording where the EEG and
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pileptic yndromes
video recordings are done at the same time. It may help
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to differentiate non-epileptic events (NEE) from seizures, It is very important to identify the syndrome wherever
and also help in identification of the type of seizure possible, for starting correct treatment and prognostication,
(Fig. 6.5.6). and to identify etiology and genetics. In the past, there
existed confusion between epilepsies and seizure types.
euroimaging Many of the epilepsies were classified and described by the
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Neuroimaging gives important information about the names of the persons who first described them. There was
etiology in cases of symptomatic epilepsies (Figs 6.5.7 no uniformity in the classification and descriptions used in
and 6.5.8). MRI is preferred since small lesions like cortical different parts of the world.
dysplasia cannot be picked up on CT scan. Generally The International League Against Epilepsy (ILAE)
neuroimaging should be done in all cases except where described a classification of seizures in 1981, and epilepsies
clinical features and EEG are suggestive of idiopathic and epileptic syndromes in 1989, which has been modified
epilepsy. in 2006. Table 6.5.4 shows classification of seizures.
Positron emission tomography and single photon
Classification of pilepsies and pileptic yndromes
emission computed tomography are functional scans that
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may be done to study the perfusion. They are used in pre- The ILAE proposed a classification of epilepsies and
epilepsy surgery workup in refractory epilepsy and help in epileptic syndromes in 1989. Earlier the epilepsies were
identifying epileptic foci. classified as localization related epilepsies, generalized
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Diseases of Central ervous ystem
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Figure 6.5.1 Hypsarrhythmia, a high voltage chaotic electroencephalogram pattern which changes, characteristic of infantile spasms
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Figure 6.5.2 Polyspike wave discharges suggestive of myoclonic seizures
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Figure 6.5.3 3/sec spike wave discharges suggestive of typical absence seizures
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Figure 6.5.4 Epileptic focus—right frontal region
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Diseases of Central ervous ystem
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Figure 6.5.5 Periodic complexes seen in subacute sclerosing pan encephalitis
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Figure 6.5.6 Video electroencephalogram. Simultaneous electroencephalogram and video recording
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Figure 6.5.7 Structural malformation of central nervous system: agenesis Figure 6.5.8 Neurocysticercosis
of corpus callosum
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Diseases of Central ervous ystem
Table 6.5.5 Information required for classifying as an epileptic able 6.5.6 Genetic and developmental epilepsy syndromes
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syndrome by age of onset (according to International League Against
• Seizure type (s) (seizure semiology plus electroencephalogram pattern) Epilepsy)
• Age of onset Neonatal period
• Developmental status • Benign familial neonatal seizures
• Etiology • Early myoclonic encephalopathy
• Anatomy • Early infantile epileptic encephalopathy (Ohtahara syndrome)
• Precipitating factors Infancy
• Prognosis (occasionally) • Migrating partial seizures of infancy
• West syndrome
• Myoclonic epilepsy of infancy
• Benign infantile seizures
epilepsies and unknown whether localization related • Dravet syndrome
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or generalized. Typically, to classify an epilepsy into an • Myoclonic epilepsy in nonprogressive disorders
epileptic syndrome, some information is required (Table Childhood
6.5.5), which may or may not be available. Practically, • Early onset benign childhood occipital epilepsy (Panayiotopoulos
it is best to use the age-wise approach in classifying the type)
epilepsies (Table 6.5.6). • Epilepsy with myoclonic astatic seizures
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• Benign childhood epilepsy with centrotemporal spikes
• Late onset childhood occipital epilepsy (Gastaut type)
Differential Diagnosis of eizures and • Epilepsy with myoclonic absences
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pilepsies • Lennox Gastaut syndrome
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• Epileptic encephalopathy with continuous spike and wave during
he onepileptic vents
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sleep including Landau Kleffner syndrome
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• Childhood absence epilepsy
Nonepileptic events are events, which resemble seizures
Adolescence
but are not the result of abnormal electrical discharges.
• Juvenile absence epilepsy
They are also known as nonepileptic attack disorder, • Juvenile myoclonic epilepsy
epilepsy imitators, epilepsy mimickers and pseudoseizures. • Epilepsy with generalized tonic clonic seizures only
These can also produce recurrent episodes of motor
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• Progressive myoclonus epilepsies
movement or apparent changes of consciousness or Relation with age less specific
behavior that are also seen in children with epilepsy. Also • Autosomal dominant nocturnal frontal lobe
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disorders that mimic seizures are more likely to occur in • Familial temporal lobe epilepsies
children who have epilepsy, associated with abnormal EEG • Autosomal dominant partial epilepsy with auditory features
or to be relieved by antiepileptic drugs (AED) making their • Generalized epilepsies with febrile seizures plus
diagnosis more difficult. • Familial focal epilepsy with variable foci
• Reflex epilepsies
Incidence – Idiopathic photosensitive occipital lobe
– Visual sensitive epilepsies
Twenty to thirty percent of all patients reporting to epilepsy
– Primary reading epilepsy
clinics are found to have NEE. As many as 30% of patients – Startle epilepsy
with NEE have real seizures as well. Nonepileptic events and Seizure disorders that are not traditionally given the diagnosis of epilepsy:
epilepsies both present at all ages and in many different • Benign neonatal seizures
forms. Therefore many conditions can mimic epilepsy at • Febrile seizures
different stages of a child’s life.
Types
pproach to Differentiation of onepileptic
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Nonepileptic events can be divided into two groups: vents from eizures
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1. Physiological : These are various physiological History and Clinical Examination
NEE
phenomena, which resemble seizures on observation or
History and clinical examination can give clues to the correct
when described by parents.
diagnosis. A description of event, especially an eyewitness
2. Psychogenic : These are seen mostly in children account is very important in obtaining a correct diagnosis.
NEE
more than 5 years of age and are either conversion A review of home videos is often the most important aid to
reactions or malingering. diagnosis. The event should typically be suggestive of some
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type of seizure. Developmental delay and neurological leading to forceful crying. They occur in children 6 months to
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deficits are more likely to be associated with true seizures, 2 years of age and disappear by 6 years age. Males are more
but may also be associated with NEEs. commonly affected than females in a ratio of 3:1. Family
history may be present in one-fourth of the cases.
Age-Based Approach
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Consider the types of seizures in a particular age group, and Pathophysiology: The spell is actually a reflex rather than
if the event does not match the type of seizures occurring in a behavior problem as was thought earlier. They are of two
that age group, one should review the NEE in that age group types:
(Table 6.5.7). For example, myoclonic jerks during sleep 1. Cyanotic (more common): There is forceful expiration
in a neonate may be confused with myoclonic seizures;
during crying, a respiratory pause (breath holding)
daydreaming in a school going child may be confused with resulting in hypoxia and cyanosis.
complex partial seizures. 2. Pallid: Vagal stimulation following a painful stimulus or
Attempts to Observe the Event during pause in respiration during expiration, results in
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cardiac asystole, hypoxia and pallor.
This is possible if the event occurs at a particular time or is
precipitated by something, e.g. breath holding spells: try to Clinical presentation: The child holds his/her breath
make the child cry. If psychogenic seizures are suspected, following a sudden painful stimulus and becomes pale
the event may be induced by suggestions. or becomes cyanosed after a prolonged expiration while
crying. He/she then loses consciousness for a brief period,
Ancillary Testing: Electroencephalogram/Video usually less than a minute. There may be stiffening of
Electroencephalogram the whole body, followed by a few clonic jerks making
Ancillary testing is done when there is doubt about the the event appear like a seizure. He/she gradually regains
diagnosis of NEE despite history and clinical observation of consciousness with return of normal color, and may remain
the patient. drowsy or sleep for sometime. The attack may occur many
Sometimes true seizures and NEEs may coexist making times in a day.
differentiation between the two very difficult.
anagement: Is as follows:
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Common onepileptic vents • Counseling regarding the benign nature of the condition
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Breath Holding Spells is a must to alleviate anxiety
• Diverting the child’s attention at the onset of crying can
Breath holding spells are stereotypic events that occur in abort an attack
response to a painful stimulus or an adverse emotional event
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• Some children have low hemoglobin levels, therefore
iron therapy may help in decreasing the frequency of • May be precipitated by an emotional event
attacks • All episodes may not be similar
• In case of severe multiple attacks, piracetam in doses of • No history of injury despite fall
50 mg/kg/day in three divided doses may be given, and • Memory of events during the episode may be present sometimes
can significantly decrease the frequency of attacks. • Thrashing movements are side to side rather than flexion extension,
and appear to vary with time
Benign Neonatal Sleep Myoclonus • Waxing and waning of movements
• Screwing up the eyes when attempts are made to examine then, and
This is a myoclonus that is sometimes seen in neonates at
uprolling of eyes on attempts to passively open the eyes
age of 1–2 weeks, up to 6 months of age. It comprises of • When hand is raised up it falls on the side rather than on the face
repetitive jerking or myoclonic movements of the different • There is usually no frothing, but saliva may trickle out from the
body parts, and occurs only during sleep. Awakening the mouth. Voluntary tongue bite may occur
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baby terminates the attacks. The baby remains neurologically • No urinary incontinence; but may occur occasionally
• Patient appears to periodically be focused and interact with
normal. They may be mistaken for seizures and put on AEDs
surroundings
to which there is no response. EEG and video EEG are normal. • Attack terminates with a particular action, e.g. sprinkling water on the
reatment: Treatment is not required. Parents should be face holding legs together or rubbing hands
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counseled about the benign nature of the condition. • Duration: Variable but is often prolonged
• Patient may start crying before, during or after the attack. Sometimes,
Syncope tears may just flow.
or when lying down. treatment or overtreatment.
If the child has vasovagal syncope, the child should avoid
situations that precipitate the attack. During an attack, the Certain ypes of eizures and
clothes should be loosened and the patient should be made
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to lie down for some time. No attempt should be made to
pileptic yndromes
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give mouth to mouth respiration. cute eizures and tatus pilepticus
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Psychogenic Seizures Most seizures terminate spontaneously without treatment
or after administration of a fast acting anticonvulsant
Psychogenic seizures are events that resemble seizures and
drug. Status epilepticus (SE) means that seizures continue
occur due to emotional or psychological reasons. There
for a prolonged period. The International League Against
is no accompanying epileptiform discharge in the brain.
Epilepsy defines SE as seizures that continue for more than
They are usually a conversion reaction, but may be a form
30 minutes or recurrent seizures for more than 30 minutes
of malingering as well. Twenty to thirty percent of children
without recovery of consciousness in between the attacks.
attending epilepsy units may have psychogenic seizures.
They are seen only after the age of 5 years. • Practical definition: Any patient who is brought with
Psychogenic seizures are mainly of two types: seizures to the hospital or whose seizures last for more
than 5 minutes is to be treated as SE
1. Unresponsiveness with no motor activity
• efractory : If seizures fail to respond to appropriate
2. Unresponsiveness with varying degrees of motor
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SE
first and second line drug treatment and persist for
activity, ranging from just shivering to thrashing around
more than 60 minutes.
violently.
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Incidence
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Table 6.5.10 Diagnostic evaluation of status epilepticus
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Overall incidence is 50 patients per 100,000 population per All cases
year. Status epilepticus in children is most likely in those less • Blood biochemistry: Glucose and electrolytes, and other metabolic
than 3 years of age. Seventy percent of children less than 1 parameters
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year with epilepsy may have SE. • Blood gases assessment
Associated fever
Classification of Status Epilepticus • Blood counts
• Cerebral spinal fluid exam
• ccording to seizure type: For example, generalized • Urine examination
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tonic clonic, partial, absence • Necessary cultures
• ccording to the clinical presentation: Studies on case to case basis
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– Convulsive status: When the seizures have a • Electroencephalogram
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predominant motor component, e.g. GTCS, clonic, • Neuroimaging
tonic, myoclonic, epilepsia partialis continua, • Drug levels
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seizures in one half of the body
– Nonconvulsive status: Absence, complex partial SE,
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continuous spike waves during slow wave sleep.
out a diagnostic evaluation (Table 6.5.10) and treat the
Pathophysiology underlying condition. A suggested management protocol
is shown in Table 6.5.11.
Convulsive SE can be life-threatening and also cause permanent
neuronal damage after 1.5–2 hours of seizure activity due to Follow-Up Advice
excessive glutamate production leading to excessive neuronal
depolarization, rise in intracellular sodium and calcium, cerebral All parents must be taught home management of seizures
edema and finally cell damage and death. Systemic changes with a benzodiazepine (nasal/buccal midazolam, rectal
include hypoxia, hypotension and hyperpyrexia. Metabolic diazepam or sublingual lorazepam). The child should be
derangements like acidosis, hypoglycemia and hyperkalemia put on long-term anticonvulsants if he is found to have EEG
can result in cardiac, respiratory and renal failure. abnormality, abnormal neuroimaging or is far from medical
facility, parents are not educated or confident about home
Etiology management of seizures.
Etiology of status is essentially the same as that of seizures
Prognosis
and epilepsy (Table 6.5.1). However, certain factors can
precipitate seizures and SE in a person with epilepsy • Mortality is 1–2% in developed countries. Improvement
(Table 6.5.9). in prognosis of convulsive SE is due to more effective
and prompt treatment
Management • orbidity: ong-term complications include epilepsy,
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The success of treatment of SE depends on how quickly focal neurological deficit, post-status encephalopathy
the seizure is brought under control. The principles of and mental retardation. Recurrence of SE can occur in
management are well defined, but the protocols vary. What up to 13% cases.
is important is that every medical care facility must have a
very clear protocol or drill in the management of SE. One ebrile eizures
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does not have to wait for 30 minutes to set into motion Definition
the treatment protocol for SE. Goals of management are
to stop the seizure activity as soon as possible and prevent These are seizures, which occur between 3 months to 5
brain damage and systemic complications, and at the years of age, associated with fever but without evidence of
same time to support airway-breathing-circulation, carry intracranial infection or defined cause for the seizure, and
without any history of seizures earlier.
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Type of Seizures in Febrile Seizures Types of Febrile Seizures
Table 6.5.11 Suggested protocol for management of status epilepticus or any patient presenting with acute seizures
Time Action
0–5 minutes Observe
Initial observation and management • Seizure activity; diagnose SE, assess patients condition
Airway
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• Suction secretions
• Administer oxygen
• Insert nasal airway
Breathing
• Intubate and provide ventilator support if required (this may done at any time throughout the
management process)
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Circulation
• Start intervenous line, draw samples for blood sugar and biochemistry. Glucose may be estimated by a
glucometer.
Start two lines if possible
• If hypoglycemic or glycemic status unknown: IV glucose 2 ml/kg—6 months 25% glucose, less than 6
months 10% glucose
Monitoring
• Vital signs monitoring especially pulse oximetry
5–15 minutes • Continue maintaining airway breathing circulation monitoring
Stabilization, monitoring and ABC • Drug administration
support IV line established: No IV access:
• Lorazepam 0.1mg/kg (max 5 mg) at 2 mg/min • Diazepam rectally 0.5 mg/kg
Drug administration OR • Midazolam intranasal /buccal 0.2–0.4 mg/kg,
• Midazolam at 2 mg/min 0.1–0.2 mg/kg intramuscular – 0.1–0.2 mg/kg.
Start first line drug: OR • Lorazepam sublingual 0.1 mg/kg
Any benzodiazepine. • Diazepam 0.2 mg/kg (max – 10 mg) at 5 mg/min Repeat twice if seizures do not stop in 5 minutes
(Rapid onset of action but short acting ) Dose can be repeated twice if seizures do not stop Followed by
after 5 minutes • Fosphenytoin IM—20 mg/kg phenytoin
equivalent (PE). Divide in half and give two
separate injections for more rapid action
15–35 minutes No response, seizures recur or initial seizures more than 10 minutes:
Monitoring and ABC support Phenytoin (PHT)
20 mg/kg@ 1 mg/kg min IV infusion (solution only in saline as PHT is incompatible with dextrose or calcium)
Drug administration OR
Fosphenytoin (FOS)
Second line drug 20 mg/kg of PE @ 3 mg/kg/min (150 mg/min)
(solution in dextrose or saline)
Phenytoin/fosphenytoin (1.5 mg of FOS = 1 mg of PHT)
(Slower onset of action but longer acting)
35–60 minutes • Continue maintaining airway breathing circulation monitoring
(Established SE) • Repeat phenytoin/fosphenytoin
5 mg/kg 2 doses to max dose of 30 mg/kg
Monitoring and ABC Support • Start third agent—phenobarbitone/midazolam infusion
– Phenobarbitone 20 mg/kg @ 2 mg/kg/min IV
Shift to ICU OR
– Midazolam drip—0.2 mg/kg bolus, followed by infusion of 0.2–2 mg/kg/hour
iv
Drug administration OR
– Valproate injection—20 mg/kg bolus over 5 minutes, then maintain at 5 mg/kg/hour for 6 hours
Repeat second line drug in smaller dose • PLUS
• Give mannitol
Start third line drug Mannitol infusion to reduce cerebral edema if there are sign of raised intracranial pressure—
5 mL/kg over 10 minutes in all patients if seizures persist for more than 30 minutes 349
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After 60 minutes (Refractory stage) More than 60 minute
Monitoring and ABC support • Continue maintaining airway breathing circulation monitoring (Ventilator support is required at this stage)
ICU care • Continuous EEG monitoring if available
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EEG monitoring • Continuous infusion of midazolam in increasing doses till seizure control
OR
Drug administration: Induce coma Pentobarbital: loading dose: 20 mg/kg over 1 hour followed by a maintenance infusion of 0.25–5 mg/kg/hour
OR
Thiopentone: loading dose: 5–10 mg/kg over 2–5 minutes, maintenance 2–10 mg/kg/hour
OR
Propofol: loading dose 1–3 mg/kg, maintenance 2–10 mg/kg/hour
Remember
• In children most SE is symptomatic, hence investigation thoroughly to find etiology.
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• LP should not be done in a convulsing patient.
• There is no place of oral administration of drugs in acute seizures; where IV access is a problem rectal/buccal/nasal routes should be used.
• Most children can be managed successfully with BZP/PHT.
• Fosphenytoin is preferred if cost is not an issue. (Cost of Fosphenytoin is 3 times cost of phenytoin; 10 kg child—cost of phenytoin loading approx Rs
25, cost of Fosphenytoin—Rs 75.)
• Start the next drug/s only after full loading doses of PHT/PB have been given.
• Give the full loading dose in one dose as this is more effective, rather than suboptimal doses many times.
• For hypotension, inotropes may be required.
• Choice of drug depends on cost and availability, as well as the ICU and monitoring facilities. It is better to give valproate rather than phenobarbitone
and midazolam rather than pentobarbitone if ventilation facility is not available.
• After seizure control: Discontinue drug infusion at 12 hours. If seizures recur reinstate drug and try weaning off at 12 hourly intervals.
• Continue maintenance doses of PHT and phenobarbitone 12–24 hours after loading dose administration.
• End point of treatment: n EEG—no electrographic seizures or burst suppression pattern; if no EEG monitoring is available—clinical seizure control.
o
• Prognosis depends on how fast the seizures are controlled.
Abbreviations: SE, Status epilepticus; EEG, Electroencephalogram; BZP, Benzodiazepines
Table 6.5.12 Types of febrile seizures • isk of epilepsy: Overall risk of epilepsy following FS
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is 2–5%. Preventing FS does not decrease the risk of
Simple Complex
• Less than 15 minutes duration • More than 15 minutes duration epilepsy
• isk of mesial temporal sclerosis ( ): There is
and and/or
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MTS
• No focal features s/o focal • Focal features present including a strong association between the development of
origin of seizure Todd’s paralysis refractory temporal lobe epilepsy/MTS and complex
• Only one attack in one febrile and/or FS (especially prolonged or focal.) However, it remains
episode of fever • More than one attack in one unclear whether the prolonged FS is the cause of MTS,
febrile episode or whether a pre-existing MTS predisposes the child to
have prolonged FS.
are recurrent. An abnormal EEG does not change the Mental and Neurological Development
management of FS, and is therefore not recommended
as part of the assessment of a child with FS. Mental and neurological development remains normal if it
• Neuroimaging is not required in simple FS but may be was normal before onset of FS.
done in:
Mortality
– Micro/macrocephaly, neurocutaneous syndrome or
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pre-existing neurological deficit Mortality is not increased in children with FS as compared
– Persistent postictal neurological deficit after the FS to the normal population.
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– Recurrent complex FS.
West yndrome
–
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Management This is an epileptic syndrome with three essential features:
Management of attack of first FS and subsequent long-term 1. Characteristic seizures called infantile spasms: The
management of FS is shown in Flow chart 6.5.1. child has a sudden spasm of the body in which the head,
neck or trunk undergoes a contraction, resulting in
Risks Following FS either flexion (flexor spasms), but sometimes extension
• isk of recurrence: Thirty-five percent of all children (extensor spasms) or flexion of one part and extension
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will have recurrence after the first FS. Management/ of the other (mixed spasms). The severity of the spasms
350 prevention of recurrences is shown in Figure 6.5.9 can be very mild when parents may notice only a mild
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Flow chart 6.5.1 Algorithm for management of febrile seizures
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• Pyridoxine should be tried early in all children in whom carbamazepine and valproate) in management of common
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a clear cause for spasms has not been identified epileptic disorders including generalized tonic clonic as well
• Epilepsy surgery for focal cortical lesions should be as focal seizures is nearly similar. The decision regarding
considered if the child has not shown a response to specific drug depends upon:
three trials of different AEDs.
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• The type of seizures and epileptic syndrome
• Side effects
Childhood bsence pilepsy
• Cost and
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This is idiopathic generalized epilepsy with a genetic basis. • Lifestyle of the patient.
Onset is at 4–8 years, girls are more affected than boys. In our set up in view of low cost, ease of administration
and low side effects, phenytoin is the drug of choice.
Seizures
Monotherapy should be the rule. Polytherapy should be
These include typical absence seizures with sudden loss of avoided because of drug interactions, and subsequent
consciousness, associated with automatisms in the form of alteration of drug efficacy.
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lip smacking, eye blinking and hand picking. The seizure
terminates suddenly as child resumes activity as if nothing Starting Antiepileptic Drugs
happened. Many attacks occur every day. The attacks can Start an AED in a small dose and build up gradually to an
be precipitated by hyperventilation. Child is neurologically optimal dose. It is best to calculate a target dose, and start
normal. with one-third of that, and increase by one-third every
week till target dose is reached in case of drugs with short
Electroencephalogram
half-lives like carbamazepine and valproate. Phenytoin
Electroencephalogram shows 3 Hz spike wave discharges and phenobarbitone may be started with the full optimum
on a normal background. Hyperventilation precipitates 3 dose at the start. If seizures continue, increase gradually till
Hz discharges on EEG and the seizure clinically. maximum tolerated dose is reached or seizure is controlled.
reating a relapse: Restart the same drug in the same
Treatment
T
dose as was effective in controlling seizures earlier.
Valproate and ethosuximide.
Changing Antiepileptic Drugs
Prognosis
Start the second drug in a small dose, and build it up to a
Response to treatment is very good. Seizures remit in most dose effective in controlling seizures. Taper off the second
children by 10–12 years of age. However, many children drug as above.
may develop infrequent generalized tonic clonic seizures.
Principles of Combination Therapy
anagement of pilepsy • Use drugs with different mechanisms of action
M
E
• Drugs should have large therapeutic index
Drug herapy
• Few side effects
T
Decision Making: Should Antiepileptic Drugs Be Started? • Keep in mind drug interactions: Combination may cause
The most important consideration in management of increased toxicity or decreased efficacy.
epilepsy is the possibility of recurrence of the seizure. Drug Drug Level Monitoring
treatment is considered only when recurrent seizures are
confirmed. The decision should be taken after counseling Drug levels may be estimated in certain specific situations
the parents, especially after a first seizure. (Table 6.5.14), but this is not usually required. Drug
Generalized tonic clonic seizures: Recur in only dosage should be decided by clinical control of seizure or
appearance of side effects. Drugs whose levels are useful
around 40% cases; hence, first episode of generalized tonic
clonic seizure does not require treatment with long-term include phenytoin, carbamazepine, phenobarbitone and
AEDs. Exceptions to this rule include; the first episode was a valproate.
SE where the patient resides in a place, which is far off from Follow-up
medical facility or parents are overanxious and unable to
administer home treatment of acute seizures. Parents should be instructed to maintain a seizure diary
Partial, absence, atonic and myoclonic seizures: (Flow chart 6.5.2) containing details of seizure type, duration
and frequency.
Because of high rates of recurrence of seizures, treatment is
indicated in these seizure types. Initial follow-up should be:
• After 4 weeks
Choice of Antiepileptic Drugs • If breakthrough seizures occur and
Choice of antiepileptic drugs has been described in • If side effects occur.
detail in Table 6.5.13 for details. The efficacy of the four Subsequent follow-up (if seizures are controlled): three
352
first line antiepileptic drugs (phenytoin, phenobarbital, monthly.
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Table 6.5.13 Drugs used in treating epilepsy
A. Conventional antiepileptic drugs
Drugs Indications Preparation Dose Side effects toxicity Remarks
Phenytoin Focal seizures Suspension 5–8 mg/kg/day Gum hypertrophy, Younger children require higher
GTCS 30 mg/5 mL Rash doses
-
125 mg/5 mL In two divided doses Steven Johnson syndrome
Toxicity Since it has a long half life, the drug
Tablets 100 mg Ataxia may be started with the target
Nystagmus dose
Blurring of vision
Make sure about which preparation
the patient is using because of wide
variation in the concentration in
different preparation
Valproate Broad spectrum, effective against Tablets 200, 400 mg 20–40 mg/kg/day Hepatotoxicity Precaution in children less than 1
any seizure type Syrup 200 mg/5 mL Doses up to 80 mg/kg/day may be Drowsiness year of age
used provided there are no side Lethargy
Idiopathic generalized epilepsies— effects Weight gain,
Childhood absence epilepsy, Hyperammonemia
juvenile myoclonic epilepsy, Three divided doses Teratogenicity
infantile spasms,
-
Lennox Gastaut syndrome Sustained release preparation: Two
divided doses
Carbamazepine Focal seizures Suspension: 100 mg/5 mL 10–30 mg/kg/day Rash Start with low dose
Generalized tonic clonic seizures Tablets 200, 400, 600 mg Three divided doses Bone marrow depression
-
Sustained release tablets are also Steven Johnson syndrome Not to be used in absence and
available 200 mg, 500 mg myoclonic, atonic and atypical
absence seizures
Contd...
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Diseases of Central ervous ystem
T d c
extbook of Pe iatri s
354
Contd...
Nitrazepam Myoclonic seizures Tab 5 mg, 10 mg 0.5 mg/kg/day two divided doses Drowsiness
Hypotonia
Ataxia
Clonazepam Myoclonic seizures, atonic, tonic, Tabs 0.5 mg, 0.03–0.1 mg/kg/day Drowsiness
-
atypical absence 2 mg two three divided doses Hypotonia
Ataxia
-
Clobazam Add on drug for any seizure type Tabs 5 mg, 0.5 mg/kg/day one two divided Drowsiness
10 mg, 20 mg doses Hypotonia
Intermittent use in Febrile Ataxia less than other
seizures, or seizures due to known benzodiazepines
precipitating causes
Contd...
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Contd...
Topiramate Monotherapy: Focal or generalized Tab 25 mg, 50 mg, 100 mg, 200 mg Start with 0.5 mg/kg/day Drowsiness Good drug with few drug
epilepsy Increase to 5 mg/kg/day Ataxia, interactions
Metabolic acidosis
Add on Focal/generalized epilepsy Max dose: Hyperammonemia especially with
West syndrome, Broad spectrum 8 mg/kg/day valproate
add on drug for epilepsy with
multiple types of seizures, e.g.
-
Lennox Gastaut syndrome
Levetiracetam Add on for myoclonic seizures Tab 250 mg, 500 mg, Start with 10 mg/kg/day Headache Safe drug for children
Focal seizures 750 mg Anorexia No drug interactions with other
Primary generalized seizures 20 mg/kg/day increase weekly Drowsiness antiepileptic drugs
Increase to 60 mg/kg/day Behavior problems
In two divided doses
Gabapentin Add on for refractory focal epilepsy Tab 100 mg, 300 mg, 400 mg, Start with 10–15 mg/kg/day Headache Worsens myoclonus and absences
without generalization 600 mg Target dose less than 5 years 40 Anorexia
Neuralgias mg/kg/day Drowsiness
More than 5 years 30 mg/kg/day Behavior problems
Three divided doses
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355
Diseases of Central ervous ystem
Flow chart 6.5.2 A sample seizure diary
extbook of Pe iatri s
c
ame of child Age Sex
N
Month Year
d
ypes of seizure: (in case the child has multiple types of seizures)
T
Type 1 Type 2 Type 3 Type 4
ntiepileptic drugs ( Ds)
A
AE
Name Dose Timing
Date Type of seizure Time of onset Time of control Precipitating factor Routine AED given Any AED given to Remarks
(in case any identified) Yes/No control acute seizure
T
Instructions:
A separate page has to be made every month.
Any skipping of doses/alteration of AED is to be recorded.
In case of multiple types of seizures, each seizure type should be assigned a number, and the number be noted.
Remarks: Anything unusual to be brought to the doctor’s notice.
Table 6.5.14 Indications for drug level monitoring Refer to Pediatric Neurologist
Uncontrolled seizures despite adequate doses of the correct antiepileptic • Children less than 2 years
drugs (through levels) • Uncontrolled seizures
Breakthrough seizures • Suspected syndromes
Antiepileptic drugs toxicity (peak levels) • Multiple seizure types.
In polytherapy
Change in antiepileptic drugs dose or regimen
Other systemic disease altering drug metabolism or excretion Counseling
To check compliance
xplain Disease
E
Indications for Hospitalization Parents should be informed about the nature of the disease
• Status epilepticus and chances of recurrence with and without treatment.
• To observe the seizure type Some epilepsies are inherently refractory to treatment, and
• Distinguish between seizure and NEE the poor outcome in such cases should be explained to the
• Serious adverse reactions parents at the outset.
• To check compliance.
ifestyle
Duration of Treatment
L
Patients should be advised to allow the child to continue
Duration of treatment is usually 18–24 months seizure free a normal lifestyle. School teachers should be informed
period. Increasing duration of AEDs therapy beyond 2 years about the nature of disease and should be specifically
does not decrease the risk of relapse. Certain other epilepsies
told not to be biased against these children. Some caution
may warrant earlier stopping, e.g. benign centrotemporal
is advocated in possibly dangerous circumstances like
epilepsy, acute symptomatic epilepsy due to inflammatory
cycling, swimming and activities near fire particularly in the
granulomas.
first year of remission.
Stopping Antiepileptic Drugs
Before tapering, the parents must be counseled about the Drug esistant pilepsy
risk of relapse after tapering.
R
E
• The drug must never be stopped abruptly; it must be Drug resistant epilepsy may be defined as failure of
tapered gradually over 4–12 weeks adequate trials of two tolerated and appropriately chosen
356 • If patient is on multiple drugs, taper one drug at a time, and used AED schedules (whether as monotherapy or in
wait for 1 month and then taper the next drug. combination) to achieve sustained seizure freedom.
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