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CURRENT Diagnosis & Treatment: Pediatrics, 21e > Chapter 25. Neurologic & Muscular Disorders > Disorders Affecting the Nervous System in Infants &Children > Seizure Disorders (Epilepsies) > Seizures & Epilepsy in Childhood >

Table 256. Seizures by Age at Onset, Pattern, and Preferred Treatment.

Seizure Type Epilepsy

Syndrome

Age at

Onset

Clinical

Manifestations

Causative Factors EEG Pattern Other

Diagnostic

Studies

Treatment and

Comments

Neonatal seizures Birth2 wk Often subtle;

sudden

limpness or

tonic

posturing, brief

apnea,

cyanosis; odd

cry; eyes

rolling up;

blinking or

mouthing or

chewing

movements;

nystagmus,

twitchiness or

clonic

movements

(focal,

multifocal, or

generalized).

Some seizures

are

nonepileptic:

decerebrate,

or otherposturings,

release from

forebrain

inhibition. Poor

response to

drugs.

Neurologic insults

(hypoxia/ischemia;

intracranial

hemorrhage)

present more in first

3 d or after 8th day;

metabolic

disturbances alone

between 3rd and 8th

days; hypoglycemia,

hypocalcemia, hyper-

and hyponatremia.

Drug withdrawal.

Pyridoxine

dependency. Other

metabolic disorders.

CNS infections.

Structural

abnormalities.

May correlate

poorly with clinical

seizures. Focal

spikes or slow

rhythms; multifocal

discharges.

Electroclinical

dissociation may

occur: electrical

seizure without

clinical

manifestations.

Lumbar

puncture; CSF

PCR for herpes,

enterovirus;

serum Ca2+,

PO4

3, serum

and CSF

glucose, Mg2+;

BUN, amino acid

screen, blood

ammonia,

organic acid

screen, TORCHS,

other metabolic

testing if

suspected.

Ultrasound or

CT/MRI for

suspected

intracranial

hemorrhage and

structural

abnormalities.

Benzodiazepines,

Phenobarbital, IV

or IM; if seizures

not controlled,

add phenytoin

IV. Recent

experience with

levetiracetam

and topiramate.

Treat underlying

disorder.

Seizures due to

brain damage

often resistant to

anticonvulsants.

When cause in

doubt, stop

protein feedings

until enzyme

deficiencies o f

urea cycle or

amino acid

metabolism ruled

out.

Infantile spasms 318 mo,

usually

about 6 mo

Abrupt, usually

but not always

symmetrical

adduction or

flexion of limbs

with flexion of

head and

trunk; or

abduction and

extensor

movements

(similar to

Moro reflex).

Occur in

clusters

typically upon

awakening.

Associated

irritability and

regression in

development.

Symptomatic in

approximately two-

thirds. Acquired CNS

injury in

approximately one-

third; biochemical,

infectious,

degenerative in

approximately one-

third; cryptogenic in

approximately one-

third. With early

onset, pyridoxine

dependency,

inherited metabolic

disorders. Tuberous

sclerosis in 510%.

TORCHS, homeobox

gene mutations,

ARX, and other

genetic mutations.

Hypsarrhythmia

(chaotic high-

voltage slow

waves or random

spikes (90%));

other

abnormalities in

10%. Rarely

normal at onset.

EEG normalization

early in course

usually correlates

with reduction of

seizures; not

helpful

prognostically

regarding mental

development.

Funduscopic and

skin

examination,

Amino and

organic acid

screen.

Chromosomes

TORCHS screen,

CT, or MRI scan

should be done

to (1) establish

definite

diagnosis, (2)

aid in genetic

counseling. Trial

ofpyridoxine.

Occasionally,

surgical

resection of

cortical

malformation.

ACTH gel (40

IU/d 150

IU/m2/d) IM once

daily. Vigabatrin,

especially if

tuberous

sclerosis. B6

(pyridoxine) trial.In resistant

cases,

topiramate,

zonisamide,

valproic acid,

lamotrigine,

ketogenic diet.

Early treatment

leads to

improved

outcome.

Febrile convulsions 3 mo5 y

(maximum

618 mo);

most

common

childhood

seizure

(incidence

Usually

generalized

seizures, < 15

min; rarely

focal in onset.

May lead to

status

epilepticus.

Nonneurologic febrile

illness (temperature

rises to 39C or

higher). Risk factors:

positive family

history, day care,

slow development,

prolonged neonatal

Normal interictal

EEG, especially

when obtained 8

10 d after seizure.

Therefore, not

useful unless

complicating

features.

Lumbar

puncture in

infants or

whenever

suspicion of

meningitis

exists.

Treat underlying

illness, fever.

Diazepam orally,

0.30.5 mg/kg,

divided 3 times

daily during

illness may be

considered.
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2%) Recurrence risk

of second

febrile seizure

30% (50% if

younger than

1 y of age);

recurrence risk

is same after

status

epilepticus.

hospitalization. Diastat rectally

for prolonged (>

5 min) seizure.

Prophylaxis with

phenobarbital or

valproic acid

rarely needed.

Cryptogenic generalized

epilepsies of earlychildhood (Lennox-Gastaut

syndrome, Myoclonic-

Astatic Epilepsy [Doose

Syndrome] and Dravet

syndrome)

Any time in

childhood(usually 27

y)

Mixed se izures

dependent onparticular

syndrome,

including tonic,

myoclonic

(shocklike

violent

contractions of

one or more

muscle groups,

singly or

irregularly

repetitive);

atonic ("drop

attacks") and

atypicalabsence with

episodes of

absence

status

epilepticus.

Multiple causes ,

usually resulting indiffuse neuronal

damage. History of

infantile spasms;

prenatal or perinatal

brain damage; viral

meningoencephalitis;

CNS degenerative

disorders; structural

cerebral

abnormalities (eg,

migrational

abnormalities).

Doose syndrome.

Dravet syndrome

associated withSCN1A mutation.

Atypical slow (1

2.5 Hz) spike-wavecomplexes and

bursts of high-

voltage

generalized

spikes, often with

diffusely s low

background

frequencies.

Electrodecremental

and fast spikes

during sleep.

As dictated by

index ofsuspicion:

genetic testing;

inherited

metabolic

disorders,

neuronal ceroid

lipofuscinosis,

others. MRI

scan, WBC

lysosomal

enzymes. Skin

or conjunctival

biopsy for

electron

microscopy,nerve

conduction

studies if

degenerative

disease

suspected.

Difficult to treat.

Topiramate,ethosuximide,

felbamate,

levetiracetam,

zonisamide,

valproate,

clonazepam,

rufinamide,

clobazam

(approval

pending)

ketogenic diet,

vagus nerve

stimulation. Avoid

phenytoin,

carbamazepine,oxcarbazepine,

gabapentin.

(Stiripentol used

in Europe but not

approved in US.)

Childhood absence

epilepsy

312 y Lapses of

consciousness

or vacant

stares, lasting

about 310 s,

often in

clusters.

Automatismsof face and

hands; clonic

activity in 30

45%. Often

confused with

complex partial

seizures but

no aura or

postictal

confusion.

Some risk for

developing

generalized

tonic clonic

seizures.

Unknown. Genetic

component.

Abnormal

thalamocortical

circuitry.

3/s bilaterally

synchronous,

symmetrical, high-

voltage spikes and

waves provoked

by

hyperventilation.

EEG alwaysabnormal. EEG

normalization

correlates closely

with control of

seizures.

Hyperventilation

often provokes

attacks. Imaging

studies rarely of

value.

Ethosuximide

most effective

and best

tolerated;

valproic acid.

Lamotrigine, in

resistant cases,

zonisamide,topiramate,

levetiracetam,

acetazolamide,

ketogenic diet.

Juvenile absence epilepsy 1015 y Absence

seizures less

frequent than

in childhood

absence

epilepsy. May

have greater

risk of

convulsive

seizures.

Unknown

(idiopathic), possibly

genetic.

3-Hz spike wave

and atypical

generalized

discharges.

Not always

triggered by

hyperventilation.

Same as

childhood

absence epilepsy

but may be more

difficult to treat

successfully.

Simple partial or focal

seizures

(motor/sensory/jacksonian)

Any age Seizure may

involve any

part of body;may spread in

fixed pattern

(jacksonian

march),

becoming

generalized. In

Often unknown;

birth trauma,

inflammatoryprocess, vascular

accidents,

meningoencephalitis,

malformations of

cortical development

(dysplasia), etc. If

EEG may be

normal; focal

spikes or slowwaves in

appropriate

cortical region;

"rolandic spikes"

(centrotemporal

spikes) are typical.

MRI, repeat if

seizures poorly

controlled orprogressive.

Oxcarbazepine,

carbamazepine;

lamotrigine,gabapentin,

topiramate,

levetiracetam,

zonisamide,

lacosamide, and

phenytoin.
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,

epileptogenic

focus often

"shifts," and

epileptic

manifestations

may change

concomitantly.

with new or

progressive

neurologic deficits, a

structural lesion (eg,

brain tumor) is likely.

If epilepsia partialis

continua (simple

partial status

epilepticus),

Rasmussen

syndrome is likely.

.

useful adjunct. If

medications fail,

surgery may be

an option.

Complex partial seizures Any age Aura

progressing to

larger event,

aura and

seizure

stereotyped

for each

patient and

related to part

of brain

seizure

originates, eg,

temporal lobe

seizures may

have a

sensation of

fear, dj vu;

epigastric

discomfort,

odd smell or

taste (usually

unpleasant).

Seizure may

consist o f

vague stare;

facial, tongue,

or swallowing

movements

and throatysounds; or

various

complex

automatisms.

Usually brief,

1590 s,

followed by

confusion or

sleep.

As above. Temporal

lobes especially

sensitive to hypoxia;

seizure may be a

sequela of birth

trauma, febrile

convulsions, viral

encephalitis,

especially herpes.

Malformations of

cortical development

(dysplasia) common

in medication

resistant patients.

Remediable causes

are small cryptic

tumors or vascular

malformations. May

be genetic.

As above. MRI; PCR of CSF

in acute febrile

situation for

herpes or

enteroviral

encephalitis.

SPECT, PET

scan, video-EEG

monitoring when

epilepsy surgery

considered.

As above.

Benign epilepsy of

childhood with

centrotemporal spikes

(BECTS/rolandic epilepsy)

516 y Simple partial

seizures of

face, tongue,

hand. With or

without

secondary

generalization.

Usually

nocturnal.

Similar seizure

patterns may

be observed in

patients with

focal cortical

lesions. Almost

always remits

by puberty.

Seizure history or

abnormal EEG

findings in relatives

of 40% of affected

probands and 18%

20% of parents and

siblings, suggesting

transmission by a

single autosomal

dominant gene,

possibly with age-

dependent

penetrance.

Centrotemporal

spikes or sharp

waves ("rolandic

discharges")

appearing

paroxysmally

against a normal

EEG background.

Seldom need CT

or MRI scan.

Often no

medication is

necessary,

especially if

seizure is

exclusively

nocturnal and

infrequent.

Oxcarbazepine,

carbamazepine

or others. (See

complex partial

seizures.)

Juvenile myoclonic epilepsy

(of Janz)

Late

childhood

andadolescence,

peaking at

13 y

Mild myoclonic

jerks of neck

and shoulderflexor muscles

after

awakening.

Usually

generalized

tonic-clonic

40% of relatives

have myoclonias,

especially in females;15% have the

abnormal EEG

pattern with clinical

attacks.

Interictal EEG

shows variety of

spike-and-wavesequences or 46-

Hz multispike-and-

wave complexes

("fast spikes").

If course is

unfavorable,

differentiatefrom progressive

myoclonic

syndromes by

appropriate

studies [eg,

b io s ies

Lamotrigine,

valproic acid,

topiramate,levetiracetam,

zonisamide.
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Your IP address is 122.200.2.50

seizures as

well. Often

absence

seizures.

Intelligence

usually normal.

Rarely resolves

but usually

remits on

medications.

(muscles , liver,

etc)].

Imaging may not

be necessary.

Generalized tonic-clonic

seizures (grand mal)

(GTCS)

Any age Loss of

consciousness;

tonic-clonic

movements,

often preceded

by vague aura

or cry.

Incontinence in

15%. Postictal

confusion and

somnolence.

Often mixed

with or

masking other

seizure

patterns.

Often unknown.

Genetic component.

May be seen with

metabolic

disturbances,

trauma, infection,

intoxication,

degenerative

disorders, brain

tumors.

Bilaterally

synchronous,

symmetrical

multiple high-

voltage spikes,

spikes waves (eg,

3/s). EEG often

normal in those

younger than age

4 y. Focal spikes

may become

"secondarily

generalized."

Imaging;

metabolic and

infectious

evaluation may

be appropriate.

Levitiracetam;

topiramate,

lamotrigine,

zonisamide,

valproic acid,

felbamate.

Combinations

may be

necessary.

Carbamazepine,

oxcarbazepine or

valproic acid;

phenytoin may

also be effective.

ACTH, adrenocorticotropic hormone; BUN, blood urea nitrogen; CNS, central nervous system; CSF, cerebrospinal fluid; CT, computed

tomography; EEG, electroencephalogram; IM, intramuscularly; IV, intravenously; MRI, magnetic resonance imaging; PCR, polymerase chain

reaction; PET, positron emission tomography; SPECT, single-photon emission tomography; TORCHS, toxoplasmosis, other infections,

rubella, cytomegalovirus, herpes simplex, and syphilis; WBC, white blood cell.
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