Chapter 11 Presented by:

dr. Budhi Febrian PJ

Nonepileptic
Moderator:
Abnormalities dr. Desin Pambudi
Sejahtera, M.Sc, SpS (K)
Electroencephalogram (EEG)
mengevaluasi fungsi otak,bukan struktur.

EEG Abnormal EEG

dapat menjadi indikator disfungsi otak,

EEG tidak bisa membedakan etiologi

atau patologi.

Dari EEG dapat ditinjau pola yang berbeda dari

EEG abnormal dan signifikansi klinisnya.
Kelainan EEG nonepilepsi yang abnormal
dapat secara luas dibagi menjadi empat kategori:

01 Kelainan ritme latar belakang

02 Pola tidur yang abnormal

03 Aktivitas lambat fokal atau general

yang abnormal

04 Pola periodik yang abnormal

 1. Kelainan ritme latar belakang

amplitudo distribusi

kecepatan Perubahan ritme

simetri reaktivitas
dari aktivitas latar
mungkin terjadi selama berbagai gangguan SSP belakang
 Perubahannya mungkin melibatkan
satu atau lebih ritme fisiologis:
ritme alfa, beta, atau mu

A. Alpha rhythm

kecemasan mengantuk
Umumnya
tidak ditemukan
Ritme alpha atau
sedikit di posterior
mata terbuka perhatian
Beberapa individu asimtomatik biasanya memiliki sedikit atau
tidak memiliki ritme alfa, mungkin dipengaruhi genetik
 Pada orang dewasa yang terjaga
--> ritme alfa kurang dari 8Hz tidak normal
--> perlambatan --> kelainan nonspesifik.

metabolik ensefalopati
pasien dengan
perlambatan bilateral
krn infeksi/
demensia dari ritme alfa sebab lain

keracunan
hipotiroidisme
Perlambatan asimetris dari ritme alfa dengan
perbedaan konsisten lebih besar dari 1,5Hz antara
kedua sisi --> tidak normal
--> kemungkinan lesi di sisi yang lebih lambat
Perbedaan amplitudo irama alfa antara kedua
hemisfer dianggap signifikan jika melebihi 50%.
Penurunan amplitudo 35% di sisi kanan mungkin
signifikan.

Lesi yang melibatkan korteks serebral, terutama di

daerah posterior atau yang menyebabkan penumpukan
cairan antara otak dan elektroda perekam,
contoh pada edema kulit kepala atau subdural, dapat
menyebabkan atenuasi ritme alfa ipsilateral
Amplitudo latar belakang yang sangat berkurang di satu
sisi EEG, dibandingkan dengan chanel homolog
sisi kontralateral, ditemukan abnormalitas kortikal grey
matter, atau dengan kelebihan
cairan antara korteks dan elektroda perekam sesuai
karakteristik stroke iskemik atau hematoma subdural.
Pada pasien dengan lesi pada gray matter dan white matter
menghasilkan aktivitas delta adalah tipikal.

Amplitudo latar belakang yang menurun juga dapat terjadi

pada lesi kongenital, seperti kista porencephalic, atau
dengan Sindrom Sturge-Weber.
Atenuasi transien latar belakang merupakan karakteristik
dari EEG postiktal pasien dengan kejang onset fokal.

Fokal supresi biasanya akan melibatkan banyak

elektroda. Penekanan fokus yang terbatas pada satu
elektroda lebih mungkin disebabkan oleh noda pasta
elektroda, atau beberapa artefak lain yang mempengaruhi
sistem pencatatan.

Peningkatan amplitudo latar belakang bentuk gelombang

(ritme alfa, spindle tidur, aktivitas beta, atau ritme mu)
dapat terlihat pada lesi ipsilateral ke serebral.
Distribusi ritme alfa yang tidak normal --> yang tersebar
luas, termasuk daerah frontal --> alfa koma,
yang mungkin disebabkan infark batang otak atau
anoksia serebral, atau efek obat.

Dalam konteks ini, ada baiknya untuk diulang kembali

bahwa ritme alfa mungkin muncul secara palsu di area
depan saat menggunakan referensi potensial rata-rata, dan
ini tidak boleh disalahartikan sebagai koma alfa pola.
Kurangnya reaktivitas ritme alfa saat membuka mata
secara konsisten di satu sisi --> lesi awal lobus oksipital .

Total lack reaktivitas ritme alfa --> koma alfa,

terutama dalam kasus anoksia serebral difus karena
gagal jantung.

Dalam kasus koma alfa akibat lesi batang otak bagian

bawah, mungkin ada beberapa derajat reaktivitas.

Ini kontras dengan temuan pada kasus psikogenik

unresponsif --> reaktivitas pembukaan mata normal.
Peningkatan fokal pada amplitudo dan atau frekuensi
ritme alfa diketahui terjadi pada pasien dengan
lesi struktural, terutama tumor

Peningkatan amplitudo terlokalisasi juga dapat dilihat pada

defek tengkorak.
Kegagalan unilateral dari pemblokiran alfa pada
pembukaan mata--> fenomena bancaud, terjadi
dengan lesi pada lobus parietal dan temporal pada
sisi yang gagal diblokir.
Lesi serebral unilateral
terletak di bagian frontal atau lobus temporal yang
menghilangkan pemblokiran alfa
biasanya dikaitkan dengan gangguan kesadaran dan
defisit neurologis yang menonjol.

Lesi terletak di parietal atau lobus oksipital -->

sering tidak terkait dengan gangguan
kesadaran atau defisit neurologis yang parah
Binocular blindness --> menyebabkan hilangnya
reaktivitas irama alfa saat membuka mata dengan
distribusi luas.

Seperti orang buta sejak lahir mungkin tidak memiliki

ritme alfa dan dapat terjadi spike oksipital tanpa adanya
lesi di oksipital.
Monocular blindness or loss of discrimiminative
vision can cause failure of alpha blocking in both
hemisphere when the blind eye is opened; opening of
the seeing eye produces normal bilateral alpha
blocking.
Beta activity
Aktivitas beta masih normal s/d 35% lebih rendah di satu
sisi,
Asimetri yang lebih besar, digabungkan dengan kelainan
lain--> indikator sensitif pada cedera kortikal yang
mendasari wilayah amplitudo yang lebih rendah.

Baik pelemahan dan aksentuasi aktivitas beta

mungkin tidak normal.
Atenuasi beta sering terlihat di:
1. Epilepsy with Generalized Tonic-Clonic
Seizures on Awakening.
EEG Findings:
Background is normal. There are rare generalized spike-waves and rare fast
polyspike-waves(2-4Hz). Changes are activated at spontaneous or provoked
awakening or during transitions between sleep stages. In some patients,
interictal changes will never be recorded.

2. West,s Syndrome
is one of the most frequent epileptic syndrome in infants, with an incidence of
2.9-4.9 per 100,000. This encephalopathy is characterized by a triad:
1.Infantile spasms
2.developmental retardation
3.hypsarrhythmia on EEG.
1. Epilepsy with Generalized Tonic-Clonic
Seizures on Awakening.
The concept of awakening epilepsy was first developed
by Janz. This type of idiopathic generalized epilepsy is
less common than JME. Onset is generally in the
second decade but earlier or later onset is possible
(range: 5-25 years). There is a slight male
predominance . A family history of epilepsy is
frequent. Generalized tonic-clonic seizures occur
within one hour of spontaneous morning awakening at
the end of the nocturnal sleep period(90%), or during
spontaneous or provoked intermediate awakenings.
A lesser peak of occurrence is found during
the evening relaxation period. Seizures are
rare and are often elicited by sleep
deprivation or excessive consumption of
alcohol on the previous evening. Some
patients may experience rare myoclonic
jerks or absences. Prognosis is usually
good, as seizures remain rare
spontaneously and treatment is effective.
EEG Findgs
Background is normal. There are rare generalized
spike-waves and rare fast polyspike-waves(2-4Hz).
Changes are activated at spontaneous or provoked
awakening or during transitions between sleep stages.
In some patients, interictal changes will never be
recorded.
2. West,s Syndrome
The west syndrome is one of the most frequent
epileptic syndrome in infants, with an incidence of 2.9-
4.9 per 100,000. This encephalopathy is characterized
by a triad: 1.Infantile spasms 2.developmental
retardation 3.hypsarrhythmia on EEG.
Onset nearly always occurs in the first year of life, usually
between the ages of 4 and 7 months . Nearly 90% of cases
are associated with neurological abnormalities arising from
a diverse array of structural, metabolic, and genetic
disorders. Only 10% to 15% of cases are cryptogenic/
idiopathic.
Spasms are brief, symmetric, bilateral tonic
contractions of muscles of trunk, neck and limbs(flexor
spasms). Contractions are often followed by crying.
Less frequently, there are extensor spasms with a
sudden extension of trunk and neck with abduction and
extension of the arms. Spasms can also be mixed
(flexor-extensor), asymmetric or unilateral, and in the
two latter cases often contralateral to a brain lesion.
Spasms occur in series, often at awakening or at sleep
onset, less commonly during nREM sleep and never
during REM sleep.
Associated focal seizures should
always be sought, as these constitute an important
element for etiological diagnosis and prognosis.
Specific etiologies can be found in half of the cases,
mainly a neurocutaneous syndrome(tuberous sclerosis),
malformations, pre-, peri-, or postnatal
encephalopathies, as well as metabolic, degenerative,
or chromosomal diseases, or prenatal infections.
Prognosis is in part related to the etiology. It has poor
prognosis in most cases, often evolving into another
epileptic encephalopathy, such as the lennox- Gastaut
syndrome, or into another severe type of epilepsy
associated with major mental retardation.
EEG findings
The interictal EEG often shows typical "hypsarrhythmia".
hypsarrhythmia is seen in 75% of patients with West syndrome.
Background is disorganized, with high-voltage, asynchronous
and arrhythmic slow waves, in association with asymmetric and
multifocal spikes and polyspikes. It is often necessary to lower the
amplitude to have a better look at the EEG tracings. Hypsarrhythmia
is mostly present at onset and can precede the occurrence of
spasms. It is seen in waking and is fragmented during sleep. It can
occur selectively during somnolence. In light nREM sleep,it becomes
discontinuous. Spikes become more frequent and tend to be more
diffuse and synchronouos. Irregular bursts of polyspike waves are
separated by apparently fairly normal segments that may include
sleep transients like spindles. Duration of REM sleep is shortened
Clinical spasms are associated with a marked suppression of the
background that lasts for the duration of the spasm. This
characteristic response is called the "electrodecremental
response”. Spasms are associated with a brief tonic muscular
contraction
evidenced by surface EMG, that is symmetric or not according to
the etiology. Serial spasms may occur at awakening, with or without
interictal hypsarrhythmia. The presence of hypsarrhythmia between
spasms may be characteristic of idiopathic cases and of a better
prognosis. Focal seizures can initiate the series of spasms, occur
during the series, or occur independently.
EEG is useful in judging successful treatment of West syndrome.
Typically, shortly after treatment with adrenocorticotropic hormone
(ACTH) or vigabatrin is initiated, the spasms stop and
hypsarrhythmia disappears.
 2. Pola tidur yang abnormal
Asimetri amplitudo sleep spindel --> sugestif lesi di sisi
dengan amplitudo lebih rendah -->hematoma subdural.
dengan amplitudo lebih tinggi --> defek tengkorak

Gelombang V amplitudo asimetris yang konsisten

--> lesi struktural, subdural hematoma atau efusi di sisi
defek tengkorak.
 2. Pola tidur yang abnormal (2)
Kelompok kelainan pola tidur lainnya termasuk gangguan
arsitektur tidur.
Seseorang biasanya melewati tahap 1 dan 2 tidur sebelum
fase pertama tidur REM terjadi, biasanya 90 menit setelah
tidur.
Fase REM yang terjadi pada awal tidur-->ciri narkolepsi
Studi polisomnografi diperlukan untuk mengevaluasi
gangguan tidur tersebut.
 3. Aktivitas lambat fokal/ general yang abnormal

Paling sering ditemukan.

Mengulang kembali slow activity yang normal:
1. delta activity terjadi sleep stages 3 and 4 ,
2. theta activity terjadi background activity of children
during wakefulness,
3. theta or delta activity yang terlihat saat hyperventilasi.
Asymmetries in amplitude and frequency may be more
significant than the mere presence of the activity.
This is due to the variable occurrence of theta activity in
drowsiness and in the waking state of normal young
and very old persons.
Aktifitas lambat dibagi menjadi:
A. Generalized intermittent slow activity
B. Focal and regional intermittent slow activity
C. Persistent slow activity
D. Encephalophatic patterns (theta coma, alpha
coma, beta coma, spindle coma, triphasic waves)

Perlambatan general paling sering pada ensefalopati.

Perlambatan fokal paling sering pada lesi struktural.
Perlambatan regional bihemisfer jarang terjadi.
A. Generalized intermittent slow activity

It consists of intermittent rhythmic, usually

monomorphic, slow activity most commonly occurring
in the delta frequency band.
The acronym IRDA (intermittent rhythmic delta activity) is
often used for this pattern.
The activity is characteristically bilateral and synchronous,
showing frontal (FIRDA) or occipital dominance(OIRDA);
rarely, it may be most prominent over the temporal areas.

TIRDA(temporal intermittent rhythmic delta activity)

is an important epileptogenic abnormality, highly
pathognomonic for temporal lobe epilepsy. These
rhythmical unilateral delta trains indicate a focal lesion.
Even when associated with a focal lesion, IRDA by
itself is nonlocalizing. The common denominator in the
wide variety of pathological processes producing IRDA is
that, when such an abnormality appears, it is likely to
be associated with the development of widespread
brain dysfunction ; the earliest clinical correlates are
fluctuating levels of alertness and attention. With focal
lesions, the mechanisms may be sufficient distortion of
the brain to produce secondary disturbances at both
the subcortical and cortical levels. With primary
intracranial encephalopathies, it appears to be due to
widespread involvement of the gray matter at
subcortical and cortical levels.
The dominance seems to be age related,
OIRDA being more common in children.
Intermittent rhythmic delta activity is usually of high
amplitude; it stands out from the background and often
has a frequency of 2to 3 Hz.
These patterns attenuate with alerting or eye opening. On
the other hand,eye closure, drowsiness, and
hyperventilation accentuate IRDA.
Although IRDA disappears in stage 2 and deeper non–
rapid eye movement (NREM) sleep, it may
reappear in REM sleep.
IRDA is not specific for a single etiology and can
occur in response to systemic toxic or metabolic
disturbances as well as to diffuse or focal intracranial
diseases. This may be due to diverse etiologies, such as
infectious, inflammatory, degenerative, traumatic,
vascular, or neoplastic disorders. IRDA is also the
nonspecific type of slowing that occurs in normal
individuals in response to hyperventilation. In such
cases, it should not be interpreted as an abnormality,
but rather as the response of a normal CNS to the stress
of an acutely changing Pco2.
Because IRDA may occur in response to systemic toxic
or metabolic disturbances, diffuse intracranial
pathology, or focal intracranial pathology, its localizing
value obviously is limited. Even when it is due to a focal
expanding lesion, the peak localization of the IRDA tends to
be age-dependent [maximal frontal in adults and maximal
posterior in children]. It is independent of the localization of
the lesion, which may be at some distance, either in the
supra- or infratentorial space, from the maximum expression
of the IRDA. The recognition that IRDA is a non localizing
rhythm, even when associated with an intracranial lesion, led
to its earlier designation as a “projected” or “distant” rhythm.
Although frequently bilateral, IRDA may occur
predominantly unilaterally. Even when it occurs
unilaterally in association with a lateralized
supratentorial lesion, the lateralization of the IRDA,
although usually ipsilateral, may even be contralateral
to the focal lesion . Therefore, when IRDA is present,
determining whether it is due to a focal lesion (and if
so, the location of the focal lesion) is the best based on
persistent localizing signs, and not on the morphology
or even the laterality of IRDA.
Summary:

IRDA is nonspecific in that it can be

seen in association with a wide variety of pathological
processes varying from systemic toxic or metabolic
disturbances to focal intracranial lesions.
B. Focal and regional intermittent slow activity
These abnormalities limited to one area or to one side of
the brain. Focal slow activity usually indicates a focal
subcortical structural lesion.
The slow activity typically has an irregular, polymorphic
appearance, hence the name polymorphic delta activity
(PDA).
Differential diagnosis focal irregular slow activity :
• Tumor
• Stroke - ischemic or hemorrhagic
• Infection - abscess or encephalitis
• Trauma - contusion or hematoma
• Epileptic focus – irregular slow activity may be associated
with an epileptic focus in the absence of
structural lesion
• Transient focal abnormality as may be seen in migraine,
ischemia, postictal dysfunction after a focal
seizure
C. Persistent slow activity
Persistent slow activity is usually in the delta frequency
band. It may occur as monomorphic, rhythmic waves
or as polymorphic, arrhythmic waves. It may be
generalized, lateralized, or focal.
In the case of the rhythmic delta activity, the waveforms
resemble each other and maintain a somewhat constant
frequency. Polymorphic delta activity (PDA) usually has a
frequency of 0.5 to 3 Hz, and the waveforms change in
frequency, amplitude, and morphology in a continuous
fashion. No reactivity to stimulation and persists both
during wakefulness and sleep. Even hyperventilation
may not have much effect on PDA.
D. Encephalopathic patterns (alpha coma, theta coma,
beta coma, spindle coma, triphasic waves)

These waves show little variation in frequency and are

either the only activity present or are clearly the dominant
activity.

Variants of these coma patterns occurs with less stable

dominant frequency and with intermixed generalized slow
waves.
1. Alpha coma:
Unremitting 8- to 13-Hz EEG activity
Unresponsive to eye opening or other stimulation.
Lack of reactivity and its spatial distribution.
Monorhythmic or diffuse, or it may
have anterior or posterior accentuation.
Only minor fluctuations in amplitude occur, and minimal to
no reactivity to external stimulation can be elicited.
Two kinds of alpha coma patterns :
a) The posterior dominant alpha coma pattern shows
either no reaction or, rarely, a variable attenuation
or increase in amplitude following altering maneuvers. -->
brain stem lesions, particularly pontine infarction.

b) Generalized or predominantly frontal alpha

activity without reaction to altering stimuli can be
seen in patients with widespread cerebral damage,
especially that following cardiac or respiratory
arrest, prolonged hypoglycemia or bilateral
destruction of midline thalamic nuclei.
2. Theta coma:
Generalized monorhythmic activity in the theta frequency
range that shows little or no evidence of either
spontaneous variability or reactivity to noxious stimulation.

The clinical correlates of the theta coma

patterns are similar to those of the generalized or
frontal dominant alpha coma pattern.

Transisi Alpha ke theta koma mengindikasikan

poor prognosis for normal recovery or survival.
3. Beta coma:
Generalized, sometimes frontal dominant, pattern of
mainly rhythmic beta waveforms. It usually occurs in
coma caused by or complicated by barbiturate or
benzodiazepine intoxication. It may also occur in acute
brainstem lesions.

Usually associated with a favorable outcome, because

in most cases it is a demonstration of the ability of cortical
structures to generate a ‘normal’ response to
pharmacological stimulation.
4. Spindle coma:
Spindle coma is a term used when diurnal EEG activity in
comatose patients contain features of stage 2 sleep,
including prominent spindle like activity.
This EEG pattern usually carries a good prognosis.
It is often accompanied by other sleep patterns such as
vertex waves or K complexes and appears to represent a
sleep stage with impaired arousal.
It is often seen following head trauma, patients
recovering from anoxic encephalopathy or
encephalitis.
5. Triphasic waves:
Frontally positive sharp transients. Amplitudo greater
than 70 microvolts. Consist of waveforms with 3
phases, each succeeding phase with longer duration
than the one before, that clearly stand out from the
background and other slow waves.
They are bilateral and occur in bursts of repetitive waves at
1-3 Hz. The total duration of each triphasic wave complex
varies between approximately 0.25 and 0.5 s. The second
phase is positive in polarity and usually has the greatest
amplitude of the 3 phases. Occasionally a relatively low
amplitude positive phase can be seen consistently
proceeding the subsequent 3 phases.
Clinical conditions associated with the triphasic
wave pattern : metabolic / toxic disturbances
with the most common being hepatic failure, renal
failure and anoxia and with other disorders
including: hypo- or hypernatremia, hypercalcemia,
hypoglycemia, stroke, hypertensive encephalopathy,
cerebral abscess, encephalitis, congestive heart
failure,
septic shock, lithium intoxication, postictal state,
nonconvulsive status epilepticus.
The prognosis mainly dependent on the degree of
background slowing, suppression or reduced
reactivity, not the presence or absence of triphasic waves.
 4. Pola periodik yang abnormal
Stereotyped recurrences of paroxysmal complexes at
relatively fixed intervals. Should be present throughout the
entire tracing or a major portion of it.
The discharges should stand out from the background.
Composed of slow waves, sharp waves, or sharp and slow
wave complexes.
Are not necessarily associated with a chronic seizure
disorder.
Often indicate severe encephalopathy and may or may
not be associated with clinical seizures.
 4. Pola periodik yang abnormal (2)

Generalized periodic paroxysmal patterns are seen

classically in subacute sclerosing panencephalitis(SSPE),
jakob-Creutzfeldt disease (JKD), and herpes simplex
encephalitis(HSE).
Electroencephalographic tracings with a burst suppression
pattern may also appear periodic, especially when the
bursts occur at regular intervals.
Lateralized and focal periodic paroxysmal patterns are
seen in acute destructive lesions involving one
hemisphere.
Generalized Periodic Paroxysmal Patterns
I. Subacute sclerosing panencephalitis (SSPE)
Subacute sclerosing panencephalitis (SSPE) is an
inflammatory disease of children and adolescents
caused by chronic infection with the measles virus. The
characteristic EEG pattern, initially described by
Radermecker and Cobb and Hill, consists of high voltage
(300-1500 µV), repetitive, polyphasic sharp
and slow wave complexes of 0.5- to 2-second duration
that recur every 4-15 seconds. Rarely, the complexes
can occur at intervals of 1-5 minutes. The interval
between complexes may shorten as the disease
progresses.
A prominent feature of SSPE is the stereotyped motor
jerks or spasms occurring with the periodic complexes.
The movements are often described as myoclonic
jerks; however, they do not have the momentary
lightning-quick nature of true myoclonus; instead, the
movements consist of an initial “shock-like
abruptness” followed by a momentary arrest of the
movement, and then a gradual melting away to the
position of the rest.
Abnormal movements, cognitive deterioration, and the
diagnostic EEG characterize the clinical disease.
II. Creutzfeldt-jacob disease(CJD)
CJD is one of the other prion diseases causing a
diffuse disorder of the CNS that is characterized by
progressive dementia, motor dysfunction, myoclonus,
and a characteristic periodic EEG pattern.
The earliest EEG changes consist of a disorganization and
decrease of normal background activity and the
development of progressive slow-wave abnormalities.
Usually generalized, but at times they occur in a more
focal or lateralized fashion. As the disease progresses,
diphasic or triphasic slow-wave discharges appear.
One characteristric feature of the periodic
discharges in CJD is the reactivity of the sharp waves
to alerting or afferent stimuli.
Loud noises and certain types of drugs such as diazepam
and the barbiturates, can temporarily abolish the periodic
sharp waves and myoclonic jerks.
As the disease progresses, the interburst interval
increases and the amplitude of the periodic sharp
waves decreases. In the late stages of the disease, the
EEG becomes almost isoelectric, with intermittent
bursts of sharp or slow waveforms that finally
disappear in the terminal stages of the disease.
On occasion CJD may progress rapidly, and the
typical EEG abnormalities may evolve over a period
of 1-3 weeks, and serial EEGs are helpful in making or
confirming the diagnosis. One should be aware,
however, that some patients with CJD may not show
the typical pattern of periodic sharp waves.
The “mad cow” variant of CJD has been described
as occurring at a younger age of onset than is typical
for CJD and without the typical EEG changes of CJD.
III. Burst-suppression pattern
Sometimes called the suppression-burst pattern when the
duration of the suppression is greater than the duration of
the burst.
This subtype of periodic pattern consists of bursts of
activity (mixture of sharp and slow waves) periodically
interrupted by episodes of suppression (activity <10
µV). Typically, the episodes of suppression are longer
(typically 5-10 s) than the bursts of activity (typically 1-3 s).
Background suppression is a "nearly flat" EEG, with very
low voltage activity (<10 µV) and no reactivity, but the
activity is still too large to meet criteria for electrocerebral
inactivity (ECI).
The bursts usually have a polymorphic appearance, but
may contain high voltage epileptiform activity in some
patients who are placed in barbiturate coma because of
refractory status epilepticus.
The duration of the intervals between the bursts is
often fairly regular in a given recording and ranges from 5
to 10s depending on the severity of the cerebral
dysfunction.
Seizure manifestations associated with this pattern
are limited to myoclonus.
Clinical conditions causing burst-suppression patterns
include a variety of severe disorders of cerebral structure
or function. Structural lesions include acute strokes,
postanoxic encephalopathy, head injury and encephalitis.
Local burst-suppression patterns can be seen over
abnormal cortical areas during surgical anesthesia.
Commonly reversible disorders causing this pattern include
deep anesthesia and coma due to barbiturates and other
CNS depressant drugs, hypothermia, and Reye,s
syndrome. The association of myoclonus, burst-
suppression patterns and postanoxic coma suggests a
very poor prognosis for survival.
IV. Periodic Lateralized Epileptiform Discharges (PLEDs)
Abnormalities consisting of repetitive spike or
sharp wave discharges, which are focal or lateralized
over one hemisphere, recur at intervals of 0.5-5
seconds, and continue through most of the duration of
the EEG study.
They are seen most frequently in the setting of acute
unilateral lesions such as cerebral infarctions,
encephalitis or tumors or in the setting of chronic
lesions or long-standing epileptic disorders.
PLEDs are usually self-limited and resolve after
the acute phase of a cerebral insult. Rarely, they may
persist on a chronic basis. Seizures often occur when
PLEDs are seen on the EEG, but clinical and
electrographic seizure manifestations typically differ
from the baseline (PLEDs) condition. The seizures
were either partial or generalized and the partial
seizures were always contralateral to the PLEDs.
Bilateral independent PLEDs (BIPLEDs) are
periodic complexes over both hemispheres.
Are not synchronous and may differ in morphology and
site of maximal expression on each side. This is an
uncommon EEG finding. In a series of 18 patients, the
most common etiologies were anoxic brain injury (28%) and
CNS infection (28%). While BIPLEDs have been associated
with herpes simplex encephalitis, the pattern can occur in
other CNS infections as well.
Incidence of coma BIPLEDs higher than PLEDs (72% vs
24%), mortality rate is higher (61% vs 29%), likelihood of
focal seizures or focal neurological deficits is lower.
TERIMAKASIH
 NEUROSAINS QURAN
Gelombang Alpha
Frekuensi:
Maturasi EEG ditunjukkan dengan
peningkatan frekuensi secara gradual
dari basic rhythm nya,
4hz  4 bln.
6Hz  12 bln
8Hz  3 tahun
10 Hz 10 tahun
Progresi alpha berhenti di usia 10th.
Akan menurun pada usia lanjut