CLINICAL ELECTROENCEPHALOGRAPHY

@1979.V0L.10,NO.3

Acute Subdural Hematoma and the Periodic Lateralized
Epileptiform Discharges
Nai-Shin Chu

Introduction
Periodic lateralized epileptiform
discharges (PLEDs) in the electroencephalogram consist of complexes of various
epileptiform waves recurring at relatively
regular intervals of one-half to three seconds
(1). This phenomenon is often associated with
an ipsilateral hemispheric structural lesion.
The most common lesions are cerebral
infarction and brain tumors (1-4). Other
neurological diseases associated with PLEDs
are intracerebral hemorrhage, encephalitis,
cerebral abscess, acute cerebral trauma
seizure disorders, neurosyphilis, and
tuberculoma (1-7). Occasionally, a small
cortical lesion appears to be responsible for
the production of PLEDs under
circumstances such as aminophylline
intoxication (8), hypoxia (8), nonketonic
hyperglycemia (9), alcohol withdrawal (10),
and systemic infection (10).The occurrence of
PLEDs in patients with subdural hematoma is
rare. Toyonaqa et al. (II) reported PLEDs in
three cases of chronic subdural hematoma,
but PLEDs associated with acute subdural
hematoma have not been reported. During the
past one and a half years at the University
Hospital two cases of PLEDs were seen in
patients with acute subdural hematoma
among a total of 10 patients with this
phenomenon. Thus, PLEDs associated with
acute subdural hematoma appear to be not as
infrequent as previously thought.

Case I

---n;e patient was a 55 year old moderately
obese white female with a long history of
alcohol abuse and hypertension. In 1972, the
patient had an acute onset of stupor and left
hemiparesis. The blood pressure was 180/115
and the cerebral angiogram revealed an
avascular mass in the right temporo-occipital
area. Right temporal craniotomy evacutated

25 cc of clotted blood. The patient was left
with residual left hemiparesis and left
homonymous hemianopsia, and continued to
receive Aldomet and Hydrochlorothiazide for
her hypertension. Pneumoencephalography
two months later revealed moderate dilation
of right occipital horn which communicated
with a porencephalic cyst. On follow-up five
years later, tile patient had been fully
functional except for the left hemianopsia.
On the day of admission, the patient tripped
over the stairs of her mobile home and fell
backwards striking the head on the concrete
floor. She immediately lost consciousness,
and in the Emergency Room a deep scalp
laceration was noted on the left parietooccipital area which was sutured. The patient
was brought to the Intensive Care Unit where
she was noted over a period of 30 minutes to
be improving with purposeful withdrawal to
painful stimulation. Subsequently, the patient
became totally unresponsive with unreactive
pupils which were 3 mm on the right and 5 mm
on the left. Diagnostic twist drills over the
temporal areas on both sides did not reveal
any hematoma. The patient was stabilized
with the use of diuretics and steroids. She
remained stuporous, moved right extremities
purposefully, but had only simple withdrawal
of left side to painful stimulation. Plantar
response was extensor on the left.
One and a half days later facial twitching
and tonic-clonic movements of the left arm
were intermittently noted for several hours.
There were brisk deep tendon reflex on the left
and decerebrate posturing of the left arm in
response to pinching. By the next day, the

Requests for reprints should be sent to Nai-Shin Chu,
M.D., Department of Neurology, University of California,
Irvine Medical Center, 101 City Drive South, Orange,
California 92668.

145
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016

CLINICAL ELECTROENCEPHALOGRAPHY

@1979.VOL.l0,NO.3

Figure 1. Case I. Recurring discharges of sharp wave complexes in the right hemisphere. Monopolar
recording with ipsilateral ear as reference. The vertical calibration is 50}JV and the horizontal
one 0.5 sec.

patient had almost continuous seizure activity
involving the eyes, face, neck, and the left
upper extremity. Arterial blood gas and blood
chemistry were within normal limits. She was
treated first with intravenous Valium, followed
with Dilantin and phenobarbital. In spite of
anticonvulsant treatment with Dilantin level of
12 J-lg/ml and phenobarbital level of 20
J-lg/ml,the patient continued to exhibit
intermittent left focal motor seizures, usually
lasting 5 to 15 seconds for the following two
days.
EEG revealed recurring polymorphic sharp
waves roughly at I Hz interspersed with
suppression of background rhythms on the
right side (Figure I). The distribution of the
sharp waves was predominantly in the frontal
and central areas. A computerized
tomographic (CT) scan revealed a large high
density mass extending all the way from the
most anterior portion of the frontal lobe to the
entire occipital lobe (Figure 2). A considerable
amount of mass was also present in the
vicinity of right lateral tentorium. The lateral
and third ventricles were shifted from right to
left approximately 2 em. The degree of shift

was more prominent anteriorly. The right
lateral ventricle was considerably
compressed. A right parietotemporal
craniectomy was performed with evacuation
of 180 cc of fresh blood clot. The seizures
subsided following the surgery.
Anticonvulsant levels were 22 J-lg/ml for
Dilantin and 29 J..Ig/ml for phenobarbital. The
patient continued to have intermittent left
decerebrate posturing, sluggish light
pupillary reflex, absent oculocephalic
response on the left. A few days later, her
clinical course was complicated by
hyperglycemia, hypokalemia, and elevated
blood urea nitrogen that were gradually
corrected.
EEG five days after surgery showed
persistence of recurring polymorphic spike
and wave complexes on the right but its
occurrence was less frequent and the interval
was more prolonged than in the previous
tracing. Sometimes burst-suppression
pattern evolved. Study of the auditory
brainstem evoked responses revealed
prolonged central conduction time following
right-sided stimulation and the absence of

146
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016

@1979.V0 L.10,NO.3

CLINICAL ELECTROENCEPHALOGRAPHY

Figure 2.

Case I. Computerized tomographic (CT) scan showed a large right subdural hematoma which
was maximal in the frontocentral region but which also extended all the way around the convexity to the entire occipital area . This was accompanied by a marked right to left midline shift
with almost obl iteration of r ight lateral ventricle.

indentifiable waves beyond Wave I on the left,
suggesting marked brainstem dysfunction.
Repeated CT scan showed absence of large
extracerebral blood collection except for a
small inc reased density in the frontal area and
a slight right to left shift. Gradually, the patient
exhibited bilateral decerebration, loss of
withdrawal to pinch in the left upper extremity,
and intermittent blink ing movements of the
eyes, cl in ically resembl ing coma vig il.
One week after the second EEG ,
oculocephal ic
response
was
absent
bilaterally, pupillary light reflex was sluggish ,
but eye blinking was still occasionally noted.
EEG showed repetitive sharp transients of
rather low ampl itudes occurring in intervals of
approx imately I to 4 seconds on the right.
Phase reversal was noted in the right central
area . Three days later, the patient developed
bilateral pneumonia and died 4 days later
fo llowi ng presumably septic shock and
cardiac arrest. Autopsy revealed bilateral

acute bronchopneumonia with abscess
formation , acute pancreatitis and left parietal
skull fracture. The dura mater was tense but
subdural collection of blood was absent.
Cerebral hemispheres were symmetr ical and
had a generalized early soften ing . The right
occipital lobe was partially obliterated with a
thin membrane which had a defect of 0.5 cm
communicating to the lateral ventricle. The
bra instem was congested without
hemorrhage and d istortion.
CASE II
A 44 year old man was found on the street,
confused , with multiple bruises over scalp ,
face , and extremities. The pat ient had a
history of excessive alcohol drink ing, and the
blood alcohol level was 61.6 mg% on
admission to a local hospital, where he had
two generalized convulsions beginning with
turn ing the head and the eyes to the right and
poss ible jerking of the right arm . The
convulsions were treated with Dilantin and

147
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016

©1979.V0L.10,NO.3

CLINICAL ELECTROENCEPHALOGRAPHY

Paraldehyde, but the patient was left with a
mild right hemiparesis and aphasia which
cleared in one or two days. The patient was
then transferred to the University Hospital
where
he
remained
confused.
The
anticonvulsant medication was discontinued,
and 3 days after admission the patient had six
or seven generalized convulsions with right
focal onset followed again by a mild right
hemiparesis and aphasia. Dilantin level was 4
jJg/ml.
An EEG showed recurring medium to high
amplitude bi- and triphasic wave complexes
which were variably sharp and predominantly
over the left hemisphere. Between the wave
complexes the background was marked by
suppression, and occasionally the epileptiform discharges were generalized. A CT scan
revealed a high density area in the left
posterior area and a rather marked left to right
midline shift. The left lateral ventricle was
compressed with obliteration of the posterior
horn. Following cerebral angiography, a left
craniotomy was performed to evacuate 65 cc
of fresh blood clot. The patient was treated
with Dilantin and phenobarbital.
Two days after the surgery the EEG
revealed left-sided PLEDs with background
suppression, although clinical seizures were
not observed. The right hemiparesis gradually
resolved, but a dense aphasia persisted. Two
weeks later, seizures recurred. Determination
of serum anticonvulsant levels revealed 4
jJg/ml for Dalantin and 10 jJg/ml for
phenobarbital. Repeated CT scan showed
persistence of a marked left-to-right midline
shift, but the extracerebral blood collection
had completely regressed. The dosage of
anticonvulsants was increased, and the EEG
repeated 3 days later revealed left
hemispheric slowing, maximal in the temporal
and parietal areas.
Two generalized seizures with right focal
onset were again observed with Dilantin level
of I J.lg/ml. The EEG showed almost
continuous spike and slow wave discharges
occurring at about one per second over the
entire left side. The slow waves were located in
the posterior temporal and occipital areas.
With readjustment of anticonvulsant dosages,
the patient had been free of seizures for the
next two weeks until he was discharged.
However, the patient was still left with some
impairment of left-right discrimination, visual
motor perception, auditory comprehension,

and word finding.
Discussion
This report demonstrates that PLEDs can be
observed in patients with acute subdural
hematoma. Both patients had a history of
alcoholism and recent head injury. They
presented with focal motor seizures with or
without secondary generalization,
concomitant with EEG manifestations of
recurring discharges of polymorphic sharp
wave complexes overthe cerebral hemisphere
where subdural hematoma was located. CT
scan revealed extracerebral collection of
dense fluid with marked midline shift. In spite
of the evacuation of subdural hematoma.
PLEDs persisted or recurred for days or
weeks.
One of the complications associated with
subdural hematoma is seizures which are
more often seen with acute subdural
hematoma (12). Although EEG alterations in
subdural hematoma are variable, asymmetry
of alpha activity or ipsilateral slowing with
suppression of background amplitude has
been stressed (13). The occurrence of PLEDs
is uncommon. Toyonaga et al (11) reported
PLEDs in 3 patients with chronic subdural
hematoma although in one patient both old
and recent hemorrhages were present. All the
patients had a history of alcoholism and their
seizures were focal contralateral to subdural
hematoma except for one patient who had in
addition secondary generalized convulsions.
PLEDs disappeared after evacuation of
hematoma, but in one patient PLEDs persisted
3 days after the surgery.
Brignolio et al (14) observed a patient with
bilateral chronic subdural hematomas who
presented with left focal motor seizures and
left hemiparesis. EEG study revealed
recurring bilateral sharp wave discharges but
maximal over the right frontal area where the
larger hematoma was located. Johnson (15)
reported a case of subdural hematoma of
unknown chronicity with right-sided
continuous focal seizures predominantly
involving the abdominal wall, but the EEG was
not obtained. Bilateral periodic slow wave
discharges resembling hepatic encephalopathy were observed in two patients with
unilateral chronic subdural hematoma (16).
Thus, PLEDs associated with acute subdural
hematoma have not yet been adequately
documented.

148
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016

CLINICAL ELECTROENCEPHALOGRAPHY

©1979.VOL.10,NO.3

The pathogensis for PLEDs is still unsettled,
although anatomical or functional
deafferentation of cerebral cortex has often
been implemented (1,3). The latter
hypothesis, however, makes it difficult to
explain the fact that in patients with focal
epilepsy or a small cortical lesion, PLEDs
occur under various toxic-metabolic
circumstances such as hypoxia (8),
aminophylline intoxication (8), alcohol
withdrawal (10), etc. In acute subdural
hematoma, compression of the underlying
cerebral cortex from the expanding subdural
mass could be an important factor for the
production of PLEDs, but there was also a
marked midline shift to suggest a significant
dysfunction of subcortical structures. It could
be argued that it was the underlying cerebral
contusion but not the subdural hematoma that
was responsible for the occurrence of PLEDs.
Autopsy study in Case I fails to support this
contention, but this possibility cannot be
completely ruled out in Case II for there was
persistent marked midline shift. However, in
cases of chronic subdural hematoma, midline
shift was either absent or minimal and PLEDs
disappeared following surgery, thus arguing
against the possibility of underlying cerebral
contusion.
In these two cases, the persistence or
recurrence of PLEDs following evacuation of
acute subdural hematoma appears to occur
under different circumstances. In Case I,
PLEDs persisted for two weeks in spite of

adequate anticonvulsant medication and
absence of clinical seizures. It is possible that
the porencephalic cyst in the right occipital
lobe aggravated by the underlying metabolic
derangements of hyperglycemia and
hypokalemia could be responsible for
persistent PLEDs. However, PLEDs continued
in spite of correction of the metabolic
conditions and there was a phase reversal in
the EEG in the central area suggesting a
possible structural etiology. In Case II, the
recurrence of PLEDs was apparently related
to inadequate anticonvulsant treatment. In
any event, when PLEDs and focal motor
seizures with or without secondary
generalization are observed in patients with
recent head trauma, acute subdural
hematoma should be strongly suspected.
Appropriate tests such as CT scan and
cerebral angiography should be performed to
ensure prompt treatment.
SUMMARY
Focal motor seizures associated with
periodic lateralized epileptiform discharges
(PLEDs) were observed in two patients with
acute subdural hematoma. Following the
surgery, one patient continued to exhibit
PLEDs but clinical seizures were absent.
PLEDs recurred in the second patient due to
inadequate anticonvulsant medication.
Autopsy study in one patient suggests that
underlying cerebral contusion was not
responsible for the occurrence of PLEDs.

REFERENCES
1. CHATRIAN, G.E., SHAW, C.M. and LEFFMAN,
H.O., The significance of periodic lateralized
epileptiform discharges in EEG: An electrographic, clinical, and pathological study,
Electroenceph. clin. Neurophysiol., 17:177193, 1964.
2.

3.

CHATRIAN, G.E., SHAW, C.M., and
LUTTRELL, C.N., Focal electroencephalographic seizure discharges in acute cerebral
infarction, Neurology (Minneap), 15:123-131,
1965.
SCHWARTZ, M.S., PRIOR, P.F., and SCOTT,
D.F., The occurrence and evolution in the EEG
of a lateralized periodic phenomenon, Brain
96:613-622,1973.

4.

ERKULVRAWATR, S., Occurrence, evolution
and prognosis of periodic lateralized epileptiform discharges in EEG, Clin. Electroenceph.,
8:89-99, 1977.

5.

JUUL-JENSEN, P., and DENNY-BROWN, D.,
EpilepsJa partialis continua, Arch. Neurol.,
15:563-578, 1966.

6.

MARKLAND, O.N., and DALY, D.O., Pseudoperiodic lateralized paroxysmal discharges in
electroencephalogram, Neurology (Minneap),
21:975-981, 1971.

7.

SMITH, J.B., WESTMORELAND, B.F., and
REAGAN, T.J., et al: A distinctive clinical EEG
profile in herpes simplex encephalitis, Mayo
Clin. Proc., 50:469-474, 1975.

149
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016

CLINICAL ELECTROENCEPHALOGRAPHY

@1979.VOL.10,NO.3

8.

YARNELL, P.R. and CHU, N-S, Focal seizures
and aminophylline, Neurology (Minneap),
25:819-822, 1975.

9.

SINGH, B.M., GUPTA, DR., and STROBOS,
R.J., Nonketotic hyperglycemia and epilepsia
partialis continua, Arch. Neurol., 29:187-190,
1973.

10.

DAUBEN, RD., and ADAMS, A.H., Periodic
lateralized epileptiform discharge in EEG: A
review with special attention to etiology and
recurrence, Clin. Electroenceph., 8:116-124,
1977.

11. TOYONAGA, K., SCHLAGENHAUF, R.E., and
SMITH, B.H., Periodic lateralized epileptiform
discharges in subdural hematoma: case
reports and review of literature, Clin. Electroenceph., 5:113-118,1974.

12.

KUNKEL, P.A., Subdural hematoma, Arch.
Surg., 38:24-54, 1939.

13.

MILLER, J.H.D., The EEG in chronic subdural
hematoma, Electroenceph. clin. Neurophysiol.,
11:603, 1959.

14.

BRIGNOLlO, F., MUTANI, R., and RICCO,
A.L., La sindrone epilepsia parziale continuacontributo personale di 3 casi, Acta Neurol.,
23:802-813, 1968.

15. JOHNSON, DA, Epilepsia partialis continua,
JAM A, 210:1756, 1969.
16.

WATSON, CW., FLYNN, R.E., and SULLIVAN,
J.F., A distinctive electroencephalographic
change associated with subdural hematoma
resembling changes which occur with hepatic
encephalopathy, Electroenceph. clin. Neurophysiol., 10:780, 1958.

150
Downloaded from eeg.sagepub.com at University of Otago Library on June 4, 2016