el991 VOL 22 NO 4

CLINICAL ELECTROENCEPHALOGRAPHY

Possible Relationship of Periodic Lateralized
Epileptiform Discharges to Thalamic Stroke
James W. Wheless, Gregory L. Holmes, Don W. King, B. B. Gallagher,
A. M. Murro, H. F. Flanigin and J. R. Smith

on the ground by her car, with her right leg in
the car. The car had not been driven the night
Epilepsy Surgery
before. She had no history of alcohol or drug
Periodic Lateralized Epileptiform Discharges
abuse, or cardiac problems. Her only medica(PLEDs)
tion is Dilantin 400 mg. at bedtime.
Thalamic Stroke
She had the onset of her seizure disorder
INTRODUCTION
(complex partial) at age 16, a couple of weeks
Periodic lateralized epileptiform discharges
after the birth of her first child. Her seizures
(PLEDs) are seen most often in diseases that
were fairly well c o n t r o l l e d (one every 2-3
produce an acute destructive cortical lesion of
months) for the first 10 years. Over the last 10
the cerebral hemisphere ipsilateral to the elecyears the seizures slowly increased in fretroencephalographic (EEG) pattern.
quency to 1 a week. The patient’sseizures begin
The most common cause in adults is an acute
with an aura of a tingling sensation involving
cerebrovascular accident.’-7 Many other neuroher right upper extremity. This is followed by
logic conditions, or systemic conditions with
unresponsiveness, mouth movements, blinkneurologic complications, are associated with
ing, and simple hand automatisms of 1-2 minute
PLEDs. Examples of these are central nervous
duration. She is then post-ictal and confused
system infection^"^ including herpes simplex
for about 5 minutes. The seizures were refracencephalitis,’ acquired immunodeficiency
tory to phenytoin, phenobarbital, primidone.
~ y n d r o m e Creutzfeldt-Jakob
,~
disease,” neucarbamazepine, and valproate. She underwent
rosyphilis,” and cerebral cysticercosis;” neoan epilepsy surgery evaluation 1%years priorto
plasms,‘ multiple s c l e r ~ s i s , ’neuro-Behcet
~
this hospitalization. Diagnostic evaluation cons y n d r ~ m e , ‘subdural
~
h e m a t o n ~ a , ~confu~”~
sisted of interictal and ictal continuous, videosional states in the elderly,17 anoxia,‘”’ alcohol
recorded, extracranial EEG monitoring (scalp
~ i t h d r a w a l , ’ ~nystagmus
”~
retractorius,“
and sphenoidal electrodes), CT scan, MRI, vistoxic-metabolic disturbance^,^'^^^^'^ sickle cell
ual field examination, neuropsychological testdisease,” status epilepticus,6 and a chronic
ing, MMPI, cerebral arteriogram, intracarotid
seizure d i ~ o r d e r . In
~ , addition,
~~
one case of
sodium amobarbital testing, and interictal and
photic induced-driven PLEDs in paroxysmal
ictal continuous, video-recorded, intracranial
dystonic choreoathetosis has been r e p ~ r t e d . ’ ~ EEG monitoring (depth electrodes). This evaAlthough cerebral infarctions are the most
luation revealed she would be a good candidate
common causes of PLEDs, these are usually
for a left anterior temporal lobectomy, and this
large lesions with cortical destruction. Subcorwas performed 1 year ago. She tolerated this
tical infarctions have not yet been described in
procedure well, and has had nofurther auras or
association with PLEDs. We report a case of a
seizures. Pathology revealed severe loss of
thalamic stroke associated with PLEDs.
~CASE REPORT
Key Words

A 38-year-old white female was admitted to
the hospital after being found unconscious
near her car. The patient was in her usual state
of health the prior evening when she went out to
her car. She was found the next morning
(approximately 12 hours later) by her parents

F r o m t h e Departments of N e u r o l o g y ( D r s Wneless
Holmes King Gallagher Murro) and Neurosurgery (Drs
Flanigin S m i t h ) Medical College of Georgia Augusta
Georgia 30912
Requests for reprints should be addressed to Dr James
Wheless Texas Comprehensive Epilepsy Program Department of Neurology
University of Texas P 0 Box 20708
Houston Texas 77225-0708
~

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‘1991 VOL 22 N O 4

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neurons and glial scarring of the hippocampal
formation.
Upon admission, her temperature was 37”C,
pulse was 68, and respirations were 14. The
blood pressure was 120/70 mm Hg. On examination the patient was obtunded. General physical examination revealed ecchymosis on the
tongue and right forearm. The remainder was
unremarkable (heart was normal, no bruits).
Neurologic examination revealed that she
would open her eyes, and groan when painful
stimuli were applied. She had no understandable speech, and could not be tested for other
language functions. Oculovestibular reflexes
were intact, and the fundi were normal. Both
pupils were 4 mm and reacted to light. Decreased movements were noted on the lower
half of the right side of the face in response to
painful stimuli. Nogag was elicited.The remaining cranial nerves that could be examined were
normal. Motor function showed a flaccid right
hemiparesis. Sensory function revealed a rightsided loss to deep pain. Gait and coordination
could not be tested. Tendon reflexes were +++
on the right and + on the left; the plantar
response was extensor on the right, and flexor
on the left.
The urine was normal. The hematocrit was
38.2%; whitecell count was 16,900 with 92%
neutrophils, 5% lymphocytes, and 3% basophils.
Platelet count was 227,000; prothrombin time
was 14.3 seconds, with a control of 10-12
seconds; partial thromboplastin time was 29.7,
with a control of 22-35 seconds. Initial electrolytes, calcium, magnesium, and general chemistry were all unremarkable except for a CPK of
3179 mu/ml (normal, 0-225; 100% mm). The
phenytoin level was 11 ng/ml, a urine drug
screen was negative. The EKG and x-ray of the
chest were normal. The lumbar puncture
showed an opening pressure of 140 mm H 2 0 ,
glucose 81 m g / d l , p r o t e i n 26 m g / d l , 11
RBC/mm,3 and a nonreactive VDRL. No organisms were seen on Gram stain, cryptococcal
antigen test was negative, acid fast bacilli smear
was negative, and the spinal fluid grew n o bacteria or fungus. The arterial blood gas on room
air was a 7.37 pH, 42.9 PCO.* The serum triglyceride was 93 mg/dl; and the total cholesterol 152 mg/dl with a VLDL cholesterol of 3
mg/dl, an LDL cholesterol of 101 mg/dl, and a
HDL cholesterol of 48 mg/dl (a normal lipoprotein profile for her age).

formed while she was obtunded disclosed the
presence of periodic lateralized epileptiform
discharges over the left hemisphere, seen maximally over the fronto-temporal area. No seizures were noted. A cranial MRI scan obtained
the next day (Figure 2) disclosed evidence of
the prior left temporal lobectomy and abnormal
signal (increased signal intensity on the T2weighted images) in the left thalamus and right
side of the brain stem (probably ischemic in
nature). Unfortunately, no further EEGs or neuroimaging studies were performed. An aortic
arch and 4-vessel cerebral arteriogram was
normal except for the left vertebral arteriogram
that demonstrated a focal decrease i n the
caliber of the distal left vertebral arteryand basilarartery consistent with diffuse vertebrobasilar
spasm. I n addition, surgical branch occlusions
in the inferior left temporal branches of the left
middle cerebral artery consistent with the previous left temporal lobectomy were seen. No
definite evidence of branch occlusions or vascular abnormalities were noted in the posterior
fossa circulation. A fetal origin of the right and
left posterior cerebral artery was noted, with
b o t h arising f r o m their respective internal
carotid arteries. The 24-hour Holter monitor
was normal; a 2-D cardiac echo showed no
thrombus; and the posterior circulation transcranial doppler was normal.
The patient steadily improved and by the
second week was more alert, and had regained
most of her strength and sensation on the right
side. Her aphasia improved slowly, and consisted primarily of asevere receptive deficit with
a moderate expressive disorder. She began
speech therapy.
It was felt as though the patient’s cerebrovascular accidents were most likely embolic in
nature, even though a definite source was not
identified, and she was placed on Coumadin.
Three to 4 weeks after this hospitalization she
had the onset of a “new” seizure type. This
consisted of staring, unresponsiveness, and
then focal clonic activity on her right side lasting 2-3 minutes, followed by a right-sided
Todd’s paralysis for 30-45 minutes.

A portable EEG (Figure 1) recording per-

DISCUSSION
Our patient’s seizures ceased after the left
temporal lobectomy. She was seizure-free on
one anticonvulsant. However, after her thalamic stroke and associated PLEDs she developed a “new“ seizure type. This finding is con-

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1991 VOL 22 NO 4

CLINICAL ELECTROENCEPHALOGRAPHY

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Drowsy, eyes closed, HFF 70 Hz, T C 0 1 Periodic lateralized epileptiform discharges (spikes polyspikes and
sharp waves) occurring every one to three seconds, over the left cerebral hemisphere maximally over the
temporal area The background activity over that hemisphere I S slower In frequency. and lower in amplitude
than the right hemisphere

sistent with prior studies that have shown the
majority of patients with PLEDs g o o n t o have
recurrent seizures after hospitalizat ion.22,23.26
There are many reports on the EEG changes
in cerebrovascular accidents, and their association with PLEDs. A stroke is the most common
etiology in patients with PLEDs. However, in
these cases PLEDs were associated with large,
destructive c o r t i c a l infarctions. Unilateral
lesions in the thalamus may produce unilateral
r h y t h m i c delta activity," b u t there are n o
reports of discrete thalarnic lesions producing
PLEDs. Schwartz reported one patient who had
PLEDs (maximally seen over the left temporal
area) and at autopsy had an extensive glioma
spreading t h r o u g h o u t the thalamus.' This
report demonstrates that PLEDs can be observed in patients with a unilateral, subcortical
stroke. The pathogenesis of PLEDs is uncertain. Lombroso and Cobb hypothesized that
there might be a thalamic or mesencephalic
origin to periodic c o r n p l e ~ e s .Others
~ ~ ' ~ ~have
hypothesized that PLEDs arise in an area of
cortex anatomically or functionally deafferentat ed f r o m the s u b c o rt ica I st r uc t u re. 7,21325
Jacome and Risko's report of photic induceddriven PLEDs in paroxysmal dystonic cho-

'

reoathetosis suggested that subcortical structures participate in the generation of P L E D s . ~ ~
Chu reported a patient with PLEDs and acute
subdural hematoma. The autopsy revealed no
underlying cerebral contusions, suggesting a
possible role of subcortical structures (due to
midline shift) in the pathogenesis of PLEDs.15
Chatrian et al believed that both cortical and
subcortical (thalarnic) structures could contribute to the genesis of PLEDs.' They felt that
the cortex must participate in the production of
PLEDs no matter what the level of origin of the
discharge was. This view was reinforced by
Markand and Daly and then by Kuroiwa and
Celesia's more recent review of the clinical significance of periodic EEG pattern^.^.^'
Our patient had both cortical and subcortical
abnormalities that could potentially contribute
to the genesis of her PLEDs. The cortical physiology surrounding a prior temporal lobectomy
is altered. This is reflected as focal slowing on
the EEG. It is possible that this change in local
cortical physiology may lower the threshold for
the production of PLEDs (by either a subsequent subcortical or cortical lesion). In addition, the embolic episode that produced the
subcortical imaging abnormalities could have

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CLINICAL ELECTROENCEPHALOGRAPHY

A

C
D
Figure 2 A - MRI obtained in the axial plane (TR 2000. TE 20) prior to the temporal lobectomy is normal (The
left cerebral hemisphere is on the right side of each photograph )
B - MRI obtained in the axial plane (TR 2000. TE 70) during this hospitalization revealsa left thalamic
abnormality (increased signal)
C - MRI obtained in the axial plane (TR 2000. TE 20) reveals the prior left temporal lobectomy
D - MRI obtained in the coronal plane (TR 2000. TE 20) during this hospitalization reveals a left
thalamic abnormality (increased signal) and evidence of the prior left temporal lobectomy

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CLINICAL ELECTROENCEPHALOGRAPHY

imaging (MRI) it will be possible to further
characterize the relationship of discrete subcortical lesions to PLEDs, something that was
not previously possible.

caused mild hypoxic-ischemic changes in the
cortex adjacent to the prior lobectomy. However, it is very unlikely that significant cortical
hypoxia occurred since nosignal abnormalities
were seen on an MRI performed more than 24
hours after the event. This occurrence of the
thalamic stroke ipsilateral to an area of prior
cortical resection may have allowed the genesis
of PLEDs without a new cortical abnormality
being seen. This suggests a possible association between subcortical structures and the
generation of PLEDs. With improved neuro-

SUMMARY
A patient with a unilateral thalamic infarct
and associated periodic lateralized epileptiforrn
discharges is described. The implications of
t h i s f o r t h e p a t h o p h y s i o l o g y of PLEDs is
discussed.

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