Epilepsy Research (2009) 86, 228—231

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Unilateral thalamic lesions and generalized or
lateralized spike wave discharges
F. Irsel Tezer a,∗, Serap Saygi b
a
b

Institue of Neurological Sciences and Psychiatry, Hacettepe University, School of Medicine, Ankara, Turkey
Department of Neurology, Hacettepe University, School of Medicine, Ankara, Turkey

Received 24 January 2009; received in revised form 27 May 2009; accepted 31 May 2009
Available online 3 July 2009

KEYWORDS
Spike wave
discharges;
Thalamic lesion;
Thalamus;
Cortex;
Idiopathic
generalized epilepsy

Summary We report four adult patients who had thalamic lesions and lateralized or generalized spike wave discharges (SWDs). The first two patients also had cortical lesions. The role of
the cortex and thalamus in the generation of SWDs is discussed. The third patient had a history
of idiopathic generalized epilepsy (IGE) with intractable seizures. The last patient had partial
seizures and absences. The coexistence of IGE with refractory focal epilepsy and the relation
with thalamic lesions are discussed.
© 2009 Elsevier B.V. All rights reserved.

1. Introduction
Spike wave discharges (SWDs), which are characteristic
EEG findings in idiopathic generalized epilepsy (IGE), are
generated through corticothalamic and thalamocortical connections (Steriade, 2005). Maintaining these discharges
requires the integrity of both the cortex and the thalamus
(Avoli and Gloor, 1982). Thalamic lesions associated with
epileptic seizures like focal or multifocal motor seizures
(Adams et al., 1988), gyratory seizures (Leiguarda et al.,
1992), infantile spasms (Incorpora et al., 1999), or epilepsy
with continuous SWDs during sleep (Incorpora et al., 1999,
Kelemen et al., 2006) have been previously reported.
Recently only four adult patients with clinical histories

compatible with IGE (Inghilleri et al., 2002; Kelemen et
al., 2006; Nguyen et al., 2006) who had unilateral thalamic lesions and generalized SWDs on electroencephalogram
(EEG), have been reported. Three of them had intractable
seizures (Kelemen et al., 2006; Nguyen et al., 2006) and one
patient had absence status (Inghilleri et al., 2002). In this
paper we present four adult patients with lateralized or generalized SWDs possibly related to unilateral thalamic lesions.
Due to the lateralization of the discharges, their clinical presentations may be important for understanding the relation
between thalamic lesions and occurrence of SWDs.

2. Patients
2.1. Patient 1

∗ Corresponding author at: Hacettepe University, School of
Medicine, Department of Neurology, O6100, Sıhhıye, Ankara, Turkey.
Tel.: +90 312 305 11 82; fax: +90 312 309 34 51.
E-mail address: irseltezer@yahoo.com.tr (F.I. Tezer).

A 23-year-old female was admitted to our clinic after she
had her first generalized tonic clonic seizure (GTCS) in the
first week of the postpartum period. She also had dysphasia
and right-sided hemiparesis. She had no history of epilepsy

0920-1211/$ — see front matter © 2009 Elsevier B.V. All rights reserved.
doi:10.1016/j.eplepsyres.2009.05.017

Unilateral thalamic lesions and generalized or lateralized spike wave discharges
or risk factor, but eclampsia had been diagnosed at the seventh month, leading to cesarean section. A venous infarction
in the left temporoparietal area and thrombosis in transverse and sigmoid sinus were seen on her cranial magnetic
resonance imaging (MRI). Her EEG revealed slow waves on
the left side. She was anticoagulated because of the high
level of factor VIII and levetiracetam was given for seizure
control. Three weeks after discharge, she was admitted due
to recurrent GTCS and difficulty in speech. Her MRI showed
a new ischemic lesion in the left pulvinar region of the thalamus (Fig. 1A) and her INR was 1.2. Her EEG showed slow
background on the left side and brief generalized spike and
multiple spikes and waves. She also had isolated spikes or
sharp waves on the left side (Fig. 1B). These lateralized
EEG findings were persistent in six EEG recordings during
the 2 years of follow up. She had a few mild seizures during
follow up and was given anticoagulation and antiepileptic
treatment.

229

mal. His EEG showed generalized SWDs for 1—2 s with frontal
dominance mostly on the right side. An acute ischemic lesion
was reported on the right cingulate gyrus on diffusion MRI.
His transthoracic echocardiography and cranial MR angiography were normal. He was treated with subcutaneous heparin
and acetyl salisylic acid; valproic acid was given for seizures.
On day 32 after admission, his left leg, with the
intractable diabetic foot ulcer, was amputated. Cranial MRI
and EEG were performed after this operation because of
lethargy. His MRI showed a new acute ischemic lesion in
the left thalamomesencephalic region (Fig. 1C) and his EEG
revealed mild slow background activity with generalized
SWDs and isolated spikes in the left centroparietal region
(Fig. 1D). Additionally pneumonia was diagnosed, antibiotic therapy was expanded but the antiepileptic treatment
was not changed. There was no recurrence of seizures but
left-sided epileptiform discharges were present in his one
follow-up EEG recording. Unfortunately we were unable to
follow him up or contact him by telephone after discharge.

2.2. Patient 2
2.3. Patient 3
A 56-year-old hypertensive, diabetic man was admitted to
hospital due to a diabetic ulcer on his left foot. During treatment of that complaint in the internal ward, 2 mg daily
risperidone was started because of his behavioral disturbances. On the fifth day, he had his first GTCS. He had no
obvious seizure risk factor. His blood biochemistry was nor-

A 27-year-old female was admitted because of generalized
convulsions that had started at the age of 14. She also
had daily attacks with loss of contact or jerks of her arms.
Her family history was unremarkable but she had a febrile
convulsion at the age of 2. She had taken phenytoin, car-

Figure 1 (A) MRI of patient 1 with a new ischemic lesion in the left pulvinar region of thalamus. (B) EEG of patient 1 with brief
generalized spike and multiple spikes and waves predominantly on the left side. She also had isolated spikes or sharp waves on the
left side. (C) MRI of patient 2 with a new acute ischemic lesion on left thalamomesencephalic region in addition to an old ischemic
lesion on the right cingulate gyrus. (D) EEG of patient 2 with generalized SWD and isolated spikes in the left centroparietal region.

230

F.I. Tezer, S. Saygi

Figure 2 (A) MRI of patient 3 with a lacunar lesion on the left medial thalamus. (B) EEG of patient 3 with generalized SWDs (ictal)
and isolated spike discharges on left side (interictal). (C) MRI of patient 4 with a sequelar left thalamic lesion and thalamic atrophy
(left side) and PET with hypoperfusion on the anteromedial part of the left thalamus. (D) EEG of patient 4 with generalized 3.5—4 Hz
SWDs.

bamazepine, and phenobarbital in different combinations
for 13 years. Due to the intractability of her seizures she
was monitored in the video-EEG monitoring unit. Absence
seizures with mild hand automatisms associated with generalized SWDs and one absence-clonic-tonic-clonic seizure
were recorded. Isolated spike discharges on the left side
were seen in her interictal EEG recordings during five days
of monitoring (Fig. 2B). Her MRI showed a lacunar lesion
on the left medial thalamus (Fig. 2A). She had no risk factor for ischemia in her history and laboratory examinations
including echocardiography. Her antiepileptic therapy was
changed to monotherapy with valproic acid. She had no further generalized convulsive seizures with valproic acid, but
absences and mild jerks persisted. Lamotrigine was added
and she became seizure free, and follow-up EEGs were
either normal or showed rare left-sided spikes.

2.4. Patient 4
A 16-year-old boy had his first GTCS at 9 years old. He had
recurrent seizures with bilateral hand and oral automatisms.
His daily attacks with loss of contact were witnessed by his
family. His mother’s and father’s cousins had a history of
epilepsy with GTCS, but there was no consanguinity between
his parents. Due to the lack of seizure control with the
combination of clonazepam, valproic acid, lamotrigine, and
carbamazepine, he was monitored for six days in the videoEEG monitoring unit. He had frequent generalized 3.5—4 Hz

SWDs for 10—30 s (Fig. 2D). In a few of these short time periods with SWDs nurses checked whether he was conscious.
Mostly he remained conscious and he was able to answer
questions or remember the given code after the end of the
paroxysm. He also had seizures with staring and automatisms. Ictal EEGs showed bilateral frontotemporal onset with
rhythmic activity prominently on the left side.
His cranial MRI showed a sequelar left thalamic lesion
with thalamic atrophy (Fig. 2C, left side) and positron
emission tomography (PET) showed hypoperfusion on the
anteromedial part of the left thalamus (Fig. 2C, right side).
Ethosuximide was added to his therapy but his seizures persisted.

3. Discussion
We report new four adult patients with unilateral thalamic
lesions that altered the integrity of the thalamocorticothalamic circuits. The difference between our cases and those
reported previously (Inghilleri et al., 2002; Kelemen et al.,
2006; Nguyen et al., 2006) was the presence of persistent and frequent lateralizing findings on EEG. That may
be related to the preceding cortical lesions leading to a
hyperexcitable cortex (Meeren et al., 2002), like in our first
two patients. However, there was a strong temporal relation with thalamic lesion and occurrence of SWDs, especially
in patient 1. SWDs were seen after the occurrence of an

Unilateral thalamic lesions and generalized or lateralized spike wave discharges
acute thalamic pulvinar lesion and lateralized to that lesion.
Involvement of the posterior—inferior part of the thalamus,
instead of the medial-anterior region, including thalamocortical cells and surrounding reticular nucleus, which are
responsible for the generation of SWDs (Steriade, 2005)
might be unexpected for the occurrence of SWDs. However,
the cytotoxic edema near the pulvinar region may affect
these structures. Furthermore, neuroimaging evidence of
pulvinar involvement in patients with temporal lobe epilepsies (Guye et al., 2006) has been reported. The pulvinar area
might be activated by the hyperexcitable temporal cortex.
Additionally, the possibility of a genetic background for IGE
in such a young patient must be considered, although she had
no history of absences or myoclonia and no family history.
Patient 2 had an acute right frontal ischemic lesion initially and SWDs lateralizing to the right. In the second
EEG with left lateralizing findings and SWDs, he had a new
ischemic lesion in the left thalamomesencephalic region.
Frontal lesions causing SWDs or secondary bilateral synchrony have been reported (Pavone and Niedermeyer, 2000).
Therefore, his first attack might have been related to the
lesion of the right cingulate gyrus. In the second EEG the
generalized SWD and localized epileptogenic activity in the
left centroparietal region showed a temporal relation with a
new left thalamic lesion. We hypothesize that the large left
thalamic lesion could easily have affected the SWD generating structures and might have been an additional factor.
The lateralizing finding in the second EEG was concordant
with the side of the recent thalamic lesion. The thalamus
and cortex, especially the perioral region of the frontal cortex, actively participate in the generation of SWDs (Meeren
et al., 2002; Steriade, 2005). Focal cortical or thalamic
lesions in this thalamocortical circuit may cause SWDs with
lateralized findings on EEG. Additionally risperidone could
facilitate the cortical and/or thalamic excitation.
The presence of absences in patient 3 and 4 was similar
to previously reported cases of intractable IGE and unilateral thalamic lesions (Nguyen et al., 2006). Importantly
our patients had SWDs with lateralizing findings compatible with the thalamic lesions. It is difficult to explain why
these destructive subcortical-thalamic lesions cause unilateral cortical discharges, but they might have activated a
superimposed hyperexcitable cortex.
In patient 4 the coexistence of IGE with refractory focal
epilepsy and/or secondary bilateral synchrony could have
been due to the presence of multiple seizure types and EEG
findings. In animal studies administration of proconvulsive
agents to caudal or rostral parts of the reticular nucleus of
the thalamus produced different semiology related to the
presence of different connections to the limbic motor area
or sensory area (Aker et al., 2006). Left thalamic atrophy

231

and hypometabolism in patient 4 may be related to partial
seizure facilitation or propagation via corticothalamic pathways (Guye et al., 2006). The presence of thalamic atrophy
or asymmetries of thalamic metabolism has been associated
with poorer outcome (Newberg et al., 2000).
In conclusion, in our patients the cause of the generalized and/or lateralized SWD may be the presence of a
hyperexcitable cortex or an irritative thalamic lesion. To
identify these mechanisms experimental animal studies may
be helpful in future.

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