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CLINICAL EEG and NEUROSCIENCE

Generalized Spike-Wave Discharges with Focal Onset in
a Patient with Head Trauma and Diffuse Cerebral Lesions:
ACase Report with EEG and Cranial MRI Findings
F. IrselTezer, Nese Dericioglu and Serap Saygi

Key Words
Absence Seizures
Electroencephalography
Head Trauma
Magnetic Resonance Imaging
ABSTRACT
The role of cerebral lesions associated with absence
seizures, outside the frontal lobe, has not been demonstrated byboth electroencephalography and neuroimaging
techniques until now, toour knowledge. We present a case
with absence seizures and EEGs with generalized 3 Hz
spike-wave patterns that were preceded by a burst of
spike-waves on the right parieto-occipital region. The
patient had a history of head trauma, and cranial MRI
revealed lesions that might be responsible for the seizures.
The patient's lateralized and localized EEG findings were
probably a representation ofsecondary bilateral synchrony
(SBS). The mechanism of SBS is considerably more complex than a simple triggering of generalized spike-wave
complexes from a single cortical focus.
INTRODUCTION
Absence seizures are defined by impairment of consciousness concomitant with generalized, synchronous 3
Hz spike-wave complexes on normal background activity
and are seen in age-related idiopathic epilepsies. t Typical
absence seizures that were symptomatic due to tumors or
other lesions have also been reported in the literature. 27
The role of localized cortical areas, especially the frontal
lobe, inthese cases has been stressed. Itwas thought that
secondary bilateral synchrony (SBS) was triggered due to
these foci.a.13 Ictal EEGs with generalized 3 Hz spike-wave
burst complexes preceded byfocal spike-wave discharges
were also reported in one patient with absence seizures. 8
Although there was a focal finding in the ictal EEGs, the
responsible lesions could not be demonstrated by neuroimaging techniques. The triggering of SBS from a lesion
located outside the frontal lobe has not been demonstrated byEEG. We recently encountered a case whose EEGs
showed a generalized 3 Hz spike-wave pattern beginning
in the right parieto-occipital area during absence seizures.
Cranial magnetic resonance imaging (MRI) showed lesions
that might be responsible forthe seizures.

Case Report
A 17-year-old male was admitted to our hospital for
intractable seizures, which started atthe age of 12. These
consisted of staring, blinking, slight elevation of the right
arm with partial loss ofconsciousness. They occurred 8-10
times a day and lasted for 10-15 seconds or more. The
patient was put on carbamezapine after the initial seizures.
Ictal behavioral characteristics changed slightly (sudden
arrest ofspeech and motion, staring with blinking and perioral myoclonia). One year later healso developed generalized tonic-clonic convulsions. Several antiepileptic medications (valproic acid, carbamazepine, primidone, clonazepam), either alone orin combinations, were tried without significant benefit.
On admission, personal history revealed severe head
trauma at the age of 9, which happened when he was
cycling. He lost consciousness for 13 days. Although
detailed records could not be obtained, the subject recovered without neurological sequela. He was able to continue his education for 6 years, but he had to leave school
when the seizures became frequent. Family history was
unremarkable. The patient had nosignificant problems during the perinatal and infantile period. There was no consanguinity between his parents and no seizure history in
his family. His neurological, physical and mental examinations were normal. Routine EEG showed frequent isolated
spikes and spike-wave discharges inthe posterior regions
of the right hemisphere and generalized 3 Hzspike-wave
complexes lasting for 10 seconds. Spike-wave discharges
were more prominent at the posterior regions of the right
hemisphere before they became generalized. The patient
did not have photosensitivity, Cranial magnetic resonance
imaging (MRI) indicated bilateral loss of periventricular
white matter especially in the frontal lobes and right parieto-occipital area and a decrease inthickness of splenium
of the corpus callosum. These were consistent with head
trauma (Figure 1).

From the Departments 01 Neurology (F. I. Tezer, S, Saygi) and the
Instrtute 01 Neurological SCiences and Psychiatry (N, Dericioglu), Hacettepe
Universrty School 01 Medicine, Ankara, Turkey.
Requests 101 reprints should be addressed to Serap Saygi, MD,
Professor of Neurology, Yuksel Caddesi, 41/5 Ankara. Turkey.
Email: ssaygi@tr.net

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Figure 1:
Cranial MRI indicates bilateral loss of periventricular white matter especially in the frontal lobes and right paneto-ocepital area with
hemosiderin deposition that was attributed to head trauma.

were already generalized atthe beginning and lasted for 820 seconds. Seven seizures occurred during sleep and
were not accompanied byany clinical findings.
The semiology was identical in all seizures but two.
Volitional activities ceased, then staring, blinking and perioral myoclonia appeared. Consciousness was disturbed;
the patient could not follow instructions and did not remember the code given during discharges. After the disappearance ofdischarges, he could follow the commands. Intwo
seizures where right parieto-occipital discharges preceded
generalized activity, the patient also had early eye deviation to the right. During sleep, isolated right parieto-occipi-

After the addition of lamotrigine to primidone and cionazepam, generalized tonic-clonic seizures disappeared,
and the frequency of absence seizures diminished to 3-4
times a day. Due tolack ofseizure control, the subject was
monitored with c1osed-circuit video-surface EEG for 2 days.
The patient had 17 seizures. In6 ofthem, generalized discharges, lasting 10-20 seconds, were preceded by right
parieto-occipital spike-wave complexes for 2.5-3 seconds
(Figure 2). The frequency of the burst remained almost
unclhanged at 3 Hz during the entire period. During one
seizure, lateralization ofdischarges tothe right hemisphere
was prominent (Figure 3). Inthe remaining seizures, bursts

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Figure 2:
Right parieto-occipital spike-wave complexes preceding 3 Hzgeneralized spike-wave discharges.

tal spikes or generalized spike-wave complexes appeared
for 1-2 seconds (Figure 4). After this investigation topiramate was added to his therapy. Frequency and duration of
seizures decreased on follow-up.

DISCUSSION
Absence seizures are included inage-related idiopathic
generalized seizures, childhood and juvenile absence
epilepsy. Symptomatic absence seizures with brain tumors,
abscesses, congenital vascular-structural abnormalities
and head injuries have also been reported," but these were
poorly documented, so it is not easy to know how many
patients had absence epilepsy. Recently, patients who had
focal lesions associated with absences have been reported.3-7·13 Except one with mUltiple subcortical white matter
lesions," all of these patients had frontal lesions. Their
EEGs were interpreted as synchronous spike-wave discharges without lateralized or localized findings. Only neuroimaging techniques supported evidence that frontal
lesions might be responsible for absence seizures.
Tuke) and Jasper" reported that insome cases, generalized 3 Hzspike-wave complexes appeared in paramedian lesions with attacks resembling petit-mal. The authors
defined the term secondary bilateral synchrony (SBS) to
describe the generalized spike-wave complex that was

seen in focal lesions. Bilateral synchronous spike-wave
discharges in patients with tumors were also reported in
the literature during the pre-CT ysars." With the stereoelectroencephalography recording, absence like partial
seizures have been described after stimulation of the
mesial frontal cortex. IS The role of the frontal lobe in
absence seizures was also demonstrated on patients' EEG
patterns. 61016-19 Frontal dominance on EEG was shown by
interictal frontal slow waves or spike-waves,'3'6'9 frontal
spikes preceding the generalized spike-wave pattern,'6.'6 or
frontal involvement in topographic mapping." But these
findings were not supported byneuroimaging techniques in
any case except two in whom interictal SPECT and ictal
PET were used todemonstrate the foci. 13,19 There was only
one case with bursts of spike-wave complexes on the left
hemisphere that spread to become generalized. 6 Few
cases of absence status with frontal lobe abnormality on
CT scans and initial frontal focal ictal discharges on EEG
have been reported."
Inthe present case, EEGs with generalized 3 Hz spikewave patterns that were preceded by a burst of spikewaves on the right parieto-occipital region were demonstrated in seizures lasting 10-20 seconds. In addition to
EEG findings, lesions that might be responsible for
seizures were also detected incranial MRI.

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©2004 VOL. 35 NO.3

CLINICAL EEG and NEUROSCIENCE

The clinical features ofour patient's seizures, especially blinking and perioral myoclonia, resembled those ofidiopathic generalized epilepsies with absences, eyelid
myoclonia with absence seizures (EMAS) and perioral
myoclonus with absence seizures (PMAS).21.22 But the
patient's absence seizures lasted for 10-20 seconds,
longer than EMAS and PMAS. He also had some absence
seizures without eyelid myoclonia or blinking and had no
family history consistent with idiopathic generalized epilepsy. On the other hand, ictal EEGs in EMAS and PMAS
show generalized discharges of spikes, more often irregularpolyspikes and slow waves at 3 Hz rather than generalized 3 Hz symmetric spike-wave discharges preceded by
lateralized-Iocalized spike-wave complexes.
Complex partial seizures that originate in the frontal
lobe may also have similar clinical features to absence
seizures. 23.25 But EEGs with 3 Hz bilateral generalized symmetrical spike-wave discharges that lack frontal predominance, especially at the beginning of discharges, are
incompatible with complex partial seizures of the frontal
lobe orfrontal absences.t" On the other hand, discharges
beginning in the right parieto-occipital region in 6 of 17
recorded seizures might suggest complex partial seizures
of the occipital lobe or absence seizures originating from
the occipital lobe. However, to the best of our knowledge,
bilateral generalized symmetrical 3 Hz spike-wave discharges have not been reported in seizures originating
from the occipital lobe.2426.27 Besides, the clinical features
of the patient's seizures were not consistent with occipital
lobe epilepsy.
In the literature, there is only one case with absence
status that developed after left occipital ischemia extending
to the ipsilateral thalamic region. 28 It was not due to the
occipital lesion. The uninjured right thalamus was thought
to generate oscillating excitation tothe whole brain. To our
knowledge, there are no reports with occipital or parietal
lesions that generate absence seizures.
Another possible explanation is that juvenile absence
seizures developed incidentally inour case after head trauma, and EEG revealed asymmetric features during
absence seizures due to widespread post-traumatic
lesions. The patient's cranial MRI findings with partial atro-

phy in splenium ofthe corpus callosum and periventricular
white matter changes with hemosiderin deposition were
compatible with head trauma. Centroaxial blows in traffic
accidents produce lesions located mostly in deep structures. 29 In the literature we believe there is only one welldefined case report of absence seizures developing after
head trauma,' but unlike our patient, in this case there
were nofocal EEG findings.
The patient's lateralized and localized EEG findings
were probably a representation of SBS that is differentiated from primary bilateral synchrony by poor symmetry
and regularity. According to Niedermeyer,JO some clinical
characteristics developing after 10 years of age and a
history of head injury suggested SBS. The mechanism of
SBS is not clear. One theory is that interhemispheric
pathways, especially the corpus callosum, are responsible fortransfer of discharges from one hemisphere to the
other; or areas maximally involved in the ictal discharge
may have projections to the thalamus, to account forthe
abrupt alteration of awareness and bilateral ictal EEG
findings. Mesial frontal cortex, rich in callosal connections
or projection to the thalamus, is the most accountable
region in the generation of SBS.7 The role of other lobes
in the generation of SBS remains to be resolved. The
temporal lobe was the second most common origin of
SBS in the study of Blume and Pillay,31 but in Marcus and
Watson's32 study occipital-temporal foci failed to produce
bisynchronous discharges.
The mechanism of SBS is considerably more complex
than a simple triggering of generalized spike-wav~ complexes from a single cortical focus. Secondary generalization might be such an alteration of inhibition. 33 Complex
interaction of excitatory-inhibitory multiple cortical epilepti·
form discharges, acting through thalamic and callosal connection in generation of SBS, may besuggested. Multiple
lesions may impair the ability of inhibitory mechanism on a
region of epileptic discharge.34 Multifocal lesions in our
patient's MRI may reflect widespread cortical-subcortical
dysfunction and SBS on EEG. The discussion whether the
seizures were idiopathic or symptomatic of a cerebral
lesion might be expanded with discovering the mechanisms of secondary bilateral synchronization.

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