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Headache Following Occipital Brain Lesion: A Case of Migraine Triggered by Occipital Spikes?
Catello Vollono, Paolo Mariotti, Anna Losurdo, Nadia Mariagrazia Giannantoni, Edoardo Mazzucchi, Piero Valentini, Paola
De Rose and Giacomo Della Marca
Clin EEG Neurosci published online 17 November 2014
DOI: 10.1177/1550059414542244
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research-article2014

EEGXXX10.1177/1550059414542244Clinical EEG and NeuroscienceVollono et al

Article

Headache Following Occipital Brain
Lesion: A Case of Migraine Triggered
by Occipital Spikes?

Clinical EEG and Neuroscience
1­–6
© EEG and Clinical Neuroscience
Society (ECNS) 2014
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DOI: 10.1177/1550059414542244
eeg.sagepub.com

Catello Vollono1, Paolo Mariotti2, Anna Losurdo1, Nadia Mariagrazia Giannantoni1,
Edoardo Mazzucchi1, Piero Valentini2, Paola De Rose2, and Giacomo Della Marca1

Abstract
This study describes the case of an 8-year-old boy who developed a genuine migraine after the surgical excision, from the
right occipital lobe, of brain abscesses due to selective infestation of the cerebrum by Entamoeba histolytica. After the surgical
treatment, the boy presented daily headaches with typical migraine features, including right-side parieto-temporal pain, nausea,
vomiting, and photophobia. Electroencephalography (EEG) showed epileptiform discharges in the right occipital lobe, although
he never presented seizures. Clinical and neurophysiological observations were performed, including video-EEG and polygraphic
recordings. EEG showed “interictal” epileptiform discharges in the right occipital lobe. A prolonged video-EEG recording
performed before, during, and after an acute attack ruled out ictal or postictal migraine. In this boy, an occipital lesion caused
occipital epileptiform EEG discharges without seizures, probably prevented by the treatment. We speculate that occipital spikes,
in turn, could have caused a chronic headache with features of migraine without aura. Occipital epileptiform discharges, even
in absence of seizures, may trigger a genuine migraine, probably by means of either the trigeminovascular or brainstem system.
Keywords
electroencephalogram, epilepsy, migraine, wavelet analysis, brain abscess, occipital lobe, Entamoeba histolytica
Received April 3, 2014; accepted May 27, 2014.

Introduction
Migraine and epilepsy are linked by very close symptom profiles, and have common treatment strategies; moreover, it has
been demonstrated that the presence of one disorder increases
the likelihood of the other.1 Migraine-like headache is frequently associated with childhood epilepsies,2 and in particular
with occipital lobe epilepsy,3 both of idiopathic4,5 or symptomatic origin.6,7 Among the idiopathic occipital epilepsies, the
late-onset variant, or “Gastaut type”,4 is more frequently associated with migraine7,8 than the early onset or “Panayiotopoulos
type.”5
Headache associated with epilepsy can occur as an ictal 8 or
postictal phenomenon.3,9 Postictal headache, following lateonset idiopathic occipital lobe epilepsy, can occur even after a
simple visual seizure and may present as a diffuse or unilateral
severe, pulsating pain; for these reasons, the occipital seizure
may be associated with migraine and clinical features which
make them virtually indistinguishable from genuine migraine.10
We describe the case of an 8-year-old boy who developed a
migraine-like headache following surgical excision of right
occipital brain abscesses due to Entamoeba histolytica. The
boy had EEG epileptiform discharges in the right occipital
lobe, but never seizures. We therefore hypothesize that

ongoing occipital lobe epileptiform EEG discharges, even in
absence of clinically overt seizures, may have triggered
migraine in this patient.

Case Report
We describe an 8-year-old child, with no relevant previous
medical history, who was referred to our center for headache
attacks. His father had migraine with aura, and his mother had
migraine without aura. At age 5 years, 3 years before our observation, the patient presented severe headache and vomiting,
and needed admission. In the emergency room, a computed
1

Unit of Neurophysiopathology and Sleep Medicine, Department of
Geriatrics, Neurosciences & Orthopedics, Catholic University, Rome, Italy
2
Paediatric Neurology Unit, Department of Paediatrics, Catholic University,
Rome, Italy
Corresponding Author:
Catello Vollono, Unit of Neurophysiopathology and Sleep Medicine,
Department of Geriatrics, Neurosciences & Orthopedics, Catholic
University, Policlinico Agostino Gemelli, Largo Agostino Gemelli 8, 00168,
Rome, Italy.
Email: lvol@libero.it
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Clinical EEG and Neuroscience 

Figure 1. Magnetic resonance (MR) scans performed 2 years after surgery. (A) T1-weighted images; (B) T2-weighted images; (C) diffusionweighted images (DWI). The MR scans show areas of altered signal in the right occipital lobe, consistent with surgery outcome. No acute
pathological process is evident; in particular, no area of altered signal, suggesting brain edema, is present in the DWI.

tomography (CT) scan showed an intracranial heterogeneous
lesion in the right posterior parietal and occipital lobes, with
perilesional edema and mass effect. Further CT and magnetic
resonance imaging (MRI) showed 3 abscesses in the right
occipital lobe. Since medical treatment with wide spectrum
antibiotics and anti-edema agents failed to reduce the volume
of the masses, the abscesses were drained surgically under
ultrasound guidance. Three weeks later, a further CT scan
showed the recurrence of the lesions (or the development of
previously undetected abscesses). Therefore, a direct surgical
excision of the abscesses was performed. Histological examination of the capsule, and of the fluid, revealed E histolytica
trophozoites. The child was not immunodepressed, and the
amoebic abscesses were attributed to one of many previous
travels in tropical areas. Therapy with metronidazole was followed by the complete resolution of the infective process. The
patient never showed any clinical or instrumental evidence of
extra cerebral amoebic lesions. After surgery, antiepileptic
prophylaxis with phenobarbital 2 mg/kg/d was started, and
never withdrawn, although the child never presented seizures.
Neuromotor development was normal before and after the
amoebic infestation. Despite the removal of brain abscesses,
the patient continued to complain of recurrent headaches, with
a frequency of 20 to 25 per month. Pain was prevalently localized in right frontotemporal region, occasionally bilateral.
During hospitalization, the pain was of moderate to severe
intensity, and associated with nausea and photophobia; attacks
lasted from minutes to 1 hour, and were usually responsive to
acetaminophen, administered only for the treatment of particularly severe attacks. Occasionally, headache was accompanied by diffuse abdominal pain, of severe intensity, also with
nausea. Visual symptoms were never reported. Typically,
attacks appeared about 1 hour before sleep, and sometimes in
the morning while awakening. Blood tests, blood count, and
erythrocyte sedimentation rate were normal. Psychological

and neuropsychological evaluation did not reveal abnormalities. Neurological examination was normal; in particular no
visual field defect was present. MRI performed 2 years after
surgery revealed signal abnormalities in the right occipital
lobe, consequent to the surgical treatment of the abscesses
(Figure 1).

Methods
A prolonged (10 hours) video-EEG and polygraphic laboratory
based recording, including awake and nocturnal sleep, were
performed to evaluate the presence of EEG abnormalities.
Since the child reported headaches in the evening, prior to nocturnal sleep, the recording was started at 9.00 pm and prolonged
up to 7.00 am the next morning. During this assessment, the
boy reported a headache similar to those he had almost daily.
The onset of the attack occurred at about 10.00 pm, lasted 15
minutes and resolved spontaneously. Montage included 19
EEG leads, in bipolar reference or referred to the mastoids,
bilateral electro-oculogram, submental muscle activity (electromyogram), and electrocardiogram. Spline frequency maps
of the wake EEG activity in the dominant alpha frequency
(9-11 Hz) were obtained, both during and after the headache
attack.

Results
Baseline wake EEG showed focal slowing over the right temporo-parieto-occipital leads, which is consistent with the site of
the surgical intervention. During wake and, more often during
sleep, clear epileptiform discharges, consisting of spike and
spike-and-slow wave complexes could be detected in the same
sites (Figure 2). Occasionally, epileptiform activities spread
over contralateral and anterior regions. During the recording,
about 30 minutes before bedtime, an acute episode of headache

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Vollono et al

Figure 2. Ten seconds of EEG and polygraphic recording from sleep stage II NREM. High-voltage spikes are present on the right temporooccipital leads, with low-amplitude contralateral projection. EMG, submental muscles surface electromyogram; EOG, electro-oculogram;
EKG, electrocardiogram; NREM, non–rapid eye movement. Calibration is in the lower right corner.

occurred. Pain was throbbing, intense, localized in the right
forehead, associated with nausea, photophobia, and phonophobia. No vomiting, visual disturbances or impairment of consciousness were observed; the patient did not show tearing,
conjunctival injection, eyelid edema or nostril congestion. The
episode remitted spontaneously after about 1 hour. EEG did not
show epileptiform discharges during the headache (Figure 3).
Moreover, neither epileptiform discharges nor isolated spikes
were detected prior to the onset of the headache, during the
acute bout, or in the 30 minutes following.
During the headache, analysis of EEG spline frequency
maps showed clear asymmetry of the dominant alpha rhythm
frequency, in the 9- to 11-Hz range, which appeared to be
markedly reduced in the right temporo-parieto-occipital regions
(Figure 4).

Discussion
We describe a child who reported, following a surgical occipital brain lesion, headaches with migraine features. EEG showed
right occipital spikes and spike-and-slow wave paroxysm, but,
despite the presence of interictal epileptiform EEG activity, the
boy never presented with clinically overt seizures. It is likely
that prophylaxis with phenobarbital, started immediately after
the surgery, prevented seizures.

The origin of the headache in our patient is questionable
since it does not match the International Classification of
Headache Disorders (ICHD-II)11 criteria either for chronic
postcraniotomy headache or chronic post–nonbacterial infection headache.
Chronic postcraniotomy headache (point 5.7.2 in the
ICHD-II, 2004)11 can be ruled out because of the clinical features of the pain. Chronic postcraniotomy headache induces
pain involving the area of craniotomy, whereas in our patient
the pain was prevalently frontotemporal, unilateral or bilateral.
Similarly, a chronic post–nonbacterial infection headache
(A9.4.2, ICHD-II)11 could be hypothesized, but the ICHD-II
itself clearly states that “there is little evidence for the existence
of chronic headache attributed to non-bacterial infections.”
We hypothesize that the ongoing epileptiform EEG discharges in the right occipital lobe, secondary to the surgical
lesion, may have triggered a genuine migraine, in the absence
of overt occipital epileptic seizures. Numerous observations
may support this hypothesis, as reported in a meticulous recent
review.12
Our patient presented headache attacks with typical migraine
features: unilateral throbbing pain, photophobia, phonophobia,
nausea, and, sometimes, vomiting. Migraine or migraine-like
headache is very frequently associated with occipital lobe epilepsies, both of idiopathic4,5 or symptomatic7 origin. In these

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Clinical EEG and Neuroscience 

Figure 3. Ten seconds of EEG and polygraphic recording in wake, during the acute headache attack. Notably, no activation of right-side
epileptiform activities is present. EMG, submental muscles surface electromiogram; EOG, electro-oculogram; EKG, electrocardiogram.
Calibration is in the lower right corner.

Figure 4. Frozen spline frequency maps of 60-second artifacts-free EEG activity in the interictal recording (A, on the left) and during the
headache attack (B, on the right). Maps show the topographic distribution of the dominant background activity (alpha band peak frequency,
frequency range 9-11 Hz). Color scale expresses the absolute power (in µV2).
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Vollono et al
cases, headaches can occur either as an ictal8,13 or a postictal
phenomenon.3,9 Some investigators have even suggested that
the headaches may be preictal.14,15 Postictal headache can occur
even after minimal, simple visual seizures; it can be lateralized,
throbbing, and completely indistinguishable from a migraine
attack.10,16
Furthermore, based on the high clinical, pathophysiological
and therapeutic overlap, Parisi et al17 recently proposed to add
to the forthcoming ICHD-3 classification18 a new entity,
namely the “ictal epileptic headache” (IEH), in order to define
a condition diagnosed when a headache attack is the only clinical feature of epileptiform discharges.
At first view, these forms of “epileptic migraine,” that is,
migraine originating as either an ictal or a postictal phenomenon, seem to be ruled out in our case. The boy never presented
any clinically overt epileptic seizure, or even simple visual
hallucination. Moreover, the video-EEG recording across the
headache episode did not show any epileptiform activity
before, during (Figure 2), or immediately after the headache
attack. Likewise, the analysis of EEG during the headache
may be consistent with a migraine attack.19 EEG, in fact,
showed a slight interictal asymmetry of the alpha rhythm, with
predominance in the left occipital lobe (Figure 4A); such alpha
asymmetry was greatly enhanced during the headache attack,
with virtually total disappearance of alpha frequencies over
the right occipital areas (Figure 4B). Various studies demonstrated that alpha asymmetry and unilateral alpha suppression
are regarded as a typical, although nonspecific, EEG features
of acute migraine.19-21
In contrast to the “ictal” findings (during the headache
attack), the prolonged video-EEG showed copious epileptiform activity, consisting of focal right occipital-temporal, highamplitude spikes, and spike-and-slow wave discharges,
particularly enhanced during non–rapid eye movement sleep
(Figure 3). Similar unequivocal epileptiform EEG activities
(spike-and-wave complexes) can be found in epilepsy, but
never in migraine (with the exception of peculiar forms, such
as basilar migraine, migraine with prolonged aura, or alternating hemiplegia).19 The pattern of occipital-posterotemporal
(O-PT) spike-wave paroxysms is an EEG abnormality observed
primarily in occipital epilepsy of childhood and basilar
migraine; occasionally O-PT spike-and-wave complexes, not
associated with epileptic seizures, may be associated with
headache.6
Consequently, we hypothesize that, even though the EEG
recording did not show epileptiform discharges during the
acute headache, the genuine migraine attack in our patient
might represent the ictal epileptic manifestation. During the
past decade, Parisi and colleagues,22-24 in numerous articles,
stressed the concept of the ictal epileptic headache (IEH) events
as “sole” ictal epileptic manifestation. In this way, the reported
migraine attack could, at least in part, follow the new IEH criteria proposed.17
Occipital lobe structures are involved in the pathogenesis of
migraine with visual aura,25 and some observations suggest

occipital involvement in migraine without aura.26,27 Modification
of excitability in the occipital cortex, whether hypoexcitability28
or hyperexcitability,29 may be involved in the pathogenesis of
migraine. These modifications of neuronal excitability are
directly linked with the phenomenon of cortical spreading
depression (CSD), which has a key role in migraine.
In 2 exhaustive recent reviews, Parisi et al12,24 clearly
defined the complex interaction between migraine attacks and
seizures, explaining that the onset and propagation of CSD
and an epileptic focus are triggered when these neurophysiological events reach a certain threshold, which is lower for
CSD than for seizure. In particular, migraine attacks can be the
result of a trigeminovascular system activation by an epileptic
discharge, which rarely can not be recorded at the scalp but
only by deep stereo-EEG recording.13,30 Thus, the fact that
EEG recording did not show epileptiform discharges during an
acute episode of headache, in the described patient, is not
enough to exclude that the migraine attack was the only ictal
epileptic manifestation.
The hypothesized pathogenesis of migraine in our patient is,
moreover, in accordance to the mechanism proposed for the
onset of postictal migraine in children with occipital lobe epilepsy. In these patients, occipital seizure discharge may trigger
genuine migraine through trigeminovascular or brainstem
mechanisms.10,31 Occipito-postero-temporal spikes may represent a nonspecific epileptiform abnormality that may occur in
children with epilepsy (idiopathic or symptomatic), absences
or even in patients with no evidence of seizures. A close association between migraine and occipito-postero-temporal spikeand-wave discharges has been reported by several authors4,32
and, as stated by Talwar et al,6 “it is not surprising that most
these patients (up to 80%) had seizures, migraine, or both.”
In conclusion, occipital epileptiform discharges, even in
absence of seizures, may trigger a genuine migraine, probably
by means of trigeminovascular or brainstem systems.
Declaration of Conflicting Interests
The author(s) declared no conflicts of interest with respect to the
research, authorship, and/or publication of this article.

Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.

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