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Historical note and Nomenclature
Reflex epilepsies are characterized by specific modes of seizure precipitation
(Commission on Classification and Terminology of the International League
Against Epilepsy 1989; Engel 2001). The most frequent forms of reflex epilepsies
are the photosensitive epilepsies, in which seizures are provoked by environmental
light stimulation. Gastaut and colleagues provided the first evidence of
the electroclinical correlates of intermittent photic stimulation in photosensitive
patients stimulated with a flash lamp (Gastaut et al 1948). Since then, numerous
studies have clarified many characteristics of visually-induced seizures
(Newmark and Penry 1979; Binnie and Jeavons 1992; Kasteleijn-Nolst Trenite
et al 2001). Visually-induced seizures are frequently seen as one element
of idiopathic generalized epilepsies also featuring other seizure types (Commission
on Classification and Terminology of the International League Against Epilepsy
1989; Engel 2001; Guerrini and Genton 2004) or as the only type of seizures
in 'pure' photosensitive epilepsies. Most often they appear to be generalized,
but in up to 17% of photosensitive patients, they may originate from the
occipital lobe (Guerrini et al 1998). Although photosensitive occipital seizures
seem to result from a cerebral lesion in a minority of patients, the more
typical pattern of recurrent photosensitive occipital seizures in otherwise
normal subjects constitutes an idiopathic epilepsy, with onset usually around
puberty (Tassinari et al 1989; Ricci and Vigevano 1993; Guerrini et al 1995;
Guerrini et al 1998). To date, about 65 such patients have been reported
in detail. However, the clinical and EEG characteristics indicating idiopathic
localization-related epilepsy were not always specifically detailed, especially
in the early reports (Davidson and Watson 1956; Herrlin 1960; Naquet et al
1960; Fischer-Williams et al 1964; De Marco and Ghersini 1985; Aso et al
1988; Maeda et al 1990; Brinciotti et al 1992; Michelucci and Tassinari 1993;
Ricci and Vigevano 1993; Ferrie et al 1994; Guerrini et al 1995; 1997; Takahashi
and Tsukahara 1998; Yalcin et al 2000).
Similar to findings on primary reading
epilepsy (Commission on Classification and Terminology of the International
League Against Epilepsy 1989), this syndrome can be defined as an idiopathic
localization-related (local, focal, partial) epilepsy with age-related
onset and a specific mode of precipitation. The syndrome is now recognized
by the ILAE task force on classification and terminology (Engel 2001).
Clinical Manifestations
The disorder is characterized clinically by partial seizures beginning around
puberty. Secondarily generalized seizures are not infrequent. Almost all
seizures appear on recognizable exposure to visual stimuli. The triggering
factors are those classically known for photosensitive epilepsies. Television
(Aso et al 1988; Tassinari et al 1989; Guerrini et al 1995) and video games
(De Marco and Ghersini 1985; Maeda et al 1990; Ferrie et al 1994; Guerrini
et al 1995) are the most commonly reported triggers. Other environmental
stimuli have been reported less often: flickering or bright sunlight, sunlight
reflected by water or other surfaces (Ricci and Vigevano 1993; Guerrini et
al 1995), discotheque lighting, and computer screens (Guerrini et al 1995).
Precipitation by visual patterns is reported by some patients. Emotional
involvement may also play a role, especially in seizures occurring in front
of the television or in relation to video games (Ferrie et al 1994). Unlike
photosensitive generalized epilepsy, there is no clear evidence for self-induction
of seizures (Guerrini et al 1995).
Visual phenomena are the initial ictal
manifestation in all patients able to describe their symptoms. These are
usually described as bright, colorful, or multicolored rings or spots that
are fixed or flashing in the periphery of the visual field, rotating or
moving slowly to the opposite half-field (Davidson and Watson 1956; Ricci and
Vigevano 1993; Guerrini et al 1995). Some patients report ictal blindness or
severe blurring of vision, limited to 1 hemifield or involving the entire visual
field, usually after the positive visual phase but occasionally as the
first symptom (Aso et al 1988; Maeda et al 1990). Visual phenomena are often
followed by a versive phase, with “conscious” head
and eye deviation most frequently towards the side of the initial visual symptoms
but occasionally contralaterally (Guerrini et al 1995).
If the seizures progress, the most frequent ictal sequence (after the initial
visual symptoms) include epigastric discomfort, unresponsiveness, and vomiting.
Some patients complain of paroxysms of sharp or piercing cephalic pain during
their seizures. Epigastric discomfort or nausea are reported in about half
of the patients, either early during the attack or later, before they become
unresponsive (Davidson and Watson 1956; Guerrini et al 1995; Walker et al
1995). Oroalimentary automatisms may occur late in the seizure. Postictal
headache is frequent and is often reported in patients who also have ictal
headache, but the ictal and postictal pain are different (Guerrini et al
1995).
In some patients, seizures may last for several minutes, with a pattern
indicating that the ictal discharge originating in the occipital cortex
may remain localized or may spread slowly to adjacent areas.
Clinical Vignette
A 24-year-old girl with normal developmental milestones, normal intelligence,
no known risk factors for epilepsy, and no family history of epilepsy had
a single focal motor secondarily generalized seizure during sleep at 4 years
of age. EEG features at that age supported a diagnosis of benign epilepsy
with centrotemporal spikes. From 12 years of age, she complained of episodes
lasting about 10 to 15 minutes, characterized by sudden vision of "phosphorescent
multicolored spots" moving in the visual field, slow sustained head
version to the left, headache, unresponsiveness, and vomiting, followed at
times by secondary generalization. Longer attacks occurred approximately
twice a year, whereas short episodes consisting of vision of colorful, moving
spots were reported monthly. All seizures were triggered by exposure to bright
light or a TV screen. From 17 years of age, EEG showed bilateral occipital
spike and wave complexes, and photic induced paroxysmal driving limited to
the occipital lobe.|{diagram:rgip1.bmp}{caption:EEG response to low frequency
intermittent photic stimulation}{label:At low frequency stimulation each
flash evokes an occipital spike.}| Habitual visual attacks were elicited
by intermittent photic stimulation during EEG.|{diagram:rgip2.bmp}{caption:Occipital
photoparoxysmal response induced by intermittent photic stimulation}{label:Top:
Eyes open, a photoparoxysmal response is driven by intermittent photic stimulation
up to 30 Hz and is accompanied by visual symptoms (see bottom). Above 30
Hz, postictal slowing of the EEG persists over the occipital areas, with
interspersed spike and wave complexes; bottom: patient’s drawing representing “phosphorescent
multicolored spots moving in the visual field.”}|
Checkboard pattern reversal, flash visual evoked potentials|{diagram:rgip3.bmp}{caption:Checkerboard
pattern reversal visual evoked potentials}{label:Visual evoked potentials at
MO electrode are of very high amplitude. Overlapped is the schematic representation
of average VEPs amplitude for 10 controls. Checks of 20 minute of arc; reversal
rate of 1.7 Hz; contrast of 57%. MO = mid occipital electrode.}| and middle
latency somatosensory evoked potentials were greatly increased in amplitude
with normal latency and morphology. Brain MRI was normal. Visually induced
seizures were not improved by phenobarbital or carbamazepine monotherapy and
promptly ceased after valproate was added to carbamazepine.
Etiology
The etiology of this epilepsy syndrome is unknown. A family history of epilepsy
and a personal history of febrile seizures are reported in about one third
of patients (Guerrini et al 1995). A few families with affected members in
different generations have been reported (Brinciotti et al 1992; Yalcin et
al 2000). Moreover, a recent report outlined the possible phenotypic overlap
between juvenile myoclonic epilepsy and idiopathic photosensitive occipital
lobe epilepsy in a few families (Taylor et al 2004). This is in accordance
with the common genetic background observed in idiopathic partial epilepsies
(Commission on Classification and Terminology of the International League
Against Epilepsy 1989) and in idiopathic photosensitivity (Jeavons and Harding
1975). Two patients have been reported who had previously presented typical
benign rolandic epilepsy, and other patients exhibiting rolandic spikes in
the EEG have been described (Guerrini et al 1995; 1997).
Pathogenesis and pathophysiology
The mechanisms underlying this disorder are likely to be similar to those involved
in the other idiopathic localization-related epilepsies. In particular, there
are some neurophysiologic analogies with benign rolandic epilepsy, the most
common form of this group. One of the classical pathophysiologic hypotheses
for the origin of benign rolandic epilepsy is that of an age-related, area-specific
hyperexcitability (Tassinari et al 1988). This hypothesis is supported by
the finding of enlarged middle latency somatosensory evoked potentials both
in benign rolandic epilepsy and in other forms of benign epilepsy of the
somatomotor cortex (Tassinari et al 1988). These somatosensory evoked potentials
could correspond to the cortical spikes evocable by tapping (Tassinari et
al 1988). Patients with idiopathic photosensitive occipital lobe epilepsy
have abnormally enlarged visual evoked potentials to both flash and checkerboard
pattern stimulation (Guerrini et al 1997; 1998). Moreover, single flash stimuli
at a low frequency can trigger occipital EEG spikes that are time-locked
to the flashes. This may indicate that an age-related hyperexcitability to
photic stimuli could become apparent at around puberty in the occipital lobe;
this is similar to the hyperexcitability to somesthetic stimuli observable
during childhood in the somatosensory cortex of children with benign rolandic
epilepsy. A visual evoked potential study using patterns of different spatial
and temporal frequency and chromaticity has revealed that the amplitude of
the response does not saturate in children and adolescents with idiopathic
photosensitive occipital lobe epilepsy, abnormally high values being reached
at moderate-high contrast (Porciatti et al 2000; Wilkins et al 2004). This
observation indicates that cortical mechanisms of contrast gain control are
severely impaired in this syndrome, because in normal controls the function
relating visual evoked potential amplitude to logarithm of stimulus contrast
typically saturates at moderate contrasts (about 20%). On the other hand,
no abnormalities were observed in the response to chromatic stimuli, suggesting
specific impairment of achromatic mechanisms.
Epidemiology
Patients with idiopathic photosensitive occipital lobe epilepsy represented
0.4% of 2447 consecutive epilepsy patients seen in 2 specialized centers
(Guerrini et al 1995). There was a 4:1 girl predominance. Age- and sex-related
trends overlap with those seen overall in photosensitive patients, with a
peak around puberty to adolescence.
Prevention
Not applicable.
Differential Diagnosis
The diagnosis of idiopathic photosensitive occipital lobe epilepsy is based
on the association of occipital seizures that appear on exposure to environmental
visual stimuli with a photoparoxysmal EEG response, usually predominating
over the occipital regions, in adolescents who have no other neurologic abnormalities.
Photic triggering of occipital seizures may also occur in the early stages
of some progressive neurologic disorders (Guerrini et al 1995). Nonprogressive
lesional epilepsies with variable outcome may also be accompanied by visually-induced
seizures (Guerrini et al 1998). However, in the presence of a lesion, photic-induced
seizures would appear to depend more on photic activation of an epileptogenic
area that is also capable of generating spontaneous seizures than on mechanisms
linked to “idiopathic” genetic photosensitivity.
The symptom cluster of visual aura, abdominal discomfort, vomiting, and headache
can make clinical differentiation between photosensitive occipital seizures
and migraine difficult, especially if the triggering role of the visual stimuli
is not recognized. However, elementary visual hallucinations of epileptic seizures
are predominantly characterized by circular or spherical multicolored patterns,
as opposed to the predominantly black and white ictal patterns of migraine
(Panayiotopoulos 1994).
When the ictal activity propagates slowly, overt symptoms may appear once the
patient is no longer confronted with the provoking stimulus. The provoking
stimulus may, therefore, be missed from the clinical history. In this case,
idiopathic photosensitive occipital lobe epilepsy may be impossible to differentiate
clinically from childhood epilepsy with occipital paroxysms (or benign occipital
epilepsy) (Gastaut 1982; Ferrie et al 1997). Appropriate EEG recordings with
photic stimulation revealing the photoparoxysmal response notably facilitate
differential diagnosis.
Rapid seizure generalization may make it impossible to distinguish clinically
between occipital and generalized photosensitivity. This limitation has no
serious practical implications, however.
Diagnostic Workup
Neurologic examination, neuropsychological testing, CT scan, and MRI are normal
in all patients with idiopathic photosensitive occipital lobe epilepsy.
Background EEG activity is normal. Spontaneous interictal spikes or spike and
wave complexes are present over the occipital region in most patients. Spikes
are unilateral or bilateral, synchronous or asynchronous, or predominant at
the Oz electrode, and are associated with generalized spike and wave complexes
in some patients. Abnormalities are enhanced by eye closure and continue for
the duration that the eyes are closed. However, some patients who appeared
to have had idiopathic photosensitive occipital lobe epilepsy have been reported
with normal interictal EEGs at rest (Herrlin 1960; Michelucci and Tassinari
1993). Intermittent photic stimulation provokes a photoparoxysmal response
that is occipital, generalized, or both. The photosensitivity range is wide
(5 Hz to 40 Hz), with marked interindividual variability (Guerrini et al 1995).
Some patients show an apparently generalized photoconvulsive response, preceded
by paroxysmal occipital driving. However, a photoparoxysmal response is not
demonstrable in all patients (De Marco and Ghersini 1985). Flash and pattern
evoked potentials show abnormally high responses even when a photoparoxysmal
response on the EEG cannot be demonstrated (Guerrini et al 1998). Pattern visual
evoked potentials can be very effective in unveiling giant potentials, in particular
when a black-and-white, high contrast (greater than 60%) pattern formed by
20 min of arc checks, alternating at 1.7 Hz is employed (Guerrini et al 1998).
Some ictal EEG findings are characteristic. The most typical initial ictal
pattern is a photoparoxysmal response followed by a progressive buildup of
ictal activity at electrodes O1, O2, or Oz. An exaggerated driving response
consisting of high amplitude sharp waves or spikes, elicited over a wide range
of flash frequencies and representing large early components of visual evoked
potentials, is also very typical. This driving response can transform into
self-sustaining rhythmic ictal activity. A shifting of the occipital ictal
discharge from side to side and a critical role of the Oz electrode in demonstrating
the ictal discharge associated with the elementary initial visual symptoms
is also typical (Guerrini et al 1995). Seizure detection by the Oz electrode
in the early stages of the seizures suggests ictal activity restricted to the
calcarine cortex, which is located mesially. This is in keeping with the giant
visual evoked potentials that are also attributable to the primary visual cortex.
Prognosis and Complications
Idiopathic photosensitive occipital lobe epilepsy carries a relatively good
prognosis. Some patients may experience only isolated seizures over several
years even if they receive no treatment. Most reported patients suffered
no more than a few seizures, becoming seizure free under antiepileptic drug
monotherapies (Guerrini et al 1995; 1997). They were, therefore, allowed
moderate use of the computer and television. Others who present a wide photosensitivity
range may continue to suffer occasional seizures on exposure to environmental
triggers despite the start of adequate drug treatment. Although drug withdrawal
has been attempted successfully in isolated cases, long-term follow-up studies
have not been reported, and the age at disappearance of photosensitivity
is not known. Outcome studies in generalized photosensitive epilepsies, conducted
regardless of the specific epileptic syndrome, indicate that although seizures
are well-controlled in most, a photoparoxysmal response persists through
early adulthood in at least two thirds of patients (Binnie and Jeavons 1992;
Harding et al 1997).
Management
The presence of a clear triggering factor should lead to restrictions concerning
exposure to the trigger. The indications for medical treatment should be
assessed on an individual basis according to the photosensitivity range of
each patient. Patients with a single seizure or a few seizures and narrow
range of photosensitivity may not require therapy. More aggressive medical
treatment should be reserved for patients with marked photosensitivity and
disabling seizures, for whom avoidance of all provoking stimuli is impractical.
Sodium valproate appears to be quite effective (Guerrini et al 1995), and the
results are similar to those observed in generalized photosensitive epilepsies
(Jeavons and Harding 1975). Phenobarbital, carbamazepine, levetiracetam, and
benzodiazepines may be helpful in some photosensitive patients who are resistant
to valproate (Kasteleijn-Nolst Trenite et al 1996; Guerrini et al 1998). The
effects of antiepileptic drugs on this form of epilepsy should be tested by
evaluating their influence on both the photoconvulsive response and the amplitude
of the visual evoked potentials.
Pregnancy
No information was provided by the author.
Anesthesia
Not applicable.
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ILAE.
ILAE Copyright Notice
Abbreviations
EEG:electroencephalogram
CT:computed tomography
MRI:magnetic resonance imaging
ICD Code
345.5
Associated Disorders
Benign rolandic epilepsy
Major Keyword Descriptors
amaurosis
contraversive seizures
eye deviation
hallucinations
head deviation
headache
intermittent photic stimulation
occipital paroxysm
partial seizures
pattern sensitivity
phosphenes
photoparoxysmal response
reflex seizures
visual evoked potentials
Minor Keyword Descriptors
complex partial seizures
EEG
illusions
light
seizures
television
tonic-clonic seizures
video games
video monitors
vomiting
Age of Presentation
06-12 years
13-18 years
Age of Typical Presentation
06-12 years
13-18 years
Population Group(s) Preferentially Affected
none selectively affected
Occupation Group(s) Preferentially Affected
none selectively affected
Sex
female>male,>2:1
female>male,>1:1
Family History
family history may be obtained
Heredity
heredity may be a factor
Glossary
Illustration captions
Title: Figure 1, EEG response to low frequency intermittent photic stimulation
Legend:
At low frequency stimulation each flash evokes an occipital spike.
Title:
Figure 2, occipital photoparoxysmal response induce by intermittent photic
stimulation
Legend: Top: Eyes open, a photoparoxysmal response is driven by intermittent
photic stimulation up to 30 Hz and is accompanied by visual symptoms (see
bottom). Above 30 Hz, postictal slowing of the EEG persists over the occipital
areas, with interspersed spike and wave complexes; bottom: patient’s
drawing representing “phosphorescent multicolored spots moving in
the visual field”
Title: Figure 3, Checkerboard pattern reversal visual
evoked potentials
Legend: visual evoked potentials at MO electrode are of very high amplitude.
Overlapped is the schematic representation of average VEPs amplitude
for 10 controls. Checks of 20 minute of arc; reversal rate of 1.7 Hz;
contrast of 57%. MO = mid occipital electrode.
Permuted Topic, Synonyms, Variants
Idiopathic photosensitive occipital lobe epilepsy
photosensitive occipital lobe epilepsy, Idiopathic
occipital lobe epilepsy, Idiopathic photosensitive
lobe epilepsy, Idiopathic photosensitive occipital
Related Topics
Early onset benign childhood occipital seizures (Panayiotopoulos syndrome)
Late onset childhood occipital epilepsy (Gastaut type)
Reflex seizures
Visual-sensitive epilepsies
Differential Diagnosis
photic-induced seizures due to progressive neurologic disorders
visually-induced seizures due to nonprogressive lesional epilepsies
childhood migraine
migraine
childhood epilepsy with occipital paroxysms (benign occipital epilepsy)
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