POSTERIOR CORTICAL EPILEPSIES
SEMINAR
The ILAE Commission (1989) classifies focal epilepsies according to their topographical/anatomical origin as:Temporal lobe epilepsiesFrontal lobe epilepsiesParietal lobe epilepsiesOccipital lobe epilepsies
These epilepsies may be idiopathic, cryptogenic or symptomatic
frontal lobe seizures prominent motor activity at
onset posturing, focal tonic activity,
and elaborate Gestures Unilateral or bilateral tonic limb
posturing, and bicycling movements
Atonic seizures (the supplementary negative motor area)
Speech arrest is often profound when it occurs
vocalizations, barking and nonverbal vocalizations
often brief, lasting under 1 minute, and typically less than 30 seconds, with little to no postictal phase
higher frequency, often have a nocturnal
Predilection more apt to secondarily
Generalize psychic symptoms- mood and
affect changes Olfactory hallucinations
temporal lobe sezures•amnesia of the event,•reactive automatisms,•duration of the seizure for longer than one minute,•prolonged postictal confusion
experiential phenomena that suggest temporal onsetIn mesial temporal onset•Autonomic- nausea and a rising epigastric sensation•psychic phenomena- panic and fear
lateral temporal lobe onset•more pronounced psychic phenomena- the sense of being in a dreamy state•Visual perceptual changes -Visual illusions ,multimodal hallucinations•Vertigo •early clonic movements
Posterior cortex epilepsies (PCEs) encompass a group of epilepsies originating from the occipital, parietal, or occipital border of the temporal lobe, or from any combination of these regions
characteristic feature of posterior neocortical seizures is the tendency to have multiple spread patterns (Salanova et al 1992, Fogarasi et al 2003).
This can occur among different patients or among different seizures in the same patient
can present with stereotyped but very different-appearing clinical seizures depending on direction of seizure spread
individual patients can have seizures that are not stereotyped from one to another, strongly suggesting multifocality
seizure propagation pathways
Seizure spread from posterior cortex
occipital focus to the ipsilateral temporal lobe through the inferior longitudinal fasciculus
Similar pathways between the occipital lobes and the
supplementary motor area and the thalamus
Between the parietal sensory cortex and the frontal motor and supplementary motor areas
Many of the disabling clinical manifestations resulted from ictal spread to adjacent cortical structures
29–88% of patients exhibited automatisms typical of temporal lobe epilepsy
38–47% had focal motor activity
seizure spread has been suggested to influence the outcome of treatment
favorable outcome when spread is to suprasylvian regions
less favorable outcome when spread is to limbic structures
Parietal lobe epilepsies
primary epileptic focus anywhere within the parietal lobe
The 1989 ILAE Commission classifies parietal lobe epilepsies among the localisation-related epilepsies
Parietal lobe epilepsies have not yet been detailed in the new ILAE diagnostic scheme
Demographic Datastart at any age Both sexes are equally affected Age at onset is much later in patients with
tumours6% of all focal epilepsies in neurosurgical
seriestwice as common as occipital lobe seizures
Clinical Manifestationsmainly simple focal without impairment of
consciousnessin order of prevalence:
somatosensorysomatic illusions (subjective disturbances of
body image)vertiginousvisual illusions or complex formed visual
hallucinationsreceptive or conductive linguistic
disturbances
Somatosensory Seizuresthe most common type (around two-thirds of
cases)Positive phenomena
tingling and a feeling of electricity, which may be confined or may spread in a Jacksonian manner
desire to move a body part or a sensation as if a part were being moved
Muscle tone may be lost
The parts most frequently involved those with the largest cortical representation
(e.g., the hand, arm, and face)
facial sensory phenomena may occur bilaterally
intraabdominal sensation of sinking, or nauseainferior and lateral parietal lobe
Negative phenomena (Non dominant parietal) numbness, a feeling that a body part is absent a loss of awareness of a part or a half of the body
(somatoagnosia)Parietal lobe visual phenomena Metamorphopsia with distortions, shortenings,
and elongations
Rarely, there may be pain superficial burning dysaesthesia, or a vague, very
severe pain
receptive or conductive language disturbancesDominant paretal
Lateralised genital sensatonsParacentral lobule
QualityTingling may be the most characteristic
symptom (76% in one study)
Pain, sometimes excruciating, is experienced by 25% of patients
Static or Jacksonian march
bilateral spread is rare
Unilateral somatosensory seizures are usually contralateral to the epileptogenic zone
Seizures ipsilateral to the side of seizure origin are exceptional
Ictal sensations in the genital areas and the rectum, and orgasmic seizures are infrequent
sexual automatisms (i.e. fondling the genitals) occur only in the postictal phase
Objective Ictal Somatosensory Deficitstwo-point discrimination was impaired in the
contralateral hand
Disturbances of Body Image and Somatic Illusions (posterior parietal lobe)
second most common ictal symptom
Ictal limb agnosia ,phantom limb sensations
Neglect is more commonly associated with the right rather than the left inferior parietal lobe
Illusions of movement
Vertigo (temporo-parietal border)about 10% as ictal manifestations
Visual illusions and complex formed visual hallucinations (non-dominant parietal regions)about 12% of patients
Linguistic Disturbances (dominant temporal-parietal lobe)alexia with agraphia and significant
calculation defects
Inhibitory motor seizures, ictal hemiplegia or negative motor manifestations,drop attacksexceptional
Seizure spreadPosterior propagation - elementary visual
hallucinations or ictal amaurosis (Williamson 1987).
Anterior spread can produce focal clonic motor activity.
spread to the supplementary motor area- asymmetrical tonic motor activity (Siegel et al 1999).
Inhibitory or hemiplegic seizures may occur, but it is not known whether this represents spread beyond the parietal lobe
posterior parietal lobe seizure spread to the temporal lobes, produce "psychoparetic" seizures (Ho et al 1994).
Parietal lobe seizures resembling panic
attacks -reflect temporal lobe seizure spread ( Sazgar et al 2003).
When seizures arise in “silent” areas of the parietal lobe and propagate anteriorly, they can be confused with frontal lobe seizures.
Frequency of seizure Spreading to Extraparietal Regions
unilateral focal clonic convulsions (57% of patients),
head and eye deviation (41% of patients),
tonic posturing of usually one extremity (28% of patients)
automatisms (21% of patients)
Secondary GTCS are usually infrequent
Duration of Seizuresfew seconds to 1–2 minProlonged isolated sensory auras
Postictal Manifestationsusually shortTodd’s paralysis (22%) dysphasia (7%)
Epileptogenic Localisationprimary sensory cortex
contralateral positive or negative symptomsalso occur with seizures emanating from
posterior parietal regionssecondary sensory area
Bilateral sensory symptoms parietal paracentral lobule
Ictal sensations in the genital areas area 5a
Ictal pain
Precipitating Factorsmovements of the affected part of the
body, tapping or other somatosensory stimuli
Sensorimotor seizures may also be triggered by music or toothbrushing
Aetiology
Non tumoural patients with parietal lobe epilepsyOut of 82 patients Salanova V reported
43% had a history of head trauma 16% a history of birth trauma the cause was unknown in 20%
• The remaining 21% – history of encephalitis– febrile convulsions– gunshot wounds to the head– forme fruste of tuberous sclerosis– hamartoma– vascular malformations– tuberculoma– arachnoid or porencephalic cysts– microgyria – post-traumatic thrombosis of the middle
cerebral artery
tumours
astrocytomas (62%)meningiomas (14%) hemangiomas (9%) oligodendrogliomas (9%)ependymoblastomas (3%).
•In reports with MRI, malformations of cortical development - the most common cause
Diagnostic Procedures
Neurological examination usually normal impaired two-point discrimination or
stereoagnosia mild limb atrophyinferior quadrantic visual field defects disturbances of written language, aphasia,
spatial orientation and right-left disorientationtumoural parietal lobe epilepsy
mild contralateral weakness is common (38%)unilateral limb atrophy is exceptional
Brain imagingHigh resolution MRI
abnormal in 60% FDG-PET and ictal SPECT
are useful in presurgical evaluations
Electroencephalography
Interictal EEGmay be normal, non-specific, or even misleadingIn symptomatic patients- localised slow waves
False localising to frontal, temporal or occipital electrodes
16% do not have epileptiform dischargessecondary bilateral synchrony is common
(32%)
• Ictal EEG• The ictal EEG may be normal in 80% of
simple focal sensory seizures• The prevalence of scalp EEG changes
– sensory seizures- 15%– as opposed to 33% when motor symptoms are
present
• Postictal EEG– focal slow wave, attenuation of background
activity or spikes
Differential DiagnosisSomatosensory seizures are misdiagnosed
as non-epileptic psychogenic fits > transient
ischaemic attacks > migraine with aura
Management
Drug treatment is similar to focal seizures and is usually effective
In intractable cases, neurosurgery achieves seizure-free state or remarkable improvement (> 65%)
Better prognostic factorsMRI abnormality concordance of different diagnostic
modalitiescompleteness of resection of the
epileptogenic zone Resection may be problematic
deficits in vision ,language, praxis, attention and higher cortical function
Occipital Lobe Epilepsies
Occipital seizures originate from an epileptic occipital focus
triggered spontaneously or by external visual stimuli
idiopathic, symptomatic or probably symptomatic
Demographic Data
Occurs at any age 5–10% of all epilepsies5% in neurosurgical series6% seen in demographic studies
Clinical Manifestations
The cardinal symptoms are mainly visual and oculomotor
Visual subjective symptoms elementary and less often complex visual
hallucinationsblindnessvisual illusionspallinopsiasensory hallucinations of ocular movementsocular pain.
Ictal objective oculomotor symptoms tonic deviation of the eyes (pursuit-like
rather than oculotonic)oculoclonic movements or nystagmusrepetitive eyelid closures or eyelid fluttering
elementary visual hallucinationsthe primary visual cortex
visual illusionsthe occipital-parietal and occipito-temporal
junctionsSeizures may spread from the occipital to
anterior regionsgenerate symptoms from the temporal, parietal
and frontal lobes secondarily hemi- or generalised convulsions
Ictal or postictal headache is frequent
Elementary Visual Hallucinations
the most common, characteristic and well-defined ictal symptoms
Often the first symptommay progress to other occipital and extra-
occipital manifestations and convulsions
mainly coloured and circulardevelop rapidly within seconds and are brief
in duration often appear in the periphery of a temporal
visual hemifield become larger and multiply in the course of
the seizure, frequently move horizontally towards the
other side
Colour, Shape and Sizeusually multicolouredShapes are mainly circular, spots, circles and
ballssquare, triangular and rectangular - less
frequentincrease in number, size or both with
progression of the seizure
Locationusually unilateraltemporal visual hemifield may appear in a normal, blind or damaged
hemifieldCentral or undefined localisation occurs in
10–30% of patients
Lateralisationcontralateral to the epileptogenic focus Conversely, this is ipsilateral to the
epileptogenic focus for unilateral visual hallucinations moving horizontally towards the other side
Visionobscured only in the area occupied by the
visual hallucinationssome patients able to read through themBlurring of vision at onset may be a form of
visual seizure
Durationdevelop rapidly within seconds usually brief, lasting from a few seconds to
1–3 minExceptionally, they last for 20–150 minutes-
focal visual status epilepticusAs a rule, last longer prior to secondarily
generalisation
Frequency and Circadian Distributionoften in multiple clusters, daily or weeklyusually diurnalRarely on awakening
Stereotypic Appearancestereotyped, particularly at onset, in all
aspects other than duration same patient experiencing different types of
seizures is exceptional
• Progression to Other Occipital or Non-Occipital Seizure Manifestations
• often progress to other ictal symptoms– complex visual hallucinations– oculoclonic seizures– tonic deviation of the eyes– eyelid fluttering or repetitive eye closures– impairment of consciousness– experiential phenomena– hemi-anaesthesia– unilateral or generalised convulsions
• extra-occipital seizure manifestations by spread to the temporal, frontal or parietal regions.
Complex Visual Hallucinations, Visual Illusions and Other Symptoms from More Anterior Ictal Spreading
Complex visual hallucinations
persons, animals, objects, figures or scenesfamiliar or unfamiliar, friendly or frighteningsmall or large area of a hemifield, or in the centre and the
whole of the visual fieldstatic, move horizontally, expand or shrink, approach or move
awaydo not have the emotional character of temporal lobe seizurescomplex visual hallucinations may appear in the defective
visual field
Ictal autoscopiaoriginate from occipito-parietal and occipito-
temporal junction areasVisual illusions
Metamorphopsia,micropsia or macropsia,achromatopsia,monochromopsia
Palinopsiapersistence or recurrence of visual images with right posterior parieto-temporal lesions.
Sensory Hallucinations of Ocular Movementssensation of ocular movement in the absence of
detectable motion - rare
Ictal Blindness often occurs as a starting or the only ictal
seizure manifestation with abrupt onsetmay follow the visual hallucinationsmay last for hours or days (status epilepticus
amauroticus).one-third of patients with symptomatic and two-
thirds of patients with idiopathic occipital epilepsy
Tonic Deviation of the Eyes, Oculoclonic Seizures and Epileptic NystagmusTonic deviation of the eyes often, followed by
ipsilateral turning of the head (40–50% of cases) – The most common non visual symptom
Consciousness is often impaired when eye deviation occurs
The epileptogenic focus is contralateral if consciousness is not impaired
Ictal nystagmus quick phase of the nystagmus is opposite to the
epileptic focusin the same direction of eye and head deviation
Repetitive eyelid closures, eyelid fluttering and eyelid blinking heralds the impending secondary GTCS
Eyelid opening, or ‘eyes widely opened’well-described symptom in occipital epilepsytypical symptom of mesial temporal lobe
seizures
ConsciousnessNot impaired during hallucinationsmay be disturbed or lost at the time of eye
deviation or eye closure
Ictal or Postictal Headachefrequently associated - 50% of casesmainly orbitaloften indistinguishable from migrainepostictal headache often occurs 3–15 min
from the end of the visual seizure, ( ‘asymptomatic interval’)
Seizure Spread
Infra-calcarine occipital foci will propagate to the temporal lobe causing
complex focal seizuressupra-calcarine foci
tend to propagate to the parietal and frontal areas giving rise to predominantly motor seizures.
Aetiology
Idiopathic, structural or metabolicMalformations of cortical development are a
common causeMetabolic or other derangements, such as
eclampsia, may have a particular predilection for the occipital lobes
Occipital seizures may be the first manifestation of celiac disease,Lafora disease or mitochondrial disorders
PathophysiologyElementary visual hallucinations
primary visual cortex complex visual hallucinations
occipito-parietal-temporal junction areasvisual illusions
non-dominant parietal regionsIctal blindness
contralateral seizure spread to involve both occipital lobes or to inhibition of the visual cortex by the seizure discharge
postictal headacheoccipital lobes are preferentially associated
with the trigeminovascular or brainstem mechanisms responsible for headache
related to serotonergic mechanisms and respond to oral sumatriptan
Another similarity with migraine - asymptomatic interval’
Diagnostic Proceduressymptomatic occipital epilepsies
haematology and biochemistry screening for metabolic disorders, molecular DNA analysis, or even skin or other tissue biopsy
High resolution MRIcalcifications of CD – CT scanf-MRI- practical value in neurosurgical cases.
Electroencephalography
• Interictal EEG• In symptomatic cases
– Background EEG is usually abnormal with posterior lateralised slow waves
– Unilateral occipital spikes or fast multiple spikes and, occasionally, occipital paroxysms occur
– There may be occipital photosensitivity
In idiopathic casesthe background interictal EEG is normal
Eg:Gastaut-type idiopathic childhood occipital epilepsy and photosensitive occipital epilepsy
Occipital spikes and occipital paroxysms, spontaneous, evoked or both, are often abundant
disappear with age
Ictal EEGparoxysmal fast activity, fast spiking or both,
localised in the occipital regions
occasional gradual anterior spreading and generalisation with irregular spike wave discharges or monomorphic spike and wave activity
Brief occipital flattening may be seen before the fast rhythmic pattern.
symptomatic occipital lobe epilepsy the ictal discharge is more widespreadpostictal localised slowing when the seizure
is prolonged or progresses to secondarily GTCS
30% of the ictal surface EEG - normal in occipital seizures
Differential Diagnosisshould be first differentiated from
migraine normal phenomenaPsychogenic
Occipital epilepsy Migraine with aura Basilar migraineVisual hallucinations
Duration for seconds to a minute Exclusive None None
Duration for 1–3 minutes Frequent Rare Rare
Duration for 4–30 minutes Rare As a rule As a rule
Daily in frequency As a rule Rare None
Mainly coloured circular patterns As a rule Rare Exceptional
Mainly achromatic or black and white linear patterns
Exceptional As a rule Rare
Moving to the opposite side of the visual field
Exclusive None None
Expanding from the centre to the periphery of a visual hemifield
Rare As a rule Frequent
Evolving to blindness Rare Rare As a rule
Evolving to tonic deviation of eyes Exclusive None None
Evolving to impairment of consciousness without convulsions
Frequent Rare Frequent
Evolving to impairment of consciousness with convulsions
Frequent Exceptional Rare
Associated with post-ictal/post-critical headache
Frequent As a rule Frequent
Blindness and hemianopia
Without other preceding or following symptoms
Frequent None Frequent
Other neurological symptoms
Brain stem symptoms None None Exclusive
Post-ictal/post-critical vomiting Rare Frequent Frequent
Post-ictal/post-critical headache
Post-ictal or post-critical severe headache Frequent As a rule Frequent
Occipital seizure Migrane with aura Basilar migrane
Differentiating Idiopathic from Symptomatic Occipital Epilepsy
symptomatic visual seizures progress to other extra-occipital seizure
manifestations and mainly temporal lobe seizures
temporal lobe symptoms are nearly exclusiveHigh resolution MRI
Prognosis
good to intractable or progressivedepends on the underlying cause and
extent of the lesions
Management
AED treatment is similar to that for any other type for focal seizures
usually effective Should be initiated as soon as possibleCarbamazepine is the drug of choicepostictal headache - oral sumatriptanNeurosurgery is effective in around 70% of
patients with 30% becoming seizure free
The Drug Treatment of Focal Epilepsies
In head-to-head comparisons among old AEDs overall treatment success was highest with
carbamazepine or phenytoin intermediate with phenobarbitone lowest with primidone
carbamazepine vs valproatecarbamazepine provided better control of
complex focal seizures CBZ had fewer long-term adverse effects
than valproateBoth drugs were comparably effective for the
control of secondarily GTCS
The new AEDsgabapentin, lamotrigine, levetiracetam,
oxcarbazepine, tiagabine, topiramate, vigabatrin and zonisamide
nearly equal efficacy to carbamazepine, phenytoin and valproate
Efficacy
Tolerability
Serious adverse events
Drug–drug interaction
Pharmacokinetics
Titration
Need for laboratory testing
Mechanism of action
Levetiracetam
High Excellent no no Ideal Fast minimal
Novel SV2A- ligand
Lamotrigine
Low Excellent
yes yes Poor Very slow
maximal
Na+
Topiramate
High Poor yes yes Satisfactory
Very slow
Maximal
multiple
Oxcarbazepine
Medium
poor yes yes Poor Slow Maximal
Na+
Zonisamide
Medium
good yes no satisfactory
slow maximal
multiple
Surgical treatment
Rasmussen (1975),first reported good outcome after removal of nontumoral epileptogenic lesions in 86 parietal cases and 25 occipital cases
Removal of a temporal lobe has also been reported to provide favorable results in some patients in whom the dominant seizure symptomatology was a result of spread of seizure discharge to that temporal lobe
Occipital epilepsy is often associated with a large epileptogenic zone
complete resections difficult
more extensive resections are a key to improved seizure control
In functionally critical areas such as the primary sensory cortex, multiple subpial transsections of the epileptogenic areas have been reported to be successful
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Clinical Features of Patients with Posterior Cortex Epilepsies and Predictors of Surgical Outcome
Charles L. Dalmagro et al
epilepsia, , 2005 Department of Neurology, Federal University of
Santa Catarina, Brazil
Surgical treatment was highly effective (p < 0.001) when compared with previous pharmacologic treatment alone.
28/44 (65.11%) patients became seizure free
Posterior cortex epilepsy: Diagnostic considerations and surgical outcome
Tao Yu et al
Seizure (2009), Beijing Institute of Functional Neurosurgery, China
Thirty-one (72.1%) had favorable surgical outcome (Engel class I and II)
26 (60.5%) seizure free patients
Cognitive changes after epilepsy surgery in the posterior cortex (R Luerding)J Neurol Neurosurg Psychiatry 2004Epilepsy surgery in the posterior cortex bears
no risk for substantial decline in general cognition
some discrete impairment in performance intelligence may occur
Thank you
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