Seizure SemiologyAbbas Tafakhori

Associate professor of Neurology

In The Name Of GOD

Semiology

• That branches of linguistics concerned with signs and symptoms

Ictus

• A sudden neurologic occurrence such as a stroke or an epileptic seizure

Detailed Analysis of Seizure Semiology

essential for the proper management of patients with epilepsy

Seizure - main symptomatology of epilepsy

definition of seizure type is important for classification of the epilepsy syndrome

The syndrome + etiology are the essential factor determining : the prognosis the most effective pharmacological treatment

Seizure control - target of treatment Presurgical workup Differentiate between epileptic and nonepileptic seizures

Seizure Semiology • 1998, Lüders et al. Semiological seizure classification

• 2001, ILAE Commission Report Glossary of descriptive terminology for ictal semiology

uses an a priori distinction between focal and generalized seizures and semiological aspects in parallel.

The clinical decision between a focal seizure and a generalized seizure is often possible only on the basis of additional information from EEG or imaging studies rather than semiological criteria.

Semiological Seizure Classification Lüders et al. (1998)

Sensorial sphere Aura

Motor sphere Motor seizure

Consciousness Dialeptic seizure

Autonomic sphere Autonomic seizure

Prominent Features Epileptic Seizure

• Seizures that cannot be assigned to any of the four groups outlined above are included in the group ‘‘special seizures.‘‘

• This category includes primarily seizures characterized as ‘‘negative” ictal phenomena:

atonic seizure

negative myoclonic seizure

etc

Semiological seizure classification

classify seizures as precise as possible

• epileptic seizure(no further information)

epileptic seizure

• characterized primarily by motor phenomena

motor seizure

• motor seizure affected the right arm

right arm motor seizure

• clonic jerking of the right arm

right arm clonic seizure

Aurasexclusively subjective symptoms without objective signs that can be documented by an observerextremely useful localizing information about the seizure onset zone

Somatosensory

Auditory

Olfactory

Abdominal

Unclassifiable

Visual

Gustatory

Autonomic

Psychic

Aura features Lateralising and localising value

Visual Flashing light of different colour ,circular, crossing midline. Ictal blindness may reflect a form of visual aura, but it can also occur as a postictal phenomenon after a visual aura

Contalateral to area 17 and 18, v illusion- v. association cortex paritotemporal

Auditory Positive-“buzz”, noise : Negative-loss hearing. Heschells gurus in STG, LTLE

Olfactory Unpleasant smells Mesial temporal lobe epilepsy (high % have amygdala neoplasm)

Gustatory Unpleasant taste (patients usually cannot identify the taste, except that it is unpleasant

insula

Somatosensory

Tingling, numbness, unpleasant heat and pain

If u/l –c/l prim. Sensory cortex If b/l-poorly described sensations of the trunk or distal extremities-supplementary sensory motor area, second sensory-motor area(superior sylvian or posterior to insula)

Aura features Lateralising and localising value

Autonomic aura Subjective sensation of palpitation, sweating, goose bumps

Insula, Epileptic activation of the basal frontal region and the anterior cingulate gyruscan evoke autonomic symptoms without the occurrence of other aura experiences or motor phenomena

Abdominal Nausea, tenseness, knot rolling, butterfly . Mainly localise to epigastriam . Sensation of increase peristalsis (van buren assesedsame with gastric balloon during aura )

Temporal (mc) frontal ,insula

Psychic Fear, elation ,déjà vu (inappropriate feeling of familiarity ) ,jamais vu .

No lateralising value , localise to mesial temporal lobe (right )

Dialeptic Seizures• “Dialeptic”, old Greek, means “to interrupt, stand still, or

pass out”•

• Alteration of consciousness (predominant semiology)• it should not be associated with any significant motor

activity

• Episodes of unresponsiveness or decreased responsiveness.

• Associated with complete or at least partial amnesia for the episode

• different terms (absence, complex partial seizure) were used, although the seizure semiology may be clinically indistinguishable.

• it can be absence seizures (dialeptic seizures with a generalized ictal EEG) and complex partial seizures (dialeptic seizures with a focal ictal EEG).

suspension of awareness and arrest of activity

Typical absence-•sudden onset without any aura ,•brief duration, typically less than 15 seconds,•sudden termination without any postictal state.•Generalized 2.5 to 4 hz spike and wave activity.

Atypical absence-•Slower loss of awareness and more gradual recoveryas well as more prominent motor manifestations.•Slower frequency less than 2.5 hz

Dialeptic seizuresfeatures Absence Complex partial

Frequency Frequent many per day Less frequent

Onset and progression Abrupt and minimal slow

automatism minor motor phenomena such as eyelid fluttering at a rate of 3 Hz and mild oral and manual automatisms

common

Aura None or rare common

duration Brief,

Autonomic seizures

• the predominant symptomatology for this type of seizure is an objectively documented alteration of the autonomic system (i.e., tachycardia documented by ECG recording) regardless of whether the patient is aware of the seizure.

• In contrast, an autonomic alteration (i.e., tachycardia) noticed by the patient without being objectively tested (i.e., ECG recording) or observed is considered an autonomic aura.

Autonimic seizures Lateralising and localising value

Pilomotor seizure- May spread in jacksonian march (spread unilaterally to adjacent body part )

Ipsilateral to seizure onset zone. Localisation poor

Ictal vomiting /retching Temporal (mainly) ,insula

Ictal spitting Right temporal lobe

Ictal hyper salivation Mesial temporal , lateralise to non dominant hemisphere

Motor Seizures 2 major subgroups

Simple :

• “Simple”

• unnatural

• Reproducible by direct stimulation of the primary motor cortex

Complex :

• Complexity of movement

• natural but Inappropriate for the situation

Simple

Myoclonic Tonic Epilepticspasm Clonic Tonic-clonic Versive

Subtypes –• duration of the muscle

contraction• rhythmicity of movement

repetition • muscles involved

Complex

Hypermotor

Automotor

Gelastic

Simple motor seizure features Lateralising and localising value

Clonic Series of recurrent regular myoclonic contractions at rate of 0.2-5/sec

Contralateral to primary motor cortex. In- frontal involve earlier . Secondary generalisation started on contralateral side and ends on ipsilateral (“end of seizure paradoxical clonus” ). Asymmetric seizure termination rare in prim. GTCS

Myoclonic Short muscle contractions lasting

Simple motor seizure

features Lateralising and localising value

Versive seizure forced and involuntary turning of the head and eyes in one direction with neck extension resulting in a sustained unnatural position .

Symptomatic zone- frontal eye field. Versive seizures appear earlier in- frontal lobe origin than TLE (can be the first sign in FLE ). Versiveseizures – lateralized to contralateral hemisphere, specially when within 10 seconds before secondary generalization.

Tonic clonic

•Generalized epilepsy - start with symmetrical tonic posturing of all the limbs followed by a “jittery” phase clonic activity of all four extremities.• Focal epilepsies – seconadary generalization almost always preceded by other seizure types and the tonic phase is usually asymmetric.

Simple motor seizure

features Lateralising and localising value

Tonic •Sustained muscle contractions >3 s that leads to tonic posturing •Tonic contraction of chest and abdominal muscle- “tonic epileptic cry” Secondarily generaliztion - have a typical “motor sequence1. The tonic face seizure and the versive seizure

lateralize to contralateral side. 2. The fencing position lateralizes to

contralateral to the raised arm 3. .The asymmetric tonic limb posturing “sign of

four” lateralizes to contralateral to the extended arm

Most commonly- frontal lobe epilepsy (62.2%) mainly bilateral and rarely temporal lobe epilepsy (1.7%) (only unilateral tonic seizures ). if clearly unilateral lateralize to contralateral

Complex motor seizure

Features Localising and lateralizing value

Hypermotor movements involve more than one articulation and resemble normal movements mainly the trunk and proximal segments of the limbs. Ex. peddling movements, running, etc. May resembles sexual activity, like violent writhing, thrusting and rhythmic movements of the pelvis, arms and legs, picking and rhythmic manipulation of the groin or genitalia. Consciousness may be preserved. Mostly during sleep

Most originate from the orbital or mesial frontal regions. may be from temporal lobe and insula.

Automotor Mainly involves distal segments of the hands, feet, mouth and tongue. Automotors can be unilateral or bilateral . Unilateral automotors is likely a manifestation of limb dystonia in the contralateral limb. 95% are associated with altered consciousness.

Typical of TLE but occasionally with FLE. Frontal automotorare shorter . Unilateral automatisms are more frequently lateralize to ipsilateral .

Gelastic Gelastic main motor manifestation is “laughing” . In 50% of the cases hypothalamic hamartomaswere detected by MRI.

.However extrahypothalamicstructures are anterior cingulate region- frontal, parietal and temporal lobes

Special Seizures

• All seizures are negative or inhibitory motor seizures except the aphasic seizures that mostly represent negative cognitive seizures

• Atonic seizures

• Astatic seizures

• Negative myoclonic seizures

• Akinetic seizures

• Aphasic seizures

• Hypomotor seizures

Special seizure Features Localization and lateralization

Atonic seizures loss of postural tone with falls or head drop. Most frequently in -symptomatic generalized epilepsies (LennoxGastautsyndrome) and are usually preceded by a generalized, proximal myoclonic seizure resulting in an abrupt fall.

Generalized. (LGS ) Focal -seen in FLE and TLE. these are slower falls and rarely significant injuries.

Astatic seizures It consist of epileptic falls. Most commonly are due to a myoclonic seizure f/ b an atonic . But it can be due to atonic seizures .

Hypomotor seizures Decrease or total absence of motor activity. Only used in whom consciousness cannot be tested during or after the seizure (newborns, infants ,children < 3 yr mentally retarded)

In focal epilepsy- temporal and parietal lobe epilepsy.

Special seizure Features Localization and lateralization

Akinetic seizures Inability to perform voluntary movements. The diagnosis only be made in patients who are conscious and cooperative, i.e. they try to perform a movement but are unable to do so (apraxia).

Localization -negative motor areas in the mesial and inferior frontal gyri.

Negative myoclonic seizures Negative myoclonic seizures A very brief loss of muscle tone of (

Summary of Lüders Classification

LRALIZATION LOCALIZATION

HEMISPHERICAL

RIGHT LEFTDOMINANT

NON DOMINANT

LOBAR

TEMPORAL EXTRATEMPORAL (FRONTAL PARIETAL OCCIPITAL)

SUBLOBAR

MESIAL TEMPOTAL/LATERAL TLE SMA/ MOTOR AREA MESIAL /LATERAL OLE

IPSILATERAL CONTRALATERAL

U/I limb automatism U/L clonic movement

Early head deviation U/L dystonia

u/l blinking Late head or eye turning

Post ictal nose wiping ictal akinesis

Asymmetrical termination of clonic jerks followed by GTCS

Post ictal paresis

Whole body turning

ATLP (asymmetric tonic limb posturing)

DOMINANT NON-DOMINANT

Ictal aphasia Ictal speech

Post ictal dysphasia b/l automatism with preserved consciousness

Ictal smile. Spitting, vomiting

Peri-ictal urinary urge

Postictal coughing

Lateralising sign Lateralising Value Symptomatogenic zone

Unilateral dystonic posturing

contra lateral Activation of BG , TLE

Hemi field visual aura contra lateral Broadman area 17-19 and adjacent area of OLE

version contra lateral Broadman area 6 and 8

Ictal aphasia and dysphasia dominant Impairment of language areas

Automatisms and preserved consciousness

Non dominant Unknown , hippocampal impairment, TLE

Lateralising sign Lateralising Value Symptomatogenic zone

Post-ictal palsy 93 % contra lateral Area 4 and 6

Post-ictal nose wiping 92% ipsilateral Unknown , TLE

Figure of 4 sign 89% contra lateral SMA , prefrontal area , TLE, ETLE

Unilateral sensory aura 89 % contra lateral Area 1,2,

Tonic activity 89% contra lateral SMA , also possibility of broadman area 6, , anterior cingulate gyrus and subcortical structures FLE

Lateralising sign Lateralising Value Symptomatogenic zone

Ictal speech 83 % non dominant Areas other than those involved language production

Clonic activity 83% contra lateral Area 4 and 6 .FLE

Unilateral ictal eye blinking 83% ipsilateral unknown

Ictal vomiting 81 % non dominant Medial ,lateral superior and inferior structure of non dominant temporal lobe and papez circuit

Ictal spitting 76 % non dominant

Frontal lobe seizures

Sudden onset and offset

Short duaration

localisation Semiological features

Primary motor cortex Clonic seizure with or without jacksonianmarch and todd’s palsy, cortical myoclonus, consciousness preserved

Dorso-lateral premotor Complex bizarre automatism ,forced acting is common

supplementary motor cortex Asymmetrical tonic seizures, well known ‘fencing posture’ I/L arm flex and C/L extended (figure of ‘4’) , short duration ,occur in cluster frequently arise out of sleep .ictalvocalisation

Mesial frontal hyperkinetic motor behaviour, ictal expression (emotions)

frontal eye field (+/- broca’s) Eye and head deviation ,ictal vocalisation or speech arrest (with broca’s)

Orbito-frontal and polar Hyperkinetic automatism with agitation , duration-short postictal –brief or nonexistent,risk of misdiagnosis as psychogenic seizure

localisation Semiological features

Rolandic or Frontal opercular area Facial clonic movement ,swallowing hyper salivation, speech arrest

non localising Rare ,staring spell, difficult to distinguish frontal absence

ADNFLE autosomal dominant nocturnal FLE Autosomal dominant ,During sleep ,Like parasomnia –jerky , dystonic posturing ,bending rocking

Insular epilepsy Specific features

•Hypersalivation is very common

•Choking

•Throat sensation

•Peri-oral paresthesia

•Autonomic –retching palpitations

•Variable semiology

TEMPORAL LOBE EPILEPSY

• AURA- Common ( epigastric )

• DURATION- 1-2 min and more

• FREQUENCY- Few per month

• ONSET- slow behavioural arrest, and stare

• AUTOMATISM- Simple oro-alimentary

• VOCALISATION- Simple speech

• GENERALISATION- Uncommon

• POSTICTAL- Confusion , aphasia up to minutes

MTLE ( aura, arrest, automatism, amnesia) LTLE

Epigastric aura (MC) ,olfactory ,psychic (fear) Auditory, cephalic (vertiginous illusion ) , complex aura

Motionless stare (behr arrest ) Anxious ,agitated behaviour

Speech arrest in dominant Vocalization

Early oro-alimetary and hand automatism Early complex automatism (gross truncal)

I/L limb automatism and C/L dystonic posturing

Less automatism, no dystonia.

Less sec. generalization Frequent sec. generalisation

Temporal Extra-temporal

Limbic aura Aura (Area specific)

Hypomotor activity , stare motionless arrest ( behr arrest )

Hypermotor ,vocalization

Dystonic posturing Tonic posturing

Slow evoluation Fast evolution

>1 min. duration brief

Temporal plus /pseudotemporal

• Early motor features (version, eye deviation)

• ET aura –sensory and throat sensation

• Early age

• No antecedent event

• High frequency ,clustering

• Frequent generalisation

CLINICAL TEMPORAL FRONTAL

AURA Common, epigastric Vague, nonspecific

DURATION 1-2 min Brief 10-60 sec

FREQUENCY Few per month Several per week

ONSET Slow behavioural arrest, and stare,sleep activation

Abrupt forceful movement,frequent sleep activation

AUTOMATISM Simple oro-alimentary Complex bipedal bizarre

SPEECH Simple verbalization speech in non dominant seizure

Complex ,loud vocalization (grunting ,screaming )

GENERALISATION Uncommon Common

POSTICTAL Confusion , aphasia

up to minutes Absent or minimal

Parietal lobe epilepsy

•Next most likely source of seizure after TLE and FLE

•Best recognized manifestation is -sensory aura –numbness, tingling, pins and needles, burning pain.

•With sensory march- post central primary sensorycortex .

•Without sensory march- second sensory area(parietal operculum )

•Seizures without parietal lobe symptoms- most ofhave no parietal symptoms but rather manifestationresulting from spread to occipital ,temporal, or frontal.

Occipital lobe epilepsy

SENSORY SYMPTOMS

•VISUAL HALLUCINATION

cardinal symptom (20-70 %)

brief, multicloured and circular

may be only manifestation

postictal headache (nonspecific -TLE)

•VISUAL ILLUSION

•BLINDNESS

MOTOR SYMPTOMS

•b/l blinking, nystagmoid eye movements, eye deviation (c/l)

•One distinctive feature –it develop and propogateposteriorly

very slowly (Eye deviation seen in OLE is much slower than in

FLE and TLE )

Clinical approach to patient with epilepsy

• Age of seizure onset-(neonatal ,childhood, juvenile, elderly)

• Warning symptoms -Aura (abdominal, sensory, visual, no aura )

• What happens during seizures -(awareness, automatism, incontinence/tongue bite )

• Post-ictal period- (confusion, aphasia, preserved speech, paralysis , immediate recovery-no confusion )

• Diurnal variation (early morning/ after awakening, any time, during sleep )

Extra temporal Seizures

FRONTAL LOBE EPILEPSY• FLE surgery is the second most

common type of epilepsy surgery performed.

• The frontal lobe occupies the largest volume of the brain and may be anatomically subdivided into:

the anterior frontopolar

orbitofrontal

mesial (or medial)

dorsolateral

opercular regions.

• Diagnosing FLE clinically may be difficult, but some features help to distinguish FLE from TLE:

seizure frequency may be higher than 30 per month, even upward of 100 per month.

patients often have seizures with an older age of onset, that is, after age 5

Semiologic features that help distinguish FLE from TLE include: bilateral limb movement at the onset of seizures

absence of oroalimentary automatisms

a very brief or absent postictal confusional state.

Vocalization is common

the seizure duration is generally shorter than the typical temporal lobe seizure, usually

Causes:

• Malformations of cortical development (MCD) (largest fraction of patients in whom epilepsy surgery is performed)

• Trauma

• stroke

• neoplasm (both benign and malignant)

• meningitis or encephalitis

• hamartomas

• vascular malformations including arteriovenous malformations, and cavernous hemangiomas

• Genetic causes Autosomal dominant nocturnal FLE

benign epilepsy with centrotemporal spikes

Seizure Types

Frontopolar Seizures

• most often due to head trauma(cause encephalomalaciaand gliosis)

• other etiologies can occur (e.g., tumor, vascular malformations)

• If auras are experienced, they may present with forced thinking, but often, auras do not occur

• secondary generalization is often the first manifestation

• Lengthy seizures with partial responsiveness similar to atypical absence can rarely be seen as well, progressing to tonic or tonic–clonic seizures.

Orbitofrontal Seizures• produce a variety of symptoms

• In children, complex partial seizures without secondary generalization can be associated with autonomic arousal including fear, flushing, piloerection and abdominal pain, and vocalizations with manual automatisms.

• EEG may demonstrate a pattern of periodic bifrontal sharp and slow waves.

• Behavior may in part be due to spread to the hypothalamus and temporal lobe.

• Other investigators have found hypermotor activity along with automatisms (and loss of awareness in some patients) and also noted asymmetric tonic posturing, frequent head and body turning, and ictal laughter.

• Olfactory hallucinations may also occur, presumably related to spread

• Scalp EEG findings may not be localized, and

intracranial EEG may be needed for diagnosis

• Sphenoidal electrodes might improve the

sensitivity of scalp EEG, but often, orbitofrontal

seizures have misleading EEG localization.

• Because of the close connections to the

temporal lobes, patients with orbitofrontal

seizures may be misdiagnosed as having TLE.

Medial Frontal Seizures

• The mesial frontal lobe consists of:

the medial aspect of the motor strip

SMA

the anterior cingulate gyrus.

Supplementary Motor Area (supplementary

sensorimotor area)

• Located immediately anterior to the motor strip on

the medial surface of the frontal lobes.

• Supplementary motor seizures have well-defined

clinical characteristics:

Patients frequently report somatosensory aura such

as numbness in a contralateral limb, which is

followed by unilateral or bilateral tonic limb

posturing.

• showing a “fencer” posture

• the “figure of four” sign

• “M2e” posturing.

• Patients may then also have whole body

movements, vocalizations, and perhaps emotional semiology, with late head and eye version.

• Negative motor seizures rarely may occur with inability to voluntarily move the extremities while the patient is awake.

• SMA seizures often are nocturnal and occur in clusters, and awareness and consciousness are usually retained unless secondary generalization occurs.

• Surgical removal of the SMA may result in transient akinetic mutism and either unilateral or bilateral weakness or apraxia (the “SMA syndrome”), which usually resolves in 1 to 4 weeks after surgery, but may last as long as 6 months.

Supplementary motor area seizures.

• A 20-year-old man has refractory GTC seizures and also SPS with left arm tonic extension occurring at night.

• The ictal surface EEG was nonlocalizing and demonstrated only diffuse attenuation during SPS.

• Cortical map showing seizure onset seen in the interhemispheric strip electrodes, primary and supplementary areas.

• Ictal IEEG with fast activity seen in the right interhemispheric electrodes

Anterior Cingulate

• The anterior cingulate gyrus has extensive connections throughout the frontal lobe as well as the limbic system, brainstem, and thalamus.

• It is involved in:

emotions

autonomic functions

perception of pain

motor planning

• Whereas the amygdala is implicated in the generation of fear in auras of TLE, the cingulate gyrus in the medial frontal lobe is thought to be the generator of fear auras in patients with FLE.

• This may relate to propagation of ictal discharges to the amygdala.

Patients with proven lesional cingulate

epilepsy have:

• complex, hypermotor behaviors

such as running, kicking, grasping, or

thrashing.

• Behavioral changes including

postictal or interictal agitation are

seen, which can resolve after

lesionectomy

Primary Motor Area

• Primary motor cortex in the medial frontal lobe (interhemispheric region)is responsible for movement of the lower extremity and sphincter control.

• Seizures arising from the leg motor cortex produce clonic movement of the thigh, leg, or foot and may produce bladder or bowel incontinence.

Dorsolateral Frontal Seizures

• The dorsolateral frontal lobe includes: the lateral primary motor strip

perirolandic region

premotor areas

• Seizures arising from premotor dorsolateral frontal cortex can cause:– tonic posturing of the arm or face– sensory phenomenon

– psychosensory auras including forced thinking (as seen with frontopolarseizures).

• Early spread to motor cortex will cause clonicactivity while still conscious, whereas temporal lobe seizures are more likely to produce experiential or epigastric auras with motor activity once consciousness is impaired .

• Seizure propagation to Broca’s area may cause speech arrest

• contralateral head and eye version commonly occur with spread to the frontal eye fields.

• The EEG more often shows localized findings than with mesial or orbitofrontal seizure origin because of the close proximity of the cortex to the scalp.

• The scalp ictal EEG often shows fast activity in the beta frequency range, in contrast to temporal lobe seizures, which more often begin with rhythmic theta discharges.

• Ictal beta at seizure onset is often well localized in dorsolateral frontal lobe seizures and predicts a good postsurgical outcome, but the same is not necessarily true for all FLE patients.

• Seizures that arise from the

primary motor strip differ clinically

from those of the SMA or

premotor area

• they usually begin with

contralateral facial or hand clonic

activity followed by spread to

the rest of that side of the body

(i.e., a jacksonian pattern of

spread), with speech arrest and

then head and eye version.

Frontal Opercular and Insular Seizures

• The operculum is the region of cortex overlying the insula and is subdivided into frontal, temporal, and parietal opercular cortices.

• Seizures arising from the frontal operculum often present with: gustatory auras

apraxias of swallowing or mastication

dysarthria.

may chew

Salivate

complain of abnormal laryngeal sensations

paresthesias in the arm and face

choking sensation

trouble breathing. Early spread in a posterior and superior direction often

causes facial clonic activity.

Localization of Frontal Lobe Seizures by

EEG

• The interictal EEG is often not helpful in the localization of

frontal lobe seizures.

• Only a small proportion of patients have spikes

restricted to the frontal lobe focus.

• Some patients have bifrontal or generalized spike-and-

wave discharges

• others may have only temporal lobe interictal spikes.

• Other individuals have multifocal spikes

• some patients have a normal interictal EEG

• The ictal EEG is often unrevealing in frontal lobe seizures:

obscured by movement and muscle artefact

negative

poorly localized.

• Focal seizure onset occasionally is noted in the scalp EEG, usually with high-frequency beta frequency onset

• More often, the ictal EEG does not provide adequate localizing information.

• This may be due to the fact that:

much frontal cortex is buried, either within sulci or in medial or basal regions that are poorly sampled by the scalp EEG

by rapid contralateral spread of ictal discharges via the corpus callosum.

• Seizures beginning in mesial frontal lobe are particularly difficult to record with scalp EEG.

• Half of patients with mesial FLE will have generalized epileptiform patterns, nonlateralized midline discharges, or no EEG findings when seizures begin.

• FLE arising in dorsolateral cortex more often appear lateralized than mesial FLE in the ictal EEG, though remain less well localized than temporal lobe seizures.

• Incorrect seizure lateralization is more often observed in lateral FLE patients than in mesial FLE patients

Differential Diagnosis

• The clinical patterns of frontal lobe seizures include bizarre behaviors, which may be confused for nonepileptic events.

• Patients may be misdiagnosed as having parasomnias or receive a diagnosis of psychogenic nonepileptic seizures (PNES) and mistakenly thought to have a primary psychiatric disease.

• It is important to recognize stereotypy of behaviorand nocturnal clustering, which suggest frontal lobe seizures rather than PNES or parasomnias.

• Patients with FLE may have preserved awareness during bilateral body movement, which may include bicycling and large thrashing movements.

• Ictal eye closure, pelvic thrusting, and prolonged seizure duration (i.e., >5 minutes) suggest PNESrather than FLE.

Surgical Considerations

• After failure of medical therapy, surgical planning for FLE should take into account the possibility of eloquent cortex (e.g., areas important for language, movement, personality) in the epileptogenic zone.

• Intracranial EEG may be performed with subdural grids to over Broca regions and the motor strip, which can be mapped either intraoperatively or extraoperatively at the bedside with electrical stimulation of the cortex.

• If the seizure focus overlies eloquent cortex, performing multiple subpial transections to preserve columnar organization can minimize postoperative functional deficits or responsive neurostimulation(RNS) can be performed.

• The addition of an anterior corpus callosotomy (ACC) may be considered for FLE patients with frequent secondary generalization, since that procedure alone often offers benefit.

• For patients who have multifocal or bilateral onset zones, RNS implantation may also be considered.

• Deep brain stimulation of the centromedian nucleus was performed experimentally in patients with FLE, but might be more suitable for patients with generalized epilepsy syndromes.

• Vagus nerve stimulation also may be considered for refractory cases that are not candidates for focal resection or fail resective therapy.

Outcome of Surgery for Frontal Lobe Epilepsy

• Frontal lobe resections have the worst seizure-free outcomes for epilepsy surgery, with 27% of patients found to be seizure free after surgery in a large metaanalysis , though some individual series demonstrate a seizure-free rate as high as 60% .

• In children, frontal lobe resections more often resulted in unsatisfactory outcomes than posterior resections in a meta-analysis of nonlesional cases.

• The authors found that complex partial seizures rather than generalized tonic–clonic seizures and focal cortical dysplasia identified on pathology were associated with better outcomes.

• recent series found 66% seizure

freedom at 1-year, 52% at 2-year,

and 44% at 5-year follow-up.

• Longer seizure duration (>5

years) was predictive of poor

outcome especially in children

and those with tumors.

• Another recent study of 58 FLE

patients who underwent focal

resection with long-term follow-up

demonstrated a favourable

OCCIPITAL LOBE EPILEPSY• Occipital lobe seizures may arise from either primary

visual or association cortex.

• Elementary visual auras such as seeing lights and

shapes arise from primary cortex, while more complex

hallucinations arise from adjacent association cortex in

occipital, posterior temporal, or parietal lobes.

• Eye blinking, eye flutter, and amaurosis are other

common clinical phenomena.

• Gaze deviation, typically ipsilateral, without

impairment of consciousness also has been reported.

In children occipital lobe epilepsy may be caused by a

variety of conditions, such as:

• trauma

• tumors

• stroke

• celiac disease

• childhood occipital epilepsy syndromes including

Panayiotopoulos and Gastaut types

• mitochondrial disease

• Posterior reversible encephalopathy syndrome

• Lafora body disease is a form of progressive

myoclonic epilepsy in which patients may experience

occipital seizures early in the course of illness.

• Celiac disease is associated with occipitoparietal lobe calcifications and epilepsy

• Children often do not have intestinal symptoms when diagnosed with epilepsy, although some may have had an intestinal syndrome in infancy.

• Folate levels are characteristically low.

• Antigliadin antibodies and intestinal biopsy help diagnose the condition, and seizures can be successfully treated with a gluten-free diet when initiated early.

• Occipital lobe epilepsy can also be difficult to

diagnose.

• The occipital lobe has three surfaces, the mesial,

lateral, and inferior surfaces.

• Mesial and inferior generators are often difficult to

identify and lateralize with scalp EEG.

• Incorrect localization and lateralization are seen

commonly, and generalized seizure patterns can be

seen in over one-quarter of patients.

• Patients with occipital epilepsy often have coexisting

temporal lobe abnormalities in the EEG and may have

dual pathology affecting both occipital and temporal lobes

Surgical Considerations

• After surgery, 46% of patients are seizure-free basedon a meta-analysis with long-term follow-up.

• Satisfactory (meaning Engel I and II) outcomes have been reported between 45% and 70% in studies done since the year 2000, and more recently published series have shown better outcomes than older series with as many as 68% achieving class I or II outcome.

• Although only small series have been reported, it has been noted that resections that include the temporal lobe and hippocampus result in favorable outcomes, which may be due to close connections to mesial temporal structures.

• ample coverage of all three surfaces of the occipital lobe with intracranial electrodes (the lateral, mesial, and tentorial surfaces) is associated with better outcome.

• Cortical mapping to determine the extent of primary visual cortex and utilizing intracranial visual evoked potentials may help minimize postoperative hemianopsias.

• The desire to spare the visual fields is the main factor limiting the extent of surgical resection, and perhaps seizure-free rates.

PARIETAL LOBE EPILEPSY

• The parietal lobe is the least common form, estimated to be the primary origin of seizures in perhaps 6% to 10% of patients.

• The diagnosis of parietal lobe epilepsy is perhaps the most challenging of all the extratemporal epilepsies when considering clinical symptoms and signs alone, because the parietal association cortex is often silent, and ictal symptoms only occur after propagation to adjacent lobes.

• Somatosensory auras, including a sensation of limb movement, and affective and vertiginous auras have been reported, as well as visual auras and rarely, painful sensations.

• Progression to tonic posturing is seen when superior or mesial parietal lobe foci spread to the SMA in the frontal lobe.

• oral and manual automatisms are seen when inferior and lateral parietal lobe seizures spread to the temporal lobes.

• The interictal EEG of PLE is often unrevealing, and localization with scalp EEG is quite challenging.

• In one study, fewer than half of PLE patients were correctly localized on scalp EEG, in part because more than one-third of PLE patients had generalized seizure patterns.

• Independent contralateral EEG discharges were also common.

• Surgical outcome is similar to FLE cases, and 46% of patients were seizure free after surgery in the largest series of 82 patients.

• Contralateral sensory loss and Gerstmannsyndrome are potential postsurgical complications.

• Cortical mapping with somatosensory evoked potentials may help define primary sensory cortex when planning the extent of surgical resection.

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