Mye Basheer, MD
Clinical Neurophysiology unit
Special medicine department
Faculty of Medicine (Kasr El-Ainy)
Secretary of the Egyptian Clinical Neurophysiology society (ECNPS)
Luxor 2017… 30 mins
Interictal discharges may be divided morphologically into sharp waves, spikes, spikewave
(also called spike-and slow wave
complexes), and polyspikewave
complexes (also called multiple spike-and- slow wave complexes)
Most important is to be distinguished from physiologic or nonspecific sharp
F7/F8 anterior temporal; T3/T4 (T7/T8 midtemporal); T5/T6 (P7/P8), posterior temporal; T1/T2, zygomatic surface electrodes, sphenoidal leads anterior or mesial temporal discharges. ; Sphenoidal leads invasive but are useful in longterm video EEG monitoring of temporal lobe epilepsy; Nasopharyngeal electrodes.
Frontopolar (Fp1/Fp2); dorsolateral frontal (F3/F4); orbitofrontal (F7/F8), or mesial (FzCz) locations.
O1/O2 are tied less strongly to clinical epilepsy.
Sometimes discharges are widespread over one hemisphere.
Independent discharges occurring in each hemisphere, arising from at least 3 distinct locations that are separated by more than one interelectrode distance.
Spike-wave or polyspikewave complexes, and involve both hemispheres more or less symmetrically, most often with a midfrontal maximum at Fz, F3 and F4. Exceptions exist, with frontopolar or occasionally posterior maxima. Although these discharges are usually bilaterally synchronous and symmetric, amplitude maxima may shift from side to side within the same record or in serial recordings in the same patient. Frequency of the spikewave bursts can be approximately 3 Hz (classical or typical), 4-6 Hz (atypical) or less than 2.5 Hz (slow). Both typical and atypical discharges occur in idiopathic/genetic syndromes, and slow spikewave complexes usually are seen in symptomatic or cryptogenic epilepsies. Those interpreting the results should recognize that, during sleep, even classic or atypical spikewave complexes usually become slower (often less than 2 Hz), occur in isolation rather than in bursts, and can include polyspikes.
Interictal Epileptiform Discharges in Persons Without A History of Seizures: What) Do They Mean? (1. Mr. X is having E.D. in his EEG with no relevant history)
Prognostic Significance of Interictal Epileptiform Discharges in Newly Diagnosed Seizure Disorders (2. Mr. X is newly diagnosed as epileptic patient)
Significance of the EEG and Epileptiform Abnormalities in Antiepileptic Drug Discontinuance (3. Mr. X is now to withdraw his AEDs)
Prognostic Significance of Interictal Epileptiform Discharges After Epilepsy Surgery (4. Mr. X made a surgery and he made a post operative EEG)
Interictal Epileptiform Discharges in Persons Without A History of Seizures: What Do They Mean?
Detection of IED in the clinical practice is invaluable for diagnosing epilepsy, classifying seizure type, and localizing the seizure focus.
However, IED are also encountered in persons with no seizure history.
Clinical Practice Settings in Which Interictal Epileptiform Discharges May Be Identified(*)
1. School-age children—screening, attention deficit and hyperactive disorder, performance issues
2. Air crew and air traffic controller candidates
3. Spell evaluations, especially psychogenic events, syncope, and sleeprelated events
4. Before electroconvulsive therapy
5. After head trauma
6. Acute encephalopathies
7. Dementia evaluations
(*)These patients do not have a history of seizures
The prevalence of IED in persons without a seizure history must be assessed according to patient age and health status. Also, a distinction should be made between IED that are spontaneous and those that are activated by photic stimulation or hyperventilation.
The important issue raised by incidentally recorded IED is how to determine the risk of subsequent epileptic seizure occurrence. The highest seizure rate reported was 14%.
??ARE IED REALLY CLINICALLY SILENT?
TCI can be observed with IED that are as brief as 0.5 seconds
??DOES AED TREATMENT OF IED HAVE A ROLE IN PERSONS WITHOUT SEIZURES?
Clinicians generally adhere to the principle of “treating the patient, not the EEG.”
Nonetheless, AED treatment of persons without a seizure history is considered for two reasons:
Prognostic Significance of Interictal Epileptiform Discharges in Newly Diagnosed Seizure Disorders
The usefulness of an EEG in patients presenting with a first unprovoked seizure is a subject of debate. the American Academy of Neurology, Child Neurology Society, and American Epilepsy Society stated “where the EEG is used as one of several variables, it can identify children with very high and very low recurrence risks.”
Furthermore, they noted that “the EEG is not used solely to determine recurrence, but also helps differentiate a seizure from other events, is essential to the diagnosis of a syndrome, and provides information on long-term prognosis; it influences the decision to perform subsequent neuroimaging studies and may influence counseling about management of the child.”
Overall, 18% to 56% of children and 12% to 50% of adults presenting with new-onset seizures showed epileptiform abnormalities on EEG.
Most studies have shown that an EEG obtained after a period of sleep deprivation improves detection of epileptiform abnormalities. However, sleep deprivation may be more important in patients with focal discharge.
The first seizure that causes a patient to seek medical attention is frequently not the patient’s actual first seizure.
Approximately 40% to 50% of patients who experience a first unprovoked seizure will have a recurrence within the subsequent 2 years. The risk of recurrence increases to 60% to 71% if epileptiform abnormalities are seen in EEG.
The strongest predictors of recurrence were seizure cause and EEG findings. As well, specific features on the initial EEG may be predictive of Intractability.
Significance of the EEG and Epileptiform Abnormalities in Antiepileptic Drug Discontinuance
Patients who are stable with treatment may wish to discontinue AED therapy for several reasons, including a. cost, b. adverse effects, c. inconvenience, d. long-term risks of therapy, e. teratogenicity, and the general sense that taking medication serves as a f. daily reminder of the condition, even after a long period of seizure freedom.
The EEG may help the decision-making process for AED discontinuation in numerous ways. It may help clarify the epilepsy a. diagnosis and allow b.prognostication about the likelihood of remission. The EEG may also help detect c. subclinical abnormal brain function. It may also provide a means of d. monitoring the patient during the period of AED discontinuation, potentially e.predicting relapse in the event of clinically significant increases in epileptiform activation.
High rate of medical intractability and a relatively low remission rate is seen with Anterior temporal sharp waves suggest the diagnosis of temporal lobe epilepsy, Generalized slow spike and wave patterns, frontal spikes in partial epilepsy of frontal origin, and Generalized polyspike and wave discharges in juvenile myoclonic epilepsy.
AED discontinuance can be considered in several types of patients:
(1) those who are seizure free for 2 to 5 years with AEDs; (2) those with a single seizure type, normal neurologic examination findings, and normal intelligence quotient;
(3) those with normal EEG findings during treatment.
Relapse occurred in 12% of patients with a normal EEG and 57% of those with an EEG labeled “definitely abnormal”
Unfavorable Clinical and EEG Risk Factors Associated With Increased Relative Risk of Relapse After AED Discontinuance
:Unfavorable clinical risk factors
Age of onset >10–11 years
Abnormal neurologic examination findings
Juvenile myoclonic epilepsy
Symptomatic partial epilepsy
Poor initial AED response
>1 AED at time of discontinuance
Family history of epilepsy
Unfavorable EEG risk factors
“Unimproved” versus baseline
Slow background, dysmaturity
Epileptiform abnormalities not otherwise specified
“Abnormal” at baseline←
Deterioration during withdrawal
Generalized epileptiform abnormalities
One factor that potentially limits the predictive value of EEG for discontinuation risk is the suppression of paroxysmal interictal EEG activity by AEDs.
Prognostic Significance of Interictal Epileptiform Discharges After
T3+ 2ry bil synchrony
a. T6 wake
b. ESES/ sleep
a. O2 ictal initiation
b. O2 ictal spread
Modern technology calls for a modern approach to classification of epileptic seizures and the epilepsies
March 2012, epilepsia.
Hans O. Lüders1,
Guadalupe Fernandez Baca-Vaca1,
Luis Carlos Mayor13,
Bernhard J. Steinhoff17,
1 article, 8 countries,18 centers, 29 authors= Perfect model of team working
FOUR DIMENSIONAL CLASSIFICATION
*Assuming that “The commission agrees that the main purpose of the classification system it is developing is to classify individual cases to help selection of therapeutic approaches and to define prognosis”.
*Suggesting that “This objective will be best accomplished by using a multidimensional system”
1.SEIZURE: the symptomatology. + frequency + triggers
2. LOCATION: Epileptogenic zone is defined (or simplifingly assumed) as the minimum brain tissue that must be removed to produce seizure freedom.
3.ETIOLOGY: expressing prognosis. Deciding some essential therapeutic strategies.
4.RELATED MEDICAL CONDITION: comprehensive clinical picture. Contributes to therapeutic decisions. QOL.
Location: Left frontal lobe
Seizures: Right hand clonic seizure → GTC
Frequency: 1-2 seizures/day
Etiology: Left frontal cortical dysplasia
Related medical condition: Mild left hand paresis
The 2017 ILAE Seizure Classification
Old Term vs New Terms for Seizures:
Absence, Petit mal – Generalized absence
Atonic or drop attack – Focal or generalized atonic
Grand mal, Tonic clonic – Generalized or unknown onset tonic clonic
Infantile spasms – Focal, generalized, unknown onset epileptic spasms
Myoclonic – Focal or generalized myoclonic
Tonic or drop attack – Focal or generalized tonic
Complex partial – Focal impaired awareness
Focal motor – Focal motor aware or impaired awareness
Focal sensory – Focal sensory aware or impaired awareness
Limbic – Focal impaired awareness
Psychomotor – Focal impaired awareness
Simple partial – Focal aware
Generalized Onset: Generalized seizures affect both sides of the brain or large networks of cells on both sides from the beginning of the event. The networks can be on the surface of the brain or involve deeper areas. Generalized seizures don’t need to involve the entire brain, just part of both sides.
Focal Onset: The term focal seizure has been used for years, but the lay public and many professionals still use the term partial seizures. In this 2017 Classification, focal seizures will replace partial seizures and refer to those that start in an area or network on one side of the brain. They may start on the surface of the brain or in deeper areas, and can be very localized or spread to larger areas. Sometimes more than one network is involved.
Unknown Onset: Seizures may be of unknown onset if the beginning of the seizure is not clear. As more information becomes available over time or through testing, the type of seizure may be changed to a generalized or focal onset seizure.
Generalized Motor Seizures
Tonic-clonic – No change (Years ago the term grand mal was used)
Clonic – No change
Tonic – No change
Myoclonic – No change
Myoclonic-tonic-clonic – New term
Myoclonic-atonic – New term
Atonic – No change
Epileptic spasms – New term
Generalized Non-Motor Seizures (Absence)
Typical Absence – No change (Years ago the term petit mal was used)
Atypical absence – No change
Myoclonic absence – New term
Eyelid myoclonia – New term
Focal Aware: During a focal aware seizure, there is no change in a person’s awareness, even if they are unable to talk or respond during the event. This replaces the term simple partial seizure.
Focal Impaired Awareness: If awareness is impaired at any time during a focal seizure, it would be called a focal impaired awareness seizure. This replaces the term complex partial seizure.
Focal to Bilateral Tonic Clonic: A focal seizure may start in one part of the brain with the person aware or with impaired awareness. It may then spread to involve both sides of the brain and the person would be unaware during the seizure. Usually other changes occur, for example the seizure may spread to cause body stiffness (tonic) and jerking movements (clonic). The term focal to bilateral tonic clonic will now be used instead of the old term secondary generalized seizure. The term generalized is being used only to describe the onset or beginning of a seizure.
Motor seizures will have a change in muscle activity of some sort, such as jerking (clonic), stiffness (tonic), loss of muscle tone (atonic), or automatisms (repeated or automatic movements).
Non-motor seizures can include changes in heart rate, breathing, or color (autonomic); blank stare, stop talking or stop moving (behavioral arrest): confusion, slowed thinking, or problems talking and understanding (cognitive changes); sudden fear, dread, anxiety or even pleasure (emotional); or changes in hearing, vision, taste, or feelings of numbness, tingling, or pain (sensory).