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					                                                  Seizure Disorders
               Notes compiled by Lisa Stroup and Kira Armstrong (and shortened by Dean Beebe 11/2004)

Seizure – (Schomer) state of pathologic hypersynchronous behavior of large number of neurons associated with an
altered neurologic function
* text defines it as – an episode of abnormally synchronized and high-frequency firing of neurons that results in
abnormal behavior or experience of the individual
Epilepsy – a condition in which there is a tendency to have recurrent unprovoked seizures (about a 1- 2% incidence)
           Lifetime risk of having a single seizure is higher, estimates ranging from 10 - 15% of population
           4th most common neurological disorder; most common neurological condition in childhood (4.3-9.3/1000)
           Onset most often during childhood and adolescence
           High incidence in prisons (4x general population):  impulse control + lower SES criminal behavior
Kindling – may account for susceptibility to electrophysiologic dysfunction in area opposite hemisphere homologous to
original site of discharge
Aura – brief, simple partial seizures of any type that are experienced by a patient with no outward behavioral
manifestations. They may occur in isolation, or they may serve as a warning for a larger seizure, when patients have
seizures that typically begin in one region of the brain before spreading
      Patients with seizures arising from medial temporal limbic structures often report a visceral sensation of rising
          in the epigastric area, a feeling of déjà vu, strange unpleasant odors, or feelings of extreme fear and panic
      Odors and panic are thought to arise from the amygdala and nearby cortex, rather than the hippocampus

                                                                     EEG

Alpha: 8-13 CPS/hertz; the normal dominant/background activity; occurs over occipital region
  Reflects an anxiety free state; used as guideline in biofeedback
  Lost with eye opening, falling asleep, medication that affects mental function
  Slows in elderly and in nearly every brain-based neurological illness
  Slows in early stage Alzheimer Disease, but remains in normal range

Beta: >13 hertz; lies over frontal lobes
  Prominent with concentration, anxiety, under effects of minor tranquilizers

Theta (4-7 hertz)/Delta (1-3 hertz):
  Detected in children and everyone entering deep sleep; generally absent in healthy, alert adults
  Presence may indicate a degenerative illness or metabolic derangement
  Focal presence may suggest a lesion in that region

   EEG is helpful in other differential diagnoses. e.g., triphasic waves present in metabolic/toxic encephalopathy and
   hepatic/renal failure delirium; periodic complexes present (seen as myoclonic jerks) in subacute sclerosing
   parencephalitis (SSPE) and Creutzfeld-Jakob disease; can differentiate between locked-in syndrome and persistent
   vegetative state (slow and disorganized)
  EEG is not useful to detect or exclude structural lesions
  EEG s/p ECT looks post-ictal (similar to GTC sz), and slow wave activity may continue for 3 months

Seizure Activity:
  Ictally, EEG reveals paroxysmal activity consisting of bursts of spikes, slow waves, or complexes of spikes and
    waves or poly-spikes and waves.
  Post ictally, EEG shows low voltage activity (“postictal depression”) followed by diffuse high voltage slowing
  Interictally, EEG often contains specific abnormalities supporting a diagnosis in 80% of epilepsy patients (20%
    have normal interictal EEGs). To evoke abnormalities, may try hyperventilation, strobe, sleep deprivation
  15% of population has nonspecific EEG changes (e.g., background slowing) – 1-2% have slow wave or spikes but
    no ictal events


                                                                       1
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                                                                  Taxonomy

Partial Seizures (a.k.a. “focal”)
- Begin in focal region of brain and semiology reflects this focus; may or may not spread; aura may be
  present. Typically last 5-10 seconds, but longer periods not uncommon

    Simple Partial
      No post-ictal deficits unless seizures are prolonged or recurrent as in Todd’s hemiparesis (see below)
      Consciousness not impaired; one mode of expression
         Motor (Jacksonian march – spreads along motor cortex. Todd’s mono or hemiparesis – accompanying
            post-ictal muscle weakness)
             Seizures in frontal motor association cortex can include “fencing posture”, bilateral leg cycling
                 movements, turning of eyes, head or body
         Sensory (unformed hallucinations in any sensory modality)
      Can have positive symptoms (e.g., hand twitching), or negative symptoms (e.g., impaired language abilities)

    Complex Partial (i.e., “psychomotor seizures”)
      Typical duration 30 seconds – 2 minutes
      Consciousness is impaired
        May have complete impairment or may only be “mild” – sometimes making the distinction between
           simple partial seizures difficult
        Can have simple partial onset followed by impairment of consciousness – or consciousness can be affected
           at onset
      complex symptoms including automatisms, subjective feelings, postural changes
      postictal - confusion (including aphasia w/dominant hemisphere involvement), amnesia, fatigue, agitation,
       aggression, and headache
      Most originate in temporal lobe
        Medial temporal lobe-onset complex partial seizures often begin with an aura of unusual, indescribable
           sensation, or with epigastric, emotional, or olfactory phenomena.
        Initial symptoms are followed by unresponsiveness and loss of awareness, during which patient may have
           automatisms (e.g., lip smacking, swallowing, or stereotyped hand or leg movements)
        Often, basal ganglia are involved – leading to contralateral dystonia/immobility. Thus, automatisms occur
           in the ipsilateral extremity --- can lead to inaccurate localizing to the “unpracticed eye”

      Usually begin in late childhood and early thirties
      Most common type of seizure (65% of all epilepsy pts)
      Difficult to recognize and interpret due to almost limitless variety of clinical findings; often mimic other
       disorders, especially psychiatric ones
        Intellectual symptomatology (aphasia, memory distortion - déjà vu [already seen], jamais vu [feeling of
            not having seen that which is familiar], deja entendu, jamais entendu, deja pensee, cognitive alterations -
            dreamy state, depersonalization, forced thinking, thought blocking)
        Affective symptomatology (fear, depression, pleasant/unpleasant experience, anxiety, embarrassment,
            anger, compulsions)
        Psychosensory symptomatology (illusions – metamorphosia [sudden distortion of a common object or
            person], micropsia [objects have become smaller, further away, or suddenly out of reach], macropsia
            [objects have become larger, closer to or “towering over” the patient], hallucinations – olfactory,
            gustatory, auditory)
        Psychomotor symptomatology (automatisms – simple, speech, affective, complex; present in 80% of
            complex partial seizure pts)

     Partial Seizures evolving to secondarily generalized seizures
      From simple or complex; spreads across corpus callosum to entire cortex
     Epilepsia partialis continua (a.k.a. focal status epilepticus) – partial seizures continue for hours/ days


                                                                       2
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Generalized Seizures
- Synchronized bilateral electrical discharge involving whole cortex. No aura, no focal semiology, no lateralized
findings, no focal EEG abnormalities. Immediate LOC. May be nonconvulsive (e.g., absence) or convulsive (e.g.,
tonic-clonic). Rarely result from tumors, infarctions, or structural lesions.
Postictal amnesia, confusion, fatigue, unresponsiveness
  Absence (petit mal)
      Onset usually 4-10 years of age, disappear in adulthood in about 40% of cases
      40% - absence replaced by GTC seizures
      characteristics: 1-10 second lapse of attention (staring) with automatisms and subtle clonic limb movements;
          maintain tone and bladder control; no significant postictal symptoms
      easily confused with inattention, dullness, or complex partial seizures (but differential diagnosis critical due to
          variable treatment)
      inherited autosomal dominant pattern
      3/second spike and wave
      often can be provoked by hyperventilation, strobe lights, or sleep deprivation
  Atypical Absence
      Usually begin in early childhood
      Frequently accompanied by other generalized seizure
      Difficult to control

     Myoclonic
      Brief, single symmetrical jerks of head and upper extremities; in series or clusters, common after waking
      No LOC (duration of generalized polyspike-wave burst usually <1 second)
    Clonic
    Tonic
    Tonic-clonic (grand mal)
     Begin at any age after infancy and persist into adulthood
     Massive motor activity (tonic stiffening of trunk followed by clonic rhythmic jerking of extremities) lasting
          less than 5 minutes, profound postictal residua
     Inherited autosomal dominant trait
     Incontinence or tongue biting is common
     Immediately postictally, patients lie immobile, flaccid, and unresponsive, with eyes closed, breathing deeply to
          compensate for the mixed metabolic and respiratory acidosis produced by seizures
     Post-ictal deficits last from minutes to hours and include profound tiredness, confusion, amnesia, headache,
          and other deficits related to location of seizure onset
  Atonic (“drop seizures”): Abrupt loss of muscle tone that produces a sudden fall
  Generalized status epilepticus – may persist for many hours and become life threatening.
  Reflex epilepsy – seizures in response to specific stimulus (e.g., light, television, music)
  Febrile seizures – occur in 2-4% of all children; recur in 1/3 of them. Tx is fever prophylaxis or oral diazepam
    with fever onset
                             Staring Spells: Complex Partial Seizures vs. Absence Seizures
Type of seizure              Aura      Duration           Automatisms       Post-ictal     Frequency      Ictal EEG
                                                                            deficits
Typical absence              None <10 sec                 None (aside from None            Multiple    Generalized
 Seizures                                                 minor mvmts of                   daily        3-4 Hz
                                                          Eyelids or mouth)
                                                          spike-wave
Typical medial               May be       30-120s         May be            May be         3-4/month      Unilateral
 temporal complex            present                      present           present                       or assym-
 partial seizures                                                                                         metric 5-8
                                                                                                          Hz – over
                                                                                                          temp lobe

                                                                       3
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                                                              Epilepsy Syndromes

     West Syndrome (infantile spasms)
              Clusters of myoclonic seizures
              Myoclonic seizures cease between 2-4 years old, but give rise to other seizure types in 25-60% of
                 cases
     Lennox-Gastaut
              Mixed seizure disorder – includes atypical absence, atonic, myoclonic
              Onset ages 2-8
              EEG – background slowing and slow spike and wave
              Seizures difficult to control and status is common

     Benign Focal Epilepsy of Childhood
              Most common type of partial seizure; centrotemporal spikes
              Rolandic Epilepsy (nocturnal seizures) – believed to have autosomal dominance with incomplete
                penetrance – EEG has characteristic centrotemporal spikes; onset b/t 3 and 13; remission nearly
                always complete by age 15
              Characteristics: unilateral parasthesias, speech arrest, T-C seizures occurring mostly at night
              Benign Occipital Epilepsy (visual symptoms)
              Onset between ages 3-10, more common in boys, often remits by puberty; inherited
              Responsive to AEDs

     Childhood Absence Epilepsy
              Onset b/t 4 and 8 (second peak of onset at puberty known as juvenile absence epilepsy
              Easy to treat and spontaneous remission in 80%
              Onset in adolescence more likely to experience generalized seizures and persist into adulthood

     Juvenile Myoclonic Epilepsy
              Onset late childhood, early adolescence
              Involves myoclonic jerks of upper extremities generally associated with morning waking. No
                 associated LOC, BUT 90-95% have generalized tonic-clonic seizures
              Responds to AED’s but resolution is infrequent
              Accounts for 10% of all epilepsies; genetically inherited (autosomal dominant)
              IQ usually ok

     Landau-Kleffner
             “Acquired aphasia with convulsive disorder”
             need abnormal EEG (usually over temporal areas) but no actual seizures are necessary for diagnosis
             Age of onset b/t 2 and 11; follows a period of normal development
             Characterized by sudden or gradual onset of auditory agnosia; may involve total unresponsiveness to
                language or progressive deterioration of expressive speech
             Usually associated with behavioral difficulties as well
             Seizure type varies, but most common is generalized motor seizures
             Seizures and language deficits unresponsive to AED’s (current: steroid tx)
             Earlier onset is related to poorer prognosis

     Continuous spike-wave discharges during sleep (CSWS)
              Continuous activity during >85% of non-REM sleep
              Neuropsychological regression associated
              Partial motor seizures, absence seizures



                                                                       4
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                                                                   Etiology

     Diagnosis = more than 1 unprovoked seizure
     Symptomatic epilepsy – origin of seizure is identified (only 30% of cases; harder to control with AEDs)
     Idiopathic – unknown seizure origin
     Risk of new onset seizures is high in infancy and childhood, declines in adulthood, and then rises again in elderly
      Most common cause in infancy and childhood are febrile seizures, congenital disorders, and perinatal injury
      Most common cause in patients > 60 – cerebrovascular disease, brain tumors and neurodegenerative conditions
     Febrile seizures – occur in 3-4% of all children, usually between ages of 6 months and 5 years; usually are brief,
     generalized tonic-clonic seizures (called simple febrile seizures).
      Increased risk of subsequent epilepsy in children with complex febrile seizures – seizures lasting more than
           15 minutes, or occurring more than once in 24 hours – some of these kids may have an underlying cause for
           epilepsy which is triggered by the fever
     Metabolic factors – hypoglycemia, hypocalcemia, electrolyte imbalance, uremia, hepatic failure, hypoxia
     Drug withdrawal – EtOH, barbiturates
     Post-traumatic – CHI, SDH, EtOH w/ multiple falls. 50% of people who develop seizure disorders will do so in
     first year post-injury; 80% within four years
     Birth injury – congenital malformations, infection, trauma, idiopathic
     Relative to age of onset:
      Perinatal – toxemia, infection, congenital defects, difficult birth
      Young children – congenital abnormality, neonatal meningitis, neurocutaneous disorders
      Adolescent – idiopathic, trauma, drug-related
      Young adult – trauma, EtOH, neoplasm, drug-related, AVM, AIDS (cerebral toxoplasmosis)
      Middle age – neoplasm, EtOH, vascular disorder, trauma
      Late life – vascular disorder, neoplasm, degenerative, cysticercosis; CVA most common after age 65
     Risk Factors:
       Genetic predisposition
       Cerebral insult
       Precipitating conditions (e.g., EtOH, physical debilitation, emotional stress, video games/TV)

                                                           Differential Diagnosis
  CT usually normal
  Normal EEG does not rule out seizure disorder; sleep EEG more sensitive than waking
  PET/SPECT: hyperperfused ictal foci; hypoperfused post-ictally; better at detecting foci than MRI/ CT
 Pseudoseizures (i.e., non-electrical events, psychogenic seizures):
  Resembles an epileptic seizure but is not caused by neuronal discharge
  Is not “voluntary”; etiology is emotional or psychological
  Possible distinguishing semiology: acute emotional disturbance may initiate, rare when sleeping or alone, gradual
    onset, crying during ictus, occasional talking, movements may be asynchronous, thrashing and may include side-to-
    side movements and pelvic thrusting, personal injury fairly rare, directed violence not unusual, react to avoidance
    testing, infrequent micturition and defecation, may be quite long, NO ictal epileptiform EEG abnormality
  More prevalent in women, children, and adolescents
  Risk Factors: h/o sexual abuse, epilepsy, psychiatric disorder (esp. depression/anxiety), or head injury/ PCS;
    model for seizure disorder (family/friend), traumatic life course, family discord/academic stress
  Important: 50% also have “real” (i.e., electrical) seizures
Other conditions that mimic seizures
  Episodic dyscontrol syndrome (i.e., recurrent rage attacks)
  Cerebrovascular disturbance (e.g., syncope, cardiac arrhythmias, TIA, transient global amnesia)
  Panic disorder
  Breath holding spells in infants
  Sleep disorders (e.g., narcolepsy, cataplexy)
  Migraine
  Metabolic disturbances (e.g., med reactions, hyperventilation, hypoglycemia)
                                                                       5
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                                                                Management

1.   Anti-epileptic drugs
      Use AED’s when seizures are prolonged or recurrent
      Seizure control can be established in up to 80% of pediatric population
2.   Surgery
      Focal resection – usually for partial complex
           In temporal lobectomies -- 80% are seizure free or have significantly reduced seizures
           improvements in behavior and psychosocial functioning have been suggested
      Corpus callosotomy
           Used to control generalized seizures by preventing their spread across the hemispheres
           Tends to decrease frequency -- but does not resolve disorder
      Functional hemispherectomy
3.   Vagus Nerve Stimulator
     VNS generator is implanted in left side of chest – stimulating lead is attached to left vagus nerve in carotid sheath
     Stimulus given off in cycles of 3 seconds on and 5 minutes off
4.   Ketogenic Diet
     1/3 experience complete control of seizures
     adherence issues
5.   Multiple subpial transection – used when seizure site is inoperable (e.g., if in motor or language cortex). Involves
     inserting a sharpened probe under the pia to sever the cortical-cortical connections…essentially disconnecting the
     epileptogenic cortex

Effects of Anticonvulsants
May cause problems with attention, motor speed, memory, and processing speed – even when AED’s are within
therapeutic range; they may compound the cognitive difficulties and behavioral problems seen in people with epilepsy
    Carbamazepine (Tegretol)
      Few cognitive side effects
      May improve speed of information processing, psychomotor speed and problem solving; may also decrease
          aggression and emotional lability
    Valproic Acid (Depakote)
      Minimal cognitive effects
      May improve alertness
      Few behavioral effects
    Phenytoin (Dilantin)
      Highest rate of side effects
      Adverse effects on psychomotor speed, memory, and problem-solving
      May result in progressive encephalopathy w/deterioration of intellection functioning, especially in children
          with MR or neuro problems
      Dilantin (phenytoin) intoxication: nystagmus, ataxia, dysarthria
    Phenobarbital
      Inconsistent cognitive findings
      Consistently related to hyperactivity, irritability and sleep disruption; may exacerbate premorbid problems
    Polytherapy treatment
      More negative impact on cognition and mood than monotherapy

                                                      Neuropsychological Findings

    IQ
      In general, not associated with intellectual decline (except in syndromes such as tuberous sclerosis, Rett
        syndrome, chromosomal disorders, etc.) – when decline is noted, often associated with AED toxicity or status
        epilepticus
      Co-occurs with MR (9-31%), autism (11-35%), and CP (18-35%)
                                                                       6
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     Language
      Expressive language more impaired than receptive
      Dysnomia is common – may contribute to verbosity and circumstantial speech
      Hypergraphia – excessive and compulsive writing
      Reported memory problems may actually reflect subtle language difficulties
     Perceptual-motor skills
      TPT has been sensitive – total time, memory, and localization scores
      Bender-gestalt – patients perform more poorly than controls
    Memory
      May reflect effects of continued abnormal activity or damage to CNS
      Memory disturbance may be related to nature, extent, and location of pathology in temporal lobes
      Long-term memory more affected than short-term memory
      Localization of onset may affect memory impairments (i.e., verbal vs visual)
    Attention
      Deficits in attention tend to be present regardless of IQ
      Generalized seizures – tend to show deficits on measures of sustained attention
      Focal seizures – greater deficits on measures of selective attention
    Executive functions
      Trail making test, WCST, Category test
      Frontal lobes affected by temporal/hippocampal discharges through temporal-frontal pathways
    Motor skills
      Decreased reaction time and psychomotor speed; overall slowing
    Learning disabilities/Achievement
      Higher risk for learning disorders
      Etiology unclear
          Seizure type, duration of disorder, severity of seizures and AED’s have NOT been found to be related to
             academic underachievement
          May be related to impairments in language, memory, and attention

Factors Affecting Cognitive Deficits
1. AED toxicity
2. Etiology
        People with idiopathic seizures score higher on IQ tests
        Symptomatic epilepsy
3. Seizure type and frequency – greater deficits seen with:
        Tonic-clonic, atypical absence, mixed seizures
        History of status epilepticus
        More frequent seizures
        Longer duration of disorder
4. Early seizure onset
5. Poor seizure control
6. TLE surgery: Non-dominant temporal lobectomy - no consistent changes in cognition; Dominant temporal
    lobectomy – depressed verbal memory fairly common. Risk factors for post-op decline in verbal memory:
    dominant resection, intact pre-op neuropsych memory testing, intact pre-op Wada memory testing, absence of
    mesial temporal sclerosis (MTS) on imaging

 Psychological findings:
      Higher prevalence of depression (especially males with complex partial)
      Higher suicide rates
      Children with epilepsy have higher rates of psychiatric disturbance than general population
      Neurological and psychosocial factors contribute to increased risk for psychological maladjustment
         Neuro variables: underlying brain damage, localized epileptogenic activity in areas regulating emotion, etc
         Family variables: significant predictors of behavior problems
                                                                       7
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                                                     Temporal Lobe Epilepsy (TLE)

   Group of conditions resulting in paroxysmal discharge within the temporal lobe; multiple etiologies
   Unifying feature: vulnerability of temporolimbic structures (amygdala, hippocampus) to epileptogenesis - vascular
   anatomy; convergent inputs from multiple sensory areas; special excitability as reflected in bursting and kindling;
   NMDA receptors and pathological plasticity
  Common denominator of TLE: temporal lobe spike focus
  Common ictal manifestations (in sum: varied, complex, and difficult to differentiate from spontaneously occurring
   behavior; complex partial seizures):
    Sensory alterations - subjective, but not necessarily any objective findings
    Motor symptoms - automatisms, twitching, eye movements, speech problems, transient weakness, etc.
    Autonomic manifestations - flushing, shortness of breath, apnea, cardiac symptoms, nausea/epigastric rising,
        etc.
    Hallucinations/illusions - in any sensory modality; includes metamorphosia, micropsia, and macropsia
    Experiential manifestations - memory flashbacks, déjà vu, jamais vu, feeling of a presence, depersonalization,
        derealization, etc.
    Emotional manifestations – often negative, sudden, unpredictable, inappropriate (fear - most common)
  “Typical” interictal behaviors** (i.e., “TLE personality”): preoccupation with religion/morality/ philosophical
   issues, hypergraphia, hyper/hypo sexuality, viscosity, increased irritability/temper outbursts, schizophrenia-like
   psychosis, fearfulness, humorlessness
    Left: intellectualized affect, thought disorder, reflective style
    Right: overemotionality, affective disorder, impulsive style; artistic creativity

     Behaviors are “opposite” that seen in Kluver-Bucy syndrome (damage to temporolimbic structures resulting in
     placidity, hypersexuality, hyperphagia, hypermetamorphosis, loss of social bonds):

**CAVEAT: I believe that current thinking and research questions the validity of a so-called “TLE personality”. In
general, it is not supported by recent evidence.


                                Complex Partial Seizures of Extratemporal Origin
- Relatively few cases documented in the literature

Clinical Characteristics of CPS of Frontal Lobe Origin:
  Frequent seizures, often in clusters with many per day
  Brief seizures lasting less than one minute
  Sudden onset and offset with little or no postictal confusion
  Prominent motor automatisms, usually complex
  Aggressive sexual automatisms as part of motor automatisms
  Vocalizations of variable complexity
  Frequent warnings, usually nonspecific
  Complex partial status epilepticus
  Bizarre attacks that appear hysterical
  Stereotyped pattern
  In Sum: similar to TLE; bizarre movements and vocalizations, behavioral automatisms

Clinical Characteristics of CPS of Occipital Lobe Origin:
  Elemental visual hallucinations
  Contralateral eye deviation
  Pulling or movement sensation in eyes in the absence of detectable motion
  Rapid forced blinking or eyelid flutter
  Ictal blindness – blackout or whiteout secondary to rapid spread via the splenium (infrequent)
  Static visual field defects
                                                                       8
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