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SEIZURE DISORDERS

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					           Seizure Disorders



PSYC4080         Seizure Disorders   1
           Seizure Disorders
 Abnormal electrical discharge in the brain.
 Neurons firing together in synchrony: paroxysmal
  depolarization shifts (PDS)
 Hyperexcitation of glutamate neurons.
 Many causes: Seizures are symptoms, not a
  disease.
 Presence of sensory or cognitive dysfunction is
  dependent on affected area(s)
 Prevalence: 0.6% of the population
 Incidence: 15,500 new cases per year (Epilepsy
  Canada)

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               Neuropathology
1. Generalized seizures – involve the entire cerebral cortex
2. Focal (partial) seizures – limited to parts of the brain

    PDS associated with a spike in the EEG




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                   Neuropathology
   Typical Muscle Movements:
1. Tonic: stage of extreme muscle tension related to PDS
   activity
2. Clonic: contractions and relaxations of muscle, occurring in
   rapid succession
     •     Rapid onset and offset of PDS activity
     •     EEG changes during and between seizures (ictal and interictal
           periods).
3. Atonic: no muscle tension

Level of Consciousness
1. Simple: No loss
2. Complex: Loss of consciousness

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               Neuropathology
 Hyper-excitability in neurons can accelerative cell
  death
 High concentration of Ca++ leads to long-term
  potentiation of synaptic responses
   • Activation of genes that cause synaptic
     reorganization
   • Axonal growth and neo-synaptogenesis
   • Lowering of seizure threshold
 Children’s brains are more resistant to these long
  term effects
     • Relative immaturity of biochemical cascades


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Childhood Seizure Disorders
1. Neonatal seizures
 Occurring up to 2 months of age
          Symptoms are acute not chronic
    Full body tonic and clonic movements
    Loss of consciousness
    More common in premature infants
    90% of patients die from these seizures.




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Childhood Seizure Disorders
Many different diseases cause infantile seizures:
 Birth trauma or head injury
 Disorders of metabolism
 Infections (I.e. herpes encephalitis)
 Anoxic episodes (loss of oxygen)
 Genetic factors (I.e. family histories)

 40% have no known cause (idiopathic epilepsy)
 90% have first onset before age 20.


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Childhood Seizure Disorders
2. Infantile spasms (West Syndrome)
 Later onset (3-6 months)
 Full body (tonic) contraction, bending over, stiff
  muscles
      May have up to 100 spasms per day
 Abnormal EEG, MR are associated with this
  syndrome.
 More common in males.
 Poor prognosis for mental development.
 Developmental disabilities are common: Only
  16% can be educated in a normal classroom
  setting
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Childhood Seizure Disorders
3. Febrile seizures
 Common response to elevated body temperature.
 2-5% of all children between 6 months and 5
  years.
 Full body seizure, tonic and clonic movements
 More common in males.
 Good prognosis: Usually no problems later in life.
      Exception to this is if the fever was due to a brain
       infection, or if there is a recurrence of seizures after a
       fever


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Childhood Seizure Disorders
 1.9% of all children have at least one epileptic
  episode.
 Most frequent onset between 6 months and 6
  years of age.




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             Adult Disorders
     Most common types of seizures:
1.   Grand mal: loss of consciousness, falling on the
     ground, and tonic-clonic movements
2.   Myoclonic seizures: clonic movements in parts of
     the body, usually no loss of consciousness
3.   Absence seizure: loss of consciousness with no
     muscle movements
4.   Complex partial seizures: loss of consciousness,
     oral automatisms, preceded by auras (sensory
     warning of seizure onset).

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           Neuropathology
Seizures may be intractable and require regular
   follow-ups

Those at increased risk:
1. Very young age of onset (< 2 years)
2. Frequent generalized seizures
3. Failure to achieve control readily
4. Evidence of brain damage
5. A specific cause
6. Severe EEG abnormality
7. Low IQ
8. Atonic, atypical absence seizures
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           Neuropathology
Why are children so vulnerable?
 GABAergic synapses develop before main
  glutamate receptors (NMDA, AMPA)
 In early development, GABA is excitatory--
  binding to GABAA receptors causes
  depolarization.
   • Shift to inhibitory effects occurs once
     glutamate receptors have matured
  Thus, the neonatal brain operates with very
  little inhibition.

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               Neuropathology
 Overt psychosocial and cognitive consequences
      Including a profound fear of having a seizure in public
 Higher incidence of adjustment, academic,
  psychiatric disorders in persons with epilepsy
  (Bennett, 1992).
 Lower IQ is associated with seizures, especially if
  the onset is early.
 Affected by underlying causes and medications
  used to treat as well.



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               Neuropathology
 Temporal lobe, and the hippocampus in
  particular, may be particularly vulnerable
      Most sensitive to effects of long term potentiation
       related to memory
      Memory and learning deficits may be associated with
       any type of seizure.
 Worst in complex partial seizures which are
  caused by temporal lobe lesions.
 Overall attention levels can be affected by most
  types of seizures.


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           Neuropathology
High “comorbidity”
1. Depression
• Major depressive episodes are common
• May be related to anticonvulsant medications
2. Anxiety Disorders
• Almost exclusively based on realistic fear of
   having a seizure in public
3. Personality and Psychotic Disorders
 Obsessive compulsive
 Personality changes
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             Other Information
  Treatment Options
 Medications
 Surgery
     • Lesioning tissue if seizures are local
     • Electrode stimulation
 Ketogenic diet (high fat, low carb) - for
  generalized seizures

 By and large, treatment does not address
  psychosocial issues directly.

PSYC4080                     Seizure Disorders   17

				
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