Epilepsy Presentation Epilepsy by mikeholy

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									Epilepsy
Subspecialty seminar
   Oct 25, 2006
defn

Two or more unprovoked seizures.
 seizure is an abnormal electrical
 activity of the brain due to hyper
 synchronous firing of aggregates of
 neurons.
CON
• Normally there are highly differentiated electrical
    signals with in the brain that sustain the normal
    life
•   “Electrical rebellion” that results in to
    monotonous discharge firing in synchrony
    across the brain
•   „Sacire‟ to take possession of
•   Most prevalent of the neurological disorders
Magnitude of the problem

• World wide incidence 0.3-.0.5%
           prevalence 5-10/1000
• Ethiopia    prevalence 5.2/1000
            GTC             81%
            Partial complex 13.9
            simple partial   5.7
 The commonest of all neurological problems
Classification
• Partial and Generalized
• Partial when the seizure arises from discreet
  area of the cortex
• Generalized when there is clinical or EEG
Manifestation of simultaneous i/v of both
  hemispheres .
• Partial sz are common ones in adults
  – Temporal lobe epilepsy commonest of the partials szs
Classification of Seizures
1. Partial seizures
a. Simple partial seizures (with motor,
sensory, autonomic, or psychic signs)
b. Complex partial seizures
c. Partial seizures with secondary
generalization
2. Primarily generalized seizures
a. Absence (petit mal)
b. Tonic-clonic (grand mal)
c. Tonic
d. Atonic
e. Myoclonic
3. Unclassified seizures
a. Neonatal seizures
b. Infantile spasms
Partial szs
• Simple partial no loss of consciousness
                  area involved →type of sz
                  Motor → convulsive
                  temporal →Auditory halln
                           →behavioral abn
                 limbic → Psychic
Post ictal paralysis 13.5%
Epilepsia partialis continua
JACKSONIAN march

•
Complex partial sz
•   Ass with alteration in consciousness
•   Stereotypical aura
•   Automatism
•   Post ictal confusion
•   Amnesia
•   Protean range of manifestations
•          Consider as DDx in any pt with paroxysmal
    abnormal behavior esp if the pt seems not to be
    fully aware of it
con
• Partial sz with sec generalizn
  Aura sterotyped clear
       Generalized szs
-Absence sz
              Common in children
               difficult to dx
               easy to treat
               transient lapses of consciousness
               Subtle motor manifestations
              70% remission rate
              classic EEG findings
..con
Tonic clonic

  the sterotype sz in the public mind
• the commonest sz of metabolic abnormalities
• 10% of the general popn at one time during their life
• Cx by: Loss of consciousness
         tonic stiffning
         clonic phase
         Post ictal confusion
         Headache/muscle pain
         usually lasts for a minute
con
Tonic /Clonic szs
Atonic sudden loss of postural tone
       predisposes to trauma
       Consciousness briefly impaired
Myoclonic
   brief reigonal or generalized contraction of the muscles
   due to metabolic disturbance
    Part of syndromes
Epilepsy syndromes

Juvenile myoclonic epilepsy
     adolescents
     benign
     ass with other sz
Lennox Gastaut syd.
      multiple sz
      Cognitive abn
      characterstic EEG
MTLE hippocampal sclerosis
       partial complex sz
       most studied
Mechanism

• Imbalance b/n excitation and inhibition of
 the neuron
        endogenous factor



Epileptogenic                 PPting
…contd
• Epileptogenic HI,stroke,malignancies
              infections,drugs..
• Endogenous family Hx
                 Genetic abnormalities
• PP factors sleep deprivation
              photo
              menses
Epileptogenesis refers to transformation of the
  normal neuronal network in to that of chronically
  hyperexcitable one
..con

Structural abnormalities

         selective loss of neurones
     (inhibitory or excitatory )


          sprouting and reorganization

               chronic hyperexcitable network
Con Partial
• Inhibitory neuronal loss
    exicitatory neurons that stimulate the inhibitory
    pathways are also lost
•   Abnormal integration of neurons with
          reorganization
•   New neuron differentiation with formation of
    new synapses
•   Alteration in the composition and expression of
    GABA receptors
MTLE
…con

• Neuronal loss
• Reorganization   gradually lowers
• Neurogenesis      sz threshold
Mechanism
Absence
 Alteration in the circuitry b/n the thalamus
  and the cortex
Normally the rhythm of cortical stimulation is
  influenced by thalamus
The thalamocortical circuit underlies the
  physiological cortical excitation including sleep
Either fires in a burst form or in a tonic manner
In turn it is influenced by the RAS
Thalamo cortical circuit
Mechanism
•   Developmental influences
•   Cortical malformations
     proliferation
     migration
     cortical organization
Being identified using high resoln neuroimaging
• Change in the neuronal microenvironment
     key buffering function
• Channelopathies
con

Focal Discreet lisions with disruption of
 the balance
Generalized Network abnormalities
         Intrinsic neuronal abnormalities
Evaluation
Is it a seizure?
 DDx for Sz
Does it have any reversible cause?
Is medication worth initiating?
HX preictal, ictal post ,ictal ,frequency
    family hx
    drugs
    systemic illnesses
•
…Con
• pptin factors
• P/E look for atherosclerotic Markers
            signs of trauma
            skin abnormalities
            neurological abn
LAB CBC,U/A, OFTs
     electrolytes
     LP
    EEG
…CON

• Neuroimaging MRI/CT
•              functional studies
evaluation
Treatment

• Treat the underlying cause
• Treat the ppting factor
• Prevent recurrence
• Address psychosocial issues
General principles
•   The lower possible dose
•   Single drug
•   Appropraite for the type
•   Start low and go slow
•      depends on the frequency of the sz
•   Side effect profile
•   Drug interaction
•   Clinical monitoring
…con

• Serum drug levels
• Switch to another class of drug if not
  controlled by one
• Use two drugs if single therapy of two
  different classes fail
• Follow up acc the control of sz
• Issue of discontinuation
Antiepileptic drugs

 mode of action ion
 channels/N.transmitters
 act on Na channels phenytoin,carbama
       lamotrigine,topiramate
 Ca channel phenytoin
 GABA potentiation Barbiturates
 Glutamate uptake Lamotrigine
             Primary         Partial         Absence         Atypical
             generalize                                      absence,
             d                                               myoclonic,
                                                             atonic


First line   Valproic acid   Carbamazepine   Valproic acid   Valproic acid
             Lamotrigine     Phenytoin       Ethosuxamide
                             Lamotrigine
                             Valproic acid



Alternativ   Phenytoin       Topiramate      Lamotrigine
                                             Clonazepam
                                                             Lamotrigine
             Carbamazepine   Levitracetam                    Topiramate
e            Topiramate      Tiagabine                       Clonazepam
             Zonisamide      Zonisamide                      Felbamate
             Felbamate       Gabapentine
             Primidone       Primidone
             Phenobarbital   Phenobarbital
New vs old drugs

• The new ones are found to be
     as effective as those of the old
     expensive
     not time tested
Side effects of AEDS
Current recommendation
(American Academy Of Neurology)
Patients with newly diagnosed epilepsy
  Who require treatment can be initiated on
 standard AEDs such as carbamazepine,
  valproic acid,phenobarbital
         OR
The new AEDs
 lamotrigine,gabapentin,oxcarbazine,or
 topiramate
 (evidence level A/B)
Status epilepticus
• Continues or repititive discreet szs without
  regaining consciousness in between which
  lasts 5 or more minutes
• Medical emergency
• As many statuses as epilepsies
• Ass with mortality rate of 20%
• The mechanism which normally aborts a
  sz is lost
Etiology

• Drug discontinuation or incompliance
• Acute structural injuries
• Remote >>       abnormalities
• Metabolic abnormalities
• Drugs intoxications
…con
• Status is Cx by
1.     self sustenance
2.     Pharmaco-resistance
3.     Neuronal damage
Which tends to worsen as time passes without
Being controlled
Pathophysiology
• Milliseconds to secs
      ionchannel opening/closing
      Neurotransmitter modulation
• Secs to minutes
        Receptor trafficing
• Minutes to Hrs
        Plastic changes in neuropeptide modulators
• Hrs to days change in gene expression
  partly explains how sz becomes self sustaining and
Pharmaco resistant
complications

• Hyperthermia
• Aspiration
• Rahbdomyolysis
• Lactic acidosis
• Brain injury
• Pulmonary edema
Treatment

• Supportive
    Airways
    BP
    Fast neurological examn
    Draw blood/secure iv line
• Ideal situations this should take <4‟
• INITIATE Rx as fast as possible
Rx
…con

Diazepam/Lorazepm
  IV stat
  Repeat another dose

Secure 2nd iv line
    Phenytoin 20mg/kg 50mg/min
                10mg/kg
..cont.

Phenobarb 20mg/kg 50mg/min
            Repeat 10mg/kg
If controlled taper for 24 hrs but maintain
  higher serum levels
G/A Propofol
When the bp is low consider midazolam drip
  .
References

Harrisons 16th edt
Uptudate 14.1
Lancet (vol 5 march 2006)
Nejm(349;13 sep 25,2003)
Nejm(2005,Tales of temporal lobe
www.neurology.com

								
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