NE URO LO GY

2 17 SEIZURES AND EPILEPSY

DR DAYRIT AND DRA DE GUZMAN

DEFINITION  OF  TERMS  

• SEIZURE  
ü Transient   &   reversible   alteration   of   behavior   caused   • Most  common  etiology  à  IDIOPATHIC  
by   a   paroxysmal,   abnormal   &   excessive   neuronal  
discharge   • 2/3  of  all  epileptic  seizures  begin  in  childhood  
ü Symptom  or  sign   • 75%  unclear  etiology  à  Idiopathic  
 
• Seizure  à  Actual  attack   CLASSIFICATION  OF  SEIZURES  
• CEREBRAL  PROBLEM  à  Not  spinal  cord  or  muscle   SEIZURES   HAVE   BEEN   GROUPED   IN   SEVERAL   WAYS:  
problem  
• IF  YOU  HAVE  RECURRENT  SEIZURES  –  YOU  HAVE   • International  League  Against  Epilepsy  (ILAE)  
EPILEPSY   • Philippine   Version:   Philippine   League   Against  
• SEIZURE   DISORDERS   –   SYNONYMOUS   WITH   Epilepsy  (PLAE)  
EPILEPSY   [the   term   epilepsy   is   usually   not   used  
because  it  brings  stigma]   ACCORDING  TO…  
• Presumed  Etiology  
ü Idiopathic  (Primary)  
 
• EPILEPSY   • Usually  childhood  onset  or  with  family  history  
ü 2   or   more   seizures   not   directly   provoked   by  
ü Symptomatic  (Secondary)  
intracranial   infection,   drug   withdrawal,   acute  
metabolic  changes  or  fever   • Secondary   to   a   tumor,   an   old   stroke,   previous  
ü OLD   DEFINITION   –   “Due   to   an   excessive   and   infection  (meningitis)  
disorderly   discharge   of     cerebral   nervous   tissue   on  
muscles”   • Site  of  Origin  
ü Diagnosis     • Example:   Coming   from   the   Temporal   Lobe   à  
Temporal  Lobe  Epilepsy  
• Epilepsy  à  Disorder/Disease  
• When  you  write  the  diagnosis,  you  put  EPILEPSY   • Clinical  Form  
• MANIFESTED  BY  SEIZURES   ü Generalized  
ü Focal  
• Frequency  
  ü Isolated  
• CONVULSION   ü Cyclic  
ü Intense   paroxysm   of   involuntary   repetitive   muscular   ü Repetitive  
contractions   ü Closely  spaced  sequence  (Status  Epilepticus)  
ü Motor  component  of  seizure   • Special  Electrophysiologic  Correlates  
• TAKE  NOTE:  Not  all  seizures  are  convulsions!   • Based  on  Electroencephalogram  (EEG)  

   
INCIDENCE  OF  EPILEPSY   DISTINCTION  IS  MADE  BETWEEN:  
• Prevalence:  5-­‐10  per  1000   • Classification   of   Seizures   (clinical   manifestations   of  
• 44  cases  per  100,000  persons  each  year  (US  data)   epilepsy;  grand  mal,  petit  mal,  etc.)  AND    
• 10%  will  experience  a  seizure  by  age  80   • Classification   of   Epilepsies   or   Epileptic   Syndromes  
• Bimodal  Distribution:   which  are  disease  constellations    
ü 1st  year  of  life    
ü Over  60  years  old    
 
• Pediatric  and  geriatric  population    
 

LEA THERESE R. PACIS + STEPHEN GABASAN J 1

   - Myoclonic  –  seen  in  patients  in  the  ICU  
CLASSIFICATION   BASED   ON   THE   INTERNATIONAL  
• “Sleep  jerks”  
CLASSIFICATION  OF  EPILEPTIC  SEIZURES:  
• PARTIAL/FOCAL:   occur   within   discrete   regions   of   the  
brain  [one  side  of  the  brain]   - Tonic  
ü Simple  Partial  –  MOST  COMMON   - Clonic  
- Atonic  –  common  in  children  
• Intact  level  consciousness  
• Suddenly  falls  down  due  to  loss  of  muscle  tone  
- Begin   with   MOTOR,   SENSORY   or   AUTONOMIC  
phenomena   depending   on   the   cortical   region  
- Tonic-­‐Clonic    
affected  
 
o MOTOR   –   MOST   COMMON   (Jacksnonian   • MOST   COMMON:   Generalized   Tonic-­‐Clonic  
 
March)   Seizures   (GTC)   à   Also   called   Grand   Mal  
 
• Can  occur  when  the  patient  is  awake  or  asleep     Seizures  J  
• As   compared   to   tremors  à   Only   seen   when   the  
patient  is  awake  
• TONIC   PHASE   –   initial   manifestations   are  
• (+)   Todd’s   Paralysis   –   transient   hemiparesis  
unconsiousness   and   tonic   contractions   of   limb  
after  an  attack  
muscles  (10-­‐30  seconds)  
o SOMATOSENSORY  or  Special  Sensory   o Expiration  induces  vocalizations  (cry  or  
moan)  
• Patient  sometimes  feel  numb  or  “goosebumps”   o Cyanosis  
o Contractions  of  masticatory  muscles  
o AUTONOMIC   o Patient  falls  to  the  ground  
o p   • CLONIC   PHASE   –   alternating   muscle  
• Vomiting     contraction     and   relaxation   of   symmetric   limb  
• Diaphoretic   jerking  (30-­‐60  secs  or  longer)  
• Cold  clammy  skin     o Ventilatory   efforts   return   immediately  
after   cessation   of   tonic   phase   and  
o PSYCHIC  –  COGNITIVE   cyanosis  clears  
ü COMPLEX  PARTIAL  -­‐  with  impaired  consciousness   o Mouth  may  froth  with  saliva  
o AURA  followed  by  impaired  consciousness   o Muscles  may  become  flaccid  
o Patient  may  appear  awake  but  lost  contact  with   o Sphincter   relaxation   may   produce  
the   environemtn   and   do   not   respond   to   urinary  incontinence    
instructions  or  questions  for  few  minutes   o May   remain   unconscious   for   variable  
o Usually   stare   or   remain   motionless   or   engage   period  of  time  
in   repetitive   semi-­‐purposeful   motor   o If  >2  mins  –  STATUS  EPILEPTICUS  
behaviours   called   AUTOMATISMS   –   chewing,   • RECOVERY   PHASE   –   regaining   consciousness  
grimacing,  gesturing,  lip  smacking,  snapping  of   maybe   followed   by   post-­‐ictal   confusion   and   or  
fingers   headache  
o May  become  hostile  or  aggressive  if  restrained   o Full   orienation   in   10-­‐30   minutes  
o Seizure   discharge   arise   form   temporal   lobe   or   (longer   with   status   or   pre-­‐existing  
medial  frontal  lobe   structural  or  metabolic  brain  disorders)  
o Symptoms   take   many   forms   but   usually  
sterotyped  
o Epigastric  symptoms  are  common   MECHANISM   OF   SEIZURE   INITIATION   AND  
o Affective   (fear),   Cognitive   (déjà   vu),   sensory   PROPAGATION:  
(olfactory  hallucinations)   1. high  frequency  of  action  potentials  
  2. hypersynchronization  
• GENERALIZED   EPILIPTOGENESIS   –   transformation   of   a   normal  
ü Rise  from  both  cerebral  hemispheres  simultaneously   neuronal   netweok   that   becomes   chronically  
ü  Bilaterally  symmetrical  and  without  local  onset     hyperexcitable,    
ü Types:   “KINDLING   PHENOMENON”   –   a   result   of   repeated  
- Absence  –  common  in  chilren   stimulation   of   subconvulsive   electrical   pulses   form  
an   established   focus   elsewhere;   controversial   in  
• Also  called  Petit  Mal  Seizure   humans  

LEA THERESE R. PACIS + STEPHEN GABASAN J 2

 o Epilepsy   may   evolve   with   increase   in   frequency,  
• NATURE   OF   THE   DISCHARGING   LESION   IN   duration  or  spread  of  the  seizures  
EPILEPSY:   o Interictal  EEG  background  is  abnormally  slow  
-­‐ SEIZURES   GENERATION   REQUIRE   THREE   o Spontaneous  resolution  of  epilepsy  is  unusual  
CONDITION   o Prognosis   depends   on   the   underlying   neurologic  
o Population   of   pathologically   condition  
excitable  neurons   II. Generalized  Epilepsies  and  Syndromes  
o An   increase   in   excitatory   ü Idiopathic,   with   age-­‐related   onset   or   Primary  
glutaminergic   activity   through   Generalized  (BNFC,  absence,  JME,  etc.)  
recurrent   connetions   to   spread   the   ü Symptomatic   or   Secondary   Generalized   (West  
discharge  -­‐  ↑  GLUTAMATE   syndrome,  Lennox-­‐Gastaut  syndrome)    
o A   reduction   in   the   activity   of   the   ü IDIOPATHIC  EPILEPSY  
normally   inhibitory   gabanergic  
projections  -­‐  ↓  GABA     • IDIOPATHIC  EPILEPSY:  
o as  a  rule,  begin  early  in  life  
• SPECIAL   EPILEPTIC   DISORDERS   –   seen   in   o not  associated  with  evidence  of  structural,  
children   nervous,  or  mental  disorders  
o Myoclonus  and  myoclonic  seizures   o normal  interictal  EEG  background  
o Reflex   e pilepsy   o favorable  response  to  anti-­‐epileptic  
o Acquired  aphasia  with  convulsive  disorder   therapy  
o Febrile   and   other   seizures   of   infancy   and   o benign  prognosis  with  spontaneous  
childhood   resolution  in  time  
o Hysterical  seizures  –  “psychogenic”    

INTERNATIONAL   CLASSIFICATION   OF   EPILEPSIES   ABSENCE  or  PETIT  MAL  SEIZURES  

AND  EPILEPTIC  SYNDROMES   ü Pyknoepilepsy  –  “Pykno”  –  compact  or  dense”  
ü Features.  brevity,  frequency,  paucity  of  motor  activity  
I. Localization-­‐related   ü "A  moment  of  absentmindedness  or  day  dreaming"  
ü Idiopathicà      IDIOPATHIC  EPILEPSY  or  “PRIMAY   o Without   a   warning....   sudden   interruption   of  
EPILEPSY”     consciousness....   stares   and   briefly   stops   talking   or  
o There   is   no   underlying   cause   indetifies   other   ceases  to  respond  
than  an  heriditary  predisposition  
o 10   percent   are   completely   motionless;   the   rest  
o Presumed  to  be  GENETIC  of  origin  
have  fine  clonic  (myoclonic)  movements  of  eyelids,  
o Ofthen  with  a  (+)  family  history  
facial  muscles  or  fingers,  at  a  rate  of  3  per  second  
o As   a   rule,   begins   early   in   life   –   20   years   old   and  
below   EEG   pattern   of   generalized   3-­‐per-­‐second   spike-­‐
o Not   associated   with   evidence   of   structural   or   and-­‐wave  pattern  
nervous  or  mental  disorders   ü After   2   to   10   seconds,   or   longer,   patient   reestablishes   full  
o Normal  interictal  EEG  background  and  MRI   contact   with   the   environment   and   resumes   pre-­‐seizure  
activity.  
• Inter-­‐ictal   à   Period   in   between   episodes   of  
seizures   (Time   wherein   the   patient   is   not   ü Hyperventilation  may  induce  an  attack  
undergoing  seizure)   ü As  many  as  several  hundred  may  occure  in  a  day  
ü Rarely  begins  before  4  years  or  after  puberty  
o Favorable  response  to  antiepileptic  therapy   ü Attacks   tend   to   diminish   during   adolescence   and  
o Benign   prognosis   with   spontaneous   resolution   in   then   disappear,   to   be   raplaced   by   other   forms   of  
time   generalized  seizure  
ü Symptomatic  à  Secondary  Epilepsy   ü "SECONDARY"  epilepsy  
o Seizures   have   an   identifiable   and   acquired   o Seizures   have   an   identifiable   and   acquired  
structural  cause  
structural  cause  
• Difficult  to  control,  treat,  and  manage   o There   is   evidence   for   focal   or   generalized  
neurological  disease  
o There   is   evidence   for   focal   or   generalized   o mental  retardation  or  deterioration  may  occur  
neurological  disease   o Rarely  begins  before  4  years,  or  after  puberty  
o Mental  retardation  or  deterioration  may  occur   o As  many  as  several  hundreds  may  occur  in  a  day  

LEA THERESE R. PACIS + STEPHEN GABASAN J 3

 o Attacks  tend  to  diminish  during  adolescence  and  then   § changes   at   the   molecular   level   -­‐   the   most  
disappear,   to   be   replaced   by   other   forms   of   prominent   of   these   are   alterations   in   the  
generalized  seizures   composition  and  expression  of  GABAA  receptors  on  
  the  surface  of  hippocampal  dentate  granule  cells  
MESIAL  TEMPORAL  LOBE  EPILEPSY   § normally,  GABAA  receptors  in  adults,  which  consist  
ü Hippocampal  sclerosis:   of  five  subunits,  serve  as  inhibitors,  hyperpolarizing  
o there   is   selective   loss   of   neurons   in   the   dentate   hilus   the   neuron   by   allowing   passage   of   chloride  
and  the  hippocampal  pyramidal-­‐cell  layer   ions  when  activated  
o relative   preservation   of   dentate   granule   cells   and   a  
small   zone   of   pyramidal   cells   (in   the   cornu   ammonis,   PATHOLOGY  OF  EPILEPSY  
field  2,  of  the  hippocampus)   ü Primary  generalized  epilepsies:  majority  are  grossly  
o the   dense   gliosis   that   accompanies   the   loss   of   neurons   and  microscopically  normal  
causes  shrinkage  and  hardening  of  tissue   ü Symptomatic  epilepsies:  neuronal  loss  and  gliosis,  
o the  term  "mesial  temporal  sclerosis"  has  also  been  used  for   porencephaly,  hamartoma,  heterotopia,  dysgenetic  cortex,  
this   lesion,   because   often   there   is   neuronal   loss   in   the   vascular  malformations,  and  tumor  
neighboring   entorhinal   cortex   and   amygdaladebate   ü Focal  epilepsies:  gliosis,  fibrosis,  vascularization,  
about  whether  hippocampal  sclerosis  is  a  cause  or  an   meningocerebral  cicatrix,  hippocampal  sclerosis  
effect  of  seizures   SEIZURE  IN  ADULTS  
o it   has   been   seen   in   a   wide   variety   of   epileptic   conditions,  
including   cryptogenic   temporal-­‐lobe   epilepsy   and   ü Secondary  to  medical  diseases  
epilepsy   that   follows   febrile   seizures   or   other   brain   o Withdrawal  seizures  —  AED  withdrawal  
insults  early  in  life,  as  well  as  in  animal  models  of  head   o Infections  —  CNS,  or  systemic  infections  
injury  and  seizures  induced  by  chemicals   o Metabolic  encephalopathies  —  hypoglycemia,  
o Hypotheses  about  the  mechanism  of  epileptogenesis   hyponatremia,  uremia,  hepatic  encephalopathy  
§ structural   r eorganization   o Medications  as  a  cause  of  seizures  —  antibiotics  
§ selective   n euronal   l oss   (carbapenem),  tricyclic  antidepressants  
§ neurogenesis   o Global  arrest  of  circulation  and  cerebrovascular  
§ molecular   alterations,   such   as   changes   in   diseases  —  hypoxic  encephalopathy  
neurotransmitter  receptors   o Acute  head  injury  
o Some   investigators   have   suggested   that   the   selective    
vulnerability  of  certain  neurons  may  be  a  mechanism  of   SEIZURE  IN  ADULTS  
epileptogenesis  in  hippocampal  sclerosis  
o In  animal  models,  excitatory  interneurons  located  within   ü Sodium  Channels  
the   dentate   gyrus,   which   normally   activate   inhibitory   o Familial  generalized  seizures  
interneurons,  appear  to  be  selectively  lost   o Benign  Familial  neonatal  convulsions  
o  Loss   of   these   excitatory   cells   would   be   expected   to   ü Potassium  Channels  
impair   the   inhibitory   feedback   and   feed-­‐forward   o Benign   i nfantile   e pilepsy  
mechanisms   that   act   on   dentate   granule   cells,   resulting   o Episodic  ataxia  type  1  
in  hyperexcitability   ü Ligand-­‐gated  Channels  
o An   intriguing   hypothesis   lies   in   the   phenomenon   of   o Autosomal  dominant  nocturnal  frontal  seizures  
neurogenesis   o Familial  generalized  and  febrile  seizures  
§ Almost   all   neurons   in   the   brain   are   postmitotic   o Juvenile  myoclonic  epilepsy    
and  do  not  divide  in  adults,  but  progenitor  cells  in   ü Calcium   C hannel  
the   dentate   gyrus   of   the   hippocampus   are   known   o Episodic  ataxia  type  2  
to  divide    
§ Postnatal   neurogenesis   in   the   hippocampus   DIAGNOSTICS  
can  occur  throughout  life   ü EEG  
§ The   potential   clearly   exists   for   an   imbalance   o Indications:  
between  excitation  and  inhibition  as  new  neurons   § To  confirm  the  diagnosis  of  epilepsy  
differentiate  and  form  synaptic  connections   § An  adequate  EEG  should  include  a  sleep  and  
awake  recording  

LEA THERESE R. PACIS + STEPHEN GABASAN J 4

 § To  classify  the  seizure  type   o Need   t o   c onfirm   d iagnosis  
§ To  make  a  diagnosis  of  non-­‐convulsive  status   o Poor  seizure  control  
epilepticus   o Severe/toxic   s ide   e ffects  
o Role  of  Interictal  EEG  in  Epilepsy   o Patients  planning  a  pregnancy  
§ Confirms  clinical  diagnosis  of  epilepsy   o Seizure  free  patient  considering  drug  withdrawal  
§ Classification  of  seizure  types  
CAUSES  OF  RECURRENT  SEIZURES  IN  DIFFERENT  AGE  
§ Definition  of  Epileptic  syndromes  
GROUPS  (Adams,  19th  Edition)  
• Monitoring  of  response  to  AED  treatment  
• Neonates  
• Evaluation   of   patients   with   single  
ü Congenital  Maldevelopment  
seizures  
ü Birth  Injury  
§ Guide   in   the   decision to discontinue AED
ü Anoxia  
treatment
ü Metabolic  Disorder  
ü BRAIN  IMAGING  (MRI  or  CT)    
- Hypocalcemia  
o Indications:  
- Hypoglycemia  
§ Partial  onset  seizures  at  any  age  
- Vitamin  B6  Deficiency  
§ Adult  onset  seizure  of  any  type  
- Biotinidase  Deficiency  
§ Presence   of   focal   neurologic   deficit   CT  and  
- Phenylketonuria  
MRI  allow  identification  of  structural  lesions    
- Others  
• MRI   higher   specificity   and   sensitivity   in  
 
diagnosing   congenital   brain   anomalies,  
• Infancy  (1-­‐6  months)  
hippocampal   sclerosis,   AV   malformations,  
ü As  above  
tumors  
ü Infantile  Spasms  (West  Syndrome)  
• CT  scan  :  if  MRI  is  not  available  or  in  those  with  
 
pacemakers.   aneurysm   clips,   severe  
• Early  Childhood  (6  months  –  3  years)  
claustrophobia  
ü Infantile  Spasms  
ü DIFFERENTIAL  DIAGNOSES  
ü Febrile  Convulsions  
o Syncope/Faints  
ü Birth  Injury  and  Anoxia  
o TIA  
ü Infections  
o Drop  attacks  
ü Trauma  
o Complicated  migraine  
ü Metabolic  Disorders  
o Hypertensive  emergency  
ü Cortical  Dysgenesis  
o Psychiatric  disorders  
ü Accidental  Drug  Poisoning  
   
• Childhood  (3—10  years)  
 
ü Perinatal  Anoxia  
TREATMENT   ü Injury  at  birth  or  later  
ü Infections  
ü CRITERIA   FOR   STARTING   ANTIEPILEPTIC   DRUG   ü Thrombosis  of  Cerebral  Arteries  or  Veins  
(AED)   ü Metabolic  Disorders  
o The  diagnosis  of  epilepsy  must  be  firm  and  definite   ü Cortical  Malformations  
o Risk  of  seizure  recurrence  must  be  sufficient   ü Lennox-­‐Gastaut  Syndrome  
o Seizure   type   or   epilepsy   syndrome   The   AIM   of   ü “Idiopathic”  (Probably  Inherited)  
Treatment   with   AEDs   is   to   prevent   seizures   for   the   ü Rolandic  Epilepsy  
following  reasons:    
§  Prevent  injury   • Adolescence  (10-­‐18  years)  
§ Avoid  disruption  to  employment  or  education   ü Idiopathic   Epilepsy   (Including   genetically   transmitted  
§ Minimize   the   social   consequences   of   the   types)  
condition   ü Juvenile  Myoclonic  Epilepsy  
§ Try  to  prevent  status  epilepticus   ü Trauma  
ü WHEN  T O  R EFER  T O  A  SPECIALIST   ü Drugs  

LEA THERESE R. PACIS + STEPHEN GABASAN J 5

   Lamotrigine  
• Early  Adulthood  (18-­‐25  years)  
MYOCLONIC   Valproate   Topiramate  
ü Idiopathic  Epilepsy  
ü Trauma   Levetiracetam  
ü Neoplasm  
Zonisamide  
ü Withdrawal  from  alcohol  or  other  sedative  drugs  
  Partial   Carbamazepine   Valproate  
• Middle  Age  (35-­‐60  years)  
ü Trauma   Phenytoin   Lamotriging  
ü Neoplasm   Oxcarbazepine  
ü Vascular  Disease  
ü Alcohol  or  other  drug  withdrawal   Levetiracetam  
  Drug   Partia Generaliz Toni Absenc Myoclon Mixe
l   ed   c   e   us   d  
• Late  Life  (Older  than  60)   secondary   Clon
ü Vascular  Disease  (usually  postinfarction)   ic  

ü Tumor  
Carbamazep +   +   +   x   x   o  
ü Abscess   ine  
ü Degenerative  Disease  
ü Trauma   Clonazepam   +   +   +   ?     ?  +  
 
Phenobarbit +   +   +   o   ?  +   ?  
 
al  

Phenytoin   +   +   +   x   x   o  

Valproate   +   +   +   +   +   +  

MEDICATION   SIDE  EFFECTS  

Phenobarbital   Sedation,  sleepiness,  

hyperactivity,  weakness  

Dilantin  –   Dizziness,  poor  balance,  

Phenyhydantoin,   weakness,  thick  gums,  
Phenytoin   excessive  hair  growth,  
allergic  rash,  SJS  

Tegretol  –   Allergic  rash,  dizziness,  

Carbamazepine   sleepiness,  weakness,  
headache,  gastric  
discomfort,  SJS,  leukopenia,  
hyponatremia  
 
WHAT  DRUG  TO  CHOOSE:   Epival/Depakene   Transient  loss  of  appetite,  
alopecia,  nausea,  vomiting,  
EFFICACY   ESTABLISHED   AED   AGAINST   COMMON   weight  gain  
SEIZURE  D RUGS:  
Rivotril  –  Clonazepam   Sleepiness,  weakness,  in  
SEIZURE  TYPE   FIRST  LINE     SECOND  LINE   chidren  –  increase  bronchial  
TONIC  CLONIC   Valproate   Lamotrigine   secretions  

 Trileptal  –   Headache,  dizziness,  

Carbamazepine  
Oxcarbazepine   sleepiness,  nausea  and  
Phenytoin   hyponatremia  

ABSENCE   Valproate   Ethosuximide  

LEA THERESE R. PACIS + STEPHEN GABASAN J 6

 Neurontin  –  Gabapentin   Sleepiness,  fatigue,  
dizziness,  weakness  and   6-­‐9   ABCs,   Establish   Fosphenytoin  
IV,   Blood   work,   (20  m g/kg  PE)  
rashes   Give   Thiamine  
and  glucose  
Lamictal  –  Lamotrigine   Allergic  rash,  drowsiness  

Topamax   Weight  loss,  mood  changes,   10-­‐20     Lorazepam   (0.1    

sleepiness,  dizziness  and   mg/kg)   or  
kidney  stones   Diazepam   (0.2  
mg/kg)  
 
21-­‐40   Phenytoin   (15-­‐ Add   phenytoind  
-­‐ start   at   the   lowest   computed   appropriate   dose   and   20  m g/kg)   (5   gm/kg)   /    
increase   slowly   until   seizure   control   is   achieved   or   fosphenytoin   (5  
side  effects  develop   mg/kg)   followed  
-­‐ Titrate  slowly  to  allow  tolerance  to  CNS  side  effects   by  Phenobarbital  
-­‐ Keep   the   regimen   simple   wth   OD-­‐   BID   dosing,   if   (20   m g/kg)   or   go  
possible   to  anesthesia  
 

SURGICAL  TREATMENT   41-­‐60     Add  

phenobarbital  
-­‐ temporal   lobectomy-­‐   50%   improvement   in   5   years   (5-­‐10  m g/kg)  
in  complex  partial  seizures  
-­‐ Corpus   callostomy   –   recommended   for   cotnrol   of  
Greater  than  60   Add   phenytoin   Anesthesia   with  
intractable   partial   and   secondary   generalized  
(5   mg.kg)   x   2   Midazolam   or  
seizures  –  especially  atonic  drop  attacks  
followed   by   Propofol  
-­‐ Hemispherectomy   –   recommended   for   severe   and  
phenobarbital  
extensive   unilateral   cerebral   disease   with  
(20   mg/kg)  
intractable  m otor  seizures  and  hemiplegia  
followed   by  
o Rasmussens   encephalitis,   Sturge-­‐Weber  
pentobarbital  
syndrome  and  Large  porencephalic  Cysts  
ROLE  OF  KETOGENIC  AND  MEDIUM  CHAIN  
FACTORS  RELATED  TO  SUCCESSFUL  WIDTHRAWAL  OF  
TRIGLYCERIDE  DIET:  
AEDs  
-­‐ exact  m echanism  –  U NKNOWN    
-­‐ Single  type  of  lesion  
-­‐ chronic  ketosis  induced  by  a  diet  high  in  fat  results  
-­‐ Normal  neurologic  examination  
in   improvement   of   cerebral   energetics   and  
-­‐ Normal  IQ  
augmentation  of  G ABA  effects  (?)  
-­‐ Normal  E EG  following  treatment  
-­‐ used  m ainly  in  children  (1-­‐10  years  old)  
COMPLICATIONS  OF  THE  DISEASE:   -­‐ 2/3   reduction   in   seizure   frequency   and   reduction  
of  A ED  usage  
-­‐ STATUS  EPILEPTICUS   -­‐ Effective  in  refractory  epilepsy  
o Recurrent   generalized   convulsions   at   a   -­‐ CHARACTERISTICS:  
frequency   that   prevents   regaining   of   o Consists  of  daily  regimen  of  1g.kg  p rotein  
conciousness  in  the  interval  between  seizures   o Enough   fat   to   make   up   desired   caloric  
o Prolonged   convulsive   status   (longer   than   30   requirements  
mins.)   carries   high   risk   for   serious   neurologic   o Very  small  amount  of  carbs  
sequelae  (“epileptic  encephalopathy”   o Ketogenic  :  antiketogenic  potential  ratio  –  3:1  
o MANAGEMENT   -­‐ Caloric  D istribution:  
o Ketogenic  –  87%  fat,  6  %  CHO  and  7%  CHON  
o MCT   –   60%   MCT,   11%   fat,   19%   CHO   and   10%  
Time  in  M inutes   Standard   Proposed   CHON    
Treatment   Treatment   o Thus  m ore  palatable  and  no  increase  in  plasma  
cholesterol  
0-­‐5   Diagnosis   and   Lorazepam   (1.0    
assessment   mg/kg)    
 
 

LEA THERESE R. PACIS + STEPHEN GABASAN J 7