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SEIZURE DAN EPILEPSI

PADA KEGANASAN
1. Partial Simplex Primary Generalized Seizu
2. Partial Complex

Modified: Crank, 2003


The pathways for seizure
propagation in partial seizures
and primary generalized
seizures (Lothman 1993)
Ionic channel
Na+, Ca++, K+, Cl-

Lignad-gated Channel
excitatory -
Glutamate
inhibitory - GABA

Excitatory
postsynaptic potential
Inhibitory
postsynaptic potential
Action potential
Excessive discharge

Result from :
Too much excitation/depolarisasi (Glutamate)
Or to little inhibition/repolarisasi (GABA)
Voltage-gated sodium channel
Open Inactivated
Na+ Na+
Ca2+ Ca2+

A
I

Carbamazepine Lamotrigine
Na + Phenytoin Na + Topiramate

A = activation gate Valproate


I = inactivation gate
Sumber: McNamara JO. Goodman & Gilmans. 9th ed. 1996:461-486.
1. Simple (without impairment of consciousness)
With motor symptoms
With special sensory or somatosensory
symptoms
With psychic symptoms
2. Complex (with impairment of consciousness)
Simple partial onset followed by impairment
of consciousness with or without
automatisms
Impaired consciousness at onset with or
without automatisms
3. Secondarily generalized (partial onset evolving
to generalized tonic-clonic seizures)
1. Absence
Generally occur in young children
through adolescence
Sudden onset
Interruption of ongoing activities
Blank stare
Upward rotation of eyes
2. Myoclonic
Sudden spasm of muscle
3. Juvenile Myoclonic Epilepsy
4. Clonic
Rhythmical muscle movements
5. Tonic
Continuous muscle tension
7. Tonic-clonic
Formerly known as grand-mal seizures
Associated with loss of sphincter tone,
biting of the tongue, moaning, crying,
and cyanosis
8. Atonic
Sudden loss of muscle tone
Head drop
Dropping of a limb
Slumping to the ground
9. Infantile spasms
10. Lennox-Gastaut
11. Unclassified Seizures
12. Status Epilepticus
EEG and Clinical Changes in Patients With Chronic Seizures
Associated With Slowly Growing Brain Tumors
John R. Hughes, MD, PhD; Steven M. Zak, MD
Arch Neurol.1987;44(5):540-543.

The goal of this study was to define the electroencephalographic (EEG)


and clinical features in 25 patients with chronic seizures (szs) associated
with slowly growing (three to 36 years) brain tumors (BTs). A matched
control group was also studied. When all EEGs were considered together
without regard to their changes, no significant differences were found
between the two groups, especially with respect to the high incidence
(60%) of EEG abnormalities both ipsilateral and contralateral to the tumor.
Exact localization of the BT by EEG (within one electrode) was found in
88% of patients. When changes in time were considered, the BT group
more often showed (1) increasing slow waves, (2) increasing sharp-wave
discharges, (3) depression of normal rhythms, (4) a change in type of sz,
(5) increase in frequency of szs, and (6) a change in neurological signs and
symptoms, especially motor. For single, double, or triple criteria, a change
in clinical signs was the most discriminative, with a deteriorating EEG as
the next best indication of a tumor. Patients with the latter signs should
then be selected for a computed tomographic or magnetic resonance
imaging scan, even if the scan was normal initially, rather than following
the expensive policy that all patients at all ages with chronic szs should
undergo these later tests.
Przegl Lek. 2003;60 Suppl 1:42-4.
[Epileptic seizures as a manifestation of brain tumors: clinical and
electroencephalographic correlations].
Abstract
Epilepsy may be the earliest and the sole clinical manifestation of brain tumours.
Different studies present epileptic seizures as the first symptom of a brain tumours
in adults in approximately 30-40% of cases and in children from 1-10%. Of 113
children, epileptic seizures as a first symptom occurred in 14 children and in 211
adults. Histopathological origin and localization of tumours changed according to
the age of patients. In all children's seizures were caused by supratentorial
tumours originated from neuroepithelial tissue and mainly astrocytomas. In adult
patients seizures were observed also mainly in supratentorial tumours (5 cases
infratentorial) which were of metasthatic origin (60%) others were glioblastomas
multiforme and sporadically meningiomas. The types of seizures in both groups
differ significantly. Children had mainly secondary generalized seizures, while
adults simple and complex partial seizures. Electroencephalographical findings
showed paroxysmal activity always associated with supratentorial brain tumours
with seizures; however, we found also abnormal EEG patterns in patients with
infratentorial tumours without seizures. Partial and secondary generalized
seizures, especially when they are intractable, should be subjected to further
investigation for exclusion of brain tumour not only in adults but also in children.
Normal EEG argues against the likehood of supratentorial lesions.

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