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POSTTRAUMATIC EPILEPSY ANDTREATMENT
Chen JWY, Ruff RL, Eavey R, Wasterlain CG. Posttraumatic epilepsy andtreatment. Journal of Rehabilitation Research !evelopment. volume "#, number
#, $%%&
Ellen J. '. Riry
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Pembimbin+
dr. 'emuel Wa+iu, 'p.', -.ed
JOURNAL READING
'eptember $%/"
Dibawakan dalam rangka tugas kepaniteraan klinik
di Bagian Neurologi Faktultas Kedokteran
Universitas Pattimura
Ambon
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01'2R0C2
Posttraumatic epilepsy 3P2E4 ma5or lon+)termcomplication of traumatic brain in5ury 32164 7ithin 8
years
Ris9 8*: penetratin+ 216
/%)$8: combat)associated closed)head trauma 7ith positive brainima+in+
8: moderately severe closed)head in5ury 7ithout ima+in+ findin+
Partial sei;ures may manifest 7ith subtle behavioralalterations mista9en for manifestations of postraumatic
stress disorder and improperly treated'udden une<pected death in epilepsy amon+ $%)"% y.o
'ei;ures social sti+ma optimal sei;ure control isessential
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!E=6>626?>
@ Epilepsy A all +roups of syndrome characteri;ed 7ith
temporary paro<ysm disorder of brain function.
3!orlandBs 6llustrated -edical !ictionary4
@ ?ther definition disease of brain defined by any of the
follo7in+ conditions
at least $ unprovo9ed sei;ures occurin+ +reater than $" hours
apart / unprovo9ed sei;ure and a probability of futher sei;ures similar
to the +eneral recurrence ris9 3at least #%:4 after $ unprovo9ed
sei;ures, occurin+ over the ne<t /% years
dia+nosis of an epilesy syndrome
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6>2R?!DC26?>
!efinition of Posttraumatic Epilepsy2raditional definition of epilepsy $ or more unprovo9ed
sei;ures after a head in5ury / 7ee9 after the head
in5ury
(#: patients 7ith / unprovo9ed posttraumatic sei;uree<perienced a $nd sei;ure 7ithin $ years
Patient 7ith / unprovo9ed posttraumatic sei;ure
e<tremely hi+h ris9 of developin+ P2E
?ther definition / or more unprovo9ed sei;ure late headin5ury need an early treatment
'ei;ures that occur 7ithin the first F days after 216 are
defined as provo9ed sei;ures
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Ris9 of Posttraumatic Epilepsy 0fter 2raumatic 1rain6n5ury
2he probability of P2E si+nificantly correlates 7ith theseverity of in5ury
6n +eneral, 216 divided into@ -ild
@ -oderate
@ 'evere-ultivariate analysis hi+h ris9 of P2E
@ depressed s9ull fracture,@ brain contusion,
@ intracranial hemorrha+e,
@ coma duration,@ lo7 Glas+o7 Coma 'cale score, and@ ?lder a+e
Patient 7ith mild 216 Presence of early sei;ure >?2increase the ris9 of P2E
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Ris9 of Posttraumatic Epilepsy in eterans
7ith 2raumatic 1rain 6n5ury
Ris9 factor for developin+ P2E 0fter penetratin+
head in5ury retained metal fra+ments,
intracranial hemorrha+e, chronic neurol+ical
deficits, brain parenchyma loss
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>atural History of Posttraumatic Epilepsy
P2E presents 7ith different sei;ure freIuency and
may evolve into remission or develop into
intractable sei;ures.
=reIuent sei;ures in the first year after penetratin+
head in5ury su++est a reduced chance of remission
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P?'22R0D-026C EP6LEP'Y 6>
C?>2E2 ?= ?6=K?E=
-edical Cost of Posttraumatic Epilepsy
-a< latent period of P2E $% years after 216
Dncontrolled sei;ures can be fatal @'ei;ures sei;ures
@ 0spirate durin+ sei;ures pneumonia and
dama+e to the air7ays and lun+s
@!isrupt blood pressure and heart control sudden
death
@!isrupt respiratory and blood temperature control
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'ocioeconomic Cost of PosttraumaticEpilepsy
'ei;ures A social sti+ma compromise society'udden une<pected death in epilepsy $%)"% y.o
Dncontrolled sei;ures become refractory tomedications
?ptimal sei;ure control A essential for the physicaland emotional health
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Ris9 of Posttraumatic Epilepsy in ?6=K?E=
eterans 7ith 2raumatic 1rain 6n5ury
ris9 for developin+ P2E M varies M type of 216
cerebral in5ury can be seen on clinical ima+in+ M
the ris9 A /%)$8:
potential ris9 M N 8:
repeated events of minimal 216 increases the ris9
of P2E un9no7n
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@ >onconvulsive 'ei;ures partial sei;ure M manifest 7ith subtle behavioral
alterations M mista9en for apathy catatonia or P2'!
presentation of a comple< partial sei;ure could befeatureless
for early detection every clinican 7ho treats patients7ith 216 is a7are of this condition.
EEG is often needed to establish a dia+nosis of non)convulsive sei;ure
the most recent report identified a little over *$.%%%in5uries and around 8.8%% individuals 7ith 216
the number of P2E cases 7ill increase if hostilitiescontinue
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P?'22R0D-026C EP6LEP'Y
2RE02-E>2
@ 6ntroduction
clinicians routinely use ne7 and effective
0E!s 7ith different mechanisms of actions
other option su+ical evaluation M Epilepsy
-onitorin+ Dnit 3E-D4
specialists consider resection sur+ery toremove the sei;ure focus to be standard of
care in patients 7ith epilepsy that is refractory
to medical treatment alone.
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@ Prevention a number of published uncontrolled,
unblinded observational studies have
investi+ated the effect of 0E!s in preventin+P2E
@ phenobarbital 3P14 O phenytoin 3PH24@ phenytoin 3PH24@
phenobarbital 3P14@ valproic acid 3P04
?nly P1OPH2 sho7ed a mar9ed differencebet7een the treated and untreated +roups
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-ost of researchers did not reproduce thebeneficial effects of prophylactic treatment7ith 0E!s in several randomi;ed trials usin+
PH2, PH2OP1, or carbama;epine 3C14 7ithfollo7)up periods of * months to 8 years
Cochrane revie7 M $.%*# patients M@ prophylactic treatment 7ith PH2 or C1 7as only
effective in reducin+ the ris9 of early provo9edsei;ures after 216
@ no beneficial effect in the prevention of P2E 7ith 0E! treatment
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@ Role of 0E!s 0fter 2raumatic 1rain 6n5ury 0E! prophyla<is seems to be effective in
controllin+ the early provo9ed sei;ures M not
the late and P2E
2he results to date do not support
prophylactic use of 0E!s in patients 7ith 216
before the development of P2E
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@Potential Pitfalls of Dsin+ ?r >ot Dsin+ 0E!Prophyla<is 0fter 2raumatic 1rain 6n5ury clinical study difficult to tease out 0E! co+nitive side
effects from the direct effects of 216 and from 0E!inhibition of recovery of brain function after 216
another limitin+ factor hetero+eneity of patientpopulations the timin+ of 0E! treatment after 216 varies amon+
studies the different types of sei;ures further complicate the
hetero+eneity issue nonepileptic sei;ures mi+ht be misdia+nosed as P2E
and the patient could be unnecessarily treated 7ith 0E!
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@ Epilepto+enesis 1asic 0spects@ epilepto+eneis describes the molecular, cellular,
and net7or9 processes
@ far from fully understood@ have emer+ed based on ressearch usin+ various
results from animal models of epilepsy
@ 0n in5ury to the superficial layers of G010er+icneurons in 216 could tilt the dedicated balancebet7een the e<citatory and inhibitory neuronsto7ard hypere<citability
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@ other observation once the 9indlin+ process is
fully established M permanent M due to certain
irreversible chan+es in the anatomical structuresand physiolo+ical functions from molecular to
net7or9 levels
@ a+ents that inhibit or reverse epilepto+enesis
antiepilepto+enic a+ents@ in contrast, dru+s that reduce hypere<citability
anticonvulsant M use to control sei;ure
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?nset@ theory / critical issue in P2E prophyla<is is
initiation of antiepilepto+enic therapy before the
epilepto+enesis process starts, or at least before it
escalates to an irreversible sta+e
@ Principle 216 could set the process of
epilepto+enesis inmotion, and many other
accessory factors 7ill also determine 7hether
epilepto+eneis could complete its course of
developin+ P2E
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@Genetic Propensity for Posttraumatic Epilepsy +enetic defects M mostly in primary +enerali;ed
epilepsies
could be vie7ed as +enetic propensity for developin+
the phenotype 3the epilepsy4 7hen the other cofactorsare present
the increased ris9 M independent of the 0P?E "
alleleBs effect on the functional outcome
role of 0P?E " allele in epilepto+enesis unclear
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@ 6ndication for !ia+nostic 'tudies for early sei;ure detection after 216 M EEG
screenin+ durin+ the first $ years 7hich patient should receive 0E! therapy
unclear 7hat clinical parameters to +uide the
continuation or termination of therapy unclear
if subtle clinical presentations correlate 7iththe epileptiform dischar+es on EEG
recordin+s M initiation of 0E! therapy
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@ Pharmacotherapy P2E in patient 3O4 M initiate 0E! therapy
follo7in+ the +eneral +uidelines used for othertypes of acIuired epilepsy.
monotherapy or polytherapy 3at least $ 0E!sof different pharmacolo+ical mechanisms4
follo7 the +eneral treatment principles usin+ the least amount of 0E!
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@ 6ndications for 'ur+ery inpatient video EEG monitorin+, PE2 scan, brain -R6
7ith epilepsy protocols futher evaluations depthK+rid intracranial electrodes,funtional -R6, cortical functional mappin+ 7ithelectrocortico+raphy
perform the Wada test
evaluate patients 7ho are refractory but fail sur+icalevaluations for placement of a deep brain stimulatoror va+us nerve stimulator
consider patients 7ho fail va+us nerve stimulation anddeep brain stimulation for enrollment in investi+ational
procedures
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C?>CLD'6?>'
@ P2E mi+ht represent a lar+e, comple<problem that should not be i+nored
@ any plans to address the problem should
be coordinated 7ith e<istin+ polytraumaand 216 pro+rams
@ e<perts are available 7ithin the 0 to
evaluate the problem and desi+n efficient,
proactive solutions
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