Posttraumatic Epilepsy

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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

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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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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



F



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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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2able /



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2able $



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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!



$/

@ 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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Posttraumatic Epilepsy

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