MODUL SEIZURE 2013.doc

8/13/2019 MODUL SEIZURE 2013.doc

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Block VII : The Nervous System & Psychiatry

Module : Seizure

Course Period : Academic Year !" # !"$

%th Semester

Name : Studet

'uidace

(aculty o) MedicieBra*i+aya ,iversity

!"$


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ST,.0NT ',I.ANC0

Course Period : %th Semester

M-.,/0 : N02V-,S SYST0M & PSYC3IAT2YS,BM-.,/0: N02V-,S SYST0M

T-PIC : S0I1,20

"4 S,B5T-PICS :

1. Introduction

2. Neurophysiology of Cerebral Cortex

3. Pathophysiology of Seizure

4. ifferential diagnosis of Seizure!. In"estigation in #pileptic Seizure

$. Seizure %anage&ent

4 C-NT2IB,T-2S

1. Nurul '( epart&ent of )nato&y 'istology

2. ian 'asanah( epart&ent of Physiology

3. %achlusil 'usna( epart&ent of Neurology

4. Nurdiana( epart&ent of Phar&acology

$4 C-MP0T0NCY A20A*his &odule is a part of the elaboration of

1. *he area of co&petence 2 ie. *he Clinical S+ill

2. *he area of co&petence 3 ie. *he Scientific,-ase of %edical Sciences .

3. *he area of co&petence 4 ie. *he %anage&ent of 'ealth Proble&s

4. *he area of co&petence ie. *he Professionalis&.

%4 C-MP0T0NCY C-MP-N0NT

1. *he Clinical S+ill / Neurological exa&ination

2. *he Scientific,-ase of %edical Sciences / *o apply the concepts and principleof -io&edical Sciences( Clinical Sciences and Public 'ealth in appropiate 0ith

Pri&ary 'ealth Care.

3. *he area of co&petence 4 i.e. %anage&ent of 'ealth Proble&s/ *o &anage

the diseases( illness and patients proble& as a indi"idual person( a part of

fa&ily and co&&unity and *o pre"ent diseases and illness

4. *he Professionalis&/ to ha"e professional attitude


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64 C/INICA/ C-MP0T0NC0

In a "ignette of a patient 0ith seizure( the student be able to/

1. &a+e a clinical diagnosis of seizure( to &a+e si&ple aids and additional

in"estigation reuested by student hi&self such as si&ple laboratory or

##5.

2. %a+e a 6udge&ent that an initial treat&ent is reuired before being referred

and describe to carry out an initial treat&ent and i&&ediately refer to the

rele"ant specialist e&ergency cases5.

74 /0A2NIN' -B80CTIV0S

)t the end of the *eaching,7earning Process of this topic( in a "ignette of a

patient 0ith a seizure the student should be able to/

1. escribe the anato&ical structure that ta+e part in seizure

2. escribe &echanis& of seizure3. escribe &echanis& of epileptogenesis

4. escribe the definition seizure and epileptic seizure

!. escribe the classification of seizure and epileptic seizure

$. escribe the pathophysiology of epileptic seizure

. escribe the signs and sy&pto&s of epilepsy

8. escribe the outline a practical approach to diagnosis and initial &anage&ent

of seizure

9. ifferentiate bet0een true seizure and psychogenic seizure

1:.e&onstrate the neurological exa&ination of seizure11. escribe antiepileptic drugs

94 /0CT,20 .0SC2IPTI-N

*his topic is a part of %odule of *he Ner"ous Syste& integratedly designed for

&edical student of the 4thse&ester through *eaching,7earning Process in the th

-loc+ both in 7ecture and S&all roup iscussion. *his part of %odule 0ill

facilitate the student to ha"e an understanding and approach to the patient 0ith

seizure.

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I4 ItroductioA4 .e)iitios) seizure fro& the 7atin sacire;to ta+e possession of5 is the clinical &anifestationof an abnor&al( excessi"e( hypersynchronous discharge of a population of corticalneurons. #pilepsy is a disorder of the central ner"ous syste& characterized byrecurrent seizures unpro"o+ed by an acute syste&ic or neurologic insult.#pileptogenesis is the seuence of e"ents that turns a nor&al neuronal net0or+ intoa hyperexcitablenet0or+.


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cells or other inhibitory neurons.


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in6ury under conditions of excessi"e neuronal acti"ation such as status epilepticusand ische&ia5( potentially leading to cell death( a process ter&ed excitotoxicity. *heother &a6or type of gluta&ate receptor is the &etabotropic receptor( 0hichfunctions by &eans of receptor,acti"ated signal transduction in"ol"ing &e&brane,associated ,proteins . *here are at least 3 subtypes of &etabotropic receptors(based on differential agonist potency( &echanis& of signal transduction( and pre,

"ersus post,synaptic localization.#xperi&ental studies using ani&al epilepsy &odels ha"e sho0n that N%)( )%P)and +ainite agonists induce seizure acti"ity( 0hereas their antagonists suppressseizure acti"ity. %etabotropic agonists appear to ha"e "ariable effects li+elydependent upon their differentlocation and &echanis&s of signal transduction. *he&a6or inhibitory neurotrans&itter( )-)( interacts 0ith 2 &a6or subtypes ofreceptor/ )-)) and )-)- receptors. )-)) receptors are foundpostsynaptically( 0hile )-)- receptors are found presynaptically( and can thereby&odulate synaptic release. In the adult brain( )-)) receptors are per&eable to Cl,ionsA upon acti"ation Cl, influx hyperpolarizes the &e&brane and inhibits actionpotentials. *herefore( substances 0hich are )-)) receptor agonists( such asbarbiturates and benzodiazepines( are 0ell +no0n to suppress seizure acti"ity.

)-)- receptors are associated 0ith second &essenger syste&s rather than Cl,channels( and lead to attenuation of trans&itter release due to their presynapticlocation. *he second &essenger syste&s often result in opening of ED channels(leading to a hyperpolarizing current. Certain )-)- agonists( such as baclofen(ha"e been reported to exacerbate hyperexcitability and seizures.


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pair of &


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of the action potential burst( and then a rapid repolarization follo0ed byhyperpolarization. *his seuence is called the paroxys&aldepolarizing shift. *he bursting acti"ity resulting fro& the relati"ely prolongeddepolarization of the neuronal &e&brane is due to influx of extracellular CaDD(0hich leads to the opening of "oltage,dependent NaD channels( influx of NaD( andgeneration of repetiti"e action potentials. *he subseuent hyperpolarizing

afterpotential is &ediated by )-) receptors and Cl, influx( or by ED efflux(depending on the cell type.Seizure propagation( the process by 0hich a partial seizure spreads 0ithin the brain(occurs 0hen there is sufficient acti"ation to recruit surrounding neurons. *his leadsto a loss of surround inhibition and spread of seizure acti"ity into contiguous areas"ia local cortical connections( and to &ore distant areas "ia long associationpath0ays such as the corpus callosu&.

*he propagation of bursting acti"ity is nor&ally pre"ented by intacthyperpolarization and a region of surrounding inhibition created by inhibitoryneurons. >ith sufficient acti"ation there is a recruit&ent of surrounding neurons "iaa nu&ber of &echanis&s.


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reorganization follo0s in6ury and creates recurrent excitatory connections( "iaaxonal ?sprouting(@ bet0een neighboring dentate granule cells. %ore recently( it hasbeen proposed that the loss( rather than being of )-)ergic inhibitory neurons( isactually of excitatory neurons 0hich nor&ally sti&ulate the inhibitory interneuronsto( in turn( inhibit the dentate granule cells. *hese &echanis&s of hyperexcitabilityof the neuronal net0or+ are not &utually exclusi"e( could act synergistically( and

&ay coexist in the hu&an epileptic brain. Seizures &ay also appear to arise fro&0idespread cortical areas "irtually si&ultaneously. *he &echanis&sunderlying such generalized seizures are uncertain. Bne type of generalized seizure(the absence seizure( also called petit &al5 is a generalized seizure consistingclinically of a brief staring spell in con6unction 0ith a characteristic burst of spi+e,0a"e co&plexes on the ##. eneralized spi+e0a"e discharges in absence seizures&ay result fro& aberrations of oscillatory rhyth&s that are nor&ally generatedduring sleep by circuits connecting the cortex and thala&us. *his oscillatorybeha"ior in"ol"es an interaction bet0een )-)- receptors( CaDD channels and EDchannels located 0ithin the thala&us. Phar&acologic &odulation of these receptorsand channels can induce absence seizures( and there is speculation that geneticfor&s of absence epilepsy &ay be associated 0ith &utations of co&ponents of this

syste&.

C4 0ileto;eesis: The Tras)ormatio o) a Normal Net*ork Ito a3yere=cita


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clinical presentations. *hese are principally/ 7oss of a0areness

eneralised con"ulsi"e &o"e&ents

rop attac+s

*ransient focal &otor attac+s

*ransient focal sensory attac+s =acial &uscle and eye &o"e&ents

Psychic experiences

)ggressi"e or "ocal outbursts

#pisodic pheno&ena in sleep

Prolonged confusional or fugue states

*he principal differential diagnoses for each presenting clinical scenario follo0 0ithbrief explanatory text the +ey diagnostic features of each diagnosis. It is notunco&&on for a patient to co&e to &edical attention after a dra&atic e"ent( butnot to do so after &inor episodes. nderstanding the occurrence and nature of&inor e"ents is crucial to &a+ing an accurate diagnosis. ) chec+list of sy&pto&s tospecifically enuire for is gi"en in *able 1.

'a"e there been any spontaneous and other0ise unexplained paroxys&al sy&pto&sJ

In particular/Sudden fallsIn"oluntary 6er+y &o"e&ents of li&bs 0hilst a0a+e-lan+ spellsnexplained incontinence of urine 0ith loss of a0areness( or in sleepBdd e"ents occurring in sleep( e.g. fall fro& bed( 6er+y &o"e&ents( auto&atis&s#pisodes of confused beha"iour 0ith i&paired a0areness( recollection

Possible si&ple partial seizures

#pigastric rising sensationK6L "uPre&onition=ear#lation( epressione,personalization( derealizationInability to understand or express language 0ritten or spo+en57oss of &e&ory( disorientationBlfactory( gustatory( "isual( auditory hallucination=ocal &otor or So&atosensory deficit( or positi"e sy&pto&s 6er+ing( tingling5.

Tahate"er the cause the patient &ay ha"e a&nesia for both the e"ent and its exactcircu&stances. *he three &ain causes are/ syncope( epilepsy( and cardiacarrhyth&ias. *ransient cerebral ischae&ia due to "ascular abnor&alities is lessco&&on. %icrosleeps "ery short dayti&e naps5 &ay occur 0ith any cause of se"eresleep depri"ation or disruption. Bther causes of diagnostic confusion are &uch rarerand include/ hypoglycae&ia or other inter&ittent &etabolic disorders( structuralano&alies of the s+ull base affecting the brainste&( or lesions affecting the CS=


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circulation.

SyncopeSyncope is the co&&onest cause of episodes of loss of a0areness. Si&plefaints or "aso"agal syncopal attac+s can usually be related to identifiableprecipitants. %ost often they occur on getting up uic+ly( or standing forprolonged periods( particularly if associated 0ith peripheral "asodilation e.g.during hot( stuffy 0eather( cro0ded trains or roo&s( or are related to drug oralcohol use5. =rightening( e&otional or unpleasant scenes( and painful sti&uli&ay also be triggers( due to increased "agal acti"ity. *here are "arious othercauses of syncopal attac+s( and classification depends on ter&inology. Coughand &icturition syncope are 0ell recognised. Changes in intrathoracicpressure cough syncope5( i&paired baroreceptors due to athero&aof the carotid carotid sinus syncope5( cardiac arrhyth&ias( or autono&icdisturbances &ay also lead to cerebral hypoperfusion and fainting. )s these&ay not be due to "aso"agal reflex changes( the typical aura of a "aso"agalsyncope &ay not be present.

#pilepsySe"eral types of seizure &ay present 0ith loss of a0areness as the solereported feature. *hese include absences( co&plex partial( tonic or atonicseizures. *ypical absences in"ol"e arrest of acti"ity( reduced or losta0areness( eyelid blin+ing or t0itching( and so&eti&es s&all &yoclonic facialor li&b 6er+s( or brief facial auto&atis&s such as lip s&ac+ing or che0ing.

*ypical absences are usually brief but often occur &any ti&es per day. *here&ay also be isolated &yoclonic 6er+s. )tonic seizures usually gi"e rise to dropattac+s but &ay appear to cause blan+ spells if the patient is sat or layingdo0n and so cannot fall. Co&plex partial seizures &ay cause loss ofa0areness 0ith fe0 if any other features. etailed enuiry &ust al0ays be

&ade for any associated psychic or &otor pheno&ena that &ay raise thepossibility of a seizure disorder.

Cardiac disorders*here are often prodro&al features si&ilar to si&ple syncope( as 0ell aspalpitations( chest pain( shortness of breath or other features ofcardio"ascular insufficiency. )ttac+s due to transient co&plete heart bloc+are abrupt and short 0ith rapid loss of consciousness. 7ac+ of cardiac output&ay be due to short episodes of "entricular tachycardia or fibrillation.Prolongation of the M* inter"al &ay lead to such e"ents. )ttac+s &ay bepreceded by palpitations( extre&e fatigue or presyncopal features. %itral"al"e prolapse and aortic stenosis &ay present 0ith episodic loss of

a0areness due to fluctuating cardiac output or associated arrhyth&ias. )orticstenosis and hypertrophic cardio&yopathy is especially prone to present 0ithepisodes of sudden collapse 0ith loss of a0areness during exercise.

%icrosleeps)ny cause of sleep depri"ation &ay lead to brief day,ti&e naps( so&eti&eslasting for only a fe0 seconds. I&paired uality of sleep &ay also be a factor.

*he &ost i&portant is obstructi"e sleep apnoea. Narcolepsy can present 0ith

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short periods of suddenly falling asleep during the day.

Panic attac+sPanic attac+s usually present 0ith feelings of fear and anxiety( associated0ith autono&ic changes and hyper"entilation. *his leads to dizziness orlightheadedness( orofacial andor peripheral paraesthesia 0hich &ay beasy&&etric5( carpopedal spas&( t0itching of the peripheries( blurred "ision(or nausea. Bccasionally these preludes &ay be forgotten( and attac+s present0ith loss of a0areness. Bften( but not al0ays( there is a clear precipitant(such as a particular situation. None of these features are consistent( ho0e"er(and differentiation fro& epilepsy can be difficult.

'ypoglycae&ia'ypoglycae&ic attac+s causing loss of consciousness are extre&ely rareexcept in patients 0ith treated diabetes &ellitus. Gery occasional cases &aybe seen due to insulin secreting tu&ours. In such cases there &ay be ahistory of a &issed &eal prior to the attac+.

Bther neurological disordersIf a head in6ury causes loss of consciousness( there is a&nesia. In accidentalhead in6ury( particularly road traffic accidents( it &ay be difficult todistinguish a&nesia caused by the in6ury fro& cases in 0hich there 0as a lossof consciousness that caused the accident. Isolated episodes of loss ofa0areness &ay also be caused by abuse of psychotropic drugs or othersubstances. Bccasionally( structural CNS abnor&alities &ay present 0ithepisodes of loss of a0areness.

Non,epileptic attac+ disorder N#)5Non,epileptic attac+ disorder( pre"iously +no0n as pseudoseizures typically

gi"es rise episodes of t0o broad types/a5 attac+s in"ol"ing &otor pheno&enab5 attac+s of lying &otionless.

*he latter are often prolonged( continuing for se"eral &inutes or so&eti&es hours.Such beha"iour is "ery rare in epileptic seizures/ there 0ill nearly al0ays be otherpositi"e pheno&ena in epileptic attac+s that last for &ore than a fe0 &inutes. Inaddition( attac+s are often triggered by external e"ents or stress. Patients 0ithN#) often ha"e a history of abnor&al illness beha"iour. Non,epileptic attac+disorder is &uch co&&oner in fe&ales than &ales( and usually co&&ences inadolescence or early adulthood see*able 25.

#pileptic attac+ N#)Precipitating cause hen alone or asleep Co&&on %ay be reportedBnset sually short %ay be short or o"er se"eral &inutes)ura Garious( usually stereotyped =ear( panic( altered &ental stateSpeech Cry( grunt at onsetA &uttering( 0ords

in auto&atis&s Se&i,"oluntary( often unintelligible%o"e&ent )tonic( tonicA if clonic( )synchronous flailing of li&bsA pel"ic

synchronouss&all a&plitude 6er+s thrustingA opisthotonousIn6ury *ongue biting( fallA directed "iolence %ay bite tongue( chee+s( lip( hands(


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subtle &o"e&ents 0hich &ay be difficult to differentiate fro& co&plex partialseizures.

'ypere+plexia)ttac+s are characterised by excessi"e startle( &ay cause stiffening( andcollapse 0ith a sudden 6er+ of all four li&bs. )ttac+s are pro"o+ed by suddenunexpected sti&uli( usually auditory. 'ypere+plexia needs to be distinguishedfro& seizures induced by startle.

Non,epileptic attac+ disorder N#)5Non,epileptic attac+s in"ol"ing pro&inent &otor pheno&ena are co&&onerthan those 0ith arrest of acti"ity. %o"e&ents are "aried but often in"ol"ese&i purposeful thrashing of all four li&bs( 0axing and 0aning o"er &any&inutes( distractibility or interaction 0ith the en"iron&ent( pro&inent pel"ic&o"e&ents and bac+ arching *able 25. Non epileptic attac+s &ay be difficultto differentiate fro& co&plex partial seizures of frontal lobe origin( 0hich canpresent 0ith "ery bizarre &otor attac+

"4"4$ .ro attacks)ny cause of loss of a0areness &ay proceed to a sudden collapse or drop attac+.#pilepsy( syncope and other cardio"ascular disorders are the co&&oner causes ofdrop attac+s.

#pilepsiesSudden drop attac+s are co&&on in patients 0ith learning disabilities andsecondary generalised epilepsies. *he falls &ay be tonic or atonic.

Cardio"ascularIf cerebral hypoperfusion is sufficient to cause sudden collapse there is

usually loss of a0areness see abo"e5. Syncope and cardiac abnor&ality arerare causes of a presentation 0ith drop attac+s.

%o"e&ent disorders%ost &o"e&ent disorders that cause drop attac+s ha"e other &orepro&inent features 0hich &a+e the diagnosis clear e.g. Par+insons disease5.Paroxys&al +inesogenic choreoathetosis &ay cause drop attac+s if there islo0er li&b in"ol"e&ent.

-rainste&( spinal or lo0er li&b abnor&alities*here are usually fixed neurological signs. *u&ours of the third "entricle &aypresent 0ith sudden episodes of collapse. Spinal cord "ascular abnor&alities

&ay present 0ith lo0er li&b 0ea+ness leading to falls 0ithout i&pair&ent ofa0areness.

CataplexyCataplexy usually occurs in association 0ith narcolepsy( although it &ay bethe presenting clinical feature. *here is no loss of consciousness 0ith attac+s.

)ttac+s &ay be precipitated by e&otion( especially laughter. Bftenthere is only loss of tone in the nec+ &uscles( 0ith slu&ping of the head


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rather than co&plete falls.

%etabolic disordersPeriodic paralysis due to sudden changes in seru& potassiu& is rare. *hecondition &ay be fa&ilial or associated 0ith other endocrine disorders ordrugs. sually there is a gradual onset( and the attac+s last for hours.

Idiopathic drop attac+s*hese attac+s are &ost co&&on in &iddle aged fe&ales. *hey ta+e the for&of a sudden fall 0ithout loss of consciousness. Characteristically the patientsre&e&ber falling and hitting the ground.


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*ransient cerebral ischae&ia*ransient ischae&ic attac+s *I)s5 usually present 0ith negati"e pheno&ena(i.e. loss of use of a li&b( he&iplegia or other deficits( although positi"epheno&ena such as paraesthesiae &ay occur. *ransient ischae&ic attac+s&ay last for a fe0 &inutes( but &ay persist for up to 24 hours. *I)s are notusually stereotyped or repeated 0ith the freuency of epileptic seizures( andthere are usually associated features to suggest "ascular disease.

*onic spas&s of &ultiple sclerosis*hese spas&s usually occur in the setting of +no0n &ultiple sclerosis( but&ay be the presenting feature( although other e"idence of &ultiple sclerosis&ay be found on exa&ination and in"estigation. *he spas&s &ay last forse"eral seconds( so&eti&es longer than one &inute.

Paroxys&al &o"e&ent disordersParoxys&al +inesogenic choreoathetosis &ay present 0ith focal &otorattac+s that are "ery si&ilar to epileptic e"ents. *re&or &ay occur in a"ariety of &o"e&ent disorders and is usually sufficiently persistent toelucidate the nonepileptic nature( but &ay be difficult to distinguish fro&certain for&s of epilepsia partialis continua. %yoclonus of subcortical origin&ay be suspected fro& the distribution of in"ol"ed &uscles e.g. spinal&yoclonus &ay be restricted to specific seg&ents( either unilateral orbilateral5. Peripheral ner"e entrap&ent usually presents 0ith 0ea+ness butoccasionally can present 0ith episodic 6er+s or t0itches.

"4"46 Trasiet )ocal sesory attacks

So&atosensory attac+s#pileptic seizures in"ol"ing the pri&ary sensory cortex are less co&&on than&otor seizures( and &ay cause spreading paraesthesia. Seizures in"ol"ingthe second sensory areas or &esial frontal cortex &ay cause sensoryillusions. *here are usually other epileptic features due to in"ol"e&ent ofad6acent or related brain structures. *ransient sensory pheno&ena &ay alsobe seen in peripheral ner"e co&pression or other abnor&alities of theascending sensory path0ays( hyper"entilation or panic attac+s and in *I)s.

*I)s are not usually stereotyped or repeated 0ith the freuency of epilepticseizures( and there are usually associated features to suggest "asculardisease.7esions of sensory path0ays cause persistent sy&pto&s( but diagnostic

confusion &ay arise in the early natural history( 0hen co&plaints areinter&ittent( or if they are posture related. 'yper"entilation &ay beassociated 0ith localised areas of paraesthesia e.g. one ar&5. Inter&ittentsensory illusions &ay be experienced in relation to a&putated or anaestheticli&bs. %igrainous episodes &ay also cause localised areas of paraesthesia(but usually ha"e the distinction of a gradual e"olution of sensory pheno&ena(both positi"e and negati"e( and associated features of &igraine.


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*ransient "estibular sy&pto&s)cute attac+s of "ertigo &ay occasionally be due to a seizure in parietal orte&poral lobes. In these cases there are generally associated features thatpoint to cerebral in"ol"e&ent( such as a focal so&atosensory sy&pto&s( de6a"u or disordered perception. Peripheral "estibular disease is a &uch &oreco&&on cause and &ay gi"e rise to paroxys&al rotational "ertigo andperception of linear &otion and there are often also other sy&pto&s ofauditory and "estibular disease such as/ deafness( tinnitus( pressure in theear and relation to head position.

Gisual sy&pto&s%igraine is a co&&on cause of episodic "isual pheno&ena. *he e"olution isusually gradual( o"er se"eral &inutes( 0ith fortification spectra( andassociated photophobia( nausea and headache. #pileptic pheno&ena areusually &uch shorter( e"ol"ing o"er seconds( and the "isual hallucinations are&ore co&&only of coloured blobs( rather than 6agged lines.

"4"47 (acial muscle ad eye movemets

Changes in facial &o"e&ents &ay occur in "arious neurological conditions includingfocal &otor seizures( co&plex partial seizures 0ith auto&atis&s( tics( dystonias orotherparoxys&al &o"e&ent disorders( especially drug induced dys+inesias andhe&ifacial spas&( as 0ell as psychological disorders.

Partial seizures-enign rolandic epilepsy usually presents 0ith seizures in childhood affecting

theface( often 0ith unilateral gri&acing( he&icorporeal sensory and &otorpheno&ena( or secondarily generalised seizures occurring in sleep. =ocal

&otorseizures &ay cause t0itching of one side of the face that &ay be restricted tospecific areas. #ye de"iation &ay be seen 0ith seizures arising in frontal(parietal or occipital cortex.Co&plex partial seizures &ay cause auto&atis&s 0ith lip s&ac+ing( che0ing(s0allo0ing( sniffing or gri&acing( 0ith a&nesia and i&paired a0areness. Ifthesefeatures are due to seizure acti"ity the attac+s are usually relati"elyinfreuent( 0hereas 0ith dystonia or other &o"e&ent disorders episodes areli+ely to occur &any ti&es per day.

%o"e&ent disorders

'e&ifacial spas& typically presents in the elderly or &iddle aged 0ithclusters of

attac+s that initially in"ol"e the eye but subseuently spread to the rest ofthat side of the face. =acial 0ea+ness &ay de"elop that persists bet0eenattac+s.-ruxis& &ay occur either during the day or in sleep( especially in children0ith learning disability. #pisodes are usually &ore prolonged than 0ith theauto&atis&s of co&plex partial seizures( and there are no associated

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features tosuggest an epileptic basis.)s 0ith dystonia and other &o"e&ent disorders affecting the face there &aybe e"idence of in"ol"e&ent else0here( and attac+s are usually &ore freuentthan is seen 0ith isolated seizures.

Bther neurological disordersefects of eye &o"e&ent control are co&&on in patients 0ith a 0ide rangeof neurological disorders. *here are usually associated features that indicatea nonepileptic basis. -izarre eye &o"e&ents also occur in blindness and &aybe &ista+en for epileptic acti"ity. Careful exa&ination is reuired to ascertainthe precise features of the eye &o"e&ent disorder( and in particular anyprecipitating factors or features of cerebellar or brainste& disease.

"4"49 Psychic e=erieces

Inter&ittent psychic pheno&ena can be seen in partial seizures especially ofte&poral lobe origin5( &igraine( panic attac+s( transient cerebral ischae&ia( druginduced flashbac+s( or 0ith illusions associated 0ith loss of a sensory &odality as0ell as psychotic illnesses.

#pilepsyPartial seizures of te&poral lobe origin are especially li+ely to be &anifest byauras in"ol"ing psychic pheno&ena. *he &ost co&&on are fear( de6a "u(&e&ory flashbac+s( "isual( olfactory or auditory hallucinations. Bther&anifestations include altered perception of the en"iron&ent 0ith adistancing

fro& reality or change in size or shape of ob6ectsA altered language functionAe&otions such as sadness( elation( and sexual arousal.Psychic experiences &ay ha"e so&e relation to past experiences. *hey areusually recalled as brief scenes( so&eti&es strung together. *hey usually lac+clarity( for exa&ple a patient &ay describe an illusion of so&eone standing infront of the& 0ho they +no0( but they cannot na&e the& or describe the& indetail. ) rising epigastric sensation &ay occur alone or in association 0ithsuch experiences. #le&ental "isual pheno&ena( such as flashing lights( are&ore often seen in occipital lobe epilepsy. )ltered thought patterns &ay beseen in both te&poral and frontal lobe seizures.

%igraine

%igrainous psychic pheno&ena &ay in"ol"e an initial heightening ofa0areness. *he principal features are usually "isual illusions that &ay beele&ental or co&plex. *hey rarely ha"e the sa&e intense e&otionalco&ponents of te&poral lobe illusions or hallucinations. *he ti&e course isusually &ore prolonged than 0ith partial seizures( and there are associatedfeatures of a pounding headache( photophobia and nausea or "o&iting. *here&ay be recognized precipitants( and there is often a rele"ant fa&ily history.

Panic attac+s


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*hese are usually associated 0ith feelings of fear and anxiety.'yper"entilation &ay lead to dizziness and light,headedness. *here are oftenunpleasant abdo&inal sensations si&ilar to the epigastric aura of partialseizures. *he e"olution( associated increases in heart rate and respiration(longer ti&e course and history of precipitating factors generally &a+e thediagnosis clear.

rug induced flashbac+s*hese share &any of the ualities of psychic te&poral lobe seizures. *hey areindi"idualised hallucinations usually related to the circu&stances of the drugabuse( often 0ith e&otional content of fear or anxiety. ) careful historyshould be ta+en for substance abuse( especially 7S and &escaline.

'allucinations or illusions caused by loss of a pri&ary sense'allucinations and illusions of an absent li&b are 0ell recognised ina&putees. Si&ilarly( people 0ho lose sight either in the 0hole or part field&ay experience "isual hallucinations or illusions in the blind field. Suchpheno&ena can be ele&ental or co&plex and include e"ol"ing scenes.Si&ilar experiences can occur 0ith deafness.

Such experiences due to the loss of a pri&ary sense present particulardiagnostic difficulty 0hen they occur in the setting of a structural lesion 0hichcould result in both pheno&ena. )n occipital infarction( for exa&ple( couldcause "isual loss and could also gi"e rise to epileptic seizures. Bften thehallucinations due t sensory loss are &ore prolonged( lasting for &inutes orhours( but can be brief.

Psychotic hallucinations and delusions'allucinations and delusions are the hall&ar+ of psychotic illnesses. *he

follo0ing features 0ould suggest a psychiatric rather than epileptic basis/co&plex nature 0ith an e"ol"ing or argued the&e( auditory nature in"ol"inginstructions or third person language( paranoid content or associated thoughtdisorder. Psychotic episodes are usually &ore long lasting than isolatedepileptic seizures( although inter&ittent psychosis &ay ha"e a si&ilar ti&ecourse to noncon"ulsi"e status.Persistent &ood changes &ay be a helpful guide( but e"en short te&porallobe seizures &ay be follo0ed by &ood changes lasting for hours or days.=urther&ore( flurries of epileptic attac+s &ay the&sel"es cause an organicpsychosis lasting for se"eral days.


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"4"4@ A;;ressive or vocal outhole body 6er+s co&&only occur in nor&al sub6ects on falling asleep.=rag&entary physiological &yoclonus usually in"ol"es the peripheries or theface( and occurs during stages 1 and 2 and


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Bther epilepsiesSeizures arising in other brain regions &ay present 0ith nocturnal attac+s.Patients &ay be aroused by an aura( although often this is not recalled 0henattac+s arise fro& sleep. Co&plex auto&atis&s( in 0hich patients get out ofbed and 0ander around &ay cause confusion 0ith paraso&nias. >ithnocturnal seizures of any type the partner is freuently a0o+en by particularco&ponents( such as "ocalisation and does not 0itness the onset.

eneralised tonic,clonic seizures not unco&&only occur on or shortlyafter a0a+ening.

Pathological frag&entary &yoclonus#xcessi"e frag&entary &yoclonus persisting into sleep stages 3 and 4 &aybe seen 0ith any cause of disrupted nocturnal sleep.


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seen in association 0ith drugs e.g. tricyclics5 or alcohol( or central ner"oussyste& diseases such as &ultisyste& atrophy. *he possibility of


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)lthough usually &ore sustained( psychiatric disorders &ay present 0ithepisodes of delusions( hallucinations or apparent confusion( lasting for hoursor days.

*ransient global a&nesia*hese episodes typically co&&ence acutely( and last for &inutes or hoursand in"ol"e both retrograde and anterograde a&nesia. Patients &ayperfor& co&plexacti"ities( but after0ards ha"e no recall of the&. *here is alac+ of other neurological features to the attac+s( and consciousness appearsto be preser"ed. *he attac+s &ay in"ol"e bilateral &edial te&poraldysfunction 0hich in so&e patients &ay be on the basis of ischae&ia( 0hilstso&e &ay ha"e an epileptic basis.

'ysterical fugue) fugue state &ay arise 0ithout an organic physical cause( as a con"ersionsy&pto&. *hese episodes &ay be brief or "ery prolonged( lasting for days ore"en 0ee+s. If seen at the ti&e of an episode inconsistencies are often foundon exa&ination of the &ental state. In so&e cases( the uestion of&alingering arises( &ost co&&only in a situation in 0hich the persons statepre"ents uestioning by 7a0 Bfficers. *he diagnosis is &ore difficult toidentify if the patient is only seen subseuently. *he &atching of 0itnessaccounts and the apparent seuence of e"ents is essential( but it &ay re&aindifficult to co&e to a fir& conclusion. In this situation( there is so&eti&es aforensic aspect( typically 0hen the person concerned is alleged to ha"eco&&itted a cri&e and they profess to ha"e no &e&ory of the e"ents. )chec+list of possible seizure,related sy&pto&s to enuire for 0henconsidering a possible diagnosis of epilepsy can be found in *able 1.

4 .i))eretial dia;osis o) eilesy i childre

*here are a range of possibilities in the differential diagnosis 0hen considering thechild 0ith a Qfunny turn. *he considerations 0ill "ary depending on certain +eyfeatures of the e"ent( as 0ell as the age of the child. *he history is +ey to anydiagnosis( and is li+ely to be far &ore useful than any in"estigation that can bereuested. )l0ays see+ the initial e"ent R a trigger or 0arning( ho0e"er young thechild. *here &ay be a typical beha"ior prior to any e"ent or a slightly older child&ay be able to relate a feeling prior to or during the e"ent. ) description of eachchange in the child should be sought( and the e"idence of loss or not of a0areness.Bther i&portant aspects of the history are &edications ta+en( de"elop&entalhistory and past &edical history but infor&ation fro& these 0ill only besupple&entary to the history of the e"ents the&sel"es. *here are a nu&ber ofpossibilities 0ithin the differential diagnosis of epilepsy in childhoodA ho0e"er a lac+

of a0areness of such alternati"es re&ains the &a6or reason for error and thepre&ature( possible &isdiagnosis( of epilepsy. *he follo0ing is a classification ofpossibilities( although not exhausti"e.

Sycoe & related disorders

isorders of orthostatic control


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Q=ainting lar+

pper air0ay obstruction

Cardiac syncope )rrhyth&ias

Co&plete heart bloc+

>olf par+inson 0hite

-rugada syndro&e

-rainste& syncope *u&our-rain ste& herniation or co&pression

Bther 'ypere+plexia

)noxic epileptic seizures

Neurolo;ical *ics

%yoclonus

Paroxys&al dystonia

Sandifers syndro&e

Paroxys&al dys+inesias

Cataplexy

-enign paroxys&al "ertigotorticollis

%igraine

)lternating he&iplegia

#ye &o"e&ent disordersB"erflo0 &o"e&ents

Behaviouralsychiatric aydrea&s

issociati"e states

Self gratification beha"iour

'yper"entilation

Panicanxiety

Non epileptic attac+ disorder

=abricated attac+s

Pseudosyncope

Stereotypiesritualistic beha"ior

Parasomias Sleep &yoclonus

'eadbanging

Confusional arousal


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"ither repetitive short duration over short period or #ith greater duration bet#een.Repetitive $er%s may imply sei&ures, although only from sleep may be sleepmyoclonus. Repetitive spasms #ill be stereotyped, in clusters. 'udden sustainedhypertonia may give a clue to hypere%plexia or brainstem syncope

)re se&i,purposeful &o"e&ents seen at any ti&eJ This may give a clue as to the

state of a#areness

>hat parts of the body are in"ol"ed in the &o"e&entsJ !or example, #hole body,eyes vs limb, all limbs vs single(multiple

Is there a beha"iour changeJoes the child stare unresponsi"elyJ)s eye movement seen in association #ith this* an they be distracted*

Is the child distressedJ)f so intermittently or continuously* +istress may suggest a#areness, particularly inbet#een spasms during clusters

Is there apparent fearJf course that may be manifest by distress, and therefore an apparent a#arenessof #hat is happening

M-.,/ S0I1,20 !"$ 6


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Is the e"ent characterised by other pheno&enaJIs there a colour changeJallor or cyanosis may be seen in cardiac arrythmias cyanotic attac%s arecommonly associated #ith reflux. !lushing may be seen #ith repetitivemovement in self gratification behavior

Is there a change in breathing patternJ+eep(stertorous breathing #ith loss of a#areness may be seen in generalisedsei&ures, compared #ith retained a#areness in self gratification behaviours.

Can the e"ent be interruptedJ)f so, then the event is probably a partial sei&ure or N"A+. )f the event cannotbe interrupted, then possibly a generalised sei&ure.

2.2 In the toddler (aged 1 to 3 years) Is the e"ent related to any particular acti"ityJ

'leep or #a%ing state parasomnias are very common at this age andin some instances mimic sei&ures. Night terrors usually occur at aspecific time each night, and during #hich the child may appearunreachable. onfusional arousals may also cause alarm as the child isinaccessible

Adverse(noxious events if the event is al#ays triggered by thisconsider

breath holding(reflex anoxic sei&ures

!ever as in febrile sei&ures

Movement / as in paroxysmal dys%inesias

!eeding / as in 'andifers syndrome

"xcitement / as in overflo# movements

Note stereotypic movements(ritualistic behaviours may be seen inchildren

#ith developmental delay(communication disorders at any time, butxcitement(stress or boredom

"motion / as in cataplexy

>hat is the &a6or &otor co&ponentJ, Is a fall the &a6or co&ponent of the e"entJ, Is the &a6or &otor co&ponent apparent hypertonia( hypotonia or dystoniaJ

o 0ypertonia consider reflex(epiratory syncope, tonic(tonic clonic

sei&ure, hypere%plexia


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o 0ypotonia consider syncope, cataplexy, 1a%inetic2 drop attac% although

thelatter unli%ely to occur in the absence of other sei&ure typeso +ystonia consider dys%inesia, benign paroxysmal torticollis 3BT4o 5nsteadiness consider benign paroxysmal vertigo 3B64, intermittent

ataxia

, Is this &o"e&ent repetiti"e or sustainedJo "ither repetitive short duration over short period or #ith greater

duration bet#een. Repetitive $er%s may imply sei&ures. Althoughrepetitive shortmovements predominantly of the face may be tics

, )re se&i,purposeful &o"e&ents seen at any ti&eJ, This may give a clue as to the state of a#areness, >hat parts of the body are in"ol"ed in the &o"e&entsJ, !or example, #hole body, eyes vs limb, all limbs vs single(multiple

Is there a beha"iour changeJ, oes the child stare unresponsi"elyJ

o

)s eye movement seen in association #ith this* an they bedistracted*, Is the child distressedJ

o )f so intermittently or continuously*

, Is there apparent fearJo f course that may be manifest by distress, and therefore an apparent

a#areness of #hat is happening.

Is the e"ent characterised by other pheno&enaJ, Is there a colour changeJ

o allor or cyanosis may be seen in cardiac arrythmias cyanotic attac%s

are commonly associated #ith expiratory apnoeic 3breath holding4

attac%s. !lushing may be seen #ith self gratification behaviour., Is there a change in breathing patternJ

o "ither an increase or decrease may give a clue to the above.

, Can the e"ent be interruptedJ

2.3 In the older child (aged 3 to 12 years)

Is the e"ent related to any particular acti"ityJ, 'leep or #a%ing state parasomnias are very common at this age and in

some instances mimic sei&ures., Movement / as in paroxysmal dys%inesias, "xcitement / as in overflo# movements

, Note stereotypic movements(ritualistic behaviours may be seen in children#ith developmental delay(communication disorders at any time, but

particularly excitement(stress or boredom., "motion / as in cataplexy

>hat is the &a6or &otor co&ponentJ, Is a fall the &a6or co&ponent of the e"entJ

M-.,/ S0I1,20 !"$ 9


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, Is the &a6or &otor co&ponent apparent hypertonia( hypotonia or dystoniaJo 0ypertonia consider reflex(epiratory syncope, tonic(tonic clonic

sei&ure, hypere%plexiao 0ypotonia consider syncope, cataplexy, 1a%inetic2 drop attac% although

thelatter unli%ely to occur in the absence of other sei&ure types

o +ystonia consider dys%inesiao 5nsteadiness consider intermittent ataxia

, Is this &o"e&ent repetiti"e or sustainedJ

o "ither repetitive short duration over short period or #ith greater

duration bet#een. Repetitive $er%s may imply sei&ures. Althoughrepetitive short movements predominantly of the face may be tics

, )re se&i,purposeful &o"e&ents seen at any ti&eJo This may give a clue as to the state of a#areness although older child

li%ely to be able to relay information about event, >hat parts of the body are in"ol"ed in the &o"e&entsJo !or example, #hole body, eyes vs limb, all limbs vs single(multiple

Is there a beha"iour changeJ, oes the child stare unresponsi"elyJ

o )s eye movement seen in association #ith this* an they be distracted

/ by touch rather than voice alone* The most common cause of 1blan%spells2 remains daydreaming. Typical absence sei&ures occur relativelyfre7uently,at any time and are of short duration 38-9: seconds4

, Is there apparent fearJ, Is there aggressi"edestructi"e beha"iourJ

o True 1rage2 attac%s in isolation are rarely, if ever epileptiform in origin.Typically they are seen in children #ith learning difficulties, but are notunseen in children #ith very specific learning problems that have not

yet been recognised. The children may become aggressive anddestructive, have little, if any recollection of the event

, Is the e"ent characterised by other pheno&enaJ, Is there a colour changeJ

o allor or cyanosis may be seen in cardiac arrythmias. allor is li%ely to

be seen in association #ith any syncope. !lushing may be seen #ithself gratification behavior

, Is there a change in breathing patternJo "ither an increase or decrease may give a clue to the above

, Is there "isual sy&pto&atologyJo 6isual disturbance, if so at #hat stage of the event / may suggest

primaryor secondary phenomenon. ;hat is the character of such 3repeated4stereotyped colours or formed ob$ect li%ely to be sei&ure late distortedvision* secondary.

, )re there sensory sy&pto&sJo )f so, then maybe partial sei&ure, or paraesthesias due to other causes


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, Is there "ocalisationJo Audible #ords or nonsense* At #hat stage of the event* +irected

speech(vocal outbursts are unli%ely to be epileptic., Can the e"ent be interruptedJ

o )f so unli%ely to be a sei&ure.

V4 INV0STI'ATI-NS IN 0PI/0PTIC S0I1,20

Infor&ation should be pro"ided to children( young people and adults and fa&iliesandor carers as appropriate on the reasons for tests( their results and &eaning( thereuire&ents of specific in"estigations( and the logistics of obtaining the&.)llin"estigations for children should be perfor&ed in a child,centred en"iron&ent.

0lectroecehalo;ram >00'?

Children( young people and adults reuiring an ## should ha"e the test perfor&edsoon after it has been reuested. )n ## should be perfor&ed only to support adiagnosis of epilepsy in adults in 0ho& the clinical history suggests that the seizureis li+ely to be epileptic in origin. *he ## should not be used to exclude a diagnosisof epilepsy in a child( young person or adult in 0ho& the clinical presentationsupports a diagnosis of a non,epileptic e"ent. )n ## &ay be used to helpdeter&ine seizure type and epilepsy syndro&e in children( young people and adultsin 0ho& epilepsy is suspected. *his enables the& to be gi"en the correct prognosis.=or children( young people and adults in 0ho& epilepsy is suspected( but 0hopresent diagnostic difficulties( specialist in"estigations should bea"ailable.

M-.,/ S0I1,20 !"$


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Neuroima;i;

Neuroi&aging should be used to identify structural abnor&alities that cause certainepilepsies. %


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recurrence5. In general ter&s( therefore( the pri&ary ob6ecti"e of treat&ent shouldbe co&plete seizure control 0here this is feasible. *his( ho0e"er( should not beachie"ed at all costs. )ntiepileptic drugs can produce se"ere ad"erse effects(particularly 0hen they are ad&inistered at high dosages or in co&bination( and thesituation should ne"er arise 0here a patient is &ade to suffer &ore fro& thead"erse effects of treat&ent than fro& the sy&pto&s of the disease. >hene"er

co&plete seizure freedo& pro"es to be a non,realistic goal( opti&al treat&entshould result fro& the best co&pro&ise bet0een the desire to &ini&ize seizurefreuency and the need to &aintain ad"erse effects 0ithin acceptable li&its.

4 2eductio o) seizure severity

)lthough &ost outco&e studies in epilepsy ha"e focused on seizure freuency(seizure se"erity( particularly 0ith respect to occurrence of potentially in6urious ictal&anifestations( is by itself an i&portant deter&inant of uality of life. In patients0hose seizures cannot be controlled co&pletely( it &a+es sense to ai& atsuppressing preferentially those seizures 0hich are &ost dis, abling. )ssessing the&ost dis, abling seizure types can reuire assistance fro& an external obser"er( but

the patients perceptions are &ore i&portant. ) seizure co&ponent that &ayappear tri"ial or negligible to an obser"er &ay be percei"ed as "ery distressing bythe patient.

$4 Avoidace o) adverse e))ects

*he prescription of antiepileptic &edication entails a significant ris+ of ad"erseeffects. >hile &any patients 0ith recently diagnosed epilepsy can be controlled atlo0 dosages( 0hich produce only &odest detectable toxicity( patients 0ith se"ereepilepsies &ay ha"e to pay a significant price in ter&s of ad"erse effects to a"oid or&ini&ize seizure recurrence.

%4 Suressio o) su


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death in epilepsy S#P5.

74 Addressi; co5morhile these ris+ factors need to be discussedand appropriate counselling gi"en( it is eually i&portant to a"oid undue restrictionson the patients lifestyle. =or exa&ple( alcohol abuse should be acti"elydiscouraged( but there is no reason to prohibit one glass of beer or 0ine at &eal

ti&es. In general( patients should be encouraged to li"e a nor&al life( 0hile a"oid,ing extre&e de"iations fro& 0hat 0ould be considered a regular lifestyle.

Prescription of &edication should also be ai&ed at &ini&izing interference 0ithdaily acti"ities. )ntiepileptic drugs 0hich can be gi"en once or t0ice daily are lessli+ely to obstruct daily rou, tines and to cause psychosocial e&barrass&ent( andthey are associated 0ith a better co&pliance. =or drugs 0hich can be gi"en once ort0ice daily but do not ha"e a long half,life( a t0ice,daily schedule &ay be preferablebecause it &ini&izes the ad"erse conseuences of &issing one dose. In general(


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once,daily dosing does not entail better co&pliance than t0ice,daily dosing( but it&ay ha"e psychological ad"antages( particularly in patients 0ho are seizure freeand percei"e each act of pill,ta+ing as the only unpleasant re&inder of theirdisease.

4 Prevetio o) eileto;eesis

#xperi&ents in ani&al &odels suggest that so&e antiepileptic drugs not only exerta sy&pto&atic effect by raising seizure threshold( but &ight also antagonizeepileptogenic processes( i.e. the &echanis&s through 0hich an epileptic conditionbeco&es established. *he suggestion has been &ade that recurrent clinical seizures&ay also lead to irre"ersible neuroanato&ical changes 0hich &ay render thedisease &ore difficult to control( but e"idence for this is contro"ersial. Ifuncontrolled seizure acti"ity leads to the Qchronicization of the disorder( a casecould be &ade for early and aggressi"e treat&ent( and for preferential use of drugs0hich putati"ely antagonize epileptogenic processes. )"ailable studies( ho0e"er(suggest that in &ost epilepsy syn, dro&es antiepileptic drugs exert &erely asy&pto&atic effect and do not affect the natural course of the disease .

Ehe should treatmet


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ta+en into account in the ne0ly proposed International 7eague )gainst #pilepsyI7)#5 definition of epilepsy as ?a disorder of the brain characterized by an enduringpredisposition to generate epileptic seizures@ and reuiring ?occurrence of at leastone unpro"o+ed seizure@.

*he +ey to opti&u& epilepsy &anage&ent is to adapt treat&ent decisions to the

characteristics of the indi"idual. In general( )# &onotherapy is indicated after t0oseizures( but in high,ris+ patients initiation of treat&ent after one seizure &ight be

6ustifiable. )# choice is deter&ined by seizure type( ad"erse,effect profile( andpatient,specific features( including age( sex 0ith special reference to childbearingpotential5( and co&orbidities. ose titration and dosing regi&ens also need to becarefully indi"idualised. =ailure to achie"e seizure freedo& should pro&ptdiagnostic reassess&ent and early consideration of the feasibility of epilepsysurgery. Co&bination therapy can be beneficial in patients 0ho did not respond tot0o or three seuential &onotherapies( although in so&e cases earlier institution ofpolytherapy &ight be 6ustified. Seizure freedo& is al0ays the ulti&ate goal( but itshould not be pursued at all costs and o"ertreat&ent should be carefully a"oided. Inpatients 0ho do achie"e seizure control( discontinuation of )#s after at least 2R4

years of seizure freedo& should be considered( after careful assess&ent ofpotential benefits "ersus the ris+ of relapse and related i&plications.

4M-.,/0 TASG

=ind out your ans0ers to the follo0ing tas+s by yourself after discuss it 0ith your

group or after reading the suggested references belo0.

1. >hat are the anato&ical structures that ta+e part in seizure J

2. #xplain the &echanis& of seizure in hyperglyce&ia U

3. #xplain the &echanis& of epileptogenesis U

4. >hat is the definition of seizure and epileptic seizure J

!. escribe the classification of seizure and epileptic seizure U

$. escribe the pathophysiology of epileptic seizure U

. escribe the signs and sy&pto&s of epilepsy U

8. 'o0 to &anage a first ti&e seizure J

9. 'o0 to differentiate bet0een true seizure and psychogenic seizure J

1:.>hat are indications to perfor& brain i&aging in seizureJ

11.>hich )# is &ost appropriate for general epileptic seizureJ

12.%a+e sche&atic algorith& to differentiate sy&pto&s of seizure in childrenU

13.%a+e sche&atic algorith& to differentiate sy&pto&s of seizure in adult U

"!4 T0AC3IN'5/0A2NIN' P2-C0SS

1. #ach student should 0or+ the tas+s in a Student,>or+sheet hand 0ritten

in )4,size boo+5 prior to S&all roup iscussion ho&e 0or+5.

2. *he Student >or+sheet 0ill be collected before S&all roup iscussion .

3. Student should discuss the tas+s in S&all roup iscussion. *he conclusion


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of the discussion 0ill be collected at the end of the discussion.

4. *he facilitators &a+e notes on things the student discuss 0hich need to

clarify at the end of each session or in lecture to achie"e the learning

ob6ecti"es and collect the report of discussion.

""4 T30 ASS0SSM0NT

1. *he =or&ati"e #"aluation 0ill be assessed through Bbser"ation Sheets

elaborating the 7earning S+ill and Content %astery

2. *he Su&&ati"e #"aluation 0ill be assesed together 0ith the other &odules

in %iddle Se&ester *est and or #nd Se&ester *est scheduled.

"4 20(020NC0S)&erican #pilepsy Society. -asic %echanis& of Seizures and #pilepsy. 2::9.

Care of the Patient 0ith Seizures. 2nded. ))NN Clinical Practice uideline Series. 2::9

#ngel V( et al eds5. #pilepsy / lobal Issue for *he Practicing Neurologist. Ne0 Wor+ / e&os %edical

Publishing. 2::!

iagnosis and %anage&ent of #pilepsy in )dults. Scottish Intercollegiate uidelines Net0or+. 2::3

Stafstro&C#. 'yperglyce&ia 7o0ers Seizure *hreshold. "pilepsy urr.( 2::3A 345/ 148R149.

rant C and >arlo0 C. =ocal epilepsy in diabetic non,+etotic hyperglycae&ia. BM


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