Evaluation of first episode of seizure in adults

EVALUATION OF FIRST EPISODE OF SEIZURE IN ADULTS

BY DR.MANUSHA,HOUSE SURGEON,

2K9 BATCH.

INTRODUCTIONSEIZURE-A SUDDEN CHANGE IN

THE BEHAVIOUR THAT IS A CONSEQUENCE OF BRAIN DYSFUNCTION.

EPILEPSY-RECURRENT SEIZURES CHARACTERISED BY THE ELECTRICAL HYPERSYNCHRONISATION OF NEURONAL NETWORKS IN THE CEREBRAL CORTEX.

PROVOKED SEIZURES-SOME SEIZURES OCCUR IN A SETTING OF METABOLIC DERANGEMENT,DRUG/ALCOHOL WITHDRAWAL,ACUTE NEUROLOGICAL DISSORDERS LIKE STROKE AND ENCEPHALITIS.

-NOT CONSIDERED AS EPILEPSY.-WOULD NOT RECUR IN THE

ABSENCE OF PROVOCATION.

NON-EPILEPTIC SEIZURES-SUDDEN CHANGES IN BEHAVIOUR-----RESEMBLE EPILEPTIC SEIZURES------BUT NOT ASS WITH TYPICAL NEUROPHYSIOLOGICAL CHANGES.

STATUS EPILEPTICUS-CONTINOUS SZ ACTIVITY WITHOUT A PAUSE I.E.,2 BACK TO BACK SZ’S WITHOUT LUCID INTERVAL OR ANY SZ LASTING MORE THAN 5-10MIN

RX-1.ES-TO RESTORE NORMAL BRAIN FNCTION2.NES-SPECIFIC TO DISORDER THAT

TRIGGERED THE SZ

PRIMARY GOALEVALUATE FIRST SZ

TREATABLE SYS PROCESS INTRINSIC

CNS DYSFNCTN UNDERLYING PATHOLOGY

EVALUATN OF SZ DETERMINES1.WHETHER THE PT WILL HAVE ADD SZ/NOT2.WHETHER TO BEGIN ANTI-CONVULSANT

THERAPY3.OR TO TREAT THE UNDERLYING CAUSESOMETIMES STATUS EPI MAY BE THE CLINICAL

PRESENTATION-------------DIAGNOSED STRAIGHT FORWARD ------TREATED ACCORDINGLY.

ETIOLOGY-EPILEPSY----1.GENETIC 2.ACQUIREDACQUIRED CAUSES-1.HEAD TRAUMA2.BRAIN TUMORS3.STROKE4.INTRACRANIAL INFCTN5.CEREBRAL DEGENRATN6.CONGENITAL BRAIN ALFRMTNS7.INBORN ERR OF META8.IDIOPATHIC

MC CAUSE IN ELDERLY----.VASCULAR ,DEGENERATIVE AND NEOPLASTIC CAUSES

IN CHILDREN------CONGENITAL BRAIN MALFRMTNS THAN IN OTHER AGE GRPS

NO SEX PREDILECTION1.ONSET OF SZ IN LATE LIFE-----RISK FACTOR FOR

STROKER:POSSSIBLE CV DISEASE CAN BE RESPONSIBLE FOR

NEW ONSET OF EPILEPSY2.HEAD INJURY----SMALL PROPORTION----MIN RISK-----CONCUSSIVE HEADD INJURY------

LOC/AMNESIA FOR LESS THAN 30 MIN----INCREASED RISK FOR------TRAUMA INDUCED

PROLONGED AMNESIA/SUBDURAL HAEMATOMA/BRAIN CONTUSION

--AED----PREVENTS SZ'S IN 1ST WK BUT DOESNT PREVENT EPILEPSY

3.ACUTE SYMPTMTC SZ'S-----PTS WTHOUT MEDI H/O EPI-----CAN PRSENT WITH SZ'S IN ACUTE CLINICAL SETTING.EG-STROKE,HEAD TRAUMA,MENINGITIS,ANOXIC ENCEPHALOPATHY.

----NOT CONSIDERED TO HAVE EPI RISK FOR FUTURE EPI----MORE IN RECOVERED PTS THAN

THOSE DEVELOPED IN ACUTE CLINICAL SETTING(WITHINSEV WKS OF STROKE/HEAD INJURY)

UNPROVOKED SZ'S OCCURING AFTER RECOVERY FRM ACUTE ILLNESS----CALLED AS REMOTESYMPTOMATIC SZ'S.

FEW OF ACUTE SYM SZ'S ----DUE TO---META DISTURBANCES

RISK FOR FUTURE EPI IS LESS THAN IN CASES OF STROKE,TRAUMA,MENINGITIS AND ANOXIC ENCEPHALOPATHY

BUT SZ RECURRENCE IN ACUTE SETTING IS POSSIBLE PROVOKED SZ ---RISK OF SZ'S---DEPENDS ON RAPIDITY

OF ONSET------THAN THE SEV OF META DISTURBANCE.

EXAMPLES- 1.HYPOGLYCEMIC SZ'S-MC IN DIA PTS TAKING EXCESSIVE

INSULIN OR ORAL HYPOGLYCEMIC DRUGS ISLET CELL TUMORS---RARE CAUSE PRODROMAL SYM-DIAPHORESIS,TACHYCARDIA,ANXIETY

AND CONFUSION. 2.NON KETOTIC HYPERGLYCEMIA------ELDERLY DIA

PTS-------FOCAL MOTOR SZ'S 3.PRECIPITOUS FALL IN S.SOD-------GTCS PRODROMAL STAGE-CONFUSION ,DEPRESSED LEVEL OF

CONSCIOUSNESS. HIGH RISK OF MORTALITY----MUST BE TREATED

URGENTLY----- BUT RAPID CORRECTION SHOLD BE AVOIDED?

4.HYPOCALCEMIA-RARE CAUSE ----MORE OFTEN IN NEONATES

ADULTS----AFTER THYROID/PARATHY SRGRY/IN ASS WTH RENAL FAILURE,HYPOPARA AND PANCREATITIS

PRODROMAL S/S-MENTAL CHANGES AND TETANY

5.HYPOMAGNESEMIA---<0.8MEQ/L------IRRRITABILITY,AGITATION,CONFUSION,MYOCLONUS,TETANY AND CONFUSION OFTEN ACC BY HYPOCAL

6.RENAL FAILURRE AND UREMIA-------MYOCLONIC SZ'S

IN ADVANCED CKD------GTCS IN PTS UNDERGOING DIALYSIS-----DIALYSIS

EQUILIBRIUM SYNDROME 7. HYPERTHY-EXACERBERATE SZ'S IN PTS WTH EPI 8.AIP------DEF OF PORPHYRIN DEAMINASE------HIGH

LEVELS OF DELTA AMINOLEVULINIC ACID AND PORPHYROBILINOGEN IN URINE

MC-----GTCS RARE-----PARTIAL SZ'S OTHER SYM ---ABD PAIN AND BEHAVIORAL CHANGES

9.CEREBRAL ANOXIA----CAUSES1.CARDIAC ARREST

2.RESP ARREST3.DROWNING4.CO POISONING 5.ANAESTH

CMPLCTNCAUSES-------GTCS NAD MYOCLONUS10.WITHDRAWAL STATES-

ALCOHOL/BENZODIAZEPENEALCOHOL WTHDRWL-----SZ'S WTHIN

7-48 HRS OF LAST DRINK11.DRUG TOXICITY

IMITATORS OF EPINONEPI PAROXYSMAL EVENTS CAN BE

MISTAKEN FOR EPIIN ADOLESCENTS AND YOUNG ADULTS-----1.SYNCOPE-----BRIEF CEREBRAL ANOXIA----

BRIEF TONIC AND/OR CLONIC MOVEMENTS WITHOUT PROLONGED POSTICTAL PHASE

2.PSYCHOLOGICAL DISORDERS(PSEUDOSZ'S)

3.SLEEP DISORDERS4.PAROXYSMAL MOVEMENT DISORDERS5.MIGRAINE AND 6.MISCELLANEOUS NEUR DISORDERS

IN ELDERLY--1.TIA2.TRANSIENT GLOBAL AMNESIA3.DROP ATTACKSTHESE MUST BE DIFFERENTIATEDPATHOPHYSIOLGY-CLINICAL FEATURES-EVALUATN OF FIRSTSZ STRTS WTH HISTORYAURAS,ICTAL AND POST ICTAL BEHAVIORS

MUST BE ASKEDSZ PPTS /TRIGGERSPARTICULAR ENV OR PHYSIOLOGICAL

TRIGGERS MAY BE PRESENT

SZ TRIGGERS INCLUDE STRONG EMOTIONS,INTENSE EXERCISE,LOUD MUSIC,FLASH LIGHTS,ETC

OTHER PHYSIOLOGICAL CNDTNS PPT SZ'S AREFEVER,MENSTRUAL PERIOD,LACK OF SLEEP, STRESS,ETC,,,

THEY LOWER THE SZ THRESHOLD RATHER THAN DIRECTLY CAUSING SZ

THESE MAY ALSO PPT NONEPI PAROXYSML SZ LIKE SYNCOPE SO PRESENCE DOESNT DIFFERENTIATE THE TWO

->PHOTO INDUCED SZ'S-NATURAL/ARTIFICIAL SOURCE(TV,VIDEO GAMES)

EG-POKEMAN CARTOON INCIDENT CHILDREN MORE SUSCEPTIBLE PHOTOSENSITIVITY DECLINES IN PHOTO INDUCED SZ'S CAN INHERITED USUALLY GENERALISED SZ'S OCCUR PTS SENSITIVE TO PARTICULAR LIGHT TRIGGERSWOMEN

MORE SUSCEPTIBLE BUT MALES DOMINATE IN REPORTS(VIDEO GAMES)

PHOTOSENSITIVITY SUGGESTS SZ'S BUT NOT SPECIFIC TO EPI

SZ S/S- 1.AURAS/SIMPLE PARTIAL SZ'S-(SIMPLE-CONSCIOUSNESS IS

NOT IMPAIRED;PARTIAL-PART OF CORTEX IS INVOLVED) AT THE BEGINNING OF SZ SZ'S NOT ENOUGH TO INTERFER WTH CONSCIOUSNESS BUT

ENOUGH TO CAUSE SYM INTERNATIONAL LEAGUE AGAINST EPI CALL AURAS AS SPS S/S VARY FRM ONE PT TO OTHER DEPEND ON WHERE THE SZ ORIGINATE SIN BRAIN EG-OCCIPITAL CORTEX---FLASHING OF LIGHRS MOTOR CORTEX-----RHYTMC JERKING MVMNTS OF

FACE,ARMS,/LEGS ON OPP HALF OF THE BODY(JACKSONIAN SZ)

THEY DO NOT TYPICALLY PRECED PROVOKED SZ'S-----SO SUPPORTS THE DIA OF EPI

WHEN NOT PRECEDED BY AURA DIFFICULT TO DIFFERENTIATE ES FRM NES

MANY EPI PTS DEV SZ ABRUPTLY WHEN THE PART OF CORTEX THAT CONTROLS MEMORY IS DISRUPTED BY SZ-----BUT NOT SPECIFIC CAN OCCUR IN NES

2.COMPLEX PARTIAL SZ'S(PREVIOUSLY CALLED TEMPORAL LOBE/PSYCHOMOTOR SZ'S)

COMPLEX-ASS WTH LOC MC TYPE IN EPI ADULTS DURING SZ PT APPEAR TO AWAKE BT NT IN CONTACT

WTH OTHERS IN THEIR ENV DO NOT RESPOND NORMALLY TO INSTUCTNS/QUES OFTEN SEEM TO STARE IN SPACE/REMAN MOTION

LESS/ENGAGE IN REPITITIVE BEHAVIORS PTS MAY BECOME HOSTILE/AGGRESSIVE WHEN

PHYSICALLY RESTRAINED TYPICALLY LAST LESSS THAN THREE MIN MAY BE PRECEDED BY SPS POSTICTAL PHASE-SOMNOLENCE CONFUSION AND

HEADACHE UPTO SEV HOURS PT HAS NO MEMORY OF WHAT HAPPENNED OTHER THAN

AURA NOT SPECIFIC

3.GENERALISED SZ-(GENERALISED-WHOLE CORTEX IS INVOLVED)

A.ABSENCE SZ'S B.GTCS C.CLONIC SZ D.MYOCLONIC E.TONIC AND F.ATONIC A.ABSENCE SZ(PETIT MAL SZ) MC DURING CHILDHOOD TYPICALLY LAST FOR 5-10 SEC FREQUENTLY OCCUR IN CLUSTERS DOZENS OR EVEN

HUNDRED TIMES A DAY DURING SZ-SUDDEN STARING WTH IMPAIRED

CONSCIOUSNESS IF SZ LAST FOR >10 SEC EYE BLINKING/LIPSMACKING

IS SEEN

B.GTCS-(GRANDMAL SZ/MAJOR MOTOR SZ/CONVULSION) MOST DRAMATIC TYPE BEGINS WITH ABRUPT LOC ASS WTH SCREAM /SHREIK MUSCLES OF EXTREMITIES.CHEST AND BACK ARE INVOLVED TWO PHASES TONIC(MUSCLE STIFFENING)AND

CLONIC(MUSCLE JERKS) PT MAY APPEAR CYANOTIC DURING TONIC PHASE---ARREST

OF RESP MVNTS----DECREASED OXYGENATN OCCURS FOR 1 MIN THEN CLONIC PHASE STARTS AND LASTS FOR ABOUT 1-2

MINUTES DURING CLONIC PHASE TONGUE CAN BE BITTEN,FROTHY

AND BLOODY SPUTUM CAN BE SEEN POSTICTAL PHASE STRTS IMMEDIATELY WHEN THE

TWITCHINGS END POSTICTAL PHASE-PT IN DEEP SLEEP,DEEP BREATHING AND

GRADUALLY WAHES UP WTH C/O HEADACHE C.CLONIC SZ-RHYTHMICAL JERKING MUSCLE CONTRCTNS

USUALLY INVOLVES ARMS,NECK AND FACE

D.MYOCLONIC SZ'S-SUDDEN BREIF MUSCLE CNTRCTNS---OCCUR SINGLY/IN CLUSTERS---CAN AFFECT ANY GRP OF MUSCLES TYPICALLY ARMS

CONSCIOUSNESS IS USUALLY NOT IMPAIRED E.TONIC SZ'S-SUDDEN MUSCLE STIFFENING OFTEN ASS WTH

LOC AND FALLING TO THE GROUND F.ATONIC SZ'S-(DROPSZ'S) OPP EFFECT TO TONIC SZ'S SUDDEN LOSSS OF CONTROL OF

MUSCLES PARTICULARLY LEGS RESULTING IN COLLAPSING TO THE GROUND AND POSSIBLE INJURIES

BEHAVIORS NOT SPECIFIC POSTICTAL PHASE-TRANSITION FRM ICTAL STATE TO NORMAL

LEVEL OF CONSCIOUSNESS SIGNIFIES RECOVERY PERIOD OF BRAIN MANIFESTATIONS-CONFUSION,SUPPRESSED ALERTNESS AND

FND MAY LAST FRM SEC---MIN--HRS DURATION DEPENDS ON SEV FACTORS LIKE PART OF BRAIN

AFFECTED,LENGTH OF SZ,WHETHER THE PT IS ON AED/NOT AND ON AGE

IF A PERSON HAVING CPS---HIS LEVEL OF CONSCIOUSNESS GRADUALLY IMPROVES MUCH LIKE A PT WAKING UP FRM ANASTHESIA AFTER OPERATN

POST ICTAL PHASE IS A PRESENTING CMPLAINT WHEN THE SZ IS BREIF

POSTICTAL PARESIS(TODDS PARALYSIS) TRANSIENT NEUROLOGICAL DEFICIT WEAKNESS OF ARM/LEG THAT FOLLOWSFOCAL MOTOR

SZ WEAKNESS USUALLY MOD RARELY SEV CAUSE OF POSTICTAL PARESIS IS UNKNOWN BUT MAY

INVOLVE PROLONGED NEURONAL HYPERPOLARISATION DUE TO ACTIVATION OF META PPUMPS OR TRANSIENT INACTIVATN CAUSE DBY NMDA RECEPTOR ACTIVATN AND EXCESSIVE CA INFLUX

MOSTLY UNILATERAL OTHER POSTICTAL SYM INCLUDE-TRANSIENT

APHASIA,AMAUROSIS,HEMIANOPSIA,SENSORY LOSSS,PSYCHOSIS,AGRESSION,ETC

EVALUATION - HISTORY- PREICTAL,ICTAL AND POSTICTAL SYM SHOULD BE ASKED FOR FEVER,TRAUMA ,INFECTIOUS ETIOLOGIES SHOULD BE RULED

OUT MEDICATION HISTORY MEDICATNS CAN CAUSE IATROGENIC SZ'S GTCS ARE MC PAST MEDICAL HIS-RISK FACTORS LIKE

TRAUMA,STROKE,INFECTN,ALCOHOL/DRUG ABUSE MUST BE ADDRESSED

FAMILY HIS-POSITIVE----- HIGHLY SUGGSTV OF EPI PARTICULARLY IN ABSENCE NAD MYOCLONIC SZ'S

PHYSICAL AND NEUROLOGIC XMNTN- GENERALLY UNREVEALING EPI SZ BUT IMP IN INFCTN AND HMRHGE NEUROLOGIC XMN SHOULD EVALUATE FOR LATERALISING

ABNORMALITIES LIKE WEAKNESS,HYPERREFLEXIA.POSITIVE BABINSKI---POINT TO CONTRALAT STRUCTRL LESION

LAB INVSTGTNA- 1.METABOLIC-INVSTGTNS FOR

ELECTROLYTES,GLU,CAL,MAG,HAEMATOLOGIC,LFTS AND TOXICOLOGIC

SCREENING 2.S.PROLACTIN LIMITED DIAGNOSTIC VALUE IN EPI RISES SHORTLY AFTER GTCS AND SOME PARTIAL SZ'S DONE AT 10-20 MIN AFTER THE EVENT 6HRS LATER (BASELINE) TWICWE THE BASELIE IS TAKEN AS POSITIVE POOLED SENSI IS HIGHER FOR GTCS THAN FOR CPS USUAL TO DIFFERENTIATE FRM PSYCHOGENIC SZ'S NORMAL S.PROLACTIN DOESNT EXCLUDE EPI SZ OR SUPPIRT THE

PSY SZ'S RISES EVEN AFTER SYNCOPE SO NOT SPECIFIC3.OTHE RSZ

BIOMARKERS HELPS DIFFERENTIATING FRM SYNCOPE,PSEUDO,AND OTHER

PHYSIOLOGIC EVENTS EG-CPK,CORTISOL,WBC COUNT,LDH,PCO2 ,NH3,NEURON SPECIFIC

ENOLASE CPK LEVELS RISED IN GTCS OUTPATIENT SETTING

4.LP-IMP WHEN ACUTE INFCTIOUS ILLNESS /MENINGEAL METASTASES ARE SUSPECTED

PROLONGED SZ'S---- PLEOCYTOSIS----MISLEADS PERFORMED ONLY AFTER SOL IS EXCLUDED 5.EEG -DIAGNOSTIC IN ES ABN INTERICTAL EEG SUPPORTS ES AND CAN HELP

DIFFERENTIATE TYPE OF SZ IF ABN EEG +NT LIKELIHOOD OF SECOND SZ IN NEXT 2 YRS NORMAL EEG DOESNT R/O EPI 6.NEUROIMAGING- TO EXCLUDE STRUCTURAL BRAIN ABN IF PT FIRST SZ IS NOT A

PROVOKED SZ MRI IS PREFERRED TO IDENTIFY SPECIFIC LESIONS SUCH AS

CORTICAL DYSPLASIAS,INFARCTS AND TUMORS CT SCAN --- IN MASS LESIONS,HMRGE,LARGE STROKE UNDER

EMERGENCY SITUATIONS,WHEN MRI IS CI IN YOUNG TO MID AGE ADULTS ---COMMON MRI FINDINGS ARE

MESIAL TEMPORAL SCLEROSIS,HEAD INJURIES,CONG ABN,TUMORS ,NCC AND VASCULAR LESIONS. ALSO REVEALS STROKE ,DEGE AND NEOPLASMS

FINDINGS SHOULD NOT BE INTERPRETED IN ISOLATION

ACUTE RX IN INPATIENT-MOST S ZREMIT SPON WTHIN 2MIN RAPID ADMNSTRTN OF AED IS NOT REQUIRED RATHER A CATH

SHOULD BE SECURD TO INJECT DRUGS IF SZ IS PROLONGED ACUTE SYMP SZ --CAUSE MUST BE QUICKLY IDENTIFIED AND

TREATED H/O EPI AED LEVELS SHULD BE CHECKED AND THE DOSE

MUST BE ADJUSTED IF SZ LAST FOR > 2MIN AED MUST BE ADMNSTRD PSYCHOSOCIAL CONSIDERATIONS--COUNSELLING PTS WTH EPI SHOULD NOT BE ALLOWED TO DRIVE HOSPITALISATION INDICATIONS--1ST SZ WITH PROLONGED POSTICTAL

STATE/INCMPLT RECOVERY 2.SE 3.SYS ILLNESS 4.HEAD TRAUM AND IF THE PT IS NOT COMPLIANT