first episode of seizures managemant

1. EVALUATION OF FIRST
EPISODE OF SEIZURE IN
ADULTS
BY DR.MANUSHA,
HOUSE SURGEON,
2K9 BATCH.

2. INTRODUCTION
 SEIZURE-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.

3.  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.

4.  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 FNCTION
2.NES-SPECIFIC TO DISORDER THAT
TRIGGERED THE SZ

5.  PRIMARY GOAL
EVALUATE FIRST SZ
TREATABLE SYS PROCESS
INTRINSIC
CNS
DYSFNCTN
UNDERLYING
PATHOLOGY

6.  EVALUATN OF SZ DETERMINES
1.WHETHER THE PT WILL HAVE ADD SZ/NOT
2.WHETHER TO BEGIN ANTI-CONVULSANT
THERAPY
3.OR TO TREAT THE UNDERLYING CAUSE
SOMETIMES STATUS EPI MAY BE THE CLINICAL
PRESENTATION-------------DIAGNOSED
STRAIGHT FORWARD ------TREATED
ACCORDINGLY.

7.  ETIOLOGY-
 EPILEPSY----1.GENETIC
 2.ACQUIRED
 ACQUIRED CAUSES-
 1.HEAD TRAUMA
 2.BRAIN TUMORS
 3.STROKE
 4.INTRACRANIAL INFCTN
 5.CEREBRAL DEGENRATN
 6.CONGENITAL BRAIN ALFRMTNS
 7.INBORN ERR OF META
 8.IDIOPATHIC

8.  MC CAUSE IN ELDERLY----.VASCULAR
,DEGENERATIVE AND NEOPLASTIC CAUSES
 IN CHILDREN------CONGENITAL
BRAIN MALFRMTNS THAN IN OTHER AGE
GRPS
 NO SEX PREDILECTION
 1.ONSET OF SZ IN LATE LIFE-----RISK
FACTOR FOR STROKE
 R:POSSSIBLE CV DISEASE CAN BE
RESPONSIBLE FOR NEW ONSET OF
EPILEPSY
 2.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

9.  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.

10.  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

11.  5.HYPOMAGNESEMIA---<0.8MEQ/L------
IRRRITABILITY,AGITATION,CONFUSION,MYOCLONU
S,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

12.  9.CEREBRAL ANOXIA----
CAUSES1.CARDIAC ARREST
 2.RESP ARREST
 3.DROWNING
 4.CO POISONING 5.ANAESTH
CMPLCTN
 CAUSES-------GTCS NAD
MYOCLONUS
 10.WITHDRAWAL STATES-ALCOHOL/
BENZODIAZEPENE
 ALCOHOL WTHDRWL-----SZ'S WTHIN
7-48 HRS OF LAST DRINK
 11.DRUG TOXICITY

13.  IMITATORS OF EPI
 NONEPI PAROXYSMAL EVENTS CAN BE
MISTAKEN FOR EPI
 IN 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 DISORDERS
 4.PAROXYSMAL MOVEMENT DISORDERS
 5.MIGRAINE AND
 6.MISCELLANEOUS NEUR DISORDERS

14.  IN ELDERLY--
 1.TIA
 2.TRANSIENT GLOBAL AMNESIA
 3.DROP ATTACKS
 THESE MUST BE DIFFERENTIATED
 PATHOPHYSIOLGY-
 CLINICAL FEATURES-
 EVALUATN OF FIRSTSZ STRTS WTH
HISTORY
 AURAS,ICTAL AND POST ICTAL
BEHAVIORS MUST BE ASKED
 SZ PPTS /TRIGGERS
 PARTICULAR ENV OR PHYSIOLOGICAL
TRIGGERS MAY BE PRESENT

15.  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

16.  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

17.  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

18.  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

19.  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

20.  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

21.  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

22.  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

23.  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

24.  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

25.  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

