Evaluation of first episode of seizure in adults

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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…
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  • 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  
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