Awareness on triggers of seizures in epilepsy among adults & its Management
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TRIGGERS OF SEIZURE IN EPILEPSY PRESENTER: DR. HERI R. MHENGA – MD (INTERN) SUPERVISOR: DR. REINHARD E. LEMA – MD, MMED (PHYSICIAN)
Introduction Seizure: is a transient disruption of brain function due to the hypersynchronous , excessive discharge of cortical neurons. Seizure can be epileptic or non epileptic such as a pseudoseizure (not due to excessive discharge) Epilepsy: a disorder resulting in recurrent seizures. A patient must have two or more unprovoked seizures to be diagnosed with epilepsy. Status Epilepticus: continuous seizure lasting > 30 minutes or several seizures occurring in succession without recovery of consciousness in between. The clinical manifestations of a seizure depend on the specific region and extent of brain involvement and may include an alteration in motor function, sensation, alertness, perception, autonomic function, or all of these .
Introduction Many children who experience a first seizure may never experience a second seizure. However, a seizure may be the initial presentation of a more serious medical condition or subsequent epilepsy. Seizure s not a disease but a symptom. Any child with seizure or H/o has to be fully evaluated. Epilepsy in children consist of wider variety of seizure types than in adults
Global Epidemiology of seizures ∞ 4 to 10% of children have an unprovoked seizure without recurrence. by age 16 years, ∞ 1% of the population will have suffered an afebrile seizure, and about half of these children will have a recurrence of seizure activity. in our settings infectious diseases and/or their sequellae are the most common causes of the seizures
pathophysiology of seizures A seizure is a temporary involuntary disturbance of brain function that may be manifested as impaired consciousness, abnormal motor activity, sensory disturbances or autonomic dysfunction. Seizures are accompanied by abnormal electrical discharges in the brain that can usually be detected by EEG. Common Denominator - increased permeability of neuronal cell membranes causes an increase in neuronal cell excitability. Things that can cause membrane instability: Deficiency in Oxygen Deficiency in Glucose Decrease/increase in other electrolytes Na , Ca , Mg , K
Duration of seizure Life threatening systemic changes Death Temporary systemic changes
Causes of sezures • Infections • Metabolic disorders • Ingestion of drugs of abuse& other toxins. • Medications • Brain/cranial abnormalities • Head trauma /intracranial bleeding • idiopathic Predisposing factors illness Fatigue Emotional stress Flashing lights Menstrual cycle Missed meals hunger Genetic predisposition
Drugs which can cause seizures Antibiotics Penicillins Isoniazid Metronidazole Anesthetics, narcotics Halothane, enflurane Cocaine, fentanyl Ketamine lignocaine Psychopharmaceuticals Antihistamines Antidepressants Antipsychotics Phencyclidine Tricyclic antidepressants , 8
Classification of seizures Partial (Focal) Seizures Abnormal electrical activity confined to a localized part of one cerebral hemisphere. Categories of partial (focal) seizures: I Without impairment of consciousness, symptoms vary based on area of origin - Motor: hand jerking, facial twitching, lip smacking - Sensory: odd taste or smell, seeing flashing lights, hearing buzzing noise - Autonomic: nausea, sweating - Emotional: anger, visual or auditory hallucinations, sense of fear Ii With impairment of consciousness Iii Partial seizures that become secondarily generalized Generalized Seizures Abnormal activity affecting the entire brain at the onset.
Categories of generalized seizures GRAND MAL - starting with a warning (aura)- sound, light, abdominal pain etc - usually tonic clonic there may be urinary incontinence, frothing and tongue biting a period of deep sleep follows episodes of mental confusion may follow(post ictal psychosis) 2 ABSENCE (PETIT MAL)- mainly disorder of children - Brief staring spells, blinking, short lapse in consciousness - No memory of incident - Recovery is usually as soon as seizure stops (no pronounced post- ictal phase) - May be mistaken as a behavioural problem Usually begin between 6-12 years old 3 MYOCLONIC - Quick muscle jerks - Consciousness generally not impaired - May occur alone, but generally occur in specific epileptic syndromes
4 CLONIC - Rapid, repetitive and rhythmic jerking of muscles (most noticeable in extremities) Consciousness impaired 5 TONIC - Stiffening of muscles (often involves rigid extension of extremities) Consciousness impaired 6 TONIC-CLONIC (GRAND MAL) - Tonic phase usually begins first (stiffening of extremities) - Clonic phase following (rhythmic jerking) - May have loss of bowel or bladder control, tongue biting, injury on falling Followed by distinct post- ictal phase (may last hours) where the patient is in a deep sleep and appears confused 7 ATONIC - Sudden loss of muscle tone causing child to suddenly drop to the floor (“drop attacks”) - Generally lasts only seconds - May or may not have loss of consciousness - High rate of injury due to falling.
Partial Seizures (focal onset seizures) — Simple partial (consciousness retained) • With motor symptoms • With somatosensory or sensory symptoms • With autonomic symptoms • With psychic symptoms — Complex partial (consciousness impaired) • Simple partial developing into a complex seizure • Consciousness impaired at onset — Partial seizure with secondary generalization Generalized Seizures — Absence seizures • Typical • Atypical — Myoclonic seizures — Clonic seizures — Tonic seizures — Tonic-clonic seizures — Atonic seizures Unclassified Seizures
DDx of seizures Many disorders can mimic seizures in children/adult and should be considered in the differential diagnosis of first seizure in a child. The most common nonepileptic paroxysmal disorders include the following Syncope or breath-holding spells Migraine Benign paroxysmal vertigo Behavioral events, such as nonepileptic staring spells, jitteriness, self-stimulation, or stereotypies Gastrointestinal reflux ( Sandifer syndrome) Movement disorders, such tics, benign myoclonus, dyskinesias , or dystonias Sleep disorders, such as night terrors or confusional arousals Psychogenic pseudoseizures or panic attacks
Detailed history of the child/adult with convulsion Mode of onset of convulsion, character, duration, any similar previous history (chronic/recurring). Triggering factors- fever, toxic substance or drug, metabolic disturbance. Family history of convulsion, inborn error of metabolism. Peri -natal/Natal history-birth asphyxia, jaundice, birth trauma, central nervous system (CNS) infection e.g. meningitis, encephalitis etc. CNS status-cerebral palsy, mental retardation (learning difficulty), any post-convulsive state .
Febrile seizures Brief, generalized tonic- clonic seizure associated with a FEBRILE illness but WITHOUT any CNS infection or other known neurological cause. Occurs children aged 6 months-6 years (VERY uncommon outside this age group) , Family h/o Generalized convulsions not more than 15min , no neurological defc i t after convulsion Risk of recurrence: 30% after 1st febrile seizure, 50% after 2nd, declines to zero by age 5 years. No anticonvulsant Rx is needed, only sponging and antipyretic agents Further evaluation is needed if: seizure occurs > 24 hours after the onset of fever, lasts > 15 minutes, appears focal , more than one seizure occurs during an illness, or there are ANY abnormalities on the neurological exam.
Neonatal seizures Subtle seizures Deviation of the eyes Eyelids are flickering Swimming or pedaling movements Apnoeic spells Tonic Clonic Myoclonic Seldom tonic clonic seizures
Aetiology of neonatal seizures Perinatal: HIE ICH Metabolic Hypoglycemia, hypocalcemia hypomagnesemia Other Infections Structural abnormalities Drug withdrawal
Treatment of neonatal seizures Optimize ventilation, cardiac output, BP, glucose, electrolytes and pH. Treat the underlying disease Intravenous line is essential Treat the seizures promptly and vigorously Phenobarbitone Phenytoin
EPILEPSY Primary (genetic epilepsy) - 65% of persons with recurrent seizures Secondary (acquired epilepsy) - 35% of persons with recurrent seizures. Most common secondary causes: Congenital abnormalities Perinatal Injuries Metabolic and Toxic Disorders Head Trauma Tumors Vascular Disease Degenerative Disorders Infectious Diseases
Specific Epilepsy Syndromes Type Age of onset EEG findings Treatment Febrile seizure 6 months to 6 years Usually normal Supportive measures Antipyretics Benign focal (rolandic seizures) 3 to 13 years Abnormal Carbamazepine (Tegretol), valproic acid (Depakene) Complex partial Any age Abnormal Various anticonvulsants Juvenile myoclonic epilepsy 12 to 18 years Abnormal Valproic acid Video game–related epilepsy Any age, although more typical in adolescents About 50 percent abnormal Abstinence from video games
Patient work up The diagnosis of seizures and epilepsy is based on history and physical exam. thorough neurological exam is mandatory. The diagnosis s supported by an EEG. Laboratory studies - blood film, culture for urine and blood – if patient has fever or irritability - full blood picture, - random blood glucose, - electrolytes (Na, Mg, K) - renal function tests ( creatinine , urea,) liver function tests, urine analysis, CSF studies (glucose, protein, RBC, WBC, gram stain and culture), Blood gases • Imaging studies - head CT/MR. These should be based on history and CF - CXR to exclude aspiration in children with status epilepticus
Treatment of sezures GENERAL RULES ABC acute management of the on-going seizure activity determine and treat the underlying cause. If seizures last > 5 minutes or if 3 or more occur in one hour, treat aggressively with medications to avoid progression to status Epilepticus
Drugs for Acute management of sezures
Drugs for Management of epilepsy
Status Epilepticus (SE)
Status epilepticus (SE) presents in a multitude of forms , dependent on etiology and patient age (myoclonic, tonic, subtle, tonic- clonic , absence, complex partial etc.) Generalized, tonic- clonic SE is the most common form of SE Conventional definition: Single seizure > 30 minutes Series of seizures > 30 minutes without full recovery
Important!!!! “If appropriate therapy is delayed, SE can cause permanent neurologic sequelae or death …” thus “ … any patient who presents actively convulsing should be assumed to have SE.” The longer SE persists, the lower is the likelihood of spontaneous cessation the harder is it to control the higher is the risk of morbidity and mortality Treatment for most seizures needs to be instituted after > 5 minutes of seizure activity
Classification Scheme for Status Epilepticus Nonconvulsive SE • Absence • Complex partial Convulsive SE • Partial (focal motor) • Generalized tonic/clonic
Non - convulsive status epilepticus Up to 20% of patient with SE have non - convulsive SE after tonic - clonic SE How do you tell that patient’s seizures have stopped? If patient does not begin to respond to painful stimuli within 20 - 30 minutes after tonic - clonic SE, suspect non - convulsive SE Urgent EEG
Common Etiologies of Status Epilepticus in Various Age Groups Neonate • Hypoxic-ischemic encephalopathy • Infection • Inborn errors of metabolism ( eg , nonketotic hyperglycemia) • Stroke or intraventricular hemorrhage • Congenital malformation • Pyridoxine deficiency and dependency Child • Infection • “Simple febrile seizure” • Metabolic disturbance • Congenital malformation • Presentation of epilepsy Adult • Stroke • Inadequate anticonvulsant concentrations • Trauma • Tumor • Unknown or undefined
………… Fever (manly 2° to infxns ) Medication change- i n epileptic pts Unknown Metabolic Congenital Anoxic Other (trauma, vascular, tumor, drugs) Mortality due to SE in children is 3 to 15% And up to 40% recover with debilitating sequellae 36% 20% 9% 8% 7% 5% 15%
Prolonged seizures Duration of seizure Life threatening systemic changes Death Temporary systemic changes
Systemic changes in SE 1. Respiratory Hypoxia and hypercarbia ß ventilation (chest rigidity from muscle spasm) Hypermetabolism ( Ý O 2 consumption, Ý CO 2 production) Poor handling of secretions Neurogenic pulmonary edema? Hypoxia/anoxia markedly increase (x3?) the risk of mortality in SE Ý pulmonary vascular pressure…… pulmonary edema…worsening resp function
2. Acidosis Impaired tissue oxygenation Increased energy expenditure Will cause Respiratory and Lactic acidocis 3.Hyperpyrexia Hyperpyrexia may develop during protracted SE, and aggravate possible mismatch of cerebral metabolic requirement and substrate delivery Treat hyperpyrexia aggressively Antipyretics, external cooling
4.Hemodynamics Sympathetic overdrive Massive catecholamine / autonomic discharge Hypertension Tachycardia Exhaustion Hypotension Hypoperfusion 0 min 60 min
5. Cerebral blood flow - Cerebral O 2 requirement Hyperdynamic phase CBF normal Exhaustion phase CBF drops as hypotension sets in Autoregulation exhausted Neuronal damage ensues Blood pressure Blood flow O 2 requirement Seizure duration
5. Glucose Hyperdynamic phase Hyperglycemia Exhaustion phase Hypoglycemia develops Hypoglycemia appears earlier in presence of hypoxia Neuronal damage ensues Glucose Seizure duration 30 min SE SE + hypoxia
7. Other alterations Blood leukocytosis Spinal fluid leukocytosis Ý K + Ý creatine kinase Myoglobinuria
A Oxygen, oral airway. Avoid hypoxia! B Consider bag-valve mask ventilation. Consider intubation C IV/IO access. Treat hypotension, but NOT hypertension What to do ?
Management of Convulsive Status Epilepticus DURATION OF SEIZURE PROCEDURES 0 to 5 minutes Ensure safety of patient, Monitor cardiopulmonary function and vital signs Give oxygen, Obtain short history and perform complete physical examination Note time 5 to 10 minutes Obtain iv access, Draw blood for laboratory tests, Give 2 mL/kg of 10% glucose Give Diazepam: 0.2 to 0.5 mg/kg, if still convulsing give the second dose of diazepam if Neonate: Phenobarbital 20 mg/kg >30 minutes Load with second long-acting agent Phenobarbital 10 mg/kg. May give additional 5- to 10-mg doses until 40 mg/kg …..Anticipate intubation 45 to 60 minutes Transfer to intensive care unit Institute general anesthesia Monitor continuously via electroencephalography
Initial investigations Labs Na, Ca, Mg, PO 2 , glucose CBC ,blood c/s ,urinalysis, urine c/s, B/s for malaria , Liver function tests, ammonia Anticonvulsant level Toxicology Lumbar puncture Always defer LP in unstable patient, but never delay antibiotic/antiviral rx if indicated CT scan Indicated for focal seizures or deficit, history of trauma or bleeding d/o
Management of status epileptics 0-5 minutes Stabilize patient (airway, oxygen, IV access, check RBG, history/physical, labs ifneeded /possible) ↓ 5-15 minutes Diazepam (rectal or IV, doses listed above) If seizures persist, repeat Diazepam 5-10 minutes after initial dose ↓ 15-35 minutes If seizures persist, give loading dose of Phenobarbital ↓ 45 minutes If seizures persist, give loading doses of Phenytoin Be prepared to support respirations ↓ 60 minutes If seizures persist, consider Thiopental drip (call anesthesia , transfer to ICU, prepare for mechanical ventilation)
Other Treatment Antibiotic for meningitis and ant malaria Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%), unless normo - or hyperglycemic Hyponatremia : Give 5 cc/kg of 3% (hypertonic saline) Hypocalcemia : Give 20-25 mg/kg of Calcium Chloride
references Paediatrics & Child health Coovadia and Wittenberg Hauser WA. The prevalence and incidence of convulsive disorders in children. Epilepsia . 1994;35( suppl 2):S1–6. Practice parameter: the neurodiagnostic evaluation of the child with a first simple febrile seizure. American Academy of Pediatrics . Provisional Committee on Quality Improvement, Subcommittee on Febrile Seizures. Pediatrics . 1996;97:769–75. Nelsons textbook of pediatrics 18th edition up to date 2009 Epilepsy syndromes in children Barry R Tharp, MD