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EPILEPSY

Dr Md MahbubulAlam

AssistantProfessor Department of Neuro-Medicine Dinajpur Medical College, Dinajpur.

• Epilepsy is one of the commonest neurological disorder • 50 million people have epilepsy at any time • 5% people in the world may have at least 1 seizure in their life time • Of 50 million 80% are in under developed countries • It has profound social physical physiological and economic consequence.
WHO’05 Neuro Asia’04

. abnormal. disorderly electrical discharge from cerebral neurons. excessive. • Epilepsy– Unprovoked recurrent seizure. i.e. seizure occurring more than once in adult & twice in children.Seizure • An abnormal clinical event cause by sudden.

• Recurrent • Stereotyped awareness to surrounding may be impaired/ behavior altered • Motor. sensory. psychic • Sudden onset. ceased spontaneously • Post.ictal phase Bradley’05 . associate with a variety of clinical and laboratory manifestation. autonomic.WHO definition of epilepsy • WHO dictionary defines epilepsy as chronic brain disorder of various aetiologies characterized by recurrent unprovoked seizure due to abnormal excessive discharge of cerebral neurons.

both clinical examination and investigation may be perfectly normal Ref.Epilepsy / Seizure – 3rd most common chronic neurological disorder after headache – Epidemiological picture is difficult to obtain because • • • • • Episodic nature Diagnosis essentially clinical Relaying on patient’s account / Eye witness description Verities of other condition can be confused Between seizure.Epilepsy • Magnitude of problem.Neuro Asia 04.Epidemiology . .

DECLINE THROUGH CHILDHOOD AND ADOLESCENCE AND RISE SHARPLY AGAIN AMONG ELDERLY .INCIDENCE • IT IS HIGHER IN UNDERDEVELOPED COUNTRIES • INCEDENCE RATE IS HIGH DURING FIRST YEAR OF LIFE.

ETIOLOGY
 FIRST 6 MONTHS OF LIFE • SEVER BIRTH INJURY • CONGENITAL DEFECTS • INBORN ERROR OF METABOLISM  BETWEEN 2 AND 20YRS BIRTH INJURY INFECTIONS TRAUMA AND GENETIC FACTORS

CONTD..
 BETWEEN 20 TO 30YRS  STRUCTURAL LESIONS SUCH AS TRAUMA, BRAIN TUMORS OR VESCULAR DISEASE

 AFTER 50YRS  CEREBROVASCULAR LESIONS  METASTATIC BRAIN TUMORS
 IDIOPATHIC

PHASES
• • • • PRODROMAL PHASE AURAL PHASE ICTAL PHASE POST ICTAL PHASE

liberia. Poor sanitation Increased CNS infection. drug/substance abuse.4 times) • Possible explanation of disparity – – – – – – Profound contrast in Socio-economic structure Poor pre/ peri-natal care.Black > White. govt.Scenario of epilepsy-Developed/underdeveloped Face to Face Developed Countries Incidence/ 1000000/ year 40-70 UK-50 USA-2 million Under developed countries 100-190 Latin America – 144-190 India.At least one seizure during their life time 4-10-/10. Nigeria – 10/1000 • 5-10% of population:.000 active epilepsy • Race:. violence Prostitution. Birth injury Malnutrition. policies and AED availability. Rural > Urban • Age – Extremes of life • Sex : Male >Female (2-2. HIV infection Treatment influence by combination of local. social perception. parasitic disease Trauma. Bradiey’05 WHO’05 .

Snake Charmer.70% – Medical access – • Very poor • High dropout.Scenario of epilepsy in-INDIA • Prevalence: 10 / 1.3 million • Treatment modality – Homeopath. Ref. sc. Spiritual Leaders --.04(4) .000 • Number of patients – 1.Neuro. Kobiraz. Ojah.

SEIZURE TYPES .

CLINICAL MANIFESTATIONS • GENERALIZED SEIZURES  TONIC CLONIC  LOSS OF CONSCIOUNESS  FALLING TO THE GROUND  STIFFENING OF THE BODY FOR 10-20SEC  SUBSEQUENT JERKING OF THE EXTREMITIES  CYNOSIS  EXESSIVE SALIVATION  TONGUE BITE OR CHEEK BITE  INCONTINENCE MAY ACCOMPANY THE SEIZURE 3/22/2013 .

CONTD. 3/22/2013 ARUN PIRAVOM .. • TYPICAL ABSENCE SEIZURES  BRIEF STARING SPELL  BRIEF LOSS OF CONSCIOUSNESS • ATYPICAL ABSENCE SEIZURES  STARING SPELL ACCOMPANIED BY OTHER SIGNS AND SYMPTOMS.

CONTD. 3/22/2013 ARUN PIRAVOM . EXESSIVE JERK OF THE BODY OR EXTREMITIES.PATIENTS OFTEN FALL.  TONIC SEIZURES SUDDEN ONSET OF MAINTAINED INCREASED TONE IN THE EXTENSOR MUSLES. • MYOCLONIC SEIZURES CHHRACTERIZED BY A SUDDEN..

• ATONIC SEIZURES IT INVOLVE EITHER A TONIC EPISODES OR A PAROXYSMAL LOSS OF MUSCLE TONE AND BEGIN SUDDENLY WITH PERSON FALLING TO THE GROUND 3/22/2013 ARUN PIRAVOM ..CONTD.

FOLLOWED BY LIMB JERKING THAT MAY OR MAY NOT BE SYMMETRIC 3/22/2013 ARUN PIRAVOM .. • CLONIC SEIZURES  BEGINS WITH LOSS OF CONSCIOUSNESS  SUDDEN LOSS OF MUSCLE TONE.CONTD.

PATIENT MAY EXPERIENCE PARASTHESIAS AND TINGLING OR NUMBNESS IN THE LEG ON THE SIDE OPPOSITE THE FOCUS.CONTD.. 3/22/2013 ARUN PIRAVOM . PARTIAL SEIZURES • EX: IF THE DISCHRGING FOCUS IS LOCATED IN MEDIAL ASPECT OF THE POST CENTRAL GYRUS.

anything from illness to brain damage to abnormal brain development . so anyone can theoretically experience a seizure Onset of a seizure may indicate a previously existing. ongoing primary neurological disease • – – – – – – Etiologic factors in seizures generally include Cerebral lesions Biochemical disorders Cerebral trauma Epilepsy In short.Etiology • – Seizures in general can be caused by any disorder that alters the neuronal environment.

Etiology. cont’ Epilepsy can result from numerous conditions depending on the age of the person experiencing the syndrome. including but not limited : • metabolic defects • congenital malformations • genetic predisposition • perinatal injury • postnatal trauma • mycological syndromes • Infection • brain tumor • vascular disease • fever • drug or alcohol abuse .

K+ & Ca2+ and causes repetitive firing of neuron & produce seizure. .Patho-physiology • Up regulation of excitatory system or • Down regulation of inhibitory system • Imbalance between excitatory system and inhibitory system facilitates cellular influx of Na+.

SYNAPTIC ARRANGEMENT inhibitory neurons stimulatory neurons .

EXCESSIVE ACTIVITY inhibitory neurons less active Stimulatory neurons overactive .

Bradley 05 .Aetiology • Gray matter lesions are mere likely to cause seizure/ epilepsy than pure white matter lesion • Etiology is often multiple combination of acquired and genetic factors • Etiology is very much age related 60 to 70% of all epilepsies are cryptogenic Ref.

protozoal. Hyponatrima. fungal • Traumatic acute. late post traumatic (PTE) • Autoimmune–SLE • Metabolic–Hypoxia. Hypoglycemia (Drugs)–Quinolones • Neoplastic–Primary/ Secondary • Degenerative MLD • Demylenating–M. congenital deformity.S • Developmental–Cortical dysphasia.Aetiology Contd……… • Vascular–CVD–late onset epilepsy • Infections–viral. bacterial. .

ILAE CLASSIFICATION Partial (Focal) Epilepsy simple partial seizures complex partial seizures partial progressing to generalized seizures Generalized Epilepsy absence seizures generalized tonic-clonic seizures tonic seizures clonic seizures atonic seizures myoclonic seizures .

MANIFESTATIONS •CAMPS A autonomic system disturbed C Consciousness altered M motor manifestations P psychic manifestations S sensory manifestations .

PARTIAL EPILEPSY .

pupil size.changes in skin color. dysamnesic. altered smell. affective.no loss of consciousness x x Occipital lobe A . taste Temporal lobe last for few seconds . numbness.dysphasic. hallucinations S . BP. pain.SIMPLE PARTIAL SEIZURES Frontal lobe Parietal lobe MAIN FEATURES C .tingling. electric shock-like feeling. burning. heat.muscle spasms (‘march’) or jerking x P . illusions. HR. cognitive. pilo-erection M .

GENERALIZED EPILEPSY .

GENERALIZED EPILEPSY .

SECONDARY GENERALIZED SEIZURES MAIN FEATURES begins like partial seizures further progression to generalized seizures .

Malignant syndromes of epilepsy • Strong evidence of cognitive impairment.weber syndrome . learning disorder and progressive in course. • Combination of multiple seizure type • Poor out come • Very difficult to control by AEDs • They includes • Infantile spasms\ west syndrome • Lennox – Gastaut syndrome • Tuberous sclerosis • Sturge.

DIAGNOSIS • History • EEG • CT scans or MRI to rule out brain lesion .

History • Birth history • About Febrile seizure • Injury & infection • Drug addiction • Past history .

PHYSICAL EXAMINATIONS • General examinations. signs of trauma.pulse. tongue bite. BP. neuro-cutaneous manifestations etc • Examination of nervous system .

• So 10% epilepsy is EEG negative • 2–3% normal person may have abnormal EEG. – Mainly done to find out the clinical type of seizure – Single interictal EEG is 30-50% sensitive – 3-4 interictal standard recording (>30mins) with provocation is 60-70% sensitive – Advanced procedure: EEG with special electrode–spheroidal or foramen ovale & telemetric EEG with video monitoring of patient 90% sensitive.Investigations • EEG – – A sensitive tools but must be used with clinical data. .

Indications of brain imaging in epilepsy • Late in onset – after 20 years of age • Partial 20 generalized in type • Refractory to drug Rx. Or deteriorates • Focal neuro-deficit • Status Epilepticus • Suspected ICSOL • EEG shows a focal seizure source .

It depends on– Types of epilepsy – Price of drug – Toxicity of drug – Drug interaction – Drug availability .Treatment • Principles of treatment • • • • Diagnosis of epilepsy including types of seizure To find out possible aetiology. Selection of drug. Indication of treatment.

water. • Person may be drowsy and confused for 30—60mins. buttons etc) • Move sharp objects away from the person. • Note the duration of attack. (fire. So. if any (Knot of tie. machinery. • If seizure continues >5mins or recur or the person is injured take medical help. . should not be left alone until fully recovered. • Move the person away from danger. road etc).Immediate care of seizures • Must be given to every epileptic patients irrespective of country or place – First aid by relatives & witness — Do’s • Loosen tight clothes. • After convulsion stops—turn into semiprone position. • Ensure airway is clear. furniture.

1. treatment with a single agent. 3.Tx A. . 2. Many seizures will stop without pharmacological intervention. is the goal. but all serve to reduce the frequency of epileptic seizures. These drugs each have a different mechanism of action. Monotherapy. Medications used to treat patients with epilepsy are called anticonvulsants.

– Take blood for anticonvulsant levels (if known epileptic and taking antiepileptic drugs) – Investigate for cause .way is clear – Give O2 to combat cerebral hypoxia. • Immediate Medical care – Ensure air. most seizures are self-limiting and not life threatening. Don’t allow crowd near the person. Don’t restrict the person’s movements. Don’t forcfully insert anything in the person’s mouth. and then send to nearby hospital.Treatment – Don’ts • • • • • Don’t panic. Don’t offer anything to eat or drink till the person is fully conscious. – Give I/V or P/ R diazepam if convulsion continues >10 mins or repeated.

. More than two unprovoked seizure for children. Single seizure with abnormal EEG.Treatment • Anticonvulsant therapy (Medical treatment)– Indications :• • • • • • • Single seizure with definite structural lesion. More than one unprovoked seizure for adult. One seizure with strong +ve family history of epilepsy Single seizure with high risk job Single seizure with mental disorder.

Try to select appropriate drug with 1/3 or ¼ th of optimum dose. consider whether any structural or metabolic lesion present or review diagnosis. gradually increase to minimum effective dose or till control of seizures or side effects. – Don’t use more than two drugs in combination at any one time. . – Use minimum division of doses. – If above fails. – Check compliance – If first drug fails (seizure continues or side effects) start 2 drug from the 1st line whilst gradually withdrawing the first.Treatment • Guide — line for AEDs Therapy – Start with 1st line drug( 80% controlled). – Try three agents singly from 1st line before using combination. test for serum drug level. – Start with low dose. If seizure is uncontrolled with highest dose.

.• About 80% of patients responds to monotherapy. • 20% need poly–therapy.

Duration of therapy • 3 – 5years after the last attack • Single drug can control 80% of epilepsy • Dose regimens should be kept as simple as possible to ensure compliance. .

• In structural lesion complete control less likely. • 50-60% seizure free after withdrawal of drugs • 20-30% seizure free with drugs • In 20-30 seizures present in spite of AEDs .Prognosis • Primary generalized than partial or 20 generalized seizure. • out come after 20 yrs.

patients should follow the general safety advices.Withdrawal of AED therapy • At least 3-5 yrs after the last attack • Then withdraw gradually over 6 months • During and 6 months after withdrawal. .

Rate of recurrence • Recurrence rate 40% within 6 months • 9% in the next 6 months • 8% in the following 12 months • Chance of recurrence–In primary generalized seizure less • Don’t withdraw – – – – If focal deficit present Seizure focal or 20 generalized Future attack may ruin is employment (e.g. driver) or endanger life. . If seizure recurs.

Intractable Epilepsy • About 5% Epilepsy are intractable • At least 5 of the major anti-epileptics have failed in adequate doses • Second level intractability is defined as failure of two drugs • Third level intractability is defined as failure of three drugs and so on .

Factors underlying • Underlying structural lesion • Mental retardation • Concomitant metabolic disorders • Cerebral Palsy .

Surgical treatment • Indication – Intractable Epilepsy – Intra-cranial structural lesion .

.Surgery Surgical resection of epileptogenic areas of the brain in patients with partial seizures is considered when seizure activity fails to respond to even the most aggressive medical management.

Epilepsy in special Situations • Epilepsy with pregnancy • Epilepsy in child bearing age • Status epilepsy • Epilepsy and driving .

Febrile convulsion • Age – 6 months to 5 yrs common between 9-20 months • Recurrent in 50% cases • Seizure usually occurs when fever is raising • Treatment – Reduction of temperature and per-rectal diazepam – Prophylaxis is debatable. but should be given in complex febrile seizure and in EEG change • Out come – Complicated (Focal.30% in develops epilepsy in later life – Simple – 2. prolonged or repeated) . .4% develops epilepsy in later life.

Status epilepticus • Predisposing factors – Sudden withdrawal of AED. – Presence Of Structural Lesion – Acute metabolic disturbances .

2 mins after another 5mg – If not control within 15 mins.TREATMENT • General– ABC – Collection of blood sample for glucose. Thiamin 100 mg if patient is alcholic – Diazepam 5mg iv stat.repeat 10 mg diazepam or Lorazepam and wait 15 mins. – Infusion of 25% glucose – Inj. if not controlled–shift the patient in icu • Specific- . electrolytes and for future analysis.

• Contu-Persisting of seizure after 30 mins- • Loading dose phenytoin or fosphenytoin iv 15mg\kg or phenobarbitone 10mg\kg • If seizure is still continues• Treatment for refractory status with intubation and GA by Propofol or thiopental • Once status controlled – Long acting AEDS should be started. .

. • Should take shallow bath in presence of relatives • No cycling till 6 months seizure free • Swimming. boating always be accompanied by others who knows about his or her illness. fire or water. fishing .Restrictions of epilepsy patients • Work or recreation above ground level • Work with dangerous machinery.

Prevention There is no way to prevent seizures… .

• Seizure control is achieved in most individual with the single medication. . • After a second and third seizure. the risk of further seizure increases to about 75% and treatment is indicated. • Principles of poly pharmacy guides the choice of drugs with different mechanisms of action.• Treatment is not always indicated after a single seizure.

but planned-checking may be needed. • Routine checking of drug levels is seldom indicated.) • After discontinuation of therapy. twothird of patients remain seizure-free. surgery may be the option of management. . • In refractory cases.Conclusion (contd.