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Epilepsy

BY SABA JAWAID SABA SULEMAN

Introduction
Definition: Epilepsy (seizure disorder): When nerve cells in the brain fire electrical impulses at a rate of up to four times higher than normal, this causes a sort of electrical storm in the brain, known as a seizure. A pattern of repeated seizures is referred to as epilepsy.

The Ayurvedic literature 400 BC: Describe epilepsy as ‘Apasmara’ means loss of consciousness. . Vedic period of 4500-1500BC : Ancient Indian Medicine refined and developed the basic concept of epilepsy Charaka Samhita. to grab or to seize. to take hold of.Historical Background Epilepsy derived from a Greek term: Epilambanei -to posses.

Ibn Sina 370 AH: describe epilepsy as a brain disease. He described some physical treatment of epilepsy and stated it is an incurable chronic illness.Historical Background contd Hippocrates 400 BC: ‘This is not a sacred disease rather disorder of brain’ . .

Historical Background contd Europe and USA 1857: Bromide was used as first anti-epileptic drugs. Jackson: Neurologist of Londondescribed relationship of electrochemical discharge of brain and seizure. . 1873 H. 1920 H. Berger: German Psychiatrist developed EEG to measure brainwaves and its application in the field of epilepsy.

1938: Use Phenytoin as AED. 1997: ILAE.Historical Background contd 1909: Formation International league against epilepsy (ILAE). 1981: ILAE classified epilepsy. 1950-1970: Developed many AED. 1912: Use Phenobarbitone as AED. . IBE and WHO jointly established Global campaign against epilepsy.

five times higher Incidence: After infancy annual incidence.1%) Developing countries. but is most frequently diagnosed in infancy.5% (0. (100/100000) The life time risk of having a single seizure: About 5%. Developing countries. adolescence and old age.20-70/100000 in developed countries.0. Prevalence: Developed countries. It occurs in men and women and can begin at any age.Incidence is double. .Epidemiology of Epilepsy Epilepsy knows no geographical. childhood. About 50 million people in World have Epilepsy. racial or social boundaries.4% .

9% in Bangalore. Sri Lanka: 0.4% in Delhi and 0.1% .Prevalence in South East Asian Countries Bangladesh: population.1% (in adult India: 0.73% Thailand: 0.72% Myanmar: 0.99% Nepal: 0.5% in Mumbai.3% in Kolkata. 0. 0.9% (In Kandy District) Pakistan: 0.) 0.

Clonic seizures D. Tonic seizures E. tonic or clonic) II. Complex Partial Seizures C. Atonic seizures (Combinations may occur: myoclonic and atonic or myoclonic and tonic) III. Absence seizures i) Typical ii) Atypical B. Generalized seizures (Convulsive and non-convulsive) A. Unclassified epileptic seizures . Simple partial seizures B.Classification of Seizures ILAE Classification (1981) I. Partial Seizures evolving to secondary generalized seizures (tonic-clonic. Partial (Focal)seizures A. Tonic-Clonic seizures F. Myoclonic seizures C.

Metabolic. Withdrawal of drugs Alcohol. Tumor.Causes of Epilepsy In 28% cases cause can be determined. Rests (72%) are Idiopathic. Infections.Epileptics .  Congenital: inborn error of metabolism. Neuro surgery. Determined causes: Inherited genetic  Acquired : trauma. Other Anti. Toxic disorders. etc. drugs.Benzodiazepine. Inflammatory. Barbiturates.

Hormonal: Prednisolone. INH. Metrizamide. Ciprofloxacin. OCP. Anti Spastic: Baclofen Stimulant: Aminophylline.Procaine.Phenformin. Theophyline. Anti Diabetic: Insulin. Oxytocin Cardiac: Lidocaine. Metronidazole.Drugs That Induce Seizures Antibiotics: Penicillin. Mefloquine. Cycloserin. Disopiramide Anesthetics: Methohexital. Radiographic contrast: Meglumine derivatives. Halothane. Proguanil. Doxapram.Propofol Antimalarial: Chroloquine. . Ketamin.

Venlafaxine. Sulpiride . Clomipramine).Reboxetine Antipsychotics: Chlorpromazine. Buproprion.Drugs That Induce Seizures Antidepressant: TCA.Depot Anti-psychotics. Imipramine.(Amitriptaline.Clozapine Mood Stabilizer: Lithium Psycho stimulant: Amphetamine Safe Psychiatric medication in Epilepsy Antidepressant: Moclobemide. Trifluphenazine. Zotepine. Duloxitine. Dosulepin. Loxapine. SSRI (with cautious) Antipsychotics: Haloperidol.

SPECT. TFT. CSF study Imaging: EEG. Prolactin. S. Video EEG telemetry. MRI of Brain. MRS. Polysomnography . CT Scan of Brain. Blood sugar. RFT. Electrolytes. LFT. PET.Diagnosis of Epilepsy Thorough History taking : From patients From reliable valid informants From observer (who observed seizures) Physical Examination: Specially neurological system Higher Psychic function Laboratory Investigation: S. CBC.

Hypoperfusion in brain 5. Drop Attacks 9. Pseudoseizure 2. Some sleep disorders 4. Syncope 3. Migraine 10.Differential Diagnosis Condition mimicking Seizures: 1. Hypoglycaemia True Seizure Vs Pseudoseizure Features & Lab findings True Seizure Pseudoseizure Resemble known seizure types Yes Tongue bite Duration Post-Ictal Phenomena Injury Occurs during sleep Can be precipitated by suggestion EEG during attack EEG after attack Serum prolactin (after attack) Anti Epileptic drug usage Yes Short Present Yes Yes No Abnormal Slowing pattern Raised Suppress seizures No No Long Absent No No Yes No Change No Change No change No Change (may worsen) . Emotional Outburst 7. Cardiac Arrhythmia 6. Dissociative fugue 8.

Pathophysiology of Epilepsy In normal brain inhibitory circuits limits synchronous discharge. When GABA receptors blocked Rhythmic and repetitive hypersynchronus discharge of neurons  seizures Excitatory NT  Ach . (Prolongation of depolarization state) . Ca-) may cause seizures. Aspartate and Glutamate also involved to develop seizures Intracellular recording shows burst of rapid action potential firing with reduction of transmembrane potential.  inhibitory system +  excitation   genesis of seizures Abnormalities in Ion Channel (Na+. GABA is particularly play this role. K+.

Pathophysiology of Epilepsy Repeated subthreshhold of a neuron generates an action potentials  seizures It has been suggested that chronic epileptic discharges may lead to secondary epileptogenesis. acidosis and other metabolic disturbance). contd . uncomplicated seizures cause no permanent/ progressive neorological dysfunctions in human brain BUT uncontrolled generalized tonic-clonic seizures or status epilepticus is associated with high neurological morbidity and permanent brain damage ( due to hypo perfusion. Short. hypoxia.

irritability.fear. Piloerection.Clinical Presentations (Partial Seizures) Simple Partial Seizures: Consciousness is fully preserved  Motor disturbance may involve any body part  Tingling .disturbance of memory. Affective symptoms. Heart rate. anger. electrical shock like feelings  Flashing light and colours.dreamy state. Blood pressure.  Psychic manifestation: Dysphasic. structured hallucination. Cognitive symptoms. Pupil size.when cortical speech area affected. elation. depression. Simple hallucinations  Changes in skin color. Illusion of size. Dysmnestic. numbness. erotic thoughts. .

Clinical Presentations Definition: Clinical Presentations (Partial Seizures) .

Gestural.  Aura may be present-short live (few seconds)  Automatism: Oro-Alimentary. Responsive and Violent.  May start as simple partial seizures then progress. . Mimicry. Ambulatory. Duration: < 3 minutes.  Majority originate in Temporal lobe (60%). but also originate another lobe – particularly Frontal(30%). Verbal.Clinical Presentations (Partial Seizures) Complex Partial Seizures (Psychomotor Seizures/Temporal lobe Epelepsy)  Always involved impairment of consciousness.

Clinical Presentations (Complex Partial Seizures) Definition: .

crying out. Duration: few minutes Post ictal period: drowsiness. apnea. deep sleep . headache. increase heart rate and blood pressure. fall. Incontinence at the end of clonic phase. followed by brief relaxations.general malaise Tonic phase: stiff. tongue bite. labored breathing. involved four limbs. salivation. confusion.cyanosed. Clonic phase: intermittent clonic movements of muscles.Clinical Presentations (Generalized Seizures) Generalized Tonic-clonic (grand mal) Convulsive seizures No Aura but have prodormal phase.

. Attacks last only a few seconds (<10 sec) and often pass unrecognized. fluttering of the eyelids. swallowing. drowsiness. flopping of the head. About 100-200 attacks may occur/day. photic stimulation or hyperventilation. Suddenly appears blank and stares. Sudden loss of consciousness and cease all motor activities.Clinical Presentations (Generalized Seizures) Typical Absence Seizures (Petit mal):  Occur almost exclusively in childhood or early adolescent. Characteristic EEG : 3 per sec generalized spike and wave Attacks precipitate by fatigue. relaxation .

Clinical Presentations Typical Absence Seizures (Petit mal) .

very brief. Force deviation of the eyes and turning head to the opposite side.Clinical Presentations Myoclonic seizures Abrupt . . hypsarrhythmic patterns of EEG. with or without loss of consciousness. involuntery flexion movements. Involve whole body or part of the body Occur most commonly at morning. Status Epilepticus Series of recurrent Tonic-Clonic seizures occurs without regaining consciousness over 30 min. Waist Syndrome: Infantile spasm. severe encepalopathy with mental retardation. May occur in healthy people (physiological) Atonic Seizures Brief loss of muscle tone. Heavy fall . Versive seizures A frontal epileptic foci may involve the frontal eye field. shortly after walking.

Under recognized syndrome with myoclonic jerks.tonic-clonic seizures or absence seizures. 20% mortality. extremities and neck. 50% have life long seizures. Mixed types of seizures and mental retardation. Juvenile myoclonic epilepsy: Inherited condition.5-6 Hz.5 Hz ) spike and wave patterns. EEG shows spike and wave pattern of 3. who survive 75% have mental retardation. Catamenial epilepsy: Epileptic women experienced that their seizures worsen during menstruation. Lennox-Gastaut syndrome: Devastating disorder in children. due to the imbalance between the proconvulsant estrogen and anticonvulsant progestogen. tonic-clonic or clonic. Usually cognitive deficit present.Clinical Presentations Infantile Spasm: Sudden brief seizures. EEG shows slow (<2. typically tonic flexor spasm of waist. .

continue to take medication. without drugs. Epilepsy outcome: After 20 years 50% seizure-free. Childhood onset epilepsy (particularly classical absence seizures) carries the best prognosis for successful drug withdrawal.Prognosis Generalized seizures are more readily controlled than partial seizures. . for last 5 years 20% seizure-free. for last 5 years 30% seizures continue in spite of adequate dose of AEDs. Refractory epilepsy: When seizure control is not achieved with the first two appropriate and well tolerated AED schedules taken as mono therapy or in combination. The presence of a structural lesion makes complete control of epilepsy less likely.

In the concern of severity.Psychiatric comorbidities in Epilepsy Mood variation: Nearly 1 in 3 patients of epilepsy report significant concern about their mood.7% patients with epilepsy in community and 19-27% of epilepsy patients who require hospitalization. . Psychosis occurs in 0. 14% in Temporal lobe epilepsy. Depression: Upto 55% prevalent in patients with epilepsy.60. Anxiety : Upto 50% prevalent in patients with epilepsy. Psychosis: Incidence of Psychosis 3.3% in patients with idiopathic generalized epilepsy. Suicide rate: In depressed patients with epilepsy is 5 times higher than that in the general population and 25 times higher in patients with complex partial seizures of temporal lobe origin.

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