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Epilepsy Pharmacotherapy

Epilepsy is a chronic neurological disorder characterized by recurrent seizures originating from abnormal neuronal discharge in the brain. It affects people of all ages globally. Seizures occur when there is sudden excessive signaling between brain cells. Epilepsy has various etiologies and can be difficult to diagnose, requiring ruling out other conditions and use of EEG or MRI to identify abnormal electrical activity or structural lesions. While 70% of epilepsy can be treated effectively, many in developing areas do not receive needed treatment. Common anti-epileptic drugs work by enhancing GABA inhibition, blocking sodium or calcium channels, or inhibiting glutamate, with phenytoin a first-line treatment for generalized and partial seizures as well as status epilepticus.

Health & Medicine◦
Epilepsy An assortment of different seizure types & syndromes originating from several mechanisms that have common sudden, excessive & synchronous discharge of cerebral neurons resulting in loss of consiousness,abnormal movements, odd behaviour /distorted perceptions.
Introduction Seizures occurs when there’s a sudden change in communication of braincells through electrical signal. During seizures,some brain cells send abnormal signals which stop other cells from working perfectly leading to temporary changes n Behaviour,Sensation,Movement/Consciousness. Onset---- During childhood & after 65 years of age. Most seizures are Benign which lasts for longtime called Status Epilepticus ,a life threatening disease characterised by Continuous seizures, sustained loss of consiousness, Respiratory distress.
Epidemiology • Epilepsy does impact on an individual's human rights, for example, access to health and life insurance is affected. • A person who suffers from epilepsy may not be able to obtain a driving licence and it has an impact on the choice of career. • Epilepsy is a chronic neurological disorder that affects people of all ages. Around 50 million people worldwide have epilepsy. Nearly 90% of the people with epilepsy are found in developing regions. Epilepsy responds to treatment 70% of the time. Despite this, approximately 75% of affected people in developing countries do not get the treatment they need. People with epilepsy and their families suffer from stigma and discrimination in many parts of the world.
Etiology
Pathogenesis of Epilepsy
There are multiple mechanisms that might contribute to synchronous hyperexcitability, including: 1) alterations in the distribution, number, type, and biophysical properties of ion channels in the neuronal membranes; (2) biochemical modifications of receptors; (3) modulation of second messaging systems and gene expression; (4) changes in extracellular ion concentrations; (5) alterations in neurotransmitter uptake and metabolism in glial cells; and (6) modifications in the ratio and function of inhibitory circuits.
Transitory imbalances between the main neurotransmitters, glutamate (excitatory) and γ -aminobutyric-acid (GABA) (inhibitory),& neuromodulators (e.g., acetylcholine, norepinephrine,and serotonin) might play a role in precipitating seizures in susceptible patients.
• Diagnosing epilepsy can be difficult as it is first necessary to demonstrate a tendency to recurrent episodes of epilepsy. There are other conditions that may cause impairment or loss of consciousness and which can be misdiagnosed as epilepsy; these include syncope, breath-holding attacks, transient ischaemic attacks, psychogenic attacks, etc. Other problems such as metabolic dysfunction, infection, head trauma or flashing lights (photosensitive seizures). These conditions have to be clearly ruled out before a diagnosis of epilepsy is made.
• The EEG is often the only examination required, particularly in generalised epilepsies, and it aims to record abnormal neuronal discharges. • Neuroimaging with magnetic resonance imaging (MRI) is the most valuable investigation when structural abnormalities such as stroke, tumour, congenital abnormalities or hydrochephalus are suspected. MRI should be carried out in anyone presenting with partial seizures or where a structural lesion on the brain may be responsible for seizures.
Neuro-imaging techniques such as: MRI,PET,SPECT. Abnormal electrcal activity during a seizure can be detected by EEG. Seizures have been categorized by site of origin, etiology, electrophysiologc correlation ,clinical presentation. Seizures have been classified in to2 broad groups: • Partial (Simple & Complex) • Generalized(Tonic-Clonic & Absence). • Others (Myoclonic, Febrile, Status epilepticus).
• Absence seizures: These involve brief, abrupt, self-limiting loss of consiousness. In 3-5 years of age patients(onset occurs) & lasts till puberty. Patient stops speaking in mid-sentence, & stares vacantly for few seconds(3-5sec).
Febrile seizures Young children may develop with illness accompanied by high fever. Intermittent muscle spasm & progressive metal deterioration.
ANTI -EPILEPTICS These are the drugs used in the treatment of EPILEPSY. Barbiturates : Phenobarbitone. Deoxybarbiturate : Primidone. Hydantoin : Phenytoin,Fosphenytoin. Immunostilbines : Carbamazepine,Carbazepine. Succimide : Ethosuximide. Aliphatic carboxylic acids: Sodium valproate, Divalproate. Phenylriazine : Lamotrigine. Cyclic GABA analogue : Gabapentin. Newer drugs :Vigabatrine, Tiagabine,Topiramate, Levetiractem. BZD’s : Diazepam,Lorazepam,Oxazepam, Clonazepam.
Mechanism of Action
The 3 mechanisms appear to be important action of Epilepsy. I. Enhancement of GABA action. II. Inhibition of Na+2 channel function. III. Inhibition of Ca+2 channel function. IV. Inhibition of Glutamate release & Blockade of receptors.
Enhancement of GABA action:( BZD’s, Barbiturates) Vigabatrin -- Inhibits enzyme“GABATransaminase”. Tiagabine --Inhibits GABAuptake & enhance action of GABA. Gabapetin – designed as an agonist @ GABAA Receptors. Inhibition of Na+2 channel function: (Phenyltriazine,Hydantoins,Immunostibines, Aliphatic –COOH’s). These drugs affect membrane excitabilty by an action on voltage- gated Na+2 channels, which carry the inward membrane current necessary for generation of Action potential. Inhibition of Ca+2 channels: (Suucimides,Gabapetin). Succimides blocks T-type Ca+2 channels . Gabapentin blocks L-type Ca+2 channels .
Pharmacokinetics: Absorption ----Slow on oral administration. Bioavailability differs in market preparations. Distribution is wide & 80-90% bound to plasma proteins. Metabolism– Liver by Hydroyxlation & Glucoronide conjugation. T1/2– 12-24hrs & increases up to 60 hrs. Only 5%Unchanged Phenytoin is excreted in urine.
Adverse Effects: @ Therapeutic levels— Due to over growth of Collagen fibres causes Gum Hypertrophy.(Can b minimized by Oral hygiene). Girls- Hirsutism,Acne,Coarsening of facial features. Hypersensitivity Reactions-Rashes,Lymphadenopathy,Neutropenia. Megaloblastic AnaemiaIt decreases Folate absorption & increases folate excretion. Osteomalacia, Hypergycemia, In pregnancy—causes FOETAL HYDANTOIN SYNDROME.
@ Higher levels– Cerebellar & Vestibular manifestations: Ataxia, Vertigo, Diplopia, Nystagmus. Drowsiness,Mental confuion, Hallucinations, Disorientation, Muscle rigidity. Epigastric pain, Nausea & vomiting (Can b minimized when taken with meals). I.V injection causes Local injury, oedema, vein thrombosis, Discolouration of injected limb,Hypotension & Cardiac arrhythmias.
Carbamazepine + Phenytoin creases each others Metabolism. Isoniazid, Cimetidine, Dicumerol,Warfarin  Inhibits Phenytoin metabolsim. Phenytoin induces Steroid degradation. Sodium Valproate Decreases metabolism & Increases Phenyton plasma levels.
USES 1st line Anti-Epileptic for Generalized Tonic-Clonic ,Simple &Complex partial seizures. In Status Epilepticus. In Trigeminal Neuralgia.
Epilepsy Pharmacotherapy