1. The Anticonvulsants

2. Seizure Classification n Partial Seizures : Focal Simple Partial SeizureSimple Partial Seizure –Consciousness Not Impaired –Convulsions limited to one limb –Sensory hallucinations –Common in older children and adults

3. n Complex Partial Seizure Consciousness is impaired brieflyConsciousness is impaired briefly Automatisms present : Automatic behaviors like lip smacking, chewingAutomatisms present : Automatic behaviors like lip smacking, chewing Post seizure confusion : 1-2 minutesPost seizure confusion : 1-2 minutes

4. n Partial Become Generalized Consciousness is impairedConsciousness is impaired Progressive seizure involvement until a generalized tonic-clonic seizure evolvesProgressive seizure involvement until a generalized tonic-clonic seizure evolves

5. n Generalized Seizures Absence Seizures (Petit Mal)Absence Seizures (Petit Mal) –Sudden, brief LOC –Amnesia for a brief period –Attacks last <30 seconds

6. –No confused state after seizure –May occur many times per day

7. n Myoclonic Seizures –Sudden, lightening fast contractions –Loss of consciousness may occur –Can last seconds to minutes

8. n Clonic Seizures –Rhythmic, synchronized contractions throughout the entire body –Loss of consciousness

9. n Tonic Seizures –generalized sustained muscle contractions throughout the body –Loss of consciousness

10. n Tonic-Clonic Seizures (Grand Mal) –Major convulsions over the entire body –Contractions occur in an alternating tonic and clonic pattern –May loose bowel & bladder control –LOC –May be preceded by an aura or an outcry

11. n Atonic Seizures –Sudden loss of postural tone –Consciousness may be lost

12. Anticonvulsants …A Plethora Of Drugs n Hydantoins n Barbiturates n Iminostilbenes n Succinimides n Benzodiazepines n Valproic Acids

13. The Hydantoins n Phenytoin (Dilantin) n Mephenytoin (Mesantoin) n Ethotoin (Peganon) n Phenacemide (Phenurone)

14. n Phenytoin (Dilantin) - Prototypic Drug Made in 1908Made in 1908 Used for seizure control in 1938Used for seizure control in 1938 In therapeutic doses, no loss of consciousnessIn therapeutic doses, no loss of consciousness

15. Dilantin - Mechanism of Action n Stabilizes neural membranes –Interferes w/ sodium ion movement across the cell –May prolong the refractory period of excitable cells by delaying the influx of potassium ions

16. Hydantoins - Adverse Side Effects n Ataxia n Hirsuitism n Headache n Dysarthria n Nystagmus n Gingival Hyperplasia

17. The Barbiturates n Phenobarbital (Luminal) n Mephobarbitol (Mebaral) n Primidone (Myosline)

18. Mechanism Of Action n Phenobarbital - The Prototype –Anticonvulsant at sub-hypnotic doses –Not addictive in therapeutic doses –Increases threshold for motor cortex stimulation

19. –Reduces neurotransmitter release thereby quieting the brain –May augment the effects of GABA –May inhibit the excitatory effects of glutamate

20. Adverse Side Effects n Ataxia n Nystagmus n Vitamin K deficiency n Folic acid deficiency n Sedation which diminishes over time

21. The Iminostilbenes n Carbamazepine (Tegretol)

22. Mechanism of Action n Identical action to the Hydantoins –Stabilizes the flux of sodium across excitable membranes –Inhibits the spread of seizure signaling –First used in 1974 in the U.S.

23. Adverse Side Effects n Diplopia n Drowsiness n Ataxia n Hematopoeitic Suppression Aplastic anemiaAplastic anemia LeukopeniaLeukopenia ThrombocytopeniaThrombocytopenia

24. n Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) –Water retention –Water intoxication –Increased intraocular pressure

25. Succinimides n Ethosuximide (Zarontin) n Methusuximide (Celontin) n Phensuximide (Milontin)

26. Mechanism of Action n Suppress nerve signal transmission in the motor cortex n Increase the threshold for stimulation n Increase glucose transport to the brain which decreases neuronal excitability

27. Adverse Side Effects n Ataxia n Dizziness n Euphoria n Headaches

28. n Aplastic Anemia n Thrombocytopenia n Agranulocytosis n Leukopenia n Decreased sexual drive

29. n Renal and hepatic toxicity n Alopecia n Hirsuitism n Gingival Hyperplasia

30. Stevens-Johnson Disease n Target Lesions On The Skin –Central dark red zone with blisters –Encompassed by a pallor area which is circumscribed by a red rim

31. –Necrotic vasculitis may be present (capillary damage) –Bloody discharge from these lesions –May involve the eyes, mouth, lips, tongue, throat, esophagus, gut, bronchopulmonary tree

32. Cause ????

33. Benzodiazepines n Diazepam (Valium) n Clonazepam (Klonopin) n Clorazapate Dipotassium (Tranxene)

34. Mechanism of Action n Enhance the effect of GABA - An inhibitory neurotransmitter n Suppresses the spread of seizure signaling produced by epileptogenic foci

35. Adverse Side Effects n Vertigo, Ataxia,Syncope n Drowsiness, Confusion n Tremor, Weakness

36. Valproic Acids n Valproate Sodium (Depakene) n Divalproex (Depakote)

37. Mechanism of Action n Mechanism of action is unknown –Inhibits GABA Transaminase –Inhibits Succinic Semialdehyde Dehydrogenase –Allows GABA to have a longer half-life

38. Anticonvulsants - Medical Uses n Used to control seizures n The Hydantoins –Trigeminal neuralgia –Cardiac arrhythmias

39. n Tegretol –Trigeminal neuralgia –Glossopharyngeal neuralgia

40. Clinical Considerations n Is the patient taking their medications regularly ???? n Time the rehab session within 30 minutes of the last dose to decrease the chances of seizures

41. n Are there any external triggers which could set off the seizure ??? (light, sound, fatigue, odors) n Are the patients changing medications or changing the dose ???

42. n Are the patients under unusual stress - divorce, family deaths, etc. n Know the side effects of the medications

43. n Have a good seizure plan in the clinic n Train personnel to appropriately respond to the seizure event