Approach to Seizure elderly adults.pptx

Seizure

1. APPROACH TO SEIZURES

2. SEIZURE : A seizure is a transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. EPILEPSY -Two or more unprovoked seizures Epilepsy describes a condition in which a person has a risk of recurrent seizures due to a chronic, underlying process A single seizure associated with clinical or EEGfeatures portending high risk of recurrence may establish the diagnosis of epilepsy incidence of epilepsy is ∼0.3–0.5% ,prevalence of epilepsy has been estimated at 5–30 persons per 1000

3. Classification

4. Focal seizures originate within networks limited to one brain region are often associated with structural abnormalities of the brain. Generalized seizures arise within and rapidly engage networks distributed across both cerebral hemispheres may result from cellular, biochemical, or structural abnormalities that have a more widespread distribution .

5. Focal Seizures with Intact Awareness Focal seizures can cause motor,sensory , autonomic, or emotional symptoms without impairment of awareness ictal EEG Abnormal discharges in a very limited region over the appropriate area of cerebral cortex if the seizure focus involves the cerebral convexity Focal motor seizures Abnormal motor movements may begin in a very restricted region, such as the fingers, and gradually progress (over seconds to minutes) to include a larger portion of the extremity “Jacksonian march,” spread of seizure activity over a progressively larger region of motor cortex Localized paresis (Todd’s paralysis) for minutes to many hours in the involved region following the seizure Seizure may continue for hours or days termed epilepsia partialis continua

6. Focal Seizures with Impaired Awareness Transient impairment of the patient’s ability to maintain normal contact with the environment -unable to respond appropriately to visual or verbal commands during the seizure -impaired recollection or awareness of the ictal phase. Aura (i.e., a focal seizure without cognitive disturbance) Motionless stare Automatisms -involuntary, automatic behaviors -basic behaviors, such as chewing, lip smacking, swallowing, or “picking” movements of the hands The patient is typically confused following the seizure -Transition to full recovery of consciousness may range from seconds up to an hour or longer -Anterograde amnesia -Transient neurologic deficits (such as aphasia, hemineglect, or visual loss )

7. Generalized onset tonic- clonic seizures Main seizure type in ∼10% of all persons with epilepsy Most common seizure type resulting from metabolic derangements The seizure usually begins abruptly without warning vague premonitory symptoms in the hours leading up to the seizure -distinct from the stereotypic auras associated with focal seizures that generalize Tonic contraction of muscles throughout the body -Muscles of expiration and the larynx -will produce a loud moan or “ictal cry.” -Respirations are impaired -secretions pool in the oropharynx -cyanosis develops Jaw muscles -biting of the tongue Marked enhancement of sympathetic tone -increases in heart rate, blood pressure, and pupillary size

8. After 10–20 s clonic phase superimposition of periods of muscle relaxation on the tonic muscle contraction periods of relaxation progressively increase until the end of the ictal phase, which usually lasts no more than 1 min postictal phase unresponsiveness, muscular flaccidity, and excessive salivation that can cause stridorous breathing and partial airway obstruction Bladder or bowel incontinence postictal confusion Headache, fatigue, and muscle ache EEG-Tonic phase of the seizure shows progressive increase in generalized low-voltage fast activity, followed by generalized high-amplitude, polyspike discharges. clonic phase , the high-amplitude activity is typically interrupted by slow waves to create a spike-and-slow-wave pattern. postictal EEG shows diffuse suppression of all cerebral activity, then slowing that gradually recovers as the patient awakens .

9. ABSENCE SEIZURES-TYPICAL AND ATYPICAL TYPICAL ABSENCE SEIZURES- sudden, brief lapses of consciousness without loss of postural control. The seizure usually lasts for only seconds, consciousness returns as suddenly as it was lost, and no postictal confusion. absence seizures are accompanied by subtle, bilateral motor signs such as rapid blinking of the eyelids, chewing movements, or small-amplitude, clonic movements of the hands. The seizures can occur hundreds of times per day, but the child may be unaware of or unable to convey their existence EEG -generalized, symmetric, 3-Hz, spike-and-slow-wave discharges that begins and ends suddenly, superimposed on a normal EEG background.

10. Atypical Absence Seizures The lapse of consciousness is usually of longer duration and less abrupt in onset and cessation, and the seizure is accompanied by more obvious motor signs that may include focal or lateralizing features. Atypical absence seizures-associated with diffuse or multifocal structural abnormalities of the brain may accompany other signs of neurologic dysfunction such as mental retardation. The seizures are less responsive to anticonvulsants compared to typical absence seizures . EEG -generalized, slow spike-and-slow-wave pattern with a frequency of ≤2.5 per second

11. Atonic Seizures -sudden loss of postural muscle tone lasting 1–2 s Consciousness is briefly impaired Usually no postictal confusion A very brief seizure may cause only a quick head drop or nodding movement, cause the patient to collapse (drop attacks)substantial risk of direct head injury with the fall EEG- B rief, generalized spike-and-wave discharges followed immediately by diffuse slow waves that correlate with the loss of muscle tone Myoclonic Seizures Myoclonus is a sudden and brief muscle contraction involve one part of the body or the entire body. A normal, physiologic form of myoclonus is the sudden jerking movement while falling asleep Pathologic myoclonus is most commonly seen in association with metabolic disorders, degenerative CNS diseases, or anoxic brain injury Myoclonic seizures are considered to be true epileptic events because they are caused by cortical dysfunction Usually coexist with other forms of generalized seizures but are the predominant feature of juvenile myoclonic epilepsy EEG -bilaterally synchronous spike-and slow-wave discharges immediately prior to the movement and muscle artifact associated with the myoclonus

12. Epileptic Spasms - Briefly sustained flexion or extension of predominantly proximal muscles, including truncal muscles During the clinical spasm, there is a marked suppression of the EEG background The electromyogram (EMG) also reveals a characteristic rhomboid pattern that may help distinguish spasms from brief tonic and myoclonic seizures Epileptic spasms occur predominantly in infants and likely result from differences in neuronal function and connectivity in the immature versus mature CNS

13. JUVENILE MYOCLONIC EPILEPSY JME is a generalized seizure disorder of unknown cause that appears in early adolescence Bilateral myoclonic jerks that may be single or repetitive Seizures are most frequent in the morning after awakening and can be provoked by sleep deprivation Consciousness is preserved Many patients also experience generalized tonic- clonic seizures, onethird have absence seizures The seizures usually respond well to appropriate anticonvulsant medication There is often a family history of epilepsy, and genetic studies suggest a polygenic cause

14. MESIAL TEMPORAL LOBE EPILEPSY SYNDROME Mesial temporal lobe epilepsy (MTLE) is the most common syndrome associated with focal seizures with impairment of consciousness

15. CAUSES ACCORDING TO AGE

16. Drugs and Other Substances That Can Cause Seizures Cocaine Phenycyclidine Methylphenidate Flumazenil

17. Evaluation of the adult patient with a seizure When a patient presents shortly after a seizure, attention to vital signs, respiratory and cardiovascular support, and treatment of seizures Life-threatening conditions such as CNS infection, metabolic derangement, or drug toxicity must be recognized and managed appropriately If this is the first seizure, then the emphasis will be Establish whether the reported episode was a seizure rather than another paroxysmal event Determine the cause of the seizure by identifying risk factors and precipitating events Decide whether antiseizure drug therapy is required in addition to treatment for any underlying illness IF the patient with prior seizures or a known history of epilepsy, the evaluation is directed toward identification of the underlying cause and precipitating factors Determination of the adequacy of the patient’s current therapy

18. HISTORY The first goal is to determine whether the event was truly a seizure Questions should focus on the symptoms before, during, and after the episode in order to differentiate a seizure from other paroxysmal events The patient may be unaware of the ictal and immediate postictal phases-witnesses to the event should be interviewed Focus on risk factors and predisposing events Clues for a predisposition to seizures include History of febrile seizures Family history of seizures Earlier auras or brief seizures not recognized as such

19. Epileptogenic factors such as prior head trauma, stroke, tumor, or CNS infection In children, a careful assessment of developmental milestones provide evidence for underlying CNS disease. Precipitating factors-Sleep deprivation Systemic diseases Sr.electrolyte or metabolic derangements Acute infection Drugs that lower the seizure threshold Alcohol or illicit drug use should also be identified

20. How to administer first aid for seizures Move the person away from danger (water, machinery, furniture) After convulsions cease, turn the person into the ‘recovery’ position (semi-prone) Ensure the airway is clear but do not insert anything in the mouth ( tonguebiting occurs at seizure onset and cannot be prevented by observers) If convulsions continue for more than 5mins or recur without the person regaining consciousness, summon urgent medical attention Do not leave the person alone until fully recovered (drowsiness and delirium can persist for up to 1hr)

21. EXAMINATION General physical examination-search for signs of infection or systemic illness Careful examination of the skin may reveal signs-tuberous sclerosis or neurofibromatosis, or chronic liver or renal disease Finding of organomegaly-indicate a metabolic storage disease Limb asymmetry-provide a clue to brain injury early in development Auscultation of the heart and carotid arteries may identify an abnormality that predisposes to cerebrovascular disease Careful assessment of mental status (including memory, language function, and abstract thinking)-suggest lesions in the anterior frontal, parietal, or temporal lobes Testing of visual fields-lesions in the optic pathways and occipital lobes Screening tests of motor function-pronator drift, deep tendon reflexes, gait, and coordination-lesions in motor (frontal) cortex cortical sensory testing (e.g., double simultaneous stimulation)-lesions in the parietal cortex

22. DIFFERENTIAL DIAGNOSIS OF SEIZURES

23. Features That Distinguish Generalized TonicClonic Seizure from Syncope

24. PSYCHOGENIC SEIZURES Psychogenic seizures are nonepileptic behaviors that resemble seizures often part of a conversion reaction precipitated by psychological distress Certain behaviors such as side-to side turning of the head ictal eye closure asymmetric large amplitude shaking movements of the limbs twitching of all four extremities without loss of consciousness pelvic thrusting are commonly associated with psychogenic than epileptic seizures Psychogenic seizures often last longer than epileptic seizures-may wax and wane over minutes to hours Measurement of sr.prolactin levels may also help to distinguish between epileptic and psychogenic seizures Most generalized seizures-some focal seizures are accompanied rise in serum prolactin in the immediate 30- min postictal period,psychogenic seizures are not Though this is not always reliable because baseline prolactin levels are rarely available and certain medications can elevate prolactin levels .

25. Serum urine toxicology should be done when Substance abuse or drug overdose is suspected In newborns and young children Metabolic screen can be requested

26. TREATMENT Therapy for a patient with a seizure disorder is almost always multimodal and includes treatment of underlying conditions that contribute to the seizures -avoidance of precipitating factors -suppression of recurrent seizures by prophylactic therapy with antiseizure medications or surgery In almost all cases, a neurologist with experience in the treatment of epilepsy should design and oversee implementation of the treatment strategy patients with refractory epilepsy or those who require polypharmacy with antiseizure drugs should remain under the regular care of a neurologist

27. TREATMENT OF UNDERLYING CONDITIONS If the cause of a seizure is a metabolic disturbance-abnormality of serum electrolytes or glucose, then treatment is aimed at reversing the problem and preventing its recurrence. Therapy with antiseizure drugs is usually unnecessary unless the metabolic disorder cannot be corrected promptly and the patient is at risk of having further seizures. If the seizure with a medication (e.g., theophylline) or illicit drug use (e.g., cocaine), therapy is avoidance of the drug; there is usually no need for antiseizure medications unless subsequent seizures occur in the absence of these precipitants. Seizures caused by a structural CNS lesion-brain tumor, vascular malformation, or brain abscess may not recur after treatment of the underlying lesion However, despite removal of the structural lesion, there is a risk of seizure that result of gliosis and other processes induced by surgery, radiation, or other therapies Most patients are therefore maintained on an antiseizure medication for at least 1 year, and an attempt is made to withdraw medications only if the patient has been completely seizure free

28. AVOIDANCE OF PRECIPITATING FACTORS An almost universal precipitating factor for seizures is sleep deprivation, so patients should do everything possible to optimize their sleep quality particular situations that appear to lower their seizure threshold; For example,association between alcohol intake and seizures-encouraged to modify their drinking habits There is often an association between stress and seizures, stress reduction techniques such as physical exercise, meditation, or counseling may be helpful .

29. When to Initiate Antiseizure Drug Therapy Recurrent seizures of unknown etiology or a known cause that cannot be reversed Patients with a single seizure due to an identified lesion such as a CNS tumor, infection, or trauma, in which there is strong evidence that the lesion is epileptogenic, should be treated. Generally accepted risk factors associated with recurrent seizures include the following: prior brain insult such as a stroke or trauma An EEG with epileptiform abnormalities A significant brain imaging abnormality (4) Nocturnal seizure. Most patients with one or more of these risk factors should be treated

30. Selection of Antiepileptic Drugs

31. MECHANISMS OF ACTION OF ANTISEIZURE DRUGS Antiseizure drugs appear to act primarily by blocking the initiation or spread of seizures Inhibition of Na+ -dependent action potentials in a frequency dependent manner (e.g., phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide, rufinamide, cenobamate ) inhibition of voltage-gated Ca2+ channels (phenytoin, gabapentin, pregabalin) Facilitating the opening of potassium channels (ezogabine) Attenuation of glutamate activity (lamotrigine, topiramate, felbamate, perampanel ) ,

32. Potentiation of GABA receptor function (benzodiazepines and barbiturates) Increase in the availability of GABA (valproic acid, gabapentin, tiagabine) Modulation of release of synaptic vesicles (levetiracetam, brivaracetam) Inhibiting T-type Ca2+ channels in thalamic neurons Ethosuximide and valproic acid

33. Antiseizure Drug Selection for Focal Seizures Carbamazepine (oxcarbazepine and eslicarbazepine ), lamotrigine, phenytoin, and levetiracetam are currently the drugs of choice Carbamazepine (which is also available in an extended-release form) follows first-order pharmacokinetics, which allows for a linear relationship between drug dose, serum levels, and toxicity leukopenia, aplastic anemia, or hepatotoxicity Oxcarbazepine avoids an intermediate metabolite also has fewer drug interactions Eslicarbazepine has a long serum half-life and is dosed once daily Lamotrigine mood-stabilizing properties that can be beneficial skin rash during the initiation of therapy Stevens-Johnson syndrome Risk can be reduced by the use of low initial doses and slow titration

34. Phenytoin long half-life once- or twice-daily dosingHowever , properties of nonlinear kinetics main causes of acute phenytoin toxicity (dizziness, diplopia, ataxia). Long-term use of phenytoin is associated with untoward cosmetic effects (e.g., hirsutism, coarsening of facial features, gingival hypertrophy) and effects on bone metabolism Levetiracetam no known clinically relevant drug-drug interactions complain of irritability, anxiety, and other psychiatric symptoms Topiramate focal and generalized seizures topiramate can cause significant psychomotor slowing and other cognitive problems Avoid in glaucoma or renal stones. Valproic acid is an effective alternative for some patients with focal seizures, especially when the seizures generalize Gastrointestinal side effects are fewer when using the delayed release formulations reversible bone marrow suppression and hepatotoxicity. high risks of women of childbearing age, including hyperandrogenism-may affect fertility and teratogenesis (e.g., neural tube defects) in offspring.

35. Zonisamide, brivaracetam, tiagabine, gabapentin, perampanel , and lacosamide additional drugs currently used for the treatment of focal seizures with or without evolution into generalized seizures Phenobarbital and other barbiturate compounds were commonly used in the past as first-line therapy for many forms of epilepsy sedation in adults hyperactivity in children subtle cognitive changes

36. Antiseizure Drug Selection for Generalized Seizures Lamotrigine, valproic acid , and levetiracetam best initial choice for the treatment of primary generalized, tonic- clonic seizures Topiramate, zonisamide, perampanel , phenytoin, carbamazepine, and oxcarbazepine are suitable alternatives Valproic acid absence, myoclonic, and atonic seizures DOC in patients with generalized epilepsy syndromes having mixed seizure types levetiracetam, rather than valproic acid , Drug of choice for women with epilepsies having mixed seizure andfor women of childbearing age Ethosuximide uncomplicated absence seizures not useful for tonic- clonic or focal seizures bone marrow suppression

37. INITIATION AND MONITORING OF THERAPY The response to any antiseizure drug is unpredictable Goal is to prevent seizures and minimize the side effects of treatment; determination of the optimal medication This process may take months or longer if the baseline seizure frequency is low Most antiseizure drugs need to be introduced relatively slowly to minimize side effects Starting doses are usually the lowest value. Subsequent increases should be made only after achieving a steady state with the previous dose

38. Start with one first line drug Start at a low dose gradually increase dose until effective control of seizures is achieved or side effects develops If first drug fails Start second first line,followed if possible by gradual withdrawl of first If second drug fails Start second line drug in combination with preferred first line drug at maximum tolerated dose If this combination fails Replace second line drug with alternative second line drug If this combination fails Check compliance and reconsider diagnosis Consider alternative,non drug treatments e.g.-surgery Use minimum number of drugs in combination at any one time Monotherapy should be the goal whenever possible .

39. WHEN TO DISCONTINUE THERAPY Withdrawl of therapy can be attempted after 2 years of seizure free interval in a patient who meets al of the following criteria complete medical control of seizures for 1–5 years single seizure type, with generalized seizures having a better prognosis than focal seizures normal neurologic examination, including intelligence no family history of epilepsy normal EEG. In most cases, it is preferable to reduce the dose of the drug gradually over 2–3 months Most recurrences occur in the first 3 months after discontinuing therapy patients should be advised to avoid potentially dangerous situations such as driving or swimming during this period Patients should be advised of the risks of recurrence, to allow them to decide whether or not they wish to withdraw Withdrawal may necessitate precautions around driving or occupation

40. TREATMENT OF REFRACTORY EPILEPSY one-third of patients with epilepsy do not respond to treatment with a single antiseizure drug Patients who have focal epilepsy related structural lesion or with multiple seizure types and developmental delay are particularly likely to require multiple drugs A combination of drugs with different mechanisms of action may be most useful Patients with myoclonic seizures resistant to valproic acid may benefit from the addition of levetiracetam, zonisamide, clonazepam, or clobazam absence seizures may respond to a combination of valproic acid and ethosuximide The same principles concerning the monitoring of therapeutic response, toxicity, and serum levels for monotherapy apply to polypharmacy, and drug interactions need to be recognized If there is no improvement, a third drug can be added while the first two are maintained If there is a response, the less effective or less well tolerated of the first two drugs should be gradually withdrawn.

41. MORTALITY OF EPILEPSY People with epilepsy have a risk of death that is roughly two to three times greater than expected Most of the increased mortality is due to the underlying etiology of epilepsy (e.g., tumors or strokes in older adults) Significant number of patients die from accidents, status epilepticus, and a syndrome known as sudden unexpected death in epilepsy (SUDEP),with convulsive seizures and tends to occur at night Genetic mutation may be the cause of both epilepsy and a cardiac conduction defect that gives rise to sudden death .

42. EPILEPSY IN PREGNANCY Most women with epilepsy who become pregnant will have an uncomplicated gestation and deliver a normal baby Pre-conception counseling Folic acid 5mg for 3 months before conception Fetal malformation Single drug Carbamazapine and lamotrigine have the lowest incidence of major fetal abnormalities Sodium valproate has relatively higher risk Levetiracetam may be safe Learning difficulties in children Lower IQ with valproate Haemorrhagic disease of newborn mother should be treated with oral vitamin K (20 mg/d, phylloquinone) in the last 2 weeks of pregnancy, and the infant should receive intramuscular vitamin K (1 mg) at birth Increased frequency of seizures: where breakthrough seizures occur, monitor antiepileptic drug levels and adjust the dose Pharmacokinetic effects of pregnancy : carbamazepine levels may fall in the third trimester Lamotrigine and levetiracetam levels may fall early in pregnancy

43. SURGICAL TREATMENT Temporal lobe epilepsy resection of the anteromedial temporal lobe (temporal lobectomy) limited removal of the underlying hippocampus and amygdala (amygdalohippocampectomy) Focal seizures arising from extratemporal regions focal neocortical resection with precise removal of an identified lesion ( lesionectomy ) Implantable device Can detect the onset of a seizure and deliver an electrical stimulation Responsive neurostimulation Stereotactic radiosurgery Laser thermoablation Deep brain stimulation