Objectives Seizure Assessment & Management Classification of seizures  Process of Diagnosing  Treatments  Maritza Lopez, RN, MSN,CNRN What is a seizure?  A seizure is an event, characterized by an excessive and synchronous discharge of cerebral neurons with associated sensory, motor, and/or behavioral changes. What is Epilepsy? Epilepsy is defined as recurrent, unprovoked seizures caused by biochemical, anatomic & physiological changes. Etiology Idiopathic- may arise from an unknown cause  Cryptogenic-may arise from an presumed cause (i.e. genetic) that is unknown or ill defined  Symptomatic-arising from a known cerebral abnormality   Conditions in the brain that produce seizures may have been present since birth, or they may develop later in life due to injury, infections, structural abnormalities in the brain, exposure to toxic agents, or for reasons that are still not well understood. 1 Risk factors for provoked seizure Risk factors for epilepsy •CNS neoplasms: gliomas/meningiomas •Vascular: Stroke, AVMs, Cavernous hemangiomas •Trauma: penetrating head injury, depressed skull fracture, LOC >24 hours, intracerebral hemorrhage •Infection: encephalitis, abscess, meningitis, neurocystercercosis •Dementia: Alzheimer’s disease •Prenatal/Perinatal: genetic syndromes, cortical malformations, hypoxia •Mental retardation ( occur in 28 % to 38% of children with epilepsy) •Cerebral palsy •Neonatal or febrile seizures? •Metabolic: Low Na/Mg/Phos/Ca/Gluc, high Na, hepatic encephalopathy, uremia •Toxic: drug or drug withdrawal (cocaine/meth v EtOH/BDZ), meds (ABX, INH, TCA, wellbutrin, clozaril, anesthetics). •Infectious: meningitis or encephalitis (bact/fungal/TB/viral/parasite), HIV, abscess. •Endocrine: hyperthyroidism •Neurodegenerative: advanced AD, VD •Trauma: penetrating head injury, depressed skull fx, ICH, LOC>24h •Tumor: mass or carcinomatous meningitis. •Vascular: hypertensive encephalopathy, eclampsia, vasculitis, SAH, ICH, ischemic stroke, SDH, EDH, AVM. Epidemiology •Almost 2 million in the U.S. have epilepsy •500,000 are medically refractory •Approximately 10% of Americans will experience a single seizure in their lifetime •Risk of a recurrent unprovoked seizure (5 years) –After single unprovoked: ~33% –After second unprovoked: ~73% Comorbidities • Mental Retardation and developmental delay occur in 28 % to 38% of children with epilepsy • Depression/mood disorders-20% • SUDEP occurs in greater proportion of patients with epilepsy compared to the general population • Memory impairment disorders • Headaches Pathophysiology Epileptogenisis originates from an imbalance between cerebral excitation and inhibition. In a sz, brain cells become abnormally linked together, leading to abnormal electrical firing. This may occur due to a loss of cells that inhibit excitatory cells or an overabundance of excitatory cells. Excitation Glutamate-most important CNS excitatory neurotransmitter involved in epilepsy  Methyl-D-asparate (MDA) is glutamate receptor  Some AEDs work by antagonizing glutamate receptors  2 Inhibition  Aminobutyric acid (GABA) – Facilitates activity of Cl- (Cl- allows cell membrane to become more neg charged, making it difficult for cells to depolarize – Opens K+ channels (which leads postsynaptic inhibition) or closes Ca++( acts as a pacemaker for nl rhythmic brain activity . (AEDs that inhibit Ca++ work for absence seizures) – Na+ channels are required for an action potential to fire. Some AEDs stabilize the inactive form of Na+ Hypersynchronization Caused by large number of neuronal cells firing together  Inhibition blockade induces polarization, leading to hyper-synchrony  Pathological conditions may compromise inhibition, leading to excitation.  Types of Seizures (International Classification of Epileptic Seizures) Generalized Seizures  Generalized seizures affect both cerebral hemispheres from the beginning of the seizure. They produce loss of consciousness, either briefly or for a longer period of time, and are sub-categorized into several major types. Tonic-Clonic Seizure Generalized tonic clonic seizures (grand mal seizures) are the most common and best known type of generalized seizure. They begin with stiffening of the limbs (the tonic phase), followed by jerking of the limbs and face (the clonic phase).  3 Absence Seizures Absence seizures (also called petit mal seizures) are lapses of awareness, sometimes with staring, that begin and end abruptly, lasting only a few seconds. There is no warning and no after-effect.  Atonic Seizure Atonic seizures produce an abrupt loss of muscle tone Myolclonic Seizures Myoclonic seizures are rapid, brief contractions of bodily muscles, which usually occur at the same time on both sides of the body. Occasionally, they involve one arm or a foot.  Partial Seizures  In partial seizures the electrical disturbance is limited to a specific area of one cerebral hemisphere. 4 Complex Partial Seizures Simple Partial Seizures  People who have simple partial seizures do not lose consciousness during the seizure. However, some people, although fully aware of what's going on, find they can't speak or move until the seizure is over. Often times aura’s are sps. CPS may be preceded by SPS  Automatisms such as lip smacking, blinking, or picking at clothes often accompany CPS  Motor phenomena such as wandering, running, or arm jerking often accompany frontal seizures.  A partial seizure may evolve to a secondarily generalized seizure  Epilepsy Syndromes  Idiopathic epilepsy w/ age-related onset  Localization-related/symptomatic epilepsies  Generalized/idiopathic epilepsies  Generalized cryptogenic or symptomatic epilepsies.  Generalized/either idiopathic or symptomatic epilepsies  Is Seizure Classification Important? Differential diagnosis Syncope  Panic attacks  TIA  Narcolepsy  Myoclonus  Multifocal chorea  Migraines  Complex partial seizures affect a larger area of the brain than simple partial seizures. Per AANN, CPS have an onset of synchronous cortical discharges resulting in symptomatology r/t brain region affected.  Yes. Accurate classification provides the key of seizure management from the initial diagnostic evaluation to decision-making about further evaluations and treatment. 5 Epilepsy Center Tests  Assessment History, neuro exam, med hx         MRI PET- positron Emissin Tomography MEG- Magnetoencephalography MSI-magnet source imaging Ictal SPECT-single photon emission computed tomography EEG-routine/sleep/sleep deprived NeuroPsych test Wada •Epileptic & behavioral events are synchronized with EEG data to establish the diagnosis and identify the treatment options. Why VET Diagnosing  Classifying seizures  Matching medications  Localizing and lateralizing focus  Seizure Safety precautions Padded side rails  Side rails up  IV  O2  Suction  Standing orders, ie. Ativan , when to notify HO  Seizure Assessment Keep patient safe. ABC’s  Position patient flat and on their side for grand mal seizures  Remove all restrictive clothing or wires or glasses.  Take blankets off.  Stay away from view of camera.  6 Tonic-Clonic Make sure patient is safe  Do not have to really have do language or motor.  Describe facial twitching, eye deviation, head deviation  Then do post ictal assesment every 5 minutes until baseline.  Simple partial Describe out loud what they feel during and after CPS Safety  How do you feel, describe  Orientation,  Ask them if they recognize object or repeat what you said.  Lip smacking, facial twitching, eye deviation, hand automatisms, is there dystonic posturing in hands, head deviation  During seizure, test… Remember word What are you feeling/impaired awareness  Language- Demonstration of Ictal speech. Are they amnestic? Comprehension(show elbow), Repetition (the train came to station a half hour late)& Naming(point to watch)  Motor response-tone?  Memory-what is the word you asked him to remember.   Post ictal NES    Orientation- Language (comprehension, naming & repetition) Motor response (upper and lower)-Todd’s paralysis Psychogenic non-epileptic seizures seem to be caused by stressful psychological experiences or emotional trauma. It is one way that the body indicates excessive stress. Repeat assessment until pt is at baseline. NOTIFY FELLOW/HO if sz lasts longer than 5 min. 7 Treatments Medications  Surgery  Vagus Nerve Stimulation  Ketogenic Diet  Complementary Treatment  “Older” Drugs       Phenobarbital 1912 Phenytoin (Dilantin) 1938 Primidone (Mysoline) 1952 Ethosuximide (Zarontin) 1960 Carbamazepine 1974 (Tegretol, Tegretol XR, Carbatrol) Valproate/Valproic Acid 1978 (Depakote, Depakene, Depakote ER) Antiepileptic Drugs - Spectrum of Activity “Newer” Drugs         Felbamate (Felbatol) Gabapentin (Neurontin) Lamotrigine (Lamictal) Topiramate (Topamax) Tiagabine (Gabatril) Levetiracetam (Keppra) Oxcarbazepine (Trileptal) Zonisamide (Zonegran) 1993 1994 1995 1996 1998 1999 2000 2000 Partial Seizures PHT, CBZ, PBR, GBP TGB, OXC, PGB They all can cause drowsiness, cognition problems, dizziness  Phenytoin-gingival hyperplasia  VPA- hair loss  Lamotrigine- rash, insomnia  Topomax and Zonisamide- kidney stones  Keppra- Behavioral issues  Felbatol- aplastic anemia ACTH ESM VPA, LTG, TPM, FBM, ZNS, LEV PHT=phenytoin; CBZ=carbamazepine; PBR=phenobarbital; GBP=gabapentin; TGB=tiagabine; OXC=oxcarbazepine; LEV=levetiracetam; VPA=valproate; LTG=lamotrigine; TPM=topiramate; FBM=felbamate; ZNS=zonisamide; ACTH=adrenocorticotropic hormone; ESM=ethosuximide; PGB=pregabalin Side effects  Generalized Seizures Absence Simple Tonic-clonic Tonic Infantile Complex Myoclonic spasms Secondarily generalized Atonic Medications         Pharmacokinetic properties-study of conc of drugs and metabolites in body Bioavailability- how much drug reaches circ Elimination- how drugs are metabolized & excreted Concentration: amt necessary to cause effect Absorption-transfer of drug from site to tissue Distrubion- rate of penetration of drug to tissue Monotherapy vs polytherapy Herbs 8 Medications- Protein binding     Determines amount of drug in plasma r/t amount in tissue Affected by age, pregnancy, amt of albumin in blood and concomitant meds. Enzyme system: Cytochrome P-140 (major drug metabolizing enzyme in body). Enzymes usually in gut and liver. Other drugs may cause inhibition or induction causing side effects or drug/drug interaction. Laboratory monitoring (more in older drugs b/c newer drugs have less protein binding Pregnancy All women of child bearing age should take Folic acid to prevent birth defects (many are folic antagonists)  Infants of mothers exposed to AED in utero are 2x likely for birth defects  Ketogenic Diet The ketogenic diet, which is very high in fats and low in carbohydrates, was first developed almost 80 years ago. It makes the body burn fat for energy instead of glucose  Invasive Monitoring  Depth electrodes: fine wires placed into the brain tissue.  Subdural strips: strands of electrodes placed on the surface of brain via burr holes in the skull. Usually 4-8 are placed in a given time, covering different pt of brains Invasive Monitoring  Subdural Grid: a rectangular sheet of electrodes placed on the surface of the brain. The grid records seizure activity, and can also be used to map speech and motor areas to help guide the surgeon in the resection. •Neuropsychological testing includes a battery of tests used to assess language, memory and intelligence. It is useful as a tool to aid in the identification of the sz focus as well as to track cognitive and behavioral functioning over time. •Wada tests (sodium amytal) determines the dominant hemisphere for language an memory •Functional brain mapping 9 Surgery Surgery Temporal lobectomy -70-80% of being sz free.  Extratemporal neocortical resection  Corpus Callosotomy-palliative  Functional hemispherectomy  Multipal Subpial Transection (MST)-offers reduction in seizures  Status Epilepticus Vagus Nerve Stimulator  Vagus nerve stimulation (VNS) is a type of treatment in which short bursts of electrical energy are directed into the brain via the vagus nerve. (50-60 thousand per year) >30 min  > 2 seizures consecutively w/o mental clearing between seizures.  Usually because of sub-therapeautic levels  Meningitis, encephalitis, eclampsia, drug w/drawal, hypoglycemia, hypoxia, trauma or stroke  S.E. Convulsive  NCSE  – Simple partial – Complex partial – Absence status  Pathophysiology-changes occur due to a massive release of epi and norepi during the seizure. Compensatory mechinisms  BP & CO  Cerebral Metabolic rate  glycemia Late Changes  CV –BP falls, decrease O2 to brain  Respiratory-Hypoxia  Metabolic-glucose rises, making pancreas work harder  10    Either continuous seizures lasting at least five minutes, or two or more discrete seizures between which there is incomplete recovery of consciousness – Tonic-clonic seizures rarely last > 2 minutes – Complex partial seizures rarely > 10 minutes Convulsive SE is a life-threatening medical emergency! Non-convulsive SE often requires aggressive management but the level of urgency is dependent on several clinical factors Subtle signs of Nonconvulsive SE Persistent coma Forced gaze deviation or nystagmus  Rhythmic twitching of one region (e.g. face, digit)  Repetitive/stereotyped language  Echolalia  Persistent confusion + seizure risk factors   Management of Status Epilepticus Time (min) Agent Dose (IV) 0-20 Lorazepam 0.1 mg/kg Rate 2 mg boluses q5 min 20-30 Fosphenytoin 20 mg/kg 150 mg/min 30-35 Fosphenytoin 5-10 mg/kg 150 mg/min Consider intubation, skipping ahead to Midazolam 35-55 Phenobarbital 20 mg/kg 50-75 mg/min 55-65 Phenobarbital 5-10 mg/kg 50-75 mg/min Midazolam OR Propofol 0.2 mg/kg load 1-2 mg/kg load 0.1 -0.4 mg/kg/hr 2-10 mg/kg/hr Pentobarbital 20 mg/kg load 50-100 mg/min Valproic acid 40 mg/kg Give over 10 mins 11