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Penney Epilepsy
BCN #2 Penney Lecture on Epilepsy 4.4.13
| Question | Answer |
|---|---|
| Epilepsy | A chronic condition characterized by spontaneous, recurrent seizures |
| Epileptic Seizure | A clinical event associated with a transient hypersynchronous neuronal discharge and represents only the symptom of a potential underlying brain pathology and not the actual disease |
| Epileptic | A descriptive term used to denote the presence of an epileptic mechanism |
| Electroencephalography | EEG used to help in the diagnosis and classification of epileptic disorders |
| Encephalopathy | Refers to cerebral dysfunction of any cause |
| Epileptiform | Distinct waves or complexes, distinguishable from the background activity, which resemble waveforms recorded in a proportion of human suffering from an epileptic disorder (EEG); Refer to Interictal EEG activity (found inbetween seizures) and not Ictal EEG |
| Clinical Neurophysiology | Brain normally produces low voltage electrical activity; Prevailing belief is that most of the activity represents dendritic synaptic potentials is Cortical Pyramidal Cells |
| EEG Brainwaves | Gamma is problem solving/concentration; Beta is busy active mind; Alpha is reflective/restful; Theta is drowsiness; Delta is sleep/dreaming |
| EEG if ab epileptic seizure | A chaotic and unregulated electrical discharge passes through the brain, causing symptoms such as physical fits or loss of consciousness. The sudden onset of the attack is shown by the abrupt increase in activity of the traces. |
| Clinical definition of Epileptic Seizure | Episode of neurologic dysfunction in which abnormal neuronal firings manifest clinically by changes in motor control, sensory perception, behavior, and/or autonomic function |
| The aberrant electrical activity that underlies epilepsy is the result of.......... | Biochemical processes at the cellular level promoting neuronal hyperexcitability and neuronal hypersynchrony (a single neuron discharging abnormally, is insufficient to produce a clinical seizure, which occurs in the context of large neuronal networks |
| Partial (Focal) Seizures | Account for almost 60% of new cases of epilepsy |
| Simple Partial Seizures | Occurs in about 15% of pt.'s with seizures; Consciousness is NOT impaired; Sxs may be motor, cognitive, sensory, autonmic, affective; Depending on the area of cerebral cortex |
| Complex Partial Seizures | Aka temporal lobe or psychomotor seizure; Occurs in approx. 35% of pt.'s with seizures; Consciousness is partially or completely impaired; There is NO initial generalized tonic-clonic activity; Pt. may have no memory of event; |
| Generalize Seizures | Account for 40% of pt.'s with epilepsy; Initial manifestations indicate involvement of BOTH hemispheres (most commonly impairment of consciousness with bilateral motor involvement); Pt.'s usually forget the events of the seizure |
| Types of Generalized Seizures | Absence (petit-mal); Myoclonic; Clonic; Tonic; Tonic-Clonic (grand-mal); Atonic |
| Absence (petit-mal) Seizures | Staring or eye flickering, some body movements may occur, no convulsions or postictal sxs |
| Myoclonic Seizures | Symmetric jerking of the extremities |
| Tonic Seizures | Rigidity |
| Tonic-Clonic (grand mal) Seizures | Tonic stiffening (extension) followed by clonic flexion motion; may produce labored respirations, cyanosis, incontinence, involuntary tongue biting, post-ictal confusion, fatigue, stupor |
| Atonic | Sudden loss of postural tone (most common in peds) |
| Distinguishing secondarily generalized partial seizure from primary generalized seizure | Preceding the seizure, period of unresponsiveness and staring, aura, automatisms, focal motor phenomena; Past occurrence of these sxs WITHOUT impairment of consciousness; Focal findings on neurological exam/MRI; Focal activity on the EEG; Adult onset |
| Semiology | The study of signs as is symptomatology |
| Causes of Non-Epileptic Seizures 1-8 | Alcohol withdrawal; Benzodiazepine withdrawal; Massive sleep deprivation; Excessive use of stimulants (cocaine); Psychogenic (pseudoseizures); Acute head trauma; CNS infection; Uremia |
| Causes of Non-Epileptic Seizures 9-16 | Eclampsia; High fever; Hypoxemia; Hyperglycemia or Hypoglycemia; Electrolyte disorders; Neurocysticerosis (common in immigrants; from uncooked pork); Malaria |
| Todd's Paralysis | After a seizure (usually a Tonic-Clonic one) pt. has confusion or any assortment of neural deficits of neurological findings that will clear to normal (time varies); Much more common after tonic-clonic! |
| What is the differential dx. for a seizure? | Syncope; Migraine; Cerebrovascular; Sleep disorder; Movement disorder; Transient global amnesia; Psychiatric |
| Syncope | Vasovagal/Noncardiogenic; Decreased cardiac output; Volume depletion; Arrhythmia |
| Migraine | Class, Basilar, Confusional, Acephalgic |
| Cerebrovascular | TIA, Amyloid angiopathy |
| Sleep disorder | REM behavior disorder, Narcolepsy, Parasomnias |
| Movement Disorder | Tics, Non-epileptic myoclonus, Tremor |
| Psychiatric | Panic, Dissociation, Conversion, Malingering |
| Psychogenic or Pseudo Seizure Sxs | Frequent triggers; Gradual onset; Thrusting/back arching/erratic movements; Closed eyes; Can be lengthy (hrs); Serum prolactin levels are normal |
| Tonic Clonic Seizure Sxs | No frequent triggers usually; Sudden onset; Synchronized and stereotyped movements; Open eyes; Tongue biting common; Self injury common; Incontinence common; Post-ictal confusion common; 1-2 minutes long usually; Serum prolactin levels elevated |
| Common Causes that Provoke Seizures | Metabolic (mostly hypos) , Hypoxia, Medications (withdrawal); Substance abuse (withdrawal) |
| Are Psychogenic non-epileptic seizures mistaken for actual seizures frequently? | PNES or Psuedoseizures are frequently mistaken for seizures and represent up to 20% of referrals to epilepsy centers |
| To treat for Anti-Epileptic Drug (AED) therapy? | Most doctors prefer not to prescribe; Controversial; Single approach cannot be recommended - varies from pt. to pt. |
| Research studies with AED | Associated with a significant reduction in recurrence risk, although the benefit persisted only for the time that the pt. was taking the medication; pt's with a high risk for seizure recurrence may choose to take medication to lessen the risk |
| Risk of seizure recurrence following an unprovoked seizure is..... | 51% |
| Two most important prognostic factors influencing risk of recurrence | Etiology of the seizures and EEG findings |
| Clinician's Responsibility in Driving/Seizure | Clinicians have an important role in evaluating pt.'s ability to drive. Clinicians neither grant nor suspend driving privileges; this is the sole legal prerogative of the state!!! Nonetheless, physicians should counsel pt.'s regarding the risks |
| Clinicians are required to report their pt.'s with seizures to driving authorities in 6 states...... which are....... | California, Delaware, Nevada, New Jersey, Oregon, Pennsylvania; Monetary fines are the most common penalty; Possibility exists for legal action for negligence |
| Four broad categories of epilepsy syndromes | Idiopathic generalized; Symptomatic generalized; Idiopathic localization-related; Symptomatic localization-related |
| Idiopathic Generalized Epilepsy Syndrome | Seizure types (absence, myoclonic, tonic-clonic); Normal neuro exam; Normal neuroimaging; EEG normal background with fast (3-6 Hz) generalized spike and wave discharges |
| Idiopathic Generalized Epilepsy Syndrome examples and tx | Childhood absence epilepsy, Juvenile myoclonic E, Epilepsy with generalized tonic-clonic seizures on awakening; Tx: Valproate (Depakote), Ethosuximide (Zarontin) effective for absence seizures only, Lamotrigne (Lamictal), Topiramate (Topamax), Felbamate |
| Symptomatic Generalized Epilepsy Syndrome | Seizure types (atypical absence, myoclinic tonic, atonic, tonic-clonic), Abnormal multifocal neuro exam, Abnormal multifocal neuroimaging, Abnormal EEG with slow (<3 Hz) generalized and/or multifocal epileptiform discharges |
| Symptomatic Generalized Epilepsy Syndrome examples and tx | Lennox-Gastaut syndrome, Progressive myoclonic epilepsies; Tx: Valproate, Lamotrigine, Topiramate, Felbamate, Ketogenic diet, Corpus callosotomy |
| Idiopathic Localization-Related Partial/Focal Epilepsy Syndrome | Seizure types-simple partial (awareness unimpaired), complex partial (awareness impaired), secondarily generalized tonic-clonic; Normal neuro exam, Normal neuroimaging, Normal EEG background with focal epileptiform discharges |
| Idiopathic Localization - Related Partial/Focal Epilepsy Syndrome examples and tx | Benign childhood epilepsy with Centro-temporal spikes (Rolandic epilepsy), Benign epilepsy with occipital paroxysms; Tx: Carbamazepine (Tegretol), Phenytoin (Dilantin) |
| Symptomatic Localization-Related Partial/Focal Epilepsy Syndrome | Seizure types-simple (awareness unimpaired), complex partial (awareness impaired) secondarily generalized tonic-clonic; Abnormal/Normal focal neuro exam, Abnormal focal neuroimaging; EEG normal or abnormal background with focal or multifocal epileptiform |
| Symptomatic Localization-Related Partial/Focal Epilepsy Syndrome examples and tx | Temporal lobe epilepsy, frontal lobe epilepsy; Carbamazepine, Phenytoin, Valproate, New agents (Gabapentin, Neurontin), Lamotrigine, Tiagabine (Gabitril), Topiramate, Felbamate, Vagus nerve stimulator, Resective surgery |
| Status Epilepticus (SE) | Clinically defined as seizures persisting or recurring without a return to consciousness for an extended period, usually 30 minutes or more; Rationale has been challenged and kinda changed to greater than 5 minutes of unrelenting seizures |
| Prehospital Tx of SE | Lab data suggest that tx is most likely to terminate seizure successfully when delivered shortly after the onset of ictus; Changes in the GABA subunit that binds Benzos occurs rapidly during prolonged seizure; Most responsive within the 1st 10 min. |
| Lorazepam vs. Diazepam | Lorazepam is more efficatious than Diazepam (both are benzos); Diazepam is a good 2nd choice if Lorazepam is not mentioned |
| Problems with Lorazepam | Heat labile compared with other benzos (needs to be refrigerated); More expensive (10%); Requires IV administration |
| New Definition of SE | Generalized convulsive status epilepticus in adults and older children (>5yo) refers to greater than 5 min. of a continuous seizure, or 2 or more discrete seizures between which there is incomplete recovery of consciousness |
| Vagus Nerve Stimulator (VNS) | Novel, non-pharmacologic tx for epileptic pt.'s whose seizures are uncontrolled by meds; Under GA bipolar lead is wrapped around the left vagus nerve and tunneled to the infraclavicular region, where it is connected to a signal generator (30 sec. q 5 min) |
| Investigators have suggested that vagus nerve stimulator increases seizure threshold by causing......... | Widespread release of GABA and glycine in the brain |
| Most common procedure performed for the tx. of epilepsy? | Anterior temporal lobe resection |
| What causes pt.'s to be considered poor candidates for seizure surgery? | Pt.'s with progressive metabolic or neurodegenerative conditions (also seizures of bilateral hemispheres) |
| What type of pt.'s should be considered for seizure surgery? | Those pt.'s in whom anti-epileptic drugs failed to completely control seizures |
| Currently what percent of pt.'s undergoing temporal lobe resections become seizure free? | 80% |
| Pt.'s with evidence of mesial temporal sclerosis on MRI have a prospect for seizure free outcome of....... | Greater than 90% |
| At present, how many epilepsy centers exist in the U.S. | over 100 |
| How long does it take before pt.'s are referred for an epilepsy surgery evaluation? | around 20 years; Delay is likely due to physician's perception of epilepsy surgery as a "last resort" procedure |
| Seizure-free surgical outcome of well selected cases is? | 70-80% |
| Post-traumatic Epilepsy | PTE is a recurrent seizure disorder that results from injury to the brain; the injury may be due to head trauma or to an operation on the brain |
| Post-traumatic Seizures | PTS is a broader spectrum term and signifies that seizures that occur as a sequele (sx or result) to brain injury; |
| Immediate PTS | Seizures that occur within 24 hours after brain injury |
| Late PTS | Seizures that occur more than 1 week after injury; Tx is not mandatory |
| Early PTS | Seizures that occur within 1 week after injury; Should be treated promptly |
| What % of ppl who have a single late post-traumatic seizure never have any further seizures? | 20% and they should not be labeled as having PTE |
| Mechanism by which trauma to brain tissue leads to recurrent seizures is...... | Unknown; but cortical lesions seem important in the genesis of epileptic activity |
| Injury related factors that increase risk for PTE | Severe trauma; Penetrating head injuries; Intracranial hematoma; Linear or depressed skull fractures; Hemorrhagic contusion; Coma lasting more than 24 hours; Early PTS; Focal neuroimaging or EEG abnormalities in the acute post injury period |
| What % of frist PTS occur within 2 years of injury? | 80%; Risk of PTS decreases with time and reaches the normal value for the population at 5 years after the head injury; About 1/2 the pt.'s who develop late PTS have 3 or fewer seizures and go into spontaneous remission thereafter |
Created by:
gsnow711