Epilepsy, Syncope, & the Unconscious Patient Flashcards

1
Q

What determines a patient’s state of arousal?

A
  • the central reticular formation, located throughout the brainstem and to the thalamus
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2
Q

Which three things should you always consider in an unconscious patient?

A
  • hypoglycemia
  • opioid overdose
  • upper airway obstruction (if the patient is cyanosed)
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3
Q

What are the most common causes of unconsciousness?

A
  • reflex syncope (such a postural hypotension)
  • concussion
  • CVAs (cerebrovascular accidents)
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4
Q

What are the five general levels of consciousness?

A
  • consciousness: awake
  • cloudy consciousness: confused
  • stupor: unconscious, awakened by shakes and shouts
  • semicomatose: unconscious, responds to pain
  • comatose: unconscious, unresponsive
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5
Q

Which three breathing patterns should be considered in the unconscious patient?

A
  • Cheyne-Stokes (periodic respiration): suggests cerebral dysfunction
  • ataxic respiration (shallow, irregular): suggests brainstem lesion
  • Kussmaul respiration (deep, rapid hyperventilation): suggests metabolic acidosis
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6
Q

What are four major causes of unconsciousness?

A
  • C.O.M.A.
  • CO2 narcosis (respiratory failure)
  • Overdose (alcohol, carbon monoxide, opioids, etc.)
  • Metabolic (diabetes, uremia, hypothyroidism)
  • Apoplexy (CVAs, also: trauma, meningitis, tumor)
  • (apoplexy is bleeding into internal organs)
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7
Q

What are blackouts? What are the major causes? Which is the most common?

A
  • blackouts are episodes of L.O.C.
  • major causes: epilepsy, reflex syncope, cardiac syncope, autonomic syncope, respiratory syncope, carotid sinus syncope, and migrainous syncope
  • epilepsy is the most common cause
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8
Q

How do we manage the unconscious patient?

A
  • maintain airway and circulation
  • “coma cocktail”: TONG (Thiamine, Oxygen, Naloxone, and Glucose); may lesson metabolic injury to the brain
  • Naloxone is an opiate antagonist
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9
Q

What is epilepsy? How common is it? What types of epilepsy are there?

A
  • epilepsy is a condition of recurrent seizures (a seizure is the symptom of paroxysmal neuronal activity) due to an enduring predisposition to generate seizures (as opposed to symptomatic seizures as an acute result of infection, etc.)
  • present in 1-2% of population, 4% in children
  • seizures can be focal (L.O.C. may or may not occur) or generalized (L.O.C. occurs; absence, tonic-clonic, myoclonic, clonic, tonic, atonic)
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10
Q

What are the major types of generalized epileptic seizures?

A
  • absence: AKA “petit mal” seizures, common in kids, frequent, brief (less than 30 seconds) loss of awareness and behavioral arrest with immediate recovery of alertness; patient may not immediately recognize what happened
  • tonic-clonic: AKA “grand mal” seizures, most severe type, rigid tonic phase (less than 1 minute) followed by a convulsive clonic phase (less than 2-3 minutes); cyanosis, tongue-biting, incontinence are common; postictal phase of confusion and amnesia
  • atonic: “drop attacks,” sudden loss of lower limb tone results in sudden falls to the ground (patient usually immediately gets right back up)
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11
Q

Following a tonic-clonic “grand mal” seizure, what may patients experience?

A
  • status epilepticus: patient experiences at least one other seizure without recovering consciousness between episodes (total even is longer than 30 minutes)
  • serial seizures: patient recovers consciousness and then experiences another seizure
  • postepileptic automatism: patient experiences abnormal behavior immediately following the seizure with no memory of the event
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12
Q

What investigations should be performed in a patient experiencing a seizure?

A
  • MRI (the best imaging for epileptic seizures)
  • if contraindicated, CT scan is OK as well
  • (imaging is indicated in the patient’s 1st seizure, often it is not done for a future seizure if the cause seems to be the same)
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13
Q

DDx of Focal Seizures and DDx of Generalized Seizures

A
  • focal: transient ischemic attack (TIA), rage attack, panic attack
  • generalized: syncope, cardiac disease, PNES (psychogenic nonepileptic seizure)
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14
Q

How do we treat epilepsy? How efficient is drug therapy?

A
  • anti-epileptic drugs (AEDs) are usually given to prevent future seizures
  • these are usually continued for at least 2 years (if the patient is seizure free for these 2 years, they can decide if they want to continue or stop therapy)
  • 50% will respond to the 1st drug, 20% to a 2nd drug, 30% will fail to respond (called pharmacoresistant epilepsy; 80% of kids fall into this category)
  • other therapies: surgery (if seizures are very focal), chronic vagal nerve stimulation, ketogenic diet (high fat, low protein)
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15
Q

Other than an epileptic disorder, what is another major cause of generalized tonic-clonic “grand mal” seizures?

A
  • alcohol withdrawal!
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16
Q

What is the most common cause of status epilepticus? What are some other causes? How do we treat it?

A
  • poor compliance with anti-epileptic drug (AED) regimen
  • others: alcohol withdrawal, intracranial infection/neoplasm, metabolic disorders, drug overdose
  • (note that status epilepticus is a medical emergency)
  • 1st line therapy is with benzodiazepines (clonazepam, diazepam)
17
Q

What is syncope?

A
  • a sudden, transient loss of consciousness and postural tone due to reduced cerebral perfusion
  • patients recover spontaneously, rapidly, and fully (vs. the slower recovery seen in the postictal phase of epilepsy)
  • if a patient does not recover: comatose
18
Q

Which two general events can cause syncope?

A
  • 1) dysfunction of the reticular activating system (RAS)
  • 2) dysfunction of BOTH cerebral hemispheres
  • (the dysfunction is due to inadequate cerebral perfusion)
19
Q

What is a focal seizure? If focal seizures are strong enough to generate a generalized seizure, which type of seizure will be generated?

A
  • focal seizures are confined to one hemisphere (usually they arise in the medial temporal lobe), and exhibit a high degree of unique stereotypy for each patient (often includes an aura, as well)
  • focal seizures (when generating a generalized seizure) will ALWAYS result in tonic-clonic “grand mal” seizures (this is called secondary generalization)
20
Q

What are the major risk factors for developing epilepsy? In patients with epilepsy, what lowers the seizure threshold?

A
  • trauma, stroke, viral encephalitis, alcohol, Alzheimer’s, bacterial meningitis, heroin use, family Hx
  • sleep deprivation, alcohol, and stress all lower the seizure threshold in epileptic patients (others: depression, menstruation, dehydration, infection, malnutrition, etc.)
21
Q

What are the major causes of epilepsy? Which is the most common

A
  • cerebrovascular disease/structural/metabolic
  • genetic
  • cryptogenic (unknown); this is the most common
22
Q

What are two major genetic causes of epilepsy?

A
  • A.D. nocturnal frontal lobe epilepsy: seizures in childhood
  • Dravet syndrome: seizures in infancy (due to mutation in SCN1A gene encoding neuronal sodium channels)
23
Q

What are the major causes of syncope? Which is the most common?

A
  • peripheral vascular syncope (the most common)
  • cardiac/central vascular syncope (the most deadly potentially)
  • cerebrovascular syncope (uncommon)
24
Q

Examples of Peripheral Vascular Syncope

A
  • (these causes of syncope usually have an immediate prodrome of “feeling faint”)
  • vasovagal: sudden onset of lowered pulse rate and vascular tone; this occurs with extreme emotion, sight of blood, etc.
  • orthostatic hypotension: loss of compensation to maintain BP when going from sitting/lying down to standing
  • cough, sneeze, and micturition syncopes
25
Q

Cardiac (Central Vascular) Syncope

A
  • these are due to myocardial dysfunction (arrhythmia, CAD, etc.) and are therefore the most potentially deadly
  • these usually lack a noticeable prodrome, and patients experience a sudden syncope
  • investigating a syncope patient is mainly to make sure it was not cardiac syncope!
26
Q

Cerebrovacular Syncope

A
  • this type of syncope is relatively rare (because hemorrhage rarely gets into the RAS and it is unlikely for a CVA to affect both hemispheres)
  • subarachnoid hemorrhage: massive headache with potential syncope
  • TIA/stroke involving the vertebrobasilar system (supplies brainstem)
27
Q

What examinations and investigations should be performed for a patient with syncope?

A
  • examination: postural hypotension, pulse rate/rhythm, cardiac murmurs, abdotenderness
  • investigations: blood sugar and ECG (all other tests are indicated only if suspicion is justifiable)
28
Q

After a patient’s 1st epileptic seizure, what is the risk for experiencing a 2nd?

A
  • 40% chance of having a 2nd seizure once the 1st occurs
29
Q

What are the main general adverse affects of anti-epileptic drugs? What about for specific drugs?

A
  • general: somnolence and sedation, cognitive impairment, ataxia (these promptly resolve after discontinuation); long-term use associated with loss of bone density; teratogenic
  • phenytoin: hirsutism, diplopia, acne, gum hypertrophy, rash/SJS
  • carbamazepine: hyponatremia, rash/SJS, weight-gain, diplopia, leukopenia
  • valproic acid: GI, weight-gain, tremor, alopecia, pancreatitis, thrombocytopenia, hepatotoxicity (rare, but fatal)
  • (SJS: Stevens-Johnson syndrome; a severe cutaneous reaction to a drug)
  • (valproate is least sedative, while the benzodiazepines are the most)
30
Q

Which patients are at an increased risk of developing Stevens-Johnson syndrome?

A
  • Asians with HLA-B1502; screen all Asians before commencing carbamazpeine
  • especially with carbamazepine
31
Q

AEDs and Contraception and Pregnancy; AEDs and Chemo/Radiotherapy

A
  • enzyme-inducing AEDs (carbamazepine and phenytoin) decrease the efficacy of the contraceptive pill by increasing estrogen clearance
  • contraceptive pill and pregnancy greatly reduce the serum level of lamotrigine (breakthrough seizures can result if the dose is not increased)
  • all AEDs are also teratogenic, doubling the risk of congenital malformations (3% chance to 6% chance); valproate is the most teratogenic of the drugs (3x-5x greater risk)
  • however, pregnant patients suffering from epilepsy ARE given AEDs as a seizure would cause potentially severe damage to the fetus; give folate to help reduce risk of malformations
  • many AEDs are excreted in breast milk (lamotrigine > levetiracetam > valproate/carbamazepine)
  • enzyme-inducing AEDs also interfere with chemotherapy and radiotherapy as they speed up the clearance of these drugs, making them less effective
32
Q

What is GEFS+ (Generalized Epilepsy w/ Febrile Seizures Plus)?

A
  • GEFS+ occurs in patients who have a history of febrile seizures as a child and who later develop epileptic seizures
33
Q

On EEG, what characterizes a generalized absence seizure?

A
  • 3Hz generalized spike-and-wave activity
34
Q

Major AEDs and Their MOAs

A
  • block Na+ channels: carbamazepine, phenytoin, valproic acid, lamotrigine, topiramate
  • block Ca2+ channels: ethosuximide, gabapentin
  • stimulate GABA transmission: benzodiazepines, phenobarbital (these allosterically enhance GABA receptors), valproic acid (inhibits GABA degradation), topiramate
  • block glutamate receptors: levetiracetam
  • (blocking ion channels, blocking glutaminergic input, and increasing GABAergic input all prevent action potential generation and NT release!)
35
Q

Epilepsy and Driving

A
  • after suffering a seizure, patients are not allowed to drive for at least 6 months (assuming they are seizure-free during this period)
  • in addition, patients are not allowed to drive for 4 months after stopping drug therapy
  • truck/bus drivers must be seizure-free for 10 years
36
Q

What are the major co-morbitidies of epilepsy? What is the mortality rate of epileptic patients?

A
  • co-morbidities: depression and anxiety (suicide is not uncommon)
  • mortality rate is 2-3x greater than normal population, due to:
  • status epilepticus (20% mortality rate)
  • injuries during seizures, aspiration pneumonia
  • sudden death (occurs in 1.7%)
37
Q

What are the first line drugs used to manage tonic-clonic seizures? Absence seizures? Partial seizures? What about status epilepticus? What about for second line drugs?

A
  • tonic-clonic: phenytoin, carbamazepine, valproic acid, phenobarbital, topiramate, lamotrigine, levetiracetam
  • absence: ethosuximide, valproic acid, lamotrigine
  • partial: carbamazepine, phenytoin, valproic acid, phenobarbital, and all others except for ethosuximide (which is ONLY used for absence seizures)
  • status epilepticus: treat acute with benzodiazepines (diazepam, lorazepam) and then give phenytoin for prophylaxis/long-term management