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Neuroscience > L57 EEG and Epilepsy > Flashcards

L57 EEG and Epilepsy Flashcards

1
Q

Define EEG

A

surface recording of the electrical activity of nerve cells of the brain

*summation of EPSPs and IPSPs

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2
Q

what are EEGs used to assess?

A
  • brain damage
  • epilepsy
  • brain death
  • sleep stages
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3
Q

what are the types of EEG electrodes?

A

surface electrodes on scalp
intracranial
strip or grid electrodes

*nasopharyngeal electrodes, foramen ovale electrodes, subdural and depth electrodes (use only when the info from routine scalp is inconsistent), sphenoidal electrodes

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4
Q

what system does EEG electrode placement use?

A

international 10/20 system - the electrodes are placed with a distance from each other of 10% or 20% of the head circumference

19 electrodes + reference electrode (farthest away from brain) + ground electrode

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5
Q

what are the electrodes connected to and what does that do?

A

electrocencephalograph (a differential amplifier - 1 amplifier for 2 electrodes)

it amplifies the brain activity and records it on a strip of paper or stores it electronically

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6
Q

what is the amplitude of the EEG when measured on the scalp?

A

100 microvolts

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7
Q

brain wave activity can be either ____ or ____

A

rhythmic or arrrhythmic

*or both!

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8
Q

brain wave activity varies in..?

A

polarity
shape
frequency

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9
Q

what does brain wave activity amplitude range from?

A

20-60 microvolts

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10
Q

name the 4 main types of normal brain waves?

A
  • beta
  • alpha
  • theta
  • delta
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11
Q

describe beta-activity

A

low amplitude
high frequency
< 12 Hz
present over frontal regions of awake person

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12
Q

describe alpha-activity

A

8-12 Hz
present over posterior (occipital) regions
background frequency of awake person with eyes closed

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13
Q

describe theta-activity

A

4-7 Hz
found in drowsy adult persons + children
detected in hypnagogic states (trances, hypnosis, light sleep and just before falling asleep)

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14
Q

describe delta-activity

A

< 4 Hz

seen in certain encephalopathies and in deep sleep in normal adults

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15
Q

what do EEGs of a normal awake person consist of?

A

alpha activity + some low amplitude beta activity

*notice clear differences between L and R and frontal and occipital

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16
Q

what EEG pattern is common in infants?

A

delta-activity

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17
Q

what EEG pattern is common in young child?

A

theta and delta activity

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18
Q

what EEG pattern is common in middle age adults?

A

alpha and beta activity

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19
Q

what EEG pattern is common in older adults?

A

low amplitude alpha activity + scattered theta and delta waves

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20
Q

the slower the waves, the more ____ the abnormality

A

severe

  • EEGs are expected to be symmetrical
  • asymmetrical EEG = indication of some kind of a lesion in the brain (bleeding, infarction, tumor etc.)
21
Q

What EEG abnormalities indicate epileptiform activity

A

sharp waves, spikes, spike + waves complexes

22
Q

What are indications for EEG

A
  • seizure disorders- locate focus + type of seizure
  • eval of transient spells - TIA, residual ischemic neurological deficit (RIND), completed infarction vs. syncope, hysterical episodes
  • intracranial disease process (tumor, access)
  • diffuse disturbances of cranial function = metabolic disorder, encephalitis, degen process like v.Creutzfeldt-Jakob disease, sleep disorders
  • coma
  • brain death (ceased activity), isoelectric EEG
23
Q

define epilepsy

A

chronic condition of repetitive seizures

  • most common ever neurological disease with 6.5% prevalence
  • in all ages, races, social classes
  • if a person has a seizure one time, its not epilepsy
  • everyone has an individual seizure threshold and might experience a seizure under certain circumstances
24
Q

what are ways seizures start?

A
  • neuronal damage (genetic, traumatic, metabolic)
  • astroglial damage (weak K+ buffering and/or glutamate uptake)
  • excessive excitiation (more glutamate released, high ext. of K+)
  • less inhibition (loss of GABAergic interneurons)
25
Q

how do seizures stop?

A
  • membrane shunting of postsynaptic neuronal currents
  • astroglial K+ biffering and/or glutamate uptake
  • reduced excitation - less glutamate release or glutamate receptors
  • inhibition - more GABAergic neuron activity
  • decrease in energy (ATP) - acidosis, block of gap junctions
26
Q

what are examples of epileptic potentials?

A
  • spikes
  • sharp waves
  • hypsarrhythmia
  • sharp and slow waves
  • spikes and waves
  • polyspikes and waves
27
Q

what are the causes of epilepsy?

A
  • primary seizures

- secondary seizures - intracranial or extracranial / focal or generalized

28
Q

what is a primary seizure?

A

idiopathic, cryptogenetic
thought to result from constitutional or genetic disposition
threshold for seizures lower than normal

29
Q

what is secondary seizure?

A

acquired (aka symptomatic, partial, focal)
results from known pathologic lesion or disease process

includes focal vs. generalized and intracranial vs. extracranial

30
Q

what are intracranial causes?

A

-primary - genetic, biochem predisposition
-secondary
tumor
vascular (infarction, hemorrhage)
ateriovenous malformation
trauma (penetrating wound, depressed fracture)
infection (abcess, encephalitis)
congenital and hereditary disease (tuberous sclerosis)

31
Q

what are extra cranial causes

A 
metabolic-electrolytes, biochem, inborn errors of metabolism
anoxia
hypoglycemia
drugs
drug withdrawal
alcohol withdrawal
32
Q

describe partial focal seizures

A

originate of a small group of neurons = seizure focus

can be simple or complex

33
Q

describe simple focal seizure

A

motor, sensory, autonomic, psychological symptoms

no alteration of consciousness

34
Q

describe complex focus seizures

A

alteration of consciousness

secondarily generalized

35
Q

define aura

A

symptoms preceding the onset of partial seizures, abnormal sensations (fear, rising feeling in abs, specific odor) originating from the seizure focus

36
Q

describe primary generalized seizures

A

no aura, no focal symptoms, both hemispheres involved

convulsive or non-convulsive

37
Q

what are the types of primary generalized seizures

A
  1. absence typical/atypical - nonconvulsive generalized seizures - absence seizure (petit mal) of children
  2. myoclonic
  3. clonic
  4. tonic
  5. tonic-clonic
  6. atonic
38
Q

describe the tonic-clonic (grand mal) seizure

A

tonic phase (30s) - begins abruptly often with a grunt or cry due to tonic contraction of the diaphragm and thorax = forced expiration. Pt may fall to ground, may lose urine, may bite his tongue, become cyanotic

Clonic phase - jerking of extremities

postictal phase - pt may be sleepy, disorientated, may complain about headache and muscle soreness

39
Q

what constitutes the minimal criteria for the dx of epilepsy?

A

recurrent seizures

40
Q

what are positive symptoms

A

sensory - seeing light flashes, feeling of fear, hearing noises or people talking
motor- jerking of arm, leg or face

41
Q

what are negative symptoms

A

sensory - slowing of normal brain function, depression of consciousness
motor - Todd paralysis

42
Q

what is Todd paralysis

A 
transcient paralysis (30 m to 36 h)
hemiparesis
seizure
speech problems
vision problems
43
Q

describe status epilepticus

A

no recovery, interictal, period between seizures

medical emergency
-metabolic derangements - hypoxia, hypotension, hypoglycemia, acidemia = brain damage!
systemic complications - cardiac arrhythmias, pulmonary edema, hyperthermia, rhabdomyolysis (rapid breakdown, lysis of skeletal muscle due to injury of muscle tissue)

44
Q

what are the tx options of epilepsy?

A

drugs that block excitation

drugs that enhance inhibition

45
Q

name and describe the drugs that block excitation

A

phenytoin, carbamazepine, lamotriginum

reduce the flow of Na and Ca ions into the neurons and increase the level of the NT GABA and suppress the release of NT glutamate = less excitability

46
Q

name and describe the drugs that enhance inhibition

A

GABAergic benzodiazepeines, barbs

potentiate inhibitory GABAa receptors and inhibit excitatory AMPA receptors

47
Q

what is the MOA of levetiracetam

A

decrease the voltage-operated delayed rectifier K current without effect on Na and A-type K currents = reduced repetitive action potential generation

reduction of N-type and P=Qtype Ca currents = decreased NT release

binds to a synaptic vesicle protein, SV2A, which is believed to impede conduction across synapses

48
Q

what are tx options for drug-resistance epilepsy

A

surgery
invasive vagus nerve stimulation
transcutaneous vagus nerve stimulation

Neuroscience (54 decks)

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