EEG stuff Flashcards

1
Q

EEG waveform and diagnosis

A

Triphasic waves
Frontally dominant, anterior to posterior phase lag, 2.5 Hz
Hepatic encephalopathy, progression of encephalopathy and elevated ammonia levels, metabolic abnormalities,

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1
Q

EEG waveform and diagnosis

A

Diffuse slowing
Acute encephalopathy: initially slow posterior dominant rhythm, reduced beta activity in frontal (with benzos or barbiturates = fast beta abundant) -> worsens to increased theta and delta -> in comatose = delta predominates -> burst suppression as worsens to flat
Also seen with anti-NMDA encephalitis in children, pediatric acute liver failure with encephalopathy

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2
Q

EEG waveform and diagnosis

A

Benzo or barbiturate causing frontally dominant, symmetric 20 Hz beta activityground 7-8 hz slowed rhythm, diffuse theta activity

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3
Q

EEG waveform and diagnosis

A

Frontally dominant generalized rhythmic delta activity - frontal intermittent rhythmic delta activity - 2-3 Hz high amplitude rhythmic to semirhythmic activity with anterior predominance
Midline cerebral pathology: 3 ventricle region tumor
Nonspecific in encephalopathic EEG

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4
Q

EEG waveform and diagnosis

A

GRDA with posterior emphasis - occipital intermittent rhythmic delta activity (ORIDA)
Children with absense epilepsy
Self-limited focal epilepsies, including childhood epilepsy with centrotemporal spikes and Panayiotopoulos syndrome.

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5
Q

EEG waveform and diagnosis

A

Lateral Periodic Discharges or Periodic Lateralized Epileptiform Discharges
Sharp waves or spikes of complexes 1-3 Hz with semirhythmic patter, no clear progression or spread
Subacute structural lesion: stroke, MC
Can be associated with the development of epilepsy
Can be seen in alcohol withdrawal, Creutzfeldt-Jakob disease, anoxic brain injury, hemiplegic migraines

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6
Q

What can be used to determine which kind of LPDs are interictal/irritative brain injury versus ictal/periictal LPDs?

A

Spiky or sharp LPDs followed by associated slow-after waves or period of flattening giving rise to triphasic morphology = LPD’s plus
LPDs-max = ictal pattern - focal nonconvulsive status epilepticus, sometimes related to subtle motor signs and epileptic seizure
LPDs-max = periodic polyspike-wave activity and focal burst-suppression-like patterns
LPDs-max have posterior predominace over temporoparietalooccipital regions - refractory to antiseizure medications

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7
Q

LPDs-max versus LPDs-plus

A

LPDs-max is a subtype of lateralized periodic discharges (LPDs) that is characterized by periodic polyspike-wave activity and/or focal burst-suppression-like patterns. LPDs-max is associated with ictal patterns, such as focal non-convulsive status epilepticus, and can sometimes be accompanied by epileptic seizures and subtle motor signs. LPDs-max is different from LPDs-plus, which are more likely to be associated with seizures and are often found along the IIC. LPDs-max, however, does not lie along the IIC.
Spiky or sharp LPDs followed by associated slow after-waves or periods of flattening giving rise to a triphasic morphology should be included in the definition of LPDs-plus. We propose defining a particular subtype of LPDs-plus that we call “LPDs-max”. The LPDs-max pattern corresponds to an ictal pattern, and therefore, a focal non-convulsive status epilepticus, sometimes associated with subtle motor signs and epileptic seizures. LPDs-max include periodic polyspike-wave activity and/or focal burst-suppression-like patterns. LPDs-max have a posterior predominance over the temporo-parieto-occipital regions and are refractory to antiseizure drugs. Interpretations of EEGs in critically ill patients require a global clinical approach, not limited to the EEG patterns. The clinical context and results of neuroimaging play key roles.

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8
Q

LPDs/PLEDS

A

LPDs, also known as periodic lateralized epileptiform discharges (PLEDs), are a common EEG pattern in patients who are critically ill and are associated with an increased risk of seizures. PLEDs are large, sharp, and repetitive potentials that are usually seen on scalp EEGs in patients who have acute structural brain lesions and serial seizures.

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9
Q

EEG waveform and diagnosis

A

Generalized Periodic Discharges
Many diseases: anoxic brain injury, hypothermia, during or after resolution of status epilepticus, infectious/toxic/metabolic encephalopathy, etc…
Disruption of the thalamocortical pathways

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10
Q

EEG waveform and diagnosis

A

SREDA: Subclinical EEG Discharges of Adults
Epileptiform: high voltage generalized fast (5-6 Hz) spike and wave activity in a recurrent pattern

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11
Q

EEG waveform and diagnosis of top box

A

Brief (potentially ictal) rhythmic epileptiform discharges - B(i)RDs/BERDs
Critically ill, neonates
Sharply contoured theta activity up to 3 seconds, can be related to epileptogenic foci in refractory epilepsy and also sites of cerebral injury in critically ill patients.

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12
Q

EEG waveform and diagnosis

A

Slowing during hyperventilation
Cerebral dysfunction: ca be “polymorphic” based on shape of waveform (structural dysfunction) or “rhythmic” based on frequency (underlying epileptiform activity)
Can be diffuse of focal

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13
Q

EEG waveform and diagnosis

A

Diffuse slowing
Global cerebral dysfunction
Theta or delta ranges
High or low amplitude
Sedatives, metabolic encephalopathy, toxic encephalopathy, cerebral infections like meningoencephalitis or deep midline brainstem structural lesions

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14
Q

EEG waveform and diagnosis

A

Frontal intermittent rhythmic delta activity (FRIDA): frontal cerebellar dysfunction
1-4 Hz, up to 2 seconds, always bilateral
Metabolic encephalopathy, neurodegenerative disease, hypoxic encephalopathy, infections and encephalitis

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15
Q

EEG waveform and diagnosis

A

Occipital intermittent rhythmic delta activity
2-3 fz Hz, high amplitude
Childhood absence Epilpesy, Childhood idopathic generalized epilepsy, juvenile huntingtons disease encephalopathy, and andi-NMDA receptor encephalitis

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16
Q

EEG waveform and diagnosis

A

Temporal intermittent rhythmic delta activity
Sinusoidal rhythmic and intermittent, antero-medial temporal regions in one or both hemispheres
1-4 hz
Seizures in temporal regions

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17
Q

EEG waveform and diagnosis

A

Alpha coma
Diffuse or widespread alpha frequencies
Diffuse in comatose patients
Posterior and vaires with noxious stimuli - brainstem lesion, poor prognosis
Diffuse with les reactivity to external stimuli - anoxic injury after cardiac arrest

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18
Q

EEG waveform and diagnosis

A

Spindle Coma
9-14 Hz, vertex sharp waves and K-complexes
on a delta background, anoxic injury, intracranial hemorrhage, diffuse ischemic insults and head trauma

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19
Q

EEG waveform and diagnosis

A

Burst Suppression
Comatose

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20
Q

Describe the EEG changes in Hepatic encephalopathy

A

Hepatic Encephalopathy
Posterior dominant rhythm, gradual slowing with appearance of theta and delta waves
Triphasic waves when encephalopathy worsens and ammonia levels increase

21
Q

Describe the eeg changes in renal (uremic) encephalopathy

A

Renal (uremic) encephalopathy
Like hepatic encephalopathy, with triphasic waves and slow background
Bursts of well-formed, smoothly contoured, negative-positive-negative, bilateral, symmetrical and synchronous, regular, reactive, periodic or rhythmic, 1.5 to 2.0 Hz, frontocentral, triphasic complexes with front occipital lag can be in any form of toxic-metabolic encephalopathy
High-voltage rhythmic delta activity with bilateral spike-slow-wave complexes is often seen in patients with dialysis disequilibrium syndrome associated with obtundation after a dialysis session

22
Q

Describe the eeg changes in hypocalcemia

A

Hypocalcemia: diffuse slowing through theta and delta frequencies, association between generalized spikes and sharp waves and burst of delta activity, 3-4 Hz spike and wave discharges in neonatals, can have absence status also

23
Q

Describe the eeg changes in hypercalcemia

A

Hypercalcemia
Increased theta and delta activity, can have spikes and sharp wave also, with increased level the background slowing increases in the frontal regions and paroxysmal bursts of theta and delta occur with TWs, can be pres like presentation
Check calcium levels to detect a CJD like syndrome in hypercalcemia

24
Q

Describe the EEG changes in hypoglycemia

A

Hypoglycemia
Slowing of background, mainly in the theta frequency range

25
Q

Describe the EEG changes in hyperglycemia

A

Hyperglycemia
Mild levels: background slows
Higher levels: increased diffuse delta slowing
>400 - sporadic spike
Nonketotic hyperglycemia can leak to continuous jerking of a body part (usually a limb) with EEG focal spikes, focal slow waves and a slower background

26
Q

EEG changes at different cerebral blood flow rates: 35-70, 25-35, 18-25, 12-18, <8-10?

A

35-70: normal - no injury
25-35: loss of beta - reversible
18-25: background slowing to theta frequencies (5-7 Hz) - reversible
12-18: background slowing to delta frequencies (1-4 Hz) - reversible
<8-10: Supression of all frequencies - neuronal death

27
Q

Methods of assessing ishcemia on EEG?

A

Fast-to-slow activity ratio assesses ischemia
Variability of relative alpha and post stiumulation alpha delta ratios correlate with DCI in SAH
Changes in alpha variability has been seen up to 2 days before onset of clinical symptoms

28
Q

How does alpha delta radio ratio and general EEG pattern change with ischemia?

A

Less alpha delta ratio
Generalized slowing (alpha -> loss beta -> loss theta -> loss delta -> suppression of all)

29
Q

Type of seizure

A

Generalized Tonic-Clonic
EEG findings include fast spike-and-wave activity at 4–5 Hz. During the tonic phase, the EEG may show a diffuse myogenic artifact, which becomes intermittent during the clonic phase

30
Q

Type of Seizure

A

Absence seizures
EEG findings include 3-Hz spike-and-wave complexes.

31
Q

Type of Seizure

A

Myoclonic seizures
EEG findings include polyspikes, which are a complex of repetitive spikes followed by a wave component.

32
Q

Type of Seizure

A

Benign focal epilepsy of childhood with centrotemporal spikes (BECTS)
EEG findings include centro-temporal spikes or Rolandic spikes.

33
Q

Type of Seizure

A

Lennox–Gastaut syndrome (LGS)
EEG findings include slow spike and waves, which are bilaterally synchronous discharges

34
Q

Type of Seizure

A

Partial seizures
EEG findings include spikes and sharp waves in a specific area of the brain, such as the temporal lobe

35
Q

Type of Seizure

A

Generalized epilepsy
EEG findings include spike-and-wave discharges that are widely spread over both sides of the brain

36
Q

Type of Encephalopathy

A

Periodic lateralized epileptiform discharges: A finding in herpes simplex encephalitis

37
Q

Type of Encephalopathy

A

CJD
Periodic sharp-wave activity: A distinctive finding in Creutzfeldt-Jakob disease (CJD), a subacute, progressive dementia caused by prion disease
Generalized periodic discharges: A finding in sporadic Creutzfeldt-Jakob disease

38
Q

Type of Encephalopathy

A

Extreme delta brushes: A finding in anti-N-methyl-D-aspartate receptor autoimmune encephalitis.

39
Q

Type of Encephalopathy

A

COVID-19 related encephalopathy: A diffuse slowing of the background activity and loss of reactivity to external stimuli

40
Q

What is this EEG of and what does it indicate?

A

Cortical Spreading Depression (with slow and prolonged peri-injury depolarization) indicates compromised metabolism
Can be used to detect infarct enlargement in MCA infarct and DCI after SAH

41
Q

What EEG findings are associated with poor outcomes after cardiac arrest?

A

Periodic epileptiform patterns
Seizures
Loss of reactivity
Absence of normal sleep architecture
Suppression burst
Flat background

42
Q

Components of quantitative EEG

A

CDSA: seizures = arch-like pattern, blue/green lower power
Asymmetry: absolute asymmetric index = absolute difference between hemispheres, relative asymmetry index = relative asymmetry over time
FFTS: three-axis array, t on x, frequency on y and power on z,
Z scores = standard deviations

43
Q

GPDs, LPDs, LRDA and GRDA - which is NOT associated with risk of seizure?

A

GRDA

44
Q

EEG findings associated with poor functional outcome at 3 months?

A

Absence of sleep architacture during 1st 24 hours of EEG
LPDs
Periodic discharges
Hunt and Hess Grade
IVH
No EEG reactivity
Absence of state change within 1st 24 hours
NCSE within 1st 24 hours
GPDs
BIPDs

45
Q

Seizure med causing hyperammonemia

A

Valproic acid

46
Q

EEG findings in SDH after cranie

A

Focal slowing, attenuation of faster frequencies and lower amplitues in region of SAH = structural dysfunction
Higher voltage and spiky waveform with irregular morphology of region = breach rhythm = after cranie
LPDs and rhythmic slowing in region = LRDA = in SDH
Rhythmic periodic patterns like LPDs and LRDA also seen

47
Q

Associated with unfavorable prognosis

A

Alpha coma

48
Q

Propylene glycol toxicity meds

A

Pentobarbital
Lorazepam
Diazepam

49
Q

Drug-induced NSCE

A

Cefepime (beta-lactam antibiotics)
Fluoroquinolones
Ifosfamide
L-asparaginase
Busulfan
Cisplatin

50
Q

RPLS and NSCE drugs

A

Tacrolimus
Cyclosporine
Bevacizumab

51
Q
A