EEG stuff Flashcards
EEG waveform and diagnosis
Triphasic waves
Frontally dominant, anterior to posterior phase lag, 2.5 Hz
Hepatic encephalopathy, progression of encephalopathy and elevated ammonia levels, metabolic abnormalities,
EEG waveform and diagnosis
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
EEG waveform and diagnosis
Benzo or barbiturate causing frontally dominant, symmetric 20 Hz beta activityground 7-8 hz slowed rhythm, diffuse theta activity
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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.
EEG waveform and diagnosis
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
What can be used to determine which kind of LPDs are interictal/irritative brain injury versus ictal/periictal LPDs?
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
LPDs-max versus LPDs-plus
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.
LPDs/PLEDS
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.
EEG waveform and diagnosis
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
EEG waveform and diagnosis
SREDA: Subclinical EEG Discharges of Adults
Epileptiform: high voltage generalized fast (5-6 Hz) spike and wave activity in a recurrent pattern
EEG waveform and diagnosis of top box
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.
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
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
EEG waveform and diagnosis
Burst Suppression
Comatose
Describe the EEG changes in Hepatic encephalopathy
Hepatic Encephalopathy
Posterior dominant rhythm, gradual slowing with appearance of theta and delta waves
Triphasic waves when encephalopathy worsens and ammonia levels increase
Describe the eeg changes in renal (uremic) encephalopathy
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
Describe the eeg changes in hypocalcemia
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
Describe the eeg changes in hypercalcemia
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
