Eeg in encephalopathy

NeurologyKota 1,904 views 40 slides May 19, 2020
Slide 1
Slide 1 of 40
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40

About This Presentation

Eeg in encephalopathy- Dr Pallav Jain


Slide Content

EEG in encephalopathies Dr Pallav Jain Senior Resident GMC,Kota

Usefulness To identify seizures or NCSE To detect functional cerebral dysfunction in patients with normal imaging To demonstrate focal or lateralized abnormalities

Patterns of EEG Diffuse slowing Intermittent delta rhythms Periodic EEG patterns(PLED,BIPLEDS,GPED) Triphasic waves Burst suppression activity Monorhythmic activity( alpha,beta,spindle coma)

Triphasic waves M edium to high amplitude (usually >70µV), diffuse, frontally predominant waves. Most prominent component is a positive sharp wave that is preceded by a short-duration negative sharp wave and followed by a long-duration negative slow wave. Duration-0.15 to 0.25 seconds and recur singly or in serial trains almost periodically GPDs with triphasic morphology- hepatic encephalopathy, uremia, sepsis, and electrolyte disturbances.

BURST-SUPPRESSION Burst suppression (BS) is an EEG pattern consisting of alternative period of slow/spike waves of high amplitude (the burst) and periods of so called flat EEG (the suppression). The amplitude of bursts is between 20-100 µV. Suppressions also vary in amplitude in the range of electro-cerebral inactivity (ECI; <20 µV to 50 µV).

As abrupt change in amplitude describes this pattern, the amplitude difference must be clearly visible and must be >50%. Bursts are usually bilateral synchronous, generalized Duration- 1-3 seconds

Pathogenesis - R esults from suppression of cortical activity via GABA- ergic mechanisms with breakthrough EEG activity due to intact glutaminergic transmission . G eneral anesthesia . M edically induced-in patients with refractory status epilepticus. Cardiopulmonary arrest who suffer from cerebral anoxia. Encountered in neonates(Severe cerebral damage)

Periodic epileptiform discharges PLEDs consist of sharp waves and/ or spikes, associated with slow waves, occurring at periodic intervals. Duration-100-300 msec , amplitude(100-300µV) and they recur every 0.5-4 sec. PLEDs stand out from the background activity due to their higher amplitudes. The periodicity of the discharges is the result of a disconnection of the cortex from the subcortical structures Significance-indicative of an acute focal brain dysfunction or unilateral brain lesion

BIPLEDs are PLEDs seen in both hemispheres, in an independent and asynchronous manner. BIPLEDs may present as asynchronous complexe . D iffering in morphology, amplitude, rate of repetition, and site of maximal involvement. A cute multifocal structural lesions, with or without metabolic disturbances. Most common-anoxic encepahalopathy,CNS infections

GPEDs Periodic complexes occupying at least 50% of a standard 30-minutes EEG, over both hemispheres in a symmetric, diffuse, and synchronous manner. Characterized by spikes/ polyspike or sharp wave of high amplitude Toxic-metabolic encephalopathies, anoxic brain injury, CJD, and nonconvulsive status epilepticus.

COMA REACTIVE EEG The EEG is said to be reactive when there is a change in cerebral rhythm to stimulation, which includes change in amplitude or frequency. Eye blink artifacts or muscle artifacts do not count. I t is important for the EEG technician to stimulate comatose patients (noxious stimulation/passive eye opening) and note the time of stimulation on EEG.

Alpha coma R hythmic alpha frequency in unconscious patient Monomorphic,symmetrical,prominently in the frontal derivations but may be diffusely represented. There is no response to external stimuli or passive opening of the eyes. Sleep wake cycles are absent. W idespread cerebral damage (as from anoxia ) Prognosis poor

Spindle coma M ono-rhythmic, non-reactive, 11-14 Hz waveforms, occurring paroxysmally on a delta background. H ead injury, midbrain strokes, drug toxicity, and cerebral anoxia. Spindle coma is associated with preserved brain stem reflexes and sparing of normal thalamo -cortical pathways C arries a better prognosis.

Beta coma Beta coma is characterized by high-amplitude beta activity, sometimes frontally predominant. Intoxication with barbiturates or benzodiazepines favorable outcome.

Hepatic - Slowing of PDR which is followed by frequency in theta and delta rhythm. Triphasic waves(25%) Uremic -Slowing of background activity. Triphasic waves(15-20%). Epileptiform activities( b/l spike and wave) more common in uremic HSE - PLED,BIPLEDS or focal temporal slowing

Hashomoto encephalopathy M ild to severe generalized slowing or frontal intermittent rhythmic delta activity, triphasic waves, photomyogenic response, and photoparoxysmal response. With clinical improvement, the EEG background activity also improves and returns to normal, R ate of resolution of the EEG abnormalities is usually slower than the rate of resolution of clinical abnormalities The EEG is useful for diagnosis.

NMDAR encepahlitis Nearly continuous combination of delta activity (1–3 Hz) with superimposed fast activity (20–30 Hz) usually in the beta range Seen in NMDA-R encephalitis It is most often symmetric and synchronous Detected broadly across all head regions with predominance in frontal regions

Creutzfeldt – Jakob disease (CJD ) B ackground rhythms become fragmented and are destroyed . Diffuse slowing appears and increases . Later , the distinctive periodic sharp wave discharges, often at 1 Hz, are recorded At first, the discharges may be more irregular and even focal, only later becoming generalized and synchronous. Background activity decreases in amplitude. Eventually the EEG is dominated by the periodic discharges with no discernible background .

Criteria Strictly periodic activity- variability of intercomplex interval is <500ms Periodic activity is continuous for atleast 1 seconds Bi/ triphasic morphology of periodic complexes Duration- 100-600 ms Periodic complex may be generalized or lateralized,but not regional or asynchronous

SSPE Periodic, stereotyped, generalized high voltage discharges I- periodic discharges seen in sleep II-In wakefulness. Bilateral synchrounus symmetrical bursts, Amplitude- 200-500mv. Each bursts consists of polyphasic , momomhorphic delta waves. Burst every 4-10 seconds(Time locked with myoclonus)

III- slow delta rhythm IV- voltage of recording gets smaller and becomes isoelectric

BRAIN DEATH Electrocerebral inactivity (ECI) is defined as the absence of any waves of cerebral origin. The record should not have activity that exceeds 2 μV , unless that activity is clear environmental artifact (e.g., an IV drip or cardiac artifact). Low-frequency filters should be set between 0.5 Hz and 1.5 Hz, and the high-frequency filter should be set at 70 Hz.

I nterelectrode impedance should be between 1000 and 10,000 Ohms. The EEG should be reviewed at a sensitivity of 2 μV /mm for at least 30 minutes D ouble-distance bipolar montage should be available to maximize the chances of detecting cerebral activity. R eversible disturbances must be excluded (toxic–metabolic perturbations, hypothermia, or sedating medication).

D/D-non-convulsive status epilepticus (NCSE). Usually no anterior-posterior delay in NCSE. GPDs that are faster in frequency (>3 Hz) or have evolution meet the criteria for electrographic seizures.
Tags