Epilepsy Report Generator
Ambulatory EEGTechnical SummaryDescription of RecordHyperventilationPhotic StimulationClinical CorrelationOther Note Snippets
Ambulatory EEG
Template 1
AMBULATORY ELECTROENCEPHALOGRAM REPORT
PATIENT NAME:
MR #:
DOB:
REFERRING PHYSICIAN:
Start Time:
End Time:
Location: Home
Introduction:
Pertinent Medications:
Technique:
An ambulatory 21-channel digital EEG, with accompanying video, using 10-20 system of electrode placement with additional A1/A2 and EKG electrodes.
EEG Findings:
The background was continuous, symmetric and medium voltage. In awake state, a well-defined 9 Hz posterior dominant rhythm was recorded in the occipital regions bilaterally. The posterior background rhythm attenuated with eye opening and enhanced with eye closure.
Drowsiness (Stage I sleep) and all stages of sleep were normal.
Hyperventilation was not performed. Photic stimulation was not performed.
Abnormalities:
Comments:
Single EKG lead:
No rhythm abnormalities were observed.
EEG Diagnosis:
This ambulatory video EEG study during awake, drowsy and sleep states recorded:
Clinical Interpretation:Template 2
CLINICAL AND EEG ANALYSIS:
Day 1 (9/21, admission – 9/22, 7 am):
Baseline EEG: In the waking state a well-defined posterior background rhythm of 8.5 Hz was recorded in the occipital regions bilaterally. The posterior background rhythm attenuated with eye opening and enhanced with eye closure. Hyperventilation for 5 minutes produced a mild generalized bisynchronous as well as asynchronous delta and theta activity. Photic stimulation produced a symmetrical bi-occipital driving response. Drowsiness and sleep were not observed. There were no epileptiform discharges.
Events: none
Interictal EEG (detections and time samples): The seizure and spike detection program was operated daily. One-half hourly time samples were reviewed. Stage 2 sleep was observed. Vertex waves, K-complexes and sleep spindles were normal in morphology and distribution.
SAMPLE CLINICAL INTERPRETATION
A. A patient with a psychogenic seizure and normal EEG:
EEG Diagnosis: This EEG is normal in waking, drowsiness and sleep. There is no EEG change in association with 1,2,3,4,5,6,7 typical spells, other than muscle and movement artifact.
Clinical Interpretation: This study recorded 1,2,3,4,5,6,7 of the patient's typical spells. The main features were (mention the most prominent features, stressing the ones that point to a psychogenic origin). There were no associated EEG changes other than muscle and movement artifact (if present). By both EEG and clinical criteria this/these spell(s) is/were non-epileptic, most probably psychogenic in nature. In addition, due to the absence of interictal EEG abnormalities, this study fails to provide support for a co-existent epilepsy.
B. Psychogenic seizure plus epileptiform abnormalities on the EEG.
EEG Diagnosis:
1. Frequent sharp waves recorded from . . .
2. Intermittent irregular slow wave activity recorded from . . .
There were no EEG changes (other than muscle and movement artifact) in association with one of the patient's typical spells.
Clinical Interpretation: This study recorded one/two/three/four/five/six of the patient's typical spells. Its/their main clinical features were . . . The EEG showed no change (other than muscle and movement artifact). By both clinical and EEG characteristics this/these spell(s) is/were non-epileptic, and most probably psychogenic in origin.
On the other hand, the interictal EEG recorded left temporal sharp waves and suggests potential epileptogenicity in the left temporal region.
C. Predominantly subjective episodes or spells without definite altered awareness or responsiveness.
Clinical Interpretation: This study recorded two episodes that were predominantly subjective. There were no associated EEG changes. This study does not support an epileptic nature for these attacks. However, since most simple partial seizures are not associated with scalp EEG changes, the possibility of simple partial seizures is not ruled out.
D. No spells & normal EEG (The Clinical Interpretation may vary depending on the reason for the request).
EEG Diagnosis: This is a normal x day or x hour EEG-CCTV study
Clinical Interpretation: No events were recorded. This normal study fails to provide support for the diagnosis of epilepsy but cannot rule it out, particularly in the absence of recorded events.
E. No spells and interictal epileptiform discharges (and slow wave activity).
EEG Diagnosis: This 4 hour EEG-CCTV study is abnormal because of 1) frequent left anterior temporal epileptiform discharges and 2) left anterior temporal intermittent irregular delta activity.
Clinical Interpretation: This study is most consistent with the interictal expression of a partial epilepsy with a left anterior temporal potential epileptogenic focus.
F. Examples of totally congruent data.
Example 1
EEG Diagnosis: This 4-day EEG-CCTV study recorded:
1- Six ictal discharges associated with clinical seizures. All had a focal onset in the right inferomesial temporal region. Two were secondarily generalized.
2- Frequent right inferomesial temporal sharp waves.
3- Intermittent right temporal 2-4 Hz irregular delta activity.
Clinical Interpretation: This study recorded 6 complex partial seizures, 2 of which were secondarily generalized. [The clinical seizure onset was with a motionless stare followed by chewing and lip smacking, favoring a temporal focus. The well formed verbal automatisms (Help me! Help me!) specifically favor a right temporal focus. The tonic head deviation to the left and focal left arm jerking prior to secondary generalization also favor a right sided focus.] or [the main clinical features were a motionless stare at onset, chewing and lip smacking, well formed verbal automatisms, and tonic left head deviation and focal left arm jerking prior to secondary generalization. These features favor a right temporal localization]. In all the seizures, the first ictal EEG changes were focal in the right inferomesial temporal region. The interictal epileptiform activity was exclusively right inferomesial temporal, and right temporal slow activity was also seen indicating a disturbance in that area.
In summary, this study provides a confident localization of the epileptogenic focus to the right inferomesial temporal region with excellent convergence of clinical seizure pattern, ictal EEG, interictal epileptiform activity, and slow wave activity.
Example 2:
EEG DIAGNOSIS: This 8-day EEG-CCTV study recorded:
1- Two ictal discharges associated with clinical seizures. Both had a focal onset in the left inferomesial temporal region.
2- Occasional left inferomesial temporal or inferomesial temporal predominant sharp waves which became extremely frequent during sleep.
3- Occasional left temporal intermittent rhythmic delta activity (TIRDA)
4- Intermittent left temporal irregular theta/delta activity.
CLINICAL INTERPRETATION: This study recorded 2 complex partial seizures none of which was secondarily generalized. The clinical onset of seizure started with cessation of normal activity, blank stare, chewing and swallowing movements favor a temporal involvement. Postictally after the first event, the patient was found to be aphasic for almost 2-3 minutes, which favors a left temporal focus. This localization was supported by the ictal EEG onset and interictal epileptiform and slow activity which was left inferomesial temporal or inferomesial temporal predominant.
In summary, this study is diagnostic of partial epilepsy with confident localization of the epileptogenic focus to the left inferomesial temporal region with excellent convergence of clinical seizure pattern, ictal EEG, interictal epileptiform activity, and slow wave activity.
G. Example of fairly congruent data, less definitive.
Example 1. Left lateral temporal
EEG DIAGNOSIS: This 3-day EEG-CCTV monitoring is abnormal because of:
1. At least 16 ictal discharges with associated clinical seizures. All ictal discharges started with theta activity in the left temporal region (at T7, T1>P7, F7).
2. Bursts of left temporal rhythmic sharp activity in sleep (F7>T7>Fp1) lasting up to 10 seconds, with some evolution raising the possibility of subclinical ictal discharges.
3. Very frequent left temporal epileptiform discharges (T7 or F7 predominance).
4. Left temporal intermittent irregular slow activity.
CLINICAL INTERPRETATION: This 3-day EEG-CCTV study recorded 16 of patient’s typical complex partial seizures. Their main characteristics were sudden crying/moaning, appearing restless and scared, mild right facial twitching, head turn to the left, and bilateral limb automatisms. The early head turning to the left and right facial twitching at onset may favor a left lateral temporal focus. This localization is supported by the ictal onset and interictal epileptiform and slow activity.
In summary, this study is diagnostic of partial epilepsy with a probable left epileptogenic focus in the left lateral temporal region.
Example 2. Left frontal
EEG DIAGNOSIS: This three day EEG-video study is abnormal because of:
1. Fifteen ictal discharges associated with clinical seizures, six of which secondary generalized. All fifteen seizures started from left frontal region (F3>Fp1,F7,C3). 10 of the seizures started with transitional sharp waves.
2. Frequent high frequency beta bursts recorded from the same region as above.
3. Interictal epileptiform discharges from the left frontal or frontotemporal region.
4. Irregular delta activity recorded from the left frontal region.
CLINICAL INTERPRETATION: This 4-day EEG-CCTV study recorded fifteen complex partial seizures, six secondarily generalized. The seizures included early head turning to the left, hypermotor automatisms of the left extremities, while the right side was motionless or posturing, and, in transition to generalization, adversive head turning to the right, and asymmetrical tonic posturing (with figure of 4). The clinical features strongly favor a left lateralization. The initial hypermotor activity may suggest frontal lobe involvement. A left frontal localization was supported by the ictal EEG onset and by the interictal epileptiform and slow activity, which were consistently left frontal.
In summary, this study is diagnostic of partial epilepsy, with strong evidence of a left frontal epileptogenic zone.
H. Examples of independent foci
Example 1
EEG DIAGNOSIS: This four days EEG is abnormal because:
1. Eight ictal discharges associated with clinical seizures, four of which recognized by the patient. Four ictal events started from the left anterior-mid temporal region and four from the right anterior-mid temporal region.
2. Frequent independent left and right anterior-mid temporal sharp waves.
3. Independent left and right temporal intermittent rhythmic (TIRDA) or irregular activity. There was overall left predominance.
CLINICAL INTERPRETATION: This four-day EEG-CCTV study recorded eight complex partial seizures without secondary generalization. Four complex partial seizures were similar, starting with lip smacking, restlessness, moaning and groaning sound as well as arm dystonic posturing affecting the right arm earlier. He has postictal aphasia and was unable to read the test sentence until after one minute from the end of the seizure. These clinical features favor a left temporal localization. This was supported by the ictal EEG onset. The other four seizures all started in sleep and were subtle to the degree that they were not recognized by the patient or his girlfriend. They included brief arousal and lip smacking only. The seizures were not tested for responsiveness or language functions. These features favor temporal localization but are not lateralizing. The ictal EEG onset was right temporal.
In summary, this study is diagnostic of partial epilepsy and indicates bilateral independent epileptogenic foci, one left temporal that generates disabling seizures and the other right temporal with only subtle seizures in sleep.
Example 2
EEG DIAGNOSIS:
This EEG is abnormal due to:
1. Eleven ictal discharges associated with clinical seizures and one subclinical ictal discharge. There were three independent onsets: right temporal [5 seizures: seizures 2, 7 (initially bitemporal), and 9-11] or right frontotemporal (with inferomesial temporal predominance within 10 seconds of onset- 3 seizures: seizures 1, 3, &8), left temporal (seizure 6 and the subclinical ictal discharge), or right occipital-posterior temporal (seizures 4&5).
2. Rare independent sharp waves in the left and right temporal regions (Sp1, F7>T7 or Sp2, F8 >T8).
3. Irregular delta activity over both left and right temporal regions.
CLINICAL INTERPRETATION: This 4 day EEG-CCTV study recorded eleven complex partial seizures, one secondary generalized. The clinical seizure onset for all seizures except 4 was with lip smacking, then she had nonmanipulative automatisms (various rhythmic motions including hand opening-closing, pill rolling or patting) of the left hand (all seizures but 4-6) and dystonic posturing of the left upper extremity (seizures 1-4). There was also well formed speech in most seizures. The lip smacking favors a temporal focus and the left arm RINCH movements and dystonic posturing favors a right lateralization. This lateralization was also supported by adversive head turning to the left and the secondary generalized seizure (#3). A right temporal localization was supported by the ictal onset in seizures 1-3 and 7-11. However, 2 seizures (#4 and 5) had a right occipital origin and one seizure (#6) had a left temporal onset.
In summary, this study is diagnostic of partial epilepsy with independent epileptogenic foci in the right temporal, right occipital, and left temporal regions. The right temporal focus was the most active with 8 seizures.
I. Example of incongruent data.
Clinical Interpretation: This study recorded 5 complex partial seizures described above. The clinical pattern of the seizures, with bilateral posturing at seizure onset favors a frontal focus. However the first ictal EEG activity is right temporal, and the interictal epileptiform discharges are bitemporal independent with a left sided predominance. Thus this study fails to localize one epileptogenic focus due to divergence between the clinical seizure pattern and ictal and interictal EEG activity.
J. Example of seizures that were clinically mesial frontal, but without clear EEG ictal discharge.
Example 1
EEG Diagnosis: This 2-day EEG-CCTV study is abnormal due to:
Numerous clinical seizures, only some of which associated with ictal discharges, particularly two secondarily generalized tonic-clonic seizures. It was usually very hard to identify a definite cerebral ictal discharge. When definite ictal EEG changes were present with more severe seizures (#24 and 56), they tended to involve the parasagittal regions (Cz>Pz). Other changes were difficult to distinguish from movement artifact.
Clinical Interpretation: This 2-day EEG-CCTV study captured numerous clinical seizures, two of which were secondarily generalized tonic-clonic seizures. The main clinical features were arousal from sleep, followed by unilateral or bilateral leg posturing +/- abduction +/- left>right leg shaking. Some of these seizures also were accompanied by bilateral arm abduction and/or left face drawing up/twitching. When the seizures generalized, there was left head and eye deviation and tonic left arm posturing before generalization. These features are most consistent with a supplementary motor area focus, not definitively lateralized, although a right lateralization is more likely. The ictal activity at the vertex is consistent with this localization (but this was rarely seen).
In summary, this study is diagnostic of partial epilepsy and is most consistent with a supplementary motor area epileptogenic zone, probably on the right.
Example 2- no clear ictal discharge
EEG DIAGNOSIS: This 5-hour EEG-CCTV study recorded one ictal discharge out of sleep. The EEG was characterized by arousal, then muscle artifact (no definite rhythmic ictal activity could be identified). There were no definitive EEG abnormalities.
CLINICAL INTERPRETATION: This 5-hour EEG-CCTV study captured one of the patient’s typical events. The main features were arousal from sleep, elevation of the right arm above and behind the head, side-to-side head movements, and hypermotor activity. Although there were no associated EEG changes other than muscle and movement artifact, this event likely represents a partial seizure with a frontal lobe epileptogenic focus due to its occurrence out of sleep, explosive motor manifestations (this was also stereotyped based on the patient’s seizures during the previous EMU admission), and brief duration. Ictal SPECT injection was attempted, but could not be completed due to technical factors. The patient refused to stay for another attempt.
In summary, this study is suggestive of partial epilepsy with a probable frontal epileptogenic zone, based on clinical features.Technical Summary
Technical Summary
Lethargic
This is a 200 Hz digital EEG with ECG monitoring performed in the lethargic state. Hyperventilation and photic stimulation were not done. Digital EEG was referentially recorded, reformatted and digitally filtered in a variety of bipolar and referential montages for optimal display.
Comatose
This is a 200 Hz digital EEG with ECG monitoring performed in the comatose state. Hyperventilation and photic stimulation were not done. Digital EEG was referentially recorded, reformatted and digitally filtered in a variety of bipolar and referential montages for optimal display.
Description of Record
Normal
Normal
Awake and Drowsy
During the maximally alert state, a XX Hz, XX microvolt posterior dominant rhythm was seen which was symmetrical, well regulated and briskly attenuated to eye opening. In the more anterior head regions, symmetric frontocentral 14-18 beta frequencies predominated. As drowsiness occurred, the posterior dominant rhythm attenuated, slow rolling eye movements appeared and increased frontocentral beta and high amplitude, and symmetrical vertex sharp transients were seen. Later stages of sleep were not attained.
Awake and Sleep
During the maximally alert state, a XX Hz, XX microvolt posterior dominant rhythm was seen which was symmetrical, well regulated and briskly attenuated to eye opening. In the more anterior head regions, symmetric frontocentral 14-18 beta frequencies predominated. As drowsiness occurred, the posterior dominant rhythm attenuated, slow rolling eye movements appeared and increased frontocentral beta and high amplitude, and symmetrical vertex sharp transients were seen. Stage 2 sleep was reached characterized by high amplitude K-complexes and 14 Hz symmetrical and synchronous frontocentral sleep spindles. Later stages of sleep were not attained.
Abnormal
Abnormal
Generalized Slowing (Delta with frequent Theta)
At the maximally alert state, there was no well-formed posterior dominant rhythm appreciated. The background consists of continuous generalized polymorphic delta (2-3 Hz) of XX microvolt. There is frequent intermixed theta (4-6 Hz) activity. The background is XX reactive to external stimuli of auditory and tactile stimulus. No electrographic or clinical seizures were recorded. No well-formed sleep architecture was seen.
Generalized Slowing (Theta)
No PDR
At the maximally alert state, there was no well-formed posterior dominant rhythm appreciated. The background consists of continuous generalized polymorphic theta (4-7 Hz) of XX microvolt. The background is XX reactive to external stimuli of auditory and tactile stimulus. No electrographic or clinical seizures were recorded. No well-formed sleep architecture was seen.
Brief PDR
During the maximally alert state, a XX Hz, XX microvolt posterior dominant rhythm was seen briefly. The background consists of continuous generalized polymorphic theta (4-7 Hz) of XX microvolt. The background is XX reactive to external stimuli of auditory and tactile stimulus. No electrographic or clinical seizures were recorded. No well-formed sleep architecture was seen.
Focal Slowing (Theta)
The background is asymmetric; with left hemisphere consists of near continuous generalized polymorphic delta (2-3 Hz) of 30-40 microvolts. There are also left temporal independent spike discharges maximum at T7. During the maximally alert state, a 8.5-9 Hz, 35-45 microvolt posterior dominant rhythm was seen which was asymmetrical seen well on right hemisphere, well regulated and briskly attenuated to eye opening. As drowsiness occurred, the posterior dominant rhythm attenuated, slow rolling eye movements appeared and increased frontocentral beta and high amplitude, and symmetrical vertex sharp transients were seen. Later stages of sleep were not attained.
Other Qualifiers
Normal
Mu rhythm at XX Hz was noted over the XX central area.
Posterior slow waves of youth were seen over the occipital regions.
POSTS were noted over the occipital regions bilaterally.
Several sharp transients were seen in the left temporal region (T7), which were likely wickets, a normal variant.
Normal variants seen during this recording include wicket spikes, rhythmic temporal theta bursts of drowsiness, 14&6 Hz positive bursts, benign epileptiform transients of sleep, 6 Hz spikes (phantom spikes, FOLD), lambda waves, shut eye waves, cone waves, rhythmic midline theta of Ciganek, subclinical rhythmic EEG discharge of adults (SREDA)
Fragments of sleep architecture, including vertex sharp waves and poorly formed sleep spindles were seen.
Abnormal
Generalized excessive beta activity was seen.
Fast and sharp activity in the left centro-temporal region at Cz, C3 and T7, was seen consistent with a breach rhythm due to the patient’s known skull defect.
Frontal intermittent rhythmic delta activity (FIRDA) was seen.
Intermittent 1-2 Hz frontally-dominant reactive triphasic waves are seen.
Continuous 1-2 Hz periodic waveforms waxing and waning were seen that were more consistent with triphasic waves prominent because of the morphology, frontal positivity, AP and PA lag, and reactivity.
Epileptic
Generalized anterior predominant synchronous 3-3.5 Hz spike and wave activity was seen lasting from 2-5 seconds.
There were several, generalized, anteriorly predominant, symmetric and synchronous, 4-5 Hz spike and slow wave discharges.
Superimposed on the delta background were relatively irregularly occurring, generalized, frontally predominant, quazi-periodic epileptiform discharges (BiPEDS/GPEDs) were seen. These occurred once every 1 to 2 seconds.
Hyperventilation
Hyperventilation
No HV
Hyperventilation was not performed.
HV Attempted
Hyperventilation was attempted but not completed successfully.
W/o Slowing
Hyperventilation was performed with good effort. HV did not induce significant EEG changes compared to baseline.
W/ Slowing
Hyperventilation was performed with good effort. XX Hz slowing was seen during HV but resolved within XX seconds of normal breathing. The slowing was paroxysmal/of gradual onset and was intermittent/continuous.
W/ Slowing
Hyperventilation was performed with good effort. XX Hz slowing was seen during HV that was paroxysmal and was intermittent.
W/Slowing and Notched Delta
Hyperventilation was performed with good effort. Initially XX Hz high-amplitude notched delta activity was seen generalized maximal bifrontal. The notched nature of the slowing is felt to be more likely due to superpositioning of frequencies rather than true spike-and-wave discharges. The slowing was of gradual onset and was intermittent. The slowing resolved within 80 seconds of normal breathing.
W/3Hz Spike-Wave Activity
Hyperventilation was performed with good effort. Generalized 3 Hz spike and wave activity lasting 10 seconds was seen without any clinical correlation (as noted by the EEG technician).
Photic Stimulation
Photic Stimulation
No PS
Photic stimulation was not performed.
W/o Driving
Photic stimulation was performed from 1-30 Hz. Photic driving was not observed. No electroretinogram artifact, photomyoclonus or photoparoxysmal responses were recorded.
W/ Driving
Photic stimulation was performed from 1-30 Hz. Photic driving was observed. Driving was bioccipital, symmetrical and best seen at flash frequencies from XX to XX Hz. No electroretinogram artifact, photomyoclonus or photoparoxysmal responses were recorded.
w/driving (no Hz specified)
Photic stimulation was performed from 1-30 Hz. Symmetric bioccipital photic driving was observed. No electroretinogram artifact, photomyoclonus or photoparoxysmal responses were recorded
Clinical Correlation
Normal
Normal
This is a normal electroencephalogram (EEG) record. A normal EEG does not exclude the possibility of epilepsy. If the clinical suspicion of epilepsy is high, a repeat EEG after sleep deprivation or a seizure may increase the frequency of detecting epileptiform discharges.
Other Qualifiers
The breach rhythm is most likely due to the patient’s known skull defect.
Abnormal Encephalopathy
Abnormal – Encephalopathy
Global Cerebral Dysfunction Mild
This EEG is consistent with mild, nonspecific and non-localizing cerebral dysfunction. No seizures or epileptiform discharges were noted.
Global Cerebral Dysfunction Moderate
This EEG is consistent with mild-to-moderate, nonspecific and non-localizing cerebral dysfunction. No seizures or epileptiform discharges were noted.
Global Cerebral Dysfunction Severe
This EEG is consistent with moderate-to-severe, nonspecific and non-localizing cerebral dysfunction. No seizures or epileptiform discharges were noted.
Global Cerebral Dysfunction Non-Reactive
The nonreactive background slowing is indicative of a severe, nonspecific and non-localizing encephalopathy. No seizures or epileptiform discharges were noted.
Global spindle coma
The nonreactive background, electro-decrements, and spindle coma are indicative of a severe, nonspecific and non-localizing encephalopathy. Spindle coma can be associated with head injury, non-traumatic intracranial hemorrhage, and cerebral anoxia in addition to other causes.
Pharmacological-induced coma
This EEG is consistent with moderate-to-severe, nonspecific and non-localizing cerebral dysfunction. The burst suppression pattern may be due to pharmacological-induced coma but may be present without the pharmacological intervention hence underlying pathological process cannot be ruled out. These findings were discussed with the primary team.
Regional Cerebral Dysfunction Moderate
This EEG is consistent with right/left XX nonspecific mild-to-moderate cerebral dysfunction and may correlate with a structural abnormality. A nonepileptiform EEG does not exclude the possibility of epilepsy. If the clinical suspicion of epilepsy is high, a repeat EEG after sleep deprivation or a seizure may increase the frequency of detecting epileptiform discharges.
Other Qualifiers
There were two generalized sharp transients which were not convincing for pathological epileptiform discharges.
Abnormal - PNES
This evaluation is consistent with a diagnosis of psychogenic non-epileptic seizures (PNES). Episodes of XX were without a scalp EEG correlate. Although the lack of an scalp EEG correlate does not exclude a simple partial seizure, the very atypical movements may suggest a nonepileptic event.
A nonepileptiform EEG does not exclude the possibility of concomitant epilepsy. If clinically indicated, an inpatient video-EEG evaluation (EMU) might be considered.
This evaluation was diagnostic for psychogenic/nonepileptic seizures. The lack of ictal and interictal epileptiform abnormalities supports this diagnosis.
More than 10 events were captured, all of which were similar but none of which were stereotypic. They consisted of tremulousness, some body jerks, upper extremitiy tremor, visual and auditory hallucinations, restlessness, and occasional gaze preference to the left lasting minutes to hours. There was no clear scalp EEG correlates.
The XXX was/were discontinued. It is recommended that the patient not be treated with any medications for treatment of epileptic seizures. The patient should also follow full seizure safety precautions until these nonepileptic/psychogenic seizures are under control. Patient not to drive until event free for 6 months. If the patient has or develops other types of spells concerning for epileptic seizures, then the patient should undergo a re-evaluation to further characterize those spells. The patient to be discharged in stable condition and plan to follow-up with neurology, psychiatry and cognitive behaviour therapy.
Abnormal - Epileptic
Abnormal – Epileptic
Simple Partial
The clinical significance of the right facial twitching is unclear. This EEG provides a non-epileptic basis for the recorded events. Simple partial motor seizures, which rarely have a scalp EEG correlate, cannot be ruled out. Clinical correlation is recommended.
Generalized
This EEG is consistent with interictal and ictal expression of symptomatic generalized epilepsy. Clinical correlation is recommended.
The presence of generalized discharges increases the risk of generalized seizures (e.g., absence, myoclonic and tonic-clonic) and with the normal background, would be most consistent with a high risk for an idiopathic generalized epilepsy syndrome. The possibility of a focal discharge (e.g., frontal) with very rapid spread (i.e., secondary bilateral synchrony) cannot be absolutely excluded but seems much less likely.
JME
This EEG is consistent with an interictal expression of an idiopathic generalized epilepsy syndrome. The morphology and frequency of the discharges is consistent with juvenile myoclonic epilepsy.
Partial
This EEG is consistent with interictal expression of partial epilepsy with left temporal epileptogenicity. Clinical correlation is recommended.
This EEG is consistent with interictal expression of partial epilepsy with independent left and right occipital epileptogenicity. Clinical correlation is recommended.
Focal Discharges
The focal epileptiform discharges (right temporo-occipital and left frontocentral) increase the risk of focal and/or secondarily generalized seizures.
TIRDA
The right temporal intermittent rhythmic delta activity (TIRDA) is thought to increase the risk of focal and/or secondary generalized seizures (similar to the risk with focal epileptiform discharges). Clinical correlation is recommended.
PLEDs
No electrographic or clinical seizures were recorded. The presence of pseudo-periodic, lateralized, epileptiform discharges (PLEDs) increases the risk of acute focal and/or secondarily generalized seizures. PLEDs are typically associated with acute/subacute structural abnormalities (stroke, abscess, etc.) and concomitant metabolic/toxic/infectious disorders. Clinical correlation is recommended.
FIRDA
Symmetric frontal intermittent rhythmic delta activity (FIRDA) was observed. Symmetric FIRDA is associated with metabolic abnormalities, midline lesions, and hydrocephalus. Clinical correlation is advised.
Asymmetric frontal intermittent rhythmic delta activity (FIRDA) was observed. Asymmetric FIRDA is associated with underlying structural brain abnormalities and also present in metabolic abnormalities, midline lesions, and hydrocephalus. Clinical correlation is advised.
Triphasic wave
The presence of triphasic waves is nonspecific but suggestive of a global toxic-metabolic encephalopathy. The diagnostic use of lorazepam to identify a change in the clinical and electrographic pattern may be of help in the differential diagnosis. Triphasic waves are a nonspecific indicator of a moderate degree of encephalopathy and can indicate renal or hepatic dysfunction. There was no clear evidence of non-convulsive status epilepticus.
Abnormal - Subclinical
One brief left temporal electrographic/subclinical seizure was seen, without obvious clinical correlate. This would be consistent with a focal epilepsy syndrome with a very high risk of focal and/or secondarily generalized seizures.
Other Qualifiers
Cerebral Dysfunction
in the setting of mild, nonspecific global cerebral dysfunction.
Excessive beta
The excessive beta is likely a medication side-effect, and can been seen with benzodiazepine and barbiturate administration.
Brain Death
This is a 200 Hz digital EEG with ECG monitoring performed in the comatose state. Hyperventilation and photic stimulation were not done. Digital EEG was referentially recorded, reformatted and digitally filtered in a variety of bipolar and referential montages for optimal display. A standard ECI protocol was used.
There was no cerebral EEG activity greater than 2mv using a standard ECI protocol.
The lack of cerebral activity greater than 2mv using a standard ECI protocol is consistent with, but not diagnostic of clinical brain death. The Neurocritical care team was informed of these findings immediately.
Other Note Snippets
Seizure Precautions
I recommended following full seizure precautions including no driving, no baths, no swimming, no working at heights, no work with potentially dangerous equipment and no activity that might injury self or others if a seizure did occur. We also discussed the Texas laws and obligations regarding driving restrictions after having had a seizure.
He was discharged in stable condition, given strict seizure precautions, and advised that he is obligated to contact the Texas DPS/DMV in order to update his medical status with respect to driving.
Seizure free
Given that *** has been seizure free for over 6 months, she does not need to follow full seizure precautions. She can start driving provided *** is compliant with her anti-seizure medications, clinical appointment and lab work relater to her epilepsy.
Given that *** has been seizure free for over 6 months, she does not need to follow full seizure precautions. However, given that she was off her medications during this evaluation, we recommended to not drive and follow full seizure precautions until ***. The patient was discharged in stable condition and will follow-up with *** in the ***.