Fig. 13.1
DWI MRI of the brain 29 h later demonstrating diffuse abnormalities, especially in the basal ganglia, thalamus, insular and occipital cortices
Fig. 13.2
DWI MRI of the brain 29 h later demonstrating diffuse abnormalities, especially in the basal ganglia, thalamus, insular and occipital cortices
Fig. 13.3
Continuous EEG monitoring demonstrating bi-hemispheric continuous runs of sharp and slow waves, which did not correlate with myoclonic jerking or clinical convulsions
Case 2.
Nonconvulsive status epilepticus . Seventy-five-year-old woman was involved in a car accident, with admission GCS of 15, and developed multi-organ failure after a protracted ICU stay. She had a cardiac arrest in the ICU, after which she never regained consciousness. An EEG was performed to rule out nonconvulsive status epilepticus (Figs. 13.4 and 13.5).
Fig. 13.4
Continuous bursts of triphasic wave activity at a rate of 1–2 Hz, occasionally intermixed with bursts of spike activity
Fig. 13.5
Significant decrease of the epileptiform activity after intravenous administration of 2 mg lorazepam. The patient did not have any clinical improvement and remained in coma
Case 3.
Seventy-year-old man s/p coronary artery bypass (×3 vessels), with complicated course in the cardiac-ICU (hemodynamic instability with prolonged hypotension). CT head was done (Fig. 13.6) and showed a small lacunar infarct. Four days after his surgery, he developed generalized tonic-clonic status epilepticus and was placed on pentobarbital coma under continuous EEG monitoring. EEG monitoring showed evolving electrographic seizures from the right (Figs. 13.7, 13.8, 13.9, and 13.10). He never regained consciousness, but the status epilepticus resolved after more than a month in barbiturate coma. Because of skin ulceration under the electrode placement areas, the continuous EEG had to be stopped.
Fig. 13.6
CT of the head showing a small centrum semiovale subacute lacune (white arrow), but paucity of other significant radiologic injuries. No MRI was ever performed due to the prolonged and severe critical condition of the patient
Fig. 13.7
Electrographic seizure , beginning from the parieto-temporo-occipital areas of the right hemisphere
Fig. 13.8
Electrographic seizure , beginning from the parieto-temporo-occipital areas and evolving
Fig. 13.9
Electrographic seizure , see in two previous figures now speading to the left hemisphere
Fig. 13.10
Electrographic seizure , seen in three previous figures now ending
Acknowledgments
The authors would like to acknowledge Dr. Ernst Niedermeyer and Dr. Peter Kaplan for their helpful suggestions and EEG tracings.
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