A 78 year old RHWM had hypertension, hypercholesterolemia, and was otherwise in good health. He complained of recent memory difficulties over the preceding 6 months prior to presentation diagnosed with cerebral amyloid angiopathy. Focal seizures were evidenced as a warning of a strange feeling, colored lights moving from left to right, brief inconsolable "reaction" of turning to the right side and curling up in a ball. Seizures typically lasted 2 minutes but could be serial and also prolonged > 5 minutes. A brain MRI brain revealed an area of cortical encephalomalacia in the left posterior temporal region involving the posterior quadrant. An EEG demonstrated left mid- and posterior temporal sharp waves. He was resistant to multiple AEDs on PHT, PB, and LEV with monthly ED visits for breakthrough serial seizures that would require hospitalization due to a prolonged "post-ictal" state.
Figure: EEG in (A) demonstrates left posterior temporal PLEDs Plus with repetitive sharp waves followed by a rhythmic ictal discharge and (B) with focal left hemispheric non-convulsive status epilepticus with rhythmic slowing. Parameters: bipolar montage, sensitivity 7 uv, and filters of 1-70 Hz.
Most epilepsy patients experience brief recurrent solitary seizures. Serial seizures and prolonged seizures > 5 minutes are coupled with seizure emergencies and potentially lead to status epilepticus (SE). SE has a higher risk of poor outcome and merit more aggressive treatment approaches. Continuous EEG monitoring has unveiled a spectrum of epileptiform abnormalities involving an interictal-ictal continuum. Certain patterns are clearly ictal while PLEDs and other periodic patterns remain may reflect interictal, post-ictal, and transitional features often seen with SE. PLEDs noted in the ED (figure A) may translate to SE in the Neurological ICU (figure B). Working criteria to separate ongoing ictal and peri-ictal EEG are available1. It remains ill-defined to what extent individual or combinations of EEG patterns contribute to brain injury and which exist as epiphenomenon. Treatment approaches varies due to our lack of understanding regarding patterns that are clearly harmful to neuronal stabilization and recovery following clinical and EEG seizures and SE2. Focal SE may result in brain atrophy without a preceding structural cause. VNS implantation was performed in our patient with improvement. Drug reduction and transition to non-enzyme inducing medication with seizure reduction (0-2/month) was possible with ED visitation virtually eliminated.
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