PMC7357055_01
Initial computed tomography (CT) scan of the head (left) showed an area of encephalomalacia in the right frontal lobe (arrow) consistent with an old stroke. Repeat CT scan of the head (middle) 12 hours after the initial CT scan revealed acute infarcts in the paramedian zone of the thalami (arrows) and CT angiogram (right) showed filling defects at the top of the basilar artery and the P1 segments of the posterior cerebral arteries.
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Computed tomography (CT) of the head showed an area of encephalomalacia in the right frontal lobe consistent with her old stroke (Figure 1). Repeat head CT 12 hours later revealed bilateral paramedian thalamic infarcts and CT angiography showed filling defects at the top of the basilar artery and the P1 segments of the posterior cerebral arteries (Figure 1).
Two days of continuous electroencephalography (days 2 and 3) showed generalized slowing, mainly rhythmic theta activity, with superimposed low-voltage semirhythmic and nonrhythmic delta activity. No epileptiform discharges, electrographic seizures, or periodic discharges were detected.
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However, cEEG recording over a 48-hour period only showed diffuse slowing and no signs of abnormal cortical hyperexcitability (Figure 2).
(A) Before convulsive movements. (B) During convulsive movements. (C) 2 minutes after lorazepam injection. (D) 5 minutes after lorazepam. Electroencephalography recorded approximately 80 minutes from the onset of stroke (before the convulsive episode) showed generalized rhythmic 2-Hz sharp wave and slow wave complexes (A). Despite abundant myogenic artifact, the EEG during convulsion continued to show similar epileptiform discharges with a slightly higher frequency of 2.5 Hz (B). Convulsive movements stopped even before lorazepam was injected. After lorazepam 2 mg was administered, the epileptiform discharges started to decrease in frequency (C) and subsequently dissipated (D).
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EEG recording (~80 minutes from onset of stupor) showed sustained generalized epileptiform discharges in the form of high-voltage rhythmic sharp and slow wave complexes (Figure 3A). The EEG, which was obscured by muscle artifact, did not show any significant change other than a slight increase in the frequency of epileptiform discharge from 2 to 2.5 Hz (Figure 3B). Lorazepam 2 mg was injected resulting in attenuation and dissipation of epileptiform discharges (Figure 3C and D).
Computed tomography (CT) scan of the head on day 12 (top row), 4 hours after the onset of stupor and 1 hour after appearance of oculomotor nerve palsy, showed the previous infarct in the paramedian zones of the thalami (arrows) with no clear-cut involvement of the midbrain. Repeat CT scan of the head on day 13 (bottom row), 22 hours after the onset of stupor, showed extension of the infarct from the paramedian zones of the thalami to the paramedian zones of the midbrain with greater involvement of the right side (arrows) consistent with the clinical findings of stupor and right oculomotor nerve palsy.
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Stat CT of the head showed the same infarct in the paramedian zones of the thalami with no midbrain infarct (Figure 4, top row). Repeat CT of the head (~22 hours after the onset of stupor) showed extension of the infarct from the paramedian zones of the thalami to the paramedian zones of the midbrain with greater involvement of the right side consistent with the clinical findings of stupor and right oculomotor nerve palsy (Figure 4, bottom row). cEEG showed waxing-waning generalized epileptiform discharges consistent with relapsing and remitting cortical hyperexcitability or NCSE (Figure 5).
(A) Generalized slowing with no epileptiform discharges. (B) Build-up of generalized rhythmic delta and sharp activity. (C) Clear-cut epileptiform discharges seen with longitudinal bipolar montage. (D) Same EEG tracing shown above displayed using transverse bipolar montage. (E) Epileptiform discharges start to break up and dissipate. (F) Next epoch with epileptiform discharges reappearing after <1 hour. Selected continuous electroencephalography epochs with compressed spectral array map (see line marker) showing waxing-waning cortical hyperexcitability. Sustained periods of generalized slowing with no epileptiform discharges (A) are followed by build-up of rhythmic delta and sharp wave activity (B) that evolve into clear-cut epileptiform discharges, as seen using longitudinal bipolar (C) and transverse bipolar montages (D), persisting over 1 to 4 hours, before breaking up and dissipating (E), only to return (F).
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Repeat CT of the head (~22 hours after the onset of stupor) showed extension of the infarct from the paramedian zones of the thalami to the paramedian zones of the midbrain with greater involvement of the right side consistent with the clinical findings of stupor and right oculomotor nerve palsy (Figure 4, bottom row). cEEG showed waxing-waning generalized epileptiform discharges consistent with relapsing and remitting cortical hyperexcitability or NCSE (Figure 5). The epileptiform discharges tend to persist for hours with minor fluctuations in frequency, amplitude, and morphology before breaking up and dissipating (Figure 5).