Table 2.
Notes. “x” indicates the presence of abnormality on brain scan, CT – Computed Tomography; MRI – Magnetic Resonance Imaging, EEG – Electroencephalography, N/A – non-applicable, * acute, surrounded by edema and caused midline shift
** became chronic
*** re-reabsorbing with persistent perilesional brain edema and midline shift
†with associated mass effect and cortical sulcal effacement
†† three focal seizures lasting approximately 30 s each
††† focal status epilepticus
‡consistent with mild microvascular disease but without acute intracranial lesion
‡‡ no evidence of brain edema
‡‡‡ no signs of cerebral vasospasm
**microhemorrhages varied between 5 and 6 to innumerable. Predominantly punctate, smaller than 3-mm in size. no concomitant larger intracranial hemorrhage. One patient with microhemorrhages has a prior brain MRI available (7 days before current hospital admission), which revealed that all hemorrhages were new. 4 in 7 patients had CT 3–7 days before MRI - no punctate microhemorrhages shown.
**No patients with altered mental status as the indication for brain imaging demonstrated acute or subacute infarct or acute intracranial hemorrhage
***the authors did not clearly state if hyperintensities comprised all cases of abnormalities.
¥ White matter microangiopathy was more than expected for age in 26 patients and in additional 108 patients as much as expected for age.
¥¥ posterior frontal and temporo-parieto-occipital symmetric bilateral hypodensity of the subcortical white matter.
¥¥¥ Default Mode Network was studied based on four nodes: the medial prefrontal cortex, the posterior cingulate cortex, and bilateral inferior parietal lobules
$ extensive and isolated WM microhemorrhages
$$ the signal alteration in the cortex completely disappeared
$$$ the olfactory bulbs were thinner and slightly less hyperintense
δ improved brain swelling