Gyriform restricted diffusion in adults: looking beyond thrombo-occlusions

Abstract

Gyriform restricted diffusion (GRD) refers to hyperintense signal involving the cerebral cortex on diffusion-weighted images (DWI) with corresponding hypointensity on apparent diffusion coefficient (ADC) images. These changes are commonly seen following a vascular occlusion, reflecting the limitation of water molecule movement across cell membranes (restricted diffusion) due to the failure of Na + /K + -ATPase pumps (cytotoxic oedema). However, GRD can occur in several other neurological conditions as well. A thorough understanding of these conditions and their anatomic predilection plays a critical role in identifying and differentiating them from vascular thrombo-occlusion, with impact towards appropriate clinical management. This review highlights the less commonly encountered, non-stroke causes of GRD in adults with case-based examples. A tabulated chart of the patterns of cortical and subcortical involvement associated with these aetiologies is provided for a quick, pattern-based reference for daily radiological reporting.

Repeat and single dose administration of gadodiamide to rats to investigate concentration and location of gadolinium and the cell ultrastructure

“…However, it appears that a small fraction persists longer-term without consequence, in agreement with the few clinical autopsy studies including direct gadolinium measurement 3 , 4 , 21 . Macrocyclic GBCAs exhibit faster clearance of gadolinium from tissues than linear agents and have been shown to have a lower propensity than linear agents for T1 signal intensity in the dentate nucleus and globus pallidus 5 , 6 , 14 , 18 .…”

“…A recent study 18 which assessed gadolinium levels in a limited number of tissues after high, repeated GBCA administration to rats, does not provide retention kinetics after a single human equivalent dose, which is more suitable a comparison to the clinical setting. Our study sought to understand not only the long-term retention kinetics following a cumulative dose, but importantly gadolinium retention after a single human equivalent dose, more relevant to the clinical use of GBCAs.…”

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome mimicking herpes simplex encephalitis: A case report

“…The gold standard for establishing the diagnosis is the detection of herpes simplex virus DNA in the CSF by PCR [13] , which was not available in our case. Of note, false-negative PCR test for HSV may occur early in the disease [14] . The absence of fever and lack of prominent alteration in consciousness in the presence of a normal CSF cell count help distinguish MELAS from typical HSE [4] .…”

“…Temporal lobe lesions that are considered strong evidence for HSE [12] can also be prominent in MELAS [5] . Classic imaging features of HSE include DWI hyperintensity and T2/FLAIR hyperintensity in the mesiotemporal and orbitofrontal lobes and insula [14] . MELAS shows that the affected areas in neuroimaging are asymmetric and do not correspond to classic vascular distribution, involve predominantly the temporal, parietal, and occipital lobes, and can be restricted to cortical areas or involve subcortical white matter [1] .…”

“…MELAS shows that the affected areas in neuroimaging are asymmetric and do not correspond to classic vascular distribution, involve predominantly the temporal, parietal, and occipital lobes, and can be restricted to cortical areas or involve subcortical white matter [1] . The lesions are hypodense on CT and hyperintense on T2-, DWI and FLAIR images and often show a slowly progressive spread [14] . Calcification in the basal ganglia, as in our case, is another common finding in MELAS, which may help to distinguish it from HSE.…”