Neurotoxic Manifestations of an Overdose Intrathecal Injection of Gadopentetate Dimeglumine

Park, Kwan-Woong; Im, Soo Bin; Kim, Bum‐Tae; Hwang, Sun Chul; Park, Jongsun; Shin, Won-Han

doi:10.3346/jkms.2010.25.3.505

Cited by 39 publications

(19 citation statements)

References 9 publications

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“…22 While there are limited data on the toxic effects of intrathecal gadolinium-based contrast agents, a 2010 report described the onset of adverse symptoms 6 hours following accidental intrathecal gadolinium contrast administration at a dose 20ϫ that used in our study. 23 Twenty-four-hour telephone follow-up and subsequent clinical notes did not reveal adverse events attributable to the MRM procedure in our cohort. Despite the apparent safety, physicians need to be mindful that intrathecal gadolinium is an FDA off-label use and should weigh the risks and benefits of the procedure carefully in each patient.…”

Section: Discussionmentioning

confidence: 91%

MR Myelography for Identification of Spinal CSF Leak in Spontaneous Intracranial Hypotension

Chazen

Talbott

Lantos

et al. 2014

AJNR Am J Neuroradiol

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Section: Discussionmentioning

confidence: 91%

MR Myelography for Identification of Spinal CSF Leak in Spontaneous Intracranial Hypotension

Chazen

Talbott

Lantos

et al. 2014

AJNR Am J Neuroradiol

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“…An increased cross-bridging of the eCBS residues by trivalent cations may lead to the generation of prolonged depolarization and bursting, resulting in imbalance in neuronal networks, culminating in the epileptiform seizure discharges. Remarkably, the accidental intrathecal administration of Gd 3ϩ -containing contrast reagents (Omniscan and Magnevist) for enhancing magnetic resonance imaging was associated with seizures in human patients (32,33).…”

Section: Discussionmentioning

confidence: 99%

Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel

Chen

Riley

et al. 2017

Journal of Biological Chemistry

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Edited by Roger J. ColbranTransient receptor potential canonical type 5 (TRPC5) is a Ca 2؉ -permeable cation channel that is highly expressed in the brain and is implicated in motor coordination, innate fear behavior, and seizure genesis. The channel is activated by a signal downstream of the G-protein-coupled receptor (GPCR)-G q/11 -phospholipase C (PLC) pathway. In this study we aimed to identify the molecular mechanisms involved in regulating TRPC5 activity. We report that Arg-593, a residue located in the E4 loop near the TRPC5 extracellular Gd 3؉ binding site, is critical for conferring the sensitivity to GPCR-G q/11 -PLC-dependent gating on TRPC5. Indeed, guanosine 5-O-(thiotriphosphate) and GPCR agonists only weakly activate the TRPC5 R593A mutant, whereas the addition of Gd 3؉ rescues the mutant's sensitivity to GPCR-G q/11 -PLC-dependent gating. Computer modeling suggests that Arg-593 may cross-bridge the E3 and E4 loops, forming the "molecular fulcrum." While validating the model using site-directed mutagenesis, we found that the Tyr-542 residue is critical for establishing a functional Gd 3؉ binding site, the Tyr-541 residue participates in fine-tuning Gd 3؉ -sensitivity, and that the Asn-584 residue determines Ca 2؉ permeability of the TRPC5 channel. This is the first report providing molecular insights into the molecular mechanisms regulating the sensitivity to GPCR-G q/11 -PLC-dependent gating of a receptor-operated channel.Transient receptor potential canonical type 5 (TRPC5) 2 channels are predominantly expressed in the nervous system. The highest levels of TRPC5 expression are found in mammalian brain regions such as the amygdala, hippocampus, cerebellum, cerebral cortex, and substantia nigra (1, 2). TRPC5 activation is implicated in regulating neurite outgrowth, growth cone morphology, and dendritic morphogenesis (3-5). In humans, TRPC5 gene mutations are associated with male mental retardation (2). TRPC5 knock-out mice exhibit deficits in motor coordination and innate fear behavior (6, 7). Genetic ablation of TRPC5 also reduces pilocarpine-induced seizures, long term potentiation, and seizure-induced neuronal cell death in the mouse hippocampus (8, 9). Plasma membrane insertion of TRPC5 in pyramidal hippocampal neurons is associated with the generation of prolonged cholinergic depolarization and bursting during epileptiform seizure discharges, suggesting that elevated TRPC5 activity may lead to an imbalance in hippocampal neuronal networks (10).Although TRPC5 channels have critical physiological roles, the molecular mechanisms involved in regulating TRPC5 activity remain not fully elucidated. TRPC5 proteins are localized to the plasma membrane and function as Na ϩ -and Ca 2ϩ -permeable channels. A TRPC5 channel consists of four subunits, each subunit containing six ␣-helical transmembrane domains (S1-S6, Fig. 1A) and a pore loop located between the S5 and S6 transmembrane domains (1, 11). The conduction pathway of the channel is formed by the S6 transmembrane domain and pore loop residues. Act...

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“…In our study, patients with an abnormal EEG were excluded due to safety concerns. Neurotoxic manifestations of gadodiamide may occur at doses 6–7 times above the recommended dose (0.5–1.0 ml) . A dose of 1 ml might not present a risk for patients, even with an abnormal EEG.…”

Section: Discussionmentioning

confidence: 99%

Intrathecal gadodiamide for identifying subarachnoid and ventricular neurocysticercosis

Higuera-Calleja

Góngora‐Rivera

Soto-Hernández

et al. 2015

Tropical Med Int Health

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Abstractobjective Some neurocysticercosis cysts may remain hidden despite novel MRI sequences. This study evaluates the diagnostic value of gadodiamide (GDD)-contrasted MRI cisternography in selected cases of neurocysticercosis.methods We included patients aged 18-65 years with a probable diagnosis of subarachnoid cysticercosis in whom previous neuroimaging studies failed to demonstrate the presence of cysts. One millilitre of GDD was administered intrathecally as a contrast agent with subsequent performance of MRI.results Fourteen patients were included. Optimal contrast diffusion was achieved in nine patients, and partial diffusion was achieved in 4. Intracranial vesicles were identified in 10 patients, with the presence of more than 60 basal subarachnoid vesicles being revealed in all, with five cysts in the fourth ventricle in four patients and a floating cyst in the lateral ventricle in one. In one case, intrathecal GDD demonstrated spinal cysticercosis. No adverse events were reported after intrathecal GDD administration.

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Neurotoxic Manifestations of an Overdose Intrathecal Injection of Gadopentetate Dimeglumine

Cited by 39 publications

References 9 publications

MR Myelography for Identification of Spinal CSF Leak in Spontaneous Intracranial Hypotension

MR Myelography for Identification of Spinal CSF Leak in Spontaneous Intracranial Hypotension

Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel

Intrathecal gadodiamide for identifying subarachnoid and ventricular neurocysticercosis

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