Long-Term Sequela of Intrathecal Gadolinium Extravasation: Symptoms Mimicking Post-concussive Syndrome

Long-Term Sequela of Intrathecal Gadolinium Extravasation: Symptoms Mimicking Post-concussive Syndrome

Patel A; Zolyan A; Itrat A

Cureus

2021

2021-03-24

Gadolinium contrast administration, usually with magnetic resonance imaging, is an important diagnostic modality in the investigation of neurological pathologies. There is little evidence in the literature suggesting repeated exposure to intrathecal gadolinium results in symptoms mimicking post-concussive syndrome (PCS). We studied one patient who received intrathecal gadolinium to investigate a pain pump malfunction and presented with encephalopathic symptoms of confusion and aphasia with imaging consistent with intracranial gadolinium extravasation. The patient was followed up regularly with repeat imaging, reassessment of persistent symptoms, and specialist evaluations; however, symptoms remained refractory and resembled PCS. Our findings indicate a need to further investigate potential associations between intrathecal gadolinium exposure and a clinical presentation consistent with PCS, irrespective of histopathological changes.

Repeated exposure to intravenous gadolinium is thought to have a cumulative effect over time with brain deposits that have been histopathologically confirmed in patients with normal renal function. Acute extravasation of gadolinium contents mimicking acute subarachnoid hemorrhage has also been described elsewhere, especially after intrathecal administration, including the patient in our case report [1,2]. There is, however, no clear consensus yet if these acute “high-dose” or gradually accumulating deposits result in long-term neurological sequelae. Recent studies have demonstrated gadolinium toxicity in preclinical in-vitro studies by pathophysiological mechanisms involving calcium homeostasis [3]. Once within the extracellular space, gadolinium is proposed to have affinity for certain other similar metals with resulting chelation and deposition in the central nervous system [4]. Animal studies have demonstrated increased markers of cellular injury after exposure to higher concentrations of gadolinium [5]. However, causal relationship is difficult to establish between gadolinium administration and neurological sequela [3]. We had the unique opportunity to study one such patient with acute toxic encephalopathy over a period of two years and report subsequent clinical findings.

Journal Article

NEOMED College of Medicine

Department fo Internal Medicine

Jan to Aug list 2021