Anterograde amnesia with hippocampal lesions following glufosinate intoxication

Park, Hee-Young; Lee, Phil Hyu; Shin, Dong Hoon; Kim, Gi Woon

doi:10.1212/01.wnl.0000233828.18399.e8

Cited by 34 publications

(26 citation statements)

References 7 publications

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“…Both had a profound inability to encode new memories. In the last decade, it has been reported that toxic exposures can be another mechanism for the development of anterograde amnesia [3]. Here, we report a novel case of a 35 year-old man who developed an immediate and apparently permanent anterograde amnesia following his exposure to a methamphetamine laboratory.…”

Section: Introductionmentioning

confidence: 84%

Anterograde Amnesia after Methamphetamine Lab Exposure

Sanders¹

2016

JNSK

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Anterograde Amnesia after Methamphetamine Lab Exposure Background: Some known toxic exposures can produce detrimental cognitive deficits. Yet, very few substances have been linked to the development of anterograde amnesia. Here, we report a novel case of a middle-age man who presented with a profound and apparently permanent anterograde amnesia following his exposure to a clandestine methamphetamine laboratory. Case Report: A 47 year-old, righthanded man presented in 2013 with a history of memory loss and seizures since 2001, when he was exposed during his work as a firefighter to the fumes of spilled material intended to synthesize methamphetamine in a clandestine laboratory. Following the exposure, he suffered a major and immediate impairment of multiple cognitive domains, with anterograde memory being most impaired. A formal neurobehavioral status examination NBSE showed a profound impairment in episodic/verbal memory and lesser impairment of executive function. The patient clinical course has to date been stable without further deterioration or improvement. Discussion: This case highlights a clear temporal relationship of methamphetamine laboratory exposure and the development of deficits in memory and executive dysfunction suggestive of involvement of both prefrontalstriatal circuits and medial temporal areas. This is in concordance with prior animal studies, and warrants further investigation in the future.

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Section: Introductionmentioning

confidence: 84%

Anterograde Amnesia after Methamphetamine Lab Exposure

Sanders¹

2016

JNSK

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“…Excessive stimulation of N-methyl-Daspartic acid (NMDA) receptors by GLA might cause hippocampal injury. 6,8 The basal ganglia are vulnerable to toxins and metabolic changes. Previous studies have shown that altered energy metabolism and the excessive stimulation of glutamate receptors are important in the pathogenesis of neuronal damage in the striatum during acute metabolic insult.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5] Although the exact mechanism of GLA toxicity remains unclear, a patient with a hippocampal lesion after GLA intoxication has been reported. 6 In this report, we describe a patient who ingested a GLAcontaining herbicide (BASTA Ò ; Bayer, Leverkusen, Germany) in an attempted suicide. Diffusion-weighted MRI (DWI) showed hyperintense lesions, not only in the hippocampus, but also in the striatum with different apparent diffusion coefficient (ADC) values.…”

Section: Introductionmentioning

confidence: 99%

Vasogenic edema in striatum following ingestion of glufosinate-containing herbicide

Lee

Song

Lee

et al. 2009

Journal of Clinical Neuroscience

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“…GLF exposure triggers convulsions and memory impairment. GLF expsoure produces moderate to severe convulsions and memory loss Watanabe and Sano, 1998;Ohtake et al, 2001;Park et al, 2006Park et al, , 2013Mao et al, 2011a andb, 2012), as well as causes structural changes to several brain regions, including the cortex and hippocampus (Calas et al, 2008;Meme et al, 2009;Park et al, 2006 ), two brain structures rich in NMDARs that play an important role in learning and memory processes.…”

Section: Glufosinate (Glf)mentioning

confidence: 99%