Acute amnestic syndromes

Alessandro, Lucas; Ricciardi, Mario; Cháves, Hernán; Allegri, Ricardo

doi:10.1016/j.jns.2020.116781

Cited by 19 publications

(38 citation statements)

References 65 publications

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“…He had no evidence of seizure activity on EEG, though EEG may not reflect prior ictal events and can sometimes be normal in subcortical seizures. Follow-up imaging did not show regional hippocampal atrophy to suggest transient epileptic amnesia [9]. Due to the patient's recent MSSA bacteremia, embolic stroke to the posterior circulation was considered a potential etiology but felt to be unlikely.…”

Section: Discussionmentioning

confidence: 92%

“…About 50% to 80% of patients with Wernicke encephalopathy may develop Korsakoff syndrome, leading to a permanent anterograde amnesia with or without confabulation, retrograde amnesia, and executive deficits [8]. MRI T2fluid-attenuated inversion recovery (FLAIR) sequences in 50% of patients may show hyperintense lesions in the fornix, medial thalamus, mammillary bodies, periventricular area around the third ventricle, and/or periaqueductal areas [9].…”

Section: Discussionmentioning

confidence: 99%

“…The differential diagnosis for this patient also includes TEA, TGA, and hippocampal stroke. These conditions lead to anterograde amnesia of variable duration [4,9]. TEA is characterized by repetitive events of shortlived anterograde amnesia and responds well to anti-seizure medication.…”

Section: Discussionmentioning

confidence: 99%

“…It is unusual for TGA to recur. In hippocampal strokes, amnesia is usually short-lived, but in a small proportion of cases, amnesia may be permanent and accompanied by cognitive symptoms such as anomia or executive difficulties [9]. Hippocampal strokes may be misdiagnosed as TGA if no MRI is obtained and symptoms improve.…”

Section: Discussionmentioning

confidence: 99%

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Complete Bilateral Hippocampal Diffusion Restriction and Reversible Amnesia Following Opiate, Cocaine, and Benzodiazepine Abuse

Huang

Lukas

2021

Cureus

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The hippocampus is a crucial component of the circuits involved in memory formation and recall. Bilateral hippocampal lesions can lead to profound anterograde amnesia. As a highly vascularized structure, the hippocampus is susceptible to ischemia from hypoxic and toxic insults. Infarction of bilateral hippocampi as a result of cocaine use, while rare, is well described in the literature. Combined opiate and stimulant abuse also cause dysfunction of this structure. We present a case of complete bilateral hippocampal diffusion restriction and anterograde amnesia after heroin, cocaine, and benzodiazepine abuse, consistent with opioid-associated amnestic syndrome, as well as a remarkable resolution of amnesia months later.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Complete Bilateral Hippocampal Diffusion Restriction and Reversible Amnesia Following Opiate, Cocaine, and Benzodiazepine Abuse

Huang

Lukas

2021

Cureus

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“…It can be observed after trauma, bleeding, ischemia, or inflammation (viral or autoimmune, e.g., in limbic encephalitis associated with adenylate kinase 5 antibodies 9 ) and may be a symptom of a psychiatric disorder (dissociative amnesia) or acute toxic metabolic disorders. 10 , 11 One of the most frequent forms is transient global amnesia (TGA) that is characterized by sudden onset of short-lasting (<24 hours) anterograde amnesia in the absence of other neurologic deficits. 12 - 14 An impaired venous blood flow affecting hippocampal function through congestive ischemia has been proposed as a possible pathophysiologic mechanism.…”

Section: Discussionmentioning

confidence: 99%

Autoimmune Global Amnesia as Manifestation of AMPAR Encephalitis and Neuropathologic Findings

Ricken

Zrzavy

Macher

et al. 2021

Neurol Neuroimmunol Neuroinflamm

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ObjectiveTo report an unusual clinical phenotype of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) encephalitis and describe associated neuropathologic findings.MethodsWe retrospectively investigated 3 AMPAR encephalitis patients with autoimmune global hippocampal amnesia using comprehensive cognitive and neuropsychologic assessment, antibody testing by in-house tissue-based and cell-based assays, and neuropathologic analysis of brain autopsy tissue including histology and immunohistochemistry.ResultsThree patients presented with acute-to-subacute global amnesia without affection of cognitive performance, attention, concentration, or verbal function. None of the patients had epileptic seizures, change of behavior, personality changes, or psychiatric symptoms. The MRI was normal in 1 patient and showed increased fluid-attenuated inversion recovery/T2 signal in the hippocampus in the other 2 patients. Two patients showed complete remission after immunotherapy. The one patient who did not improve had an underlying adenocarcinoma of the lung and died 3.5 months after disease onset because of tumor progression. Neuropathologic analysis of the brain autopsy revealed unilateral hippocampal sclerosis accompanied by mild inflammatory infiltrates, predominantly composed of T lymphocytes, and decrease of AMPAR immunoreactivity.ConclusionAMPAR antibodies usually associate with limbic encephalitis but may also present with immune responsive, acute-to-subacute, isolated hippocampal dysfunction without overt inflammatory CSF or MRI changes.

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