scholarly journals “Vascular” Korsakoff Syndrome With Bilaterally Damaged Mammillothalamic Tracts: Insights Into the Pathogenesis of “Acute” Korsakoff Syndrome As Acute-Onset Irreversible Anterograde Amnesia

Cureus ◽  
2021 ◽  
Author(s):  
Yuichiro Yoneoka ◽  
Yasuhiro Seki ◽  
Katsuhiko Akiyama
Keyword(s):  
Anterograde Amnesia ◽  
Acute Onset ◽  
Korsakoff Syndrome

scholarly journals Wernicke-Korsakoff Syndrome following Small Bowel Obstruction

2002 ◽  
Vol 13 (3-4) ◽  
pp. 89-94 ◽  
Author(s):  
Shoumitro Deb ◽  
Richard Law-Min ◽  
David Fearnley
Keyword(s):  
Small Bowel ◽  
Small Bowel Obstruction ◽  
Bowel Obstruction ◽  
Anterograde Amnesia ◽  
Delayed Recall ◽  
Korsakoff Syndrome ◽  
History Of ◽  
Objective Tests ◽  
Subjective Evidence ◽  
Materials Planning

We report a case of a 64-year-old lady who developed clinical features of Wernicke-Korsakoff syndrome following a laparotomy for small bowel obstruction. Following the operation she developed paralytic ileus and required total parenteral nutrition for one month. A suspected history of average 40 units of weekly alcohol consumption prior to the operation could not be confirmed and the patient did not show any sign of alcohol dependence. Within a few months of treatment with a daily oral dose of thiamine 200 mgs supplemented by multivitamins the patient showed subjective evidence of improvement in confusion, confabulation, and anterograde amnesia, although objective tests showed residual deficits in many areas of cognitive functioning, including immediate and delayed recall of verbal and non-verbal materials, planning and switching of attention.

scholarly journals Transient global amnesia: Isolated event or healthy predictor? Clinical experience of an Italian Emergency Department

2019 ◽  
Vol 15 (3) ◽  
Author(s):  
Greta Barbieri ◽  
Alessandro Cipriano ◽  
Simona Luly ◽  
Viola Del Nista ◽  
Eugenio Orsitto ◽  
...  
Keyword(s):  
Emergency Department ◽  
Neurological Diseases ◽  
Transient Global Amnesia ◽  
Anterograde Amnesia ◽  
Acute Onset ◽  
Clinical Syndrome ◽  
Neurological Symptoms ◽  
Self Awareness ◽  
Benign Pathology ◽  
Global Amnesia

Transient global amnesia (TGA) is a clinical syndrome characterized by reversible anterograde amnesia, in which the patient is alert, self-awareness appears intact and other neurological symptoms are absent. The diagnosis is based on the following criteria: i) witnessed event; ii) acute onset of anterograde amnesia; iii) no accompanying neurological symptoms; iv) no alteration of consciousness; v) no epileptic features; vi) resolution within 24 hours; vii) exclusion of other causes. We conducted a cohort study at the Department of Emergency Medicine on 119 patients with TGA diagnosis from 2010 to 2014, with follow-up evaluation by telephone interview. The objectives of our study were to evaluate the frequency of subsequent episodes, to identify predisposing factors, and to investigate whether TGA is a possible predictor of neurological disease. The frequency of comorbidity in our population was in line with literature. We observed a recurrence rate of 9.5%, with a prevalence for the male gender, while no other factor correlates with TGA recurrence. TGA was not a predictor of further neurological diseases. In conclusion, TGA is a benign pathology with a low probability of relapse. Accordingly, management in Emergency Department should be based on a correct initial clinical classification for rapid discharge.

scholarly journals Acute-Onset Anterograde Amnesia Caused by Isolated Bilateral Fornix Infarction

2013 ◽  
Vol 40 (5) ◽  
pp. 738-739 ◽  
Author(s):  
Philippe Rizek ◽  
Stephen Pasternak ◽  
Andrew Leung ◽  
Mary E. Jenkins
Keyword(s):  
Anterograde Amnesia ◽  
Acute Onset

scholarly journals Transient global amnesia with bilateral hippocampal findings in magnetic resonance imaging

2020 ◽  
Vol 3 (1) ◽  
pp. 01-03
Author(s):  
Sonia P. Rodriguez ◽  
Alfredo Fernandez de Castro ◽  
Carlos Enrique Trillos Peña
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Personal Identity ◽  
Transient Global Amnesia ◽  
Anterograde Amnesia ◽  
Acute Onset ◽  
Unknown Etiology ◽  
Imaging Findings ◽  
Resonance Imaging ◽  
Global Amnesia

Transient global amnesia (TGA) is an unusual neurological syndrome of unknown etiology that affects individuals between 50 and 75 years old. We describe the case of a 61-year-old woman, who experienced an episode of two hours of anterograde amnesia. The event had an acute onset and was observed by a reliable witness. It lacked motor or sensory symptoms, compromised consciousness, or personal identity. A brain magnetic resonance was performed 22 hours after the onset of symptoms depicting foci of restricted diffusion in both hippocampi. Taking into account clinical and imaging findings, the diagnosis of transient global amnesia was made.

Acute amnestic syndrome and ischemic stroke: A case series

2020 ◽  
pp. 10.1212/CPJ.0000000000000928
Author(s):  
Malik Ghannam ◽  
Qasem Alshaer ◽  
Hope Ukatu ◽  
Mohammed Alkuwaiti ◽  
Christopher Streib
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Memory Impairment ◽  
Case Series ◽  
Anterograde Amnesia ◽  
Acute Onset ◽  
Stroke Treatment ◽  
Long Term Follow Up ◽  
High Degree

AbstractPurposeof Review: Stroke is an uncommon cause of amnesia. We describe in detail three cases of anterograde amnesia and confabulation secondary to acute ischemic stroke and review the available literature.Recent Findings:In our case series, all three patients presented with anterograde amnesia and two of three co-presented with prominent confabulation. These symptoms were recognized in delayed fashion and no patients received IV tPA. Although stroke infarct topology was variable, all three patients had infarction of the fornix. Long-term follow-up was obtained in two of three patients: both had persistent memory impairment and were no longer functionally independent.Summary:Acute onset anterograde amnesia and confabulation may uncommonly represent acute ischemic stroke. Delays in this diagnosis typically exclude patients from emergent stroke treatment or timely diagnostic stroke evaluation. Physicians should maintain a high degree of suspicion, especially in patients with comorbid vascular risk factors. Memory impairment secondary to ischemic stroke can produce considerable long-term disability.

scholarly journals Neural Correlate of Anterograde Amnesia in Wernicke–Korsakoff Syndrome

2014 ◽  
Vol 28 (5) ◽  
pp. 760-770 ◽  
Author(s):  
Louis Nahum ◽  
Jean-Michel Pignat ◽  
Aurélie Bouzerda-Wahlen ◽  
Damien Gabriel ◽  
Maria Chiara Liverani ◽  
...  
Keyword(s):  
Anterograde Amnesia ◽  
Neural Correlate ◽  
Korsakoff Syndrome

scholarly journals Optic tract and internal capsule lesion in a patient with Wernicke-Korsakoff syndrome

2020 ◽  
Vol 1 (1) ◽  
pp. 101-103
Author(s):  
Micaela Anahí Hernández ◽  
Francisco Varela ◽  
Catalina Bensi
Keyword(s):  
Brain Mri ◽  
Lactate Concentration ◽  
Anterograde Amnesia ◽  
Serum Levels ◽  
Remote Memory ◽  
Hyperintense Lesion ◽  
Adequate Treatment ◽  
Posterior Limb ◽  
Korsakoff Syndrome ◽  
Increased Risk

A 72-year-old man, presented with a one-week history of confusion and an anterograde amnesic disorder accompanied by confabulation, with lack of insight to his symptoms. Medical history included alcohol abuse and admitted twenty-years of alcohol ingestion (approximately 186 gr/day). Neurologic examination was notable for slightly decreased consciousness, disorientation to time, severe anterograde amnesia and unsteadiness of stance and gait with four limb ataxia. A metabolic blood panel including liver profile showed alanine aminotransferase mildly elevated (66 UI/L) with elevated gamma-glutamyl-transpeptidase (gGT: 426 UI/L). Tests for HIV, syphilis and vitamin B12 levels were negative. Review of initial brain MRI showed a symmetrical, increased fluid-attenuated inversion recovery (FLAIR) signal lesion extending through the hypothalamus, periaqueductal area, mamillary bodies, bilateral anterior thalami, chiasm, both optic tracts and posterior limbs of both internal capsules with restricted diffusion and patchy contrast enhancement (figure 1  1a-1b). A possible Wernicke-Korsakoff syndrome diagnosis was achived. Following the initial examination, the patient was initiated on prophylactic parenteral thiamine reposition. CSF analysis showed elevated proteins (174 mg/dl) and lactate concentration (2.9 mmol/L). Cytologic and immunocytochemical study showed no neoplastic processes. Screening of autoimmune antibodies in CSF and paraneoplastic antibodies in serum were negative. EEG and full-body CT scans were unremarkable. Thiamine serum levels were normal (16,5 ug/L) (blood sample collected previous to reposition).  Finally, a neurocognitive test indicated malperformance in tasks related to immediate and delayed recall and disturbances in recent and remote memory with confabulation. A new brain MRI after supplementation showed regression of the previous lesion (figure 1  2a-2b). He was discharged one month later with residual anterograde amnesia and gait instability that are still present eleven months later, at the last follow up.   Figure 1: (1) Axial FLAIR MRI sequence showing extensive, symmetrical, hyperintense lesion in chiasm and both optic tracts (1.a) and periaqueductal area, hypothalamus and posterior limb of internal capsules (1.b). (2) Axial FLAIR MRI sequence showing regression of the hyperintense lesion one month after thiamine reposition in chiasm and both optic tracts (2.a) and periaqueductal area, hypothalamus and posterior limb of internal capsules (2.b)   Wernicke’s encephalopathy (WE) prototypical clinical triad consists of motor problems such as ataxia or gait incoordination, ocular signs (commonly ophthalmoparesis and nystagmus) and mental status changes1-3. Thiamine (vitamin B1) deficiency secondary to alcoholism is the most common etiologic factor3. If left untreated or undertreated, there is an increased risk of developing a chronic sequelae: the Korsakoff’s syndrome (KS), characterized with loss of working memory and confabulation with sparing of remote memories2-4. Both syndromes together are termed Wernicke-Korsakoff syndrome (WKS). Even though diagnosis of WKS remains primarily clinical3, brain MRI findings in previously reported typical locations1-3are highly specific of this syndrome, suggesting MRI is a valuable confirmation tool. Normal thiamine serum levels shouldn’t dismiss the initial suspicion, as its blood concentration does not necessarily reflect brain tissue’s concentration4. Our case suggests that, even when MRI lesions are not characteristic, intravenous thiamine reposition should be immediately initiated if WKS is suspected, considering the patient's outcome depends on prompt diagnosis and adequate treatment.

The Korsakoff Syndrome

1995 ◽  
Vol 166 (2) ◽  
pp. 154-173 ◽  
Author(s):  
Michael D. Kopelman
Keyword(s):  
Memory Loss ◽  
Anterograde Amnesia ◽  
Metabolic Abnormalities ◽  
Memory Disorder ◽  
Mammillary Bodies ◽  
Korsakoff Syndrome ◽  
Retrograde Memory ◽  
Neuro Imaging ◽  
Relationship Of ◽  
The Relationship

BackgroundInvestigations of the Korsakoff syndrome by researchers from different disciplines have proliferated in recent years, making it apposite to review the various findings.MethodThis review is based on the author's knowledge of reports in the major clinical and neuropsychological journals, supplemented by Medline searches to update particular subtopics.ResultsThe Korsakoff syndrome is defined as a disproportionate impairment in memory, relative to other aspects of cognitive function, resulting from a nutritional (thiamine) depletion. The initial manifestations of the disorder are variable, and a persistent memory impairment can result from a non-alcoholic aetiology, although this seems to happen much less commonly than in the past – presumably because of generally higher standards of nutrition. Although there is agreement on the underlying neuropathology, the critical lesion sites for memory disorder have been debated. Recent evidence suggests that the circuit involving the mammillary bodies, the mammillo-thalamic tract and the anterior thalamus, rather than the medial dorsal nucleus of the thalamus, is particularly critical in the formation of new memories. The relationship of these deficits to thiamine depletion remains a topic of current investigation, as does the purported role of neurotransmitter depletions in the cholinergic, glutamate/GABA and catecholamine and serotonergic systems. Neuro-imaging studies have confirmed autopsy findings of more widespread structural and metabolic abnormalities, particularly involving the frontal lobes.ConclusionsThe relationship of these neuropathological, neurochemical, and metabolic abnormalities to cognitive functioning, with particular reference to specific aspects of memory processing, has been considered in some detail. Whereas structural and/or neurochemical abnormalities within the limbic/diencephalic circuits account for anterograde amnesia, some other factor, such as frontal lobe dysfunction, must underlie the severe retrograde memory loss which is characteristically found in this syndrome.

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