Elevated cerebrospinal fluid tau in Wernicke encephalopathy

Frijlink, Daphne W.; Tilanus, Joachim J; Roks, Gerwin

doi:10.1136/bcr-2012-006661

Cited by 6 publications

(3 citation statements)

References 10 publications

(14 reference statements)

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“…Thus, depressed patients may be at high risk for WKS. To our knowledge, there are 12 previous reports of major depression causing malnutrition and WE 9,10,12–18,20,21. Two of these patients had concomitant alcohol use disorder 20,21.…”

Section: Discussionmentioning

confidence: 92%

<p>A patient with Korsakoff syndrome of psychiatric and alcoholic etiology presenting as DSM-5 mild neurocognitive disorder</p>

Nikolakaros

Kurki

Myllymäki

et al. 2019

NDT

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Background: Wernicke’s encephalopathy (WE) and Korsakoff syndrome (KS) are underdiagnosed. The DSM-5 has raised the diagnostic threshold by including KS in the major neurocognitive disorders, which requires that the patient needs help in everyday activities. Methods: We report clinical, neuropsychological, and radiological findings from a patient who developed Wernicke-Korsakoff syndrome as a result of alcohol use and weight loss due to major depression. We assess the diagnosis in the context of the scientific literature on KS and according to the DSM-IV and the DSM-5. Results: The patient developed ataxia during a period of weight loss, thus fulfilling current diagnostic criteria of WE. WE was not diagnosed, but the patient partially improved after parenteral thiamine treatment. However, memory problems became evident, and KS was considered. In neuropsychological examination, the Logical Memory test and the Word List test were abnormal, but the Verbal Pair Associates test was normal (Wechsler Memory Scale-III). There were intrusions in the memory testing. The Wisconsin Card Sorting Test was broadly impaired, but the other test of executive functions (difference between Trail Making B and Trail Making A tests) was normal. There was atrophy of the mammillary bodies, the thalamus, the cerebellum, and in the basal ganglia but not in the frontal lobes. Diffusion tensor imaging showed damage in several tracts, including the uncinate fasciculi, the cinguli, the fornix, and the corona radiata. The patient remained independent in everyday activities. The patient can be diagnosed with KS according to the DSM-IV. According to the DSM-5, the patient has major neurocognitive disorders. Conclusions: Extensive memory testing is essential in the assessment of KS. Patients with a history of WE and typical clinical, neuropsychological, and radiological KS findings may be independent in everyday activities. Strict use of the DSM-5 may worsen the problem of Wernicke-Korsakoff syndrome underdiagnosis by excluding clear KS cases that do not have very severe functional impairment.

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Section: Discussionmentioning

confidence: 92%

<p>A patient with Korsakoff syndrome of psychiatric and alcoholic etiology presenting as DSM-5 mild neurocognitive disorder</p>

Nikolakaros

Kurki

Myllymäki

et al. 2019

NDT

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“…In patients with isolated tau increase, we observed 8 patients with Wernicke’s syndrome and 3 patients with an epileptic seizure during or following alcohol withdrawal. The CSF tau level increase in Wernicke’s encephalopathy, which has already been described in a few publications, results in extensive neuronal cell loss (Frijlink et al, 2012; Matsushita et al, 2008). Its increase after an epileptic seizure is also described (Matsui et al, 2007; Palmio et al, 2009); however, to the best of our knowledge, never specifically in patients with AUD and complicated withdrawal syndrome.…”

Section: Discussionmentioning

confidence: 79%

Cerebrospinal Fluid Biomarkers in Patients With Alcohol Use Disorder and Persistent Cognitive Impairment

Azuar

Bouaziz‐Amar

Cognat

et al. 2021

Alcoholism Clin & Exp Res

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Background The prevalence of cognitive impairment is high among alcohol‐dependent patients. Although the clinical presentation of alcohol‐related cognitive disorder (ARCD) may resemble that of Alzheimer’s disease (AD), the prognosis and treatment of the 2 diseases are different. Cerebrospinal fluid (CSF) biomarkers (tau, phosphorylated tau, and amyloid β) have high diagnostic accuracy in AD and are currently being used to discriminate between psychiatric disorders and AD, but are not used to diagnose ARCD. The aim of this study was to characterize CSF biomarkers in a homogeneous, cognitively impaired alcohol‐dependent population. Methods This single‐center study was conducted in an addiction medicine department of a Parisian Hospital. We selected patients with documented persistent cognitive impairment whose MoCA (Montreal Cognitive Assessment) score was below 24/30 after at least 1 month of documented inpatient abstinence from alcohol. We measured the CSF biomarkers (tau, phosphorylated tau, and amyloid β 1‐42 and 1‐40) in 73 highly impaired alcohol‐dependent patients (Alcohol Use Disorders Identification Test score over 11 for women and 12 for men) with. Results Patients' average age was 60 ± 9.1 years and 45 (61.6%) had a normal CSF profile, 8 (11.0%) had a typical CSF AD profile, and 20 (27.4%) had an intermediate CSF profile. Conclusions This study revealed a high prevalence of AD in alcohol‐dependent patients with persistent cognitive deficits and several anomalies in their CSF profiles. Thus, it is important to consider AD in the differential diagnosis of persistent cognitive deficits in patients with alcohol dependence and to use CSF biomarkers in addition to imaging and neuropsychological testing to evaluate alcohol‐related cognitive impairment.

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“…The sizes and localization of the lesion generally affects the profile of CSF t-tau levels after stroke which vary to a great extent, generally reaching maximum levels after 3 weeks to 1 month and returning to normal levels after 3-5 months [69,73]. Other neurological conditions with transiently elevated t-tau levels include acute Wernicke's disease [74,75], after chemotherapy treatment for hematologic malignancies [76], and patients with temporary neurologic dysfunction after aortic surgery [77]. Altogether, these studies support the idea of CSF t-tau reflects the degree of brain injury and harbors a prognostic value in transient acute neuronal damage syndromes.…”

Section: Total Taumentioning

confidence: 99%

Tau Protein as a Biological Fluid Biomarker in Neurodegenerative Dementias

Llorens¹,

Villar‐Piqué²,

Candelise³

et al. 2019

Cognitive Disorders

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Tau is a microtubule-associated protein, whose main function is the modulation of the stability of axonal microtubules. In physiological conditions tau is abundant in neurons while its expression in glial populations is low and restricted to astrocytes and oligodendrocytes. The aggregation of tau in neurofibrillary or gliofibrillary tangles is the main hallmark of tauopathies, a complex group of human neurodegenerative conditions where tau hyper-phosphorylation causes its increased insolubility and aggregation leading to tangle formation and microtubule destabilization. Tau can be detected in biological fluids in physiological and pathological conditions. In several neurodegenerative dementias, either associated or not to a primary tauopathy, tau levels are altered in a diseasespecific pattern, which can be used as a biomarker for disease diagnosis and prognosis. The study of tau levels in biological fluids has been mainly performed in the cerebrospinal fluid (CSF), although the recent development of ultrasensitive techniques allows the robust quantification of tau in blood-based biofluids such as serum and plasma. The presence of elevated total-tau in the CSF is assumed to reflect the degree of axonal damage in the brain tissue. Consequently, highest total-tau CSF levels are found in sporadic Creutzfeldt-Jakob disease, which is characterized by massive neuronal damage and a rapid progressive course. Elevated total-tau is also detected in Alzheimer's disease and dementia with Lewy bodies, while in other dementia conditions such as vascular dementia, frontotemporal dementia and corticobasal degeneration are unchanged, inconclusive or not determined. Additionally, total-tau rises temporarily due to cerebral infarction. In contrast, elevated phospho-tau levels seem to be restricted to Alzheimer's disease pathology, most likely mirroring the presence of the hyper-phosphorylated form in the brain tissue, although phospho-tau levels are mainly unaffected in tauopathies. Additionally, isoforms and different structural and truncated tau forms have also been reported to be altered in neurodegenerative dementias. In this complex scenario the diagnostic accuracy of diverse tau forms as disease-specific biomarkers needs to be established. In this chapter, we summarize the current knowledge on the alterations of diverse tau forms

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Elevated cerebrospinal fluid tau in Wernicke encephalopathy

Cited by 6 publications

References 10 publications

<p>A patient with Korsakoff syndrome of psychiatric and alcoholic etiology presenting as DSM-5 mild neurocognitive disorder</p>

<p>A patient with Korsakoff syndrome of psychiatric and alcoholic etiology presenting as DSM-5 mild neurocognitive disorder</p>

Cerebrospinal Fluid Biomarkers in Patients With Alcohol Use Disorder and Persistent Cognitive Impairment

Tau Protein as a Biological Fluid Biomarker in Neurodegenerative Dementias

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