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Elevated cerebrospinal fluid tau in Wernicke encephalopathy
Daphne W Frijlink1, Joachim J Tilanus, Gerwin Roks
1Department of Neurology, St Elisabeth Hospital, Tilburg, Netherlands.
BMJ Case Reports
|August 11, 2012
Summary
Wernicke encephalopathy can mimic Creutzfeldt-Jakob disease with high CSF tau. Prompt thiamine treatment led to recovery, highlighting WE as a treatable cause of rapid dementia.
Area of Science:
- Neurology
- Neuroscience
- Biochemistry
Background:
- Wernicke encephalopathy (WE) presents with neurological deficits and can mimic rapidly progressive dementia syndromes like Creutzfeldt-Jakob disease (CJD).
- Cerebrospinal fluid (CSF) tau protein levels are utilized in diagnosing dementia subtypes, particularly CJD and Alzheimer's disease.
- Elevated CSF tau with normal phosphorylated tau (p-tau) is typically indicative of aggressive neurological diseases, such as CJD.
Observation:
- A case study involving a woman with symptoms mimicking CJD, including confusion and gait ataxia.
- The patient exhibited highly elevated CSF tau and normal p-tau levels, initially suggesting an aggressive neurological condition.
- Clinical presentation and CSF biomarkers raised suspicion for CJD.
Findings:
- Immediate thiamine treatment resulted in significant clinical improvement.
- The patient recovered well within 2.5 months, indicating a reversible condition.
- The case demonstrates WE presenting with biomarker profiles typically associated with CJD.
Implications:
- This case underscores the importance of considering treatable conditions like Wernicke encephalopathy in the differential diagnosis of rapidly progressive dementia.
- Clinicians should maintain a high index of suspicion for WE, even when CSF tau levels are markedly elevated.
- Early recognition and treatment of WE are crucial for favorable patient outcomes, preventing misdiagnosis as incurable neurodegenerative diseases.
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