1. Wernicke’s encephalopaty: the best way to make early diagnosis D.MACHADO* – A.BOCCHIO *– A.M.ROSANO’*- M.OGGERO*- N.MILLOZ° – G.DOVERI°– T.MELONI* *Radiology Department, °General Medicine Department Regional Hospital of Valle d’Aosta

2. Wernicke’s encephalopathy is an acute, neuropsychiatric syndrome described for the first time in 1881 by doctor Carl Wernicke as a thriad characterised by nystagmus and ophthalmo- plegia, mental-status changes and unsteadiness of stance and gait Prevalence of Wernicke’s encephalopathy lesions at autopsy : (0·8–2·8%) clinical studies : (0·04–0·13%)

3. The disorder results from a deficiency in vitamin B1 (thiamine), which, in its biologically active form, is an essential coenzyme in several biochemical pathways in the brain, mainly involved in the glucose metabolism and cerebral energy utilization

4. Metabolic changes

5. In the Western world, thiamine deficiency is characteristically associated with chronic alcoholism However, Wernicke encephalopathy has been described in many other situations where nutrition has been compromised.

6. two of four items The classical triad nystagmus and ophthalmo- plegia mental-status changes unsteadiness of stance and gait is recognised in only 1/3 of cases oculomotor abnormalities (usually affect 29%of patients) altered mental state or mild memory impairment cerebellar dysfunction (20%) dietary deficiencies two of the four criterias should be present

7. Patient 59, presented with confusion; Remote history: breast Ca (2001), diabetes mellitus type II, hypertension, liver disease of unknown origin Clinical history

9. After a few days from admission: LP: liquor normal, no signs of infection CT was repeated: unchanged from the previous sepsis (blood culture positive for Gram +) and worsening mental status (GCS = 9) EEG: diffuse slowing EMG: axonal polyneuropathy Routine blood tests: liver distress, signs of malnutrition (decreased prealbuminemia), possible alcohol abuse (increased transferrin desialata and macrocytosis) Clinical history

10. Hyperintense outbreaks in FLAIR sequences at floor of the IV ventricle, periacqueductal white matter, qudrigeminal plate, mammillary bodies, medial dorsal thalamus and lateral walls of the third ventricle.

11. Hyperintense outbreaks in T2 and FLAIR sequences at periacqueductal white matter, mammillary bodies, parts of the medial dorsal thalamus and lateral walls of the third ventricle.

13. No contrast enhancement was shown after Gadolinium administration

14. The signal abnormalities in MRI were suggestive for the presence of a WS. The patient was given thiamine (1 vial x 3 / day) and folate Within 1 week : progressive improvement in clinical status, with return of consciousness. Residual attentional deficits and weakness in all four limbs

15. Conclusion Wernicke encephalopaty (WE) must be considered as a medical emergency, as it is associated with significant morbidity and mortality Because the condition is potentially reversible, early diagnosis is important Diagnosis may be difficult because of either a non specifical clinical presentation or because of unrecognised clinical datas and neurological signs. The diagnosis is clinical and is mainly supported by the dramatic response of neurological signs to parenteral thiamine

16. Among paraclinical studies MRI is currently considered the most valuable for diagnosis, with a sensitivity of only 53%, but a specificity of 93%, which means that it can be used to rule out the disorder Conclusion Althoug atypical MRI findings have been described, as involvment of cerebellum, cranial nerve nuclei, red nuclei, dentate nuclei, caudate nuclei, splenium, and cerebral cortex

17. Lo cation and distribution of the lesions Remote history (alcohol abuse) Clinical presentation Correlated with literature

18. Thank you