1. A Case of Memory Loss and Poor Balance

2. Presenting Complaint
56 yo male presenting with memory loss and poor balance

3. History of Presenting Complaint
Memory Loss – 4/7 hx short term memory loss e.g. unable to recall if ate a meal + recollection of past events in present time e.g. though mother still alive even though past away 5yrs ago
Altered balance – unsteady gait, had x2 falls the night before, recalls events, nil LOC. Stated legs felt weak

4. HPC Cont. Poor oral intake – 1/52
Increased sleep patterns - 4/7, sleeps 15hrs/day, denies daytime fatigue
Previously well
Nil cough, CP, abdo pain, diarrhoea/vomiting, fevers, sweats or urinary symptoms
Nil visual/hearing disturbances, dizziness, paraesthesia, headache, neck pain or photophobia

5. PMHx
STEMI 2011
Prostate adenocarcinoma 2012 – underwent prostatectomy, PSA 19/1/12 <0.01
Appendiceal adenocarcinoma 2009
Dyslipidaemia
Depression

6. PSHx FHx Prostatectomy Aug 2012 Appendectomy 2009 Stent 2011
Mother – x2 MIs 55yrs
Father – MI in 60s

7. Medications Aspirin 100mg Perindopril 5mg Metoprolol 25mg
Clopidogrel 75mg
Atrovastatin 80mg
Fluoxetine 20mg (commenced 6/7 ago)

8. Social Hx Lives with wife + 2 children
Ex-truck driver – ceased work since prostectomy
Smokes ½ - 1 pack/day
Alcohol – varriable, 6-12/day. Since onset of symptoms has reduced to 2/day
Denies recreational drug use
Denies recent travel or exposures

9. Examination Afebrile, BP 129/74, HR 62, RR 18, Sats 100% RA
Alert, nil distress
ECG NAD
CVS
Warm and well perfused
HSDN, nil murmurs or added
JVPNE
Nil peripheral oedema

10. Examination Cont. Resp GIT Chest clear, EA Nil wheezes or creps
Abdo soft, non-tender
Nil jaundice, nil asterixis
Nil organomegally

11. Examination Cont. CNS Normal speech – comprehendable but vague
Alert and compliant
Nil neck stiffness
Disoriented to time and place (refers to previous hospital admission)
Knows name, DoB & address but not age
19/30 on MMSE
Able to name objects
Impaired memory – unable to retain new information, able to recall past events but gaps in long term memory
Nil confabulation

12. Examination Cont. CN II-XII intact Left lateral nystagmus Nil diplopia
Power 5/5 globally, L=R upper & lower limbs
Normal sensation and proprioception
Past pointing on finger-nose test
Nil dysdiadochokinesis
Wide based gait
Truncal ataxia

13. Differentials?

14. Differentials

15. Investigations?

16. Investigations

22. What Else?
CT Head Normal

23. MRI

24. MRI Chronic deep white matter ischaemia
The degree of ventricular dilatation and prominence of the subarachnoid spaces is most likely related to involutional change. However, the differential of normal pressure hydrocephalus needs to be considered clinically, particularly given the degree of periventricular white matter hyperintensity

25. Management
AWS
Neuro Obs
IV Thiamine 500mg TDS

26. Progress – Day 5 Feeling better Gait much improved
Still not oriented to time and place
Still ongoing short term memory impairment
Continued IV thiamine
Continued Physio/OT rv

27. Diagnosis Wernicke’s Encephalopathy ?Menengitis/Encephalitis
?Other drug/medication related

28. Outcome
Patient transferred to Wynnum Hospital for ongoing rehabilitation
Continue course of thiamine and switching to oral dose
Will review in clinic with repeat MRI in 2 weeks

29. Wernicke’s
Wernicke's encephalopathy (WE) is a common, acute neurologic disorder caused by thiamine deficiency. Clinical triad of encephalopathy, oculomotor dysfunction, and gait ataxia
Korsakoff's syndrome (KS) is a late, neuropsychiatric manifestation of Wernicke's encephalopathy (WE) in which there is a striking disorder of selective anterograde and retrograde amnesia

30. Wernicke’s Encephalopathy
Described in 1881 after Carl Wernicke (Polish Physician), also named Wernicke’s area & Sergei Korsakoff (Russian psychiatrist)
inadequate intake or absorption of thiamine (Vitamin B1)
Thiamine plays a vital role in the metabolism of carbohydrates. Thiamine is a cofactor for several essential enzymes in the Krebs cycle and the pentose phosphate pathway

31. The male-to-female ratio 1
The male-to-female ratio 1.7:1, likely owing to alcoholism being 3-4 times more frequent in men than in women.
Average age at onset is 50 years

32. Conditions associated with WE include:
Chronic alcoholism
Anorexia nervosa or dieting
Hyperemesis of pregnancy
Prolonged intravenous feeding without proper supplementation
Prolonged fasting or starvation, or unbalanced nutrition, especially with refeeding
Gastrointestinal surgery (including bariatric surgery)
Systemic malignancy
Transplantation
Hemodialysis or peritoneal dialysis
Acquired immunodeficiency syndrome

33. Wernicke-Korsakoff Syndrome
Different stages of the disease
Wernicke's encephalopathy (WE) is an acute syndrome
Korsakoff's syndrome (KS) refers to a chronic neurologic condition that usually occurs as a consequence of WE

34. Clinical Features
Clinical triad = ophthalmoplegia, ataxia, and global confusion
Only 1/3 present this way
Confusion most common presentation
Most Patients profoundly disoriented, indifferent, and inattentive, although rarely they have an agitated delirium related to ethanol withdrawal
Stupor, coma, and death may ensue if left untreated

35. Differentials Psychosis Normal pressure hydrocephalus
Cerebrovascular accident
Chronic hypoxia
Closed-head injury
Hepatic encephalopathy
Postictal state
Other substance abuse
Alcohol withdrawl
Delerium/Dementia
Stroke/Ischemia

36. Investigations Clinical Diagnosis
FBC – exclude anemias and leukemias as causes of altered mental status
Serum glucose levels - Exclude hypoglycemia and hyperglycemia
ABG
Toxic drug screening
Consider lumbar puncture (LP) - Consider LP to exclude CNS infections
Erythrocyte transketolase levels – but not necessary for diagnosis

37. Wernicke's disease. MRI reveals abnormal enhancement of the mammillary bodies (atrophy), typical of acute Wernicke's encephalopathy

38. Management Require immediate administration of thiamine
Usually 500mg IV tds for 2-3 days than reduce dose
Administration of glucose without thiamine can precipitate or worsen WE
Thiamine should be administered before glucose
Oral thiamine absorption often unreliable initially

39. Prognosis
Significantly disabling but can be prevented or reversed if treated early
Persistent neurologic dysfunction is common
Significant morbidity and mortality rate, especially if no early signs of neurologic improvement are present after repletion of thiamine
A worse outcome may be expected in late-stage Wernicke encephalopathy

40. The End ???