A Case of Memory Loss and Poor Balance

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

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

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

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

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

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

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

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

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

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

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

Differentials?

Differentials

Investigations?

Investigations

What Else? CT Head Normal

MRI

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

Management AWS Neuro Obs IV Thiamine 500mg TDS

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The End ???