 Acute neurological disorder induced by

Thiamine deficiency(Vitamin B1)

 More prevalent in males (1.7: 1)
 Average onset age is 50 years
(range: 30-70 years)
 First described in 1881 by Dr. Carl Wernicke
 Rate has been found to be significantly
higher in specific populations, i.e., homeless
people, older people (especially those living
alone or in isolation), and psychiatric
inpatients, where alcohol use and poor
nutritional states predominate.
 Prevalence at autopsy exceeds clinical
detection.
 Water soluble vitamin absorbed from the gut.
 Serves as a cofactor to several enzymes that
are responsible for lipid and carbohydrate
metabolism, production of amino acids and
production of glucose derived
neurotransmitters.
 Also have a role in axonal conduction esp. of
acetylcholinergic and serotoninergic
neurons.
 Cellular impairment and injury occur within 2-
3 weeks of decreased intake and thiamine
depletion.
 Acute thiamine deficiency leads to
mitochondrial dysfunction resulting in
oxidative toxicity in areas of brain.
 Chronic alcoholism
 Malnutrition or prolonged starvation
 Hyperemesis Gravidarum
 Bariatric surgery
 Gastric malignancy (inflammatory bowel
disease)
 Intestinal obstruction (abscess)
 Thyrotoxicosis
 Iatrogenic (IV glucose without thiamine
supplement or chronic hemodialysis)
 Systemic diseases (AIDS, disseminated TB)
 Thiamine deficient formula/ breastfeeding by
mothers with inadequate thiamine intake
 Infection( precipitating factor)- pneumonia,
meningitis
 Clinical Triad - ocular abnormalities (29%)
- encephalopathy (82%)
- ataxia (23%)
 Occurs in 1/3 of cases.
 Hallmark of WE
 Nystagmus, bilateral rectal
palsies and conjugate gaze
palsies (involvement of
oculomotor, abducens and
vestibular nuclei)
 Less common manifestations
are pupillary abnormalities,
ptosis, sctomata and
anisocoria
 Global confusion state, disinterest,
inattentiveness or agitation.
 Most common presentation is mental state
changes.
 Stupor and coma observed in severe cases
 Due to polyneuropathy, cerebellar damage
and vestibular paresis.
 Wide based stance
 Slow and uncertain short stepped gait.
 Inability to walk without support in severe
cases.
 Peripheral neuropathy (weakness, foot drop
& decreased proprioception)
 GI symptoms (nausea, vomiting, lactic
acidosis)
 Hypotension
 Hypothermia
 Memory disturbances
 Acute symmetrical lesions in thalamus,
mamillary bodies, tectal plate,
periaqueductal area, floor of 4th ventricle
(includes oculomotor and vestibular nuclei
and cerebellar vermis)

 Lesions are in form of vascular congestion,

microglial proliferation and petechial
hemorrhages.
 Chronic complication of WE
 Occurs in 2/3 of patients with untreated WE
 Only 25% of patients fully recover.
 Lesions are similar to WE expect they are
not hemorrhagic.
 Results in cerebellar atrophy (irreversible
change).
 Characteristics:
 Anterograde amnesia (inability to form new
memories)
 Retrograde amnesia ( inability to recall past
events)
 Confabulations
 Detailed patient history
 Physical and neurological examination
 Laboratory evaluation
 CBC (rule out infections, severe anemia)
 Serum thiamine levels
 Erythrocyte transketolase levels
 Serum glucose levels
 Toxic drug screening
 Lumbar puncture (rule out CNS infections)
 Imaging
 MRI (fluid attenuated inversion recovery
{FLAIR} images)
 CT ( not specific)
 EEG ( rule out non- convulsive status
epilepticus)
 Hepatic encephalopathy
 Hypoglycemia
 Anorexia nervosa
 Alcohol related psychosis
 Withdrawal syndromes
 Delirium tremens
 Considered a medical emergency
 Emergency care : Parenteral Thiamine (multiple
daily doses – 500mg/dose)
 Alcohol withdrawal
 In case of WKS, use of oral Thiamine to prevent
further complications.
 Parenteral magnesium sulfate in case of
hypomagnesaemia
 Balanced diet with high thiamine containing
foods.
THANK YOU..