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
Ocular motor signs are attributable to lesions in the brainstem affecting the abducens nuclei and eye movement centers in the pons and midbrain.Ataxia is a manifestation of damage to the cerebellum, particularly the superior vermis and also the vestibular apparatus
Idea is to exclude alternate or coexisting medical conditions.
Confabulation - Patient fills in gaps of memory with data that can be recalled at that moment
Dr Carl Wernicke
A Polish neurologist, who
in 1881 as a triad of acute
mental confusion, ataxia,
Deﬁciency of vitamin B1 (thiamine)
An essential coenzyme in several
biochemical pathways in the brain,
Krebs cycle and the pentose phosphate
α-ketoglutarate dehydrogenase, pyruvate
dehydrogenase, and transketolase.
Mainly involved in the glucose metabolism
and cerebral energy utilization
Failure of thiamine-dependent
Inhibition of metabolism in brain regions
with higher metabolic demands and
high thiamine turnover.
Energy production drops, and
neuronal damage ensues
BRAIN TISSUE INJURY
Failure of GABA
Chronic alcoholism – Malnutrition –
reduced thiamine uptake and utilization
Bariatric Surgery (Bariatric BeriBeri)
Infants on formula diet deficient in
incidence can be as high as
12.5% in a population of alcoholics.
The prevalence approximately 2%.
The male-to-female ratio is 1.7 : 1
Average age at onset is 50 years.
The classical triad of symptoms – only 1/3rd
Evidence of long-term alcohol abuse or
Other symptoms could include memory
disturbance, hypothermia with
hypotension, and delirium tremens.
Special clinical scenarios as previously
Ocular abnormalities – nystagmus , bilateral
lateral rectus palsies, conjugate gaze palsies,
sluggish pupils, ptosis, and anisocoria
Encephalopathy – global confusional state,
disinterest, inattentiveness, or agitation; Coma is
Gait ataxia – cerebellar damage, and
Peripheral neuropathy – foot drop, and
CBC – R/o severe anemias and leukemias as
causes of altered mental status
O2 Saturation and ABG - Exclude hypoxia/
hypercarbia; Metabolic Acidosis may be+
Toxic drug screening - Excludes some causes
of drug-induced altered mental status.
Lumbar puncture (LP)
infections, if indicated
CT/MRI – exclude ICSOLs etc.
particular Changes in acute
encephalopathy - excessive
mamillary body and cerebellar
Erythrocyte transketolase activity assay,
Thiamine assay – very specific tests – not
widely available – reserved for
Emergency department care – Parenteral thiamine –
Requirement in chronic alcoholics may be as high as
500mg single dose or multiple daily doses.
Never start on Dextrose
Parenteral magnesium sulfate as thiamine therapy
ineffective in presence of hypomagnesemia
In-Patient care – Watch for complications – Korsakoff
psychosis – Alcohol withdrawal – Congestive heart
failure – Lactic acidosis
Out-Patient Care – Thiamine 100 mg PO daily, start
alcohol cessation program, Advise on importance of
85% of the survivors of the acute phase of
Wernicke encephalopathy who remain
untreated go on to develop WernickeKorsakoff syndrome.
It manifests with
About 20% eventually recover completely
during long-term follow-up care.
considered as a medical emergency, as it is
associated with signiﬁcant morbidity and
Because the condition is potentially
reversible, early diagnosis is important.
The diagnosis is clinical and is mainly
supported by the dramatic improvement of
neurological signs on parenteral thiamine