⚠️ Untreated Wernicke's encephalopathy → Korsakoff's syndrome. Early recognition and prompt treatment are critical. Delay leads to irreversible cognitive decline.

ℹ️ About

Wernicke’s Encephalopathy is an acute, reversible neurological emergency caused by thiamine deficiency, most often seen in chronic alcoholism, severe malnutrition, or hyperemesis gravidarum.
If untreated, it can progress to Korsakoff’s syndrome, which causes permanent amnesia and confabulation.
Both conditions reflect different stages of the same disease process, linked by neuronal energy failure.

Aetiology & Pathophysiology

Caused by deficiency of thiamine (vitamin B1), an essential coenzyme in carbohydrate metabolism.
Thiamine pyrophosphate (TPP) is required for:
- Pyruvate dehydrogenase – links glycolysis to the Krebs cycle.
- α-ketoglutarate dehydrogenase – within the Krebs cycle.
- Transketolase – in the pentose phosphate pathway.
Deficiency → impaired ATP generation in neurons → oxidative stress → selective neuronal death (especially in mammillary bodies, thalamus, and periaqueductal grey matter).
Alcohol impairs thiamine absorption, storage, and phosphorylation, worsening deficiency.

🩺 Clinical Features

Wernicke’s Encephalopathy (acute phase) – “Classic Triad”:
- 👁️ Ocular signs: Nystagmus, diplopia, ophthalmoplegia (e.g. abducens palsy).
- 🚶 Cerebellar dysfunction: Ataxia, unsteady gait.
- 🧠 Confusion: Acute confusion, disorientation.
Note: All three features occur together in <20% of cases → underdiagnosis is common.
Korsakoff’s Syndrome (chronic phase):
- Profound anterograde amnesia (cannot form new memories).
- Some retrograde amnesia (loss of recent past events).
- Confabulation – filling memory gaps with fabricated stories.
- Personality change and apathy, but relatively preserved other cognitive functions.
Beri-Beri (systemic thiamine deficiency):
- Dry Beri-Beri: Peripheral neuropathy, areflexia.
- Wet Beri-Beri: High-output cardiac failure, oedema.

🔎 Investigations

Bloods: ↓ thiamine, ↓ RBC transketolase activity, ↑ pyruvate and lactate; ↑ GGT if alcohol-related.
MRI: T2 hyperintensity in mammillary bodies, thalami, and periaqueductal grey.
LP: Usually normal, helps exclude infection.
Post-mortem: Necrosis and gliosis in mammillary bodies, thalamus, brainstem.

💊 Management

🎯 Immediate IV thiamine (e.g., Pabrinex) BEFORE any glucose administration (to avoid precipitating acute Wernicke’s).
Acute regimen:
- Pabrinex 2 pairs IV TDS for 3–5 days → then oral thiamine long-term.
- Thiamine 400-500 mg TDS for 3 days → then oral thiamine long-term.
Also replace magnesium (essential for thiamine-dependent enzymes).
Supportive care: nutritional support, alcohol withdrawal management.
Prognosis: Wernicke’s can reverse with early treatment; Korsakoff’s has poor recovery, with permanent memory impairment in most cases.

Comparison Table

Condition	Main Features	Reversibility
Wernicke’s Encephalopathy	Confusion, ophthalmoplegia, ataxia	Reversible with urgent thiamine
Korsakoff’s Syndrome	Anterograde amnesia, confabulation, apathy	Often permanent
Beri-Beri	Dry: neuropathy \| Wet: heart failure	Improves with thiamine

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Vitamin B1 Thiamine deficiency