Korsakoff psychosis (KP) is a disorder of declarative learning and memory that results from thiamine deficiency, largely (90%) secondary to chronic alcohol abuse in industrialized nations. It is classically, but not always, seen following the presentation of Wernicke encephalopathy (see “Wernicke Syndrome”).

Korsakoff syndrome

KPF

Wernicke-Korsakoff syndrome

Alcoholic polyneuritic psychosis

• The incidence of KP is declining as a result of improved patient nutrition and awareness by health professionals
• More common in males
• Age of onset evenly distributed between ages 30 and 70 yr

• Impaired anterograde memory as a core feature, and commonly retrograde memory is impaired to a varying extent as well.
• Remote memory is relatively less impaired on neuropsychiatric testing.
• Confabulation (the fabrication of false memories to fill memory gaps) is common.
• Severe declarative amnesia and concomitant deficits in executive function result in compromised autonomy.

KP is the result of thiamine deficiency. Thiamine deficiency is commonly seen in chronic alcoholism and other malnourished populations (anorexia, bariatric surgery, malignancy). It may also occur from prolonged infusion of dextrose-containing fluids without thiamine repletion.

• Stroke, trauma, or tumor affecting the temporal lobes or hippocampi
• Cerebral anoxia
• Transient global amnesia
• Dementia of multiple causes

A high index of suspicion should be maintained in chronic alcoholism and malnourished states.

• CBC
• Serum chemistries
• Erythrocyte thiamine transketolase concentration before and after replacement with thiamine pyrophosphate

MRI brain may show nonspecific T₂ hyperintensities in the diencephalon and mesencephalon but is not pathognomonic. However, MRI/CT may be helpful in ruling out other diagnoses.

A supervised environment may be required.

• Acute: Treatment should be initiated in all patients with clinical suspicion of Wernicke encephalopathy (WE). Thiamine supplementation should precede glucose administration in all patients at risk for WE lest they develop Korsakoff syndrome.
• Alcoholics with WE: Treat with 500 mg of thiamine hydrochloride (dissolved in 100 ml of normal saline) infused intravenously over 30 min three times daily for 2 to 3 days.
• If a response is observed, continue with 250 mg of thiamine hydrochloride intravenously or intramuscularly daily until clinical improvement ceases.
• Nonalcoholics with WE: Treat with 200 mg of thiamine hydrochloride (dissolved in 100 ml of normal saline) infused intravenously over 30 minutes three times daily for 2 to 3 days.
• Parenteral magnesium must be infused concurrently with thiamine.
• Side effects of parenteral thiamine hydrochloride may include generalized pruritus, transient local irritation, or, rarely, anaphylactic or anaphylactoid reactions.

Recommended oral dose after completed parenteral treatment for WE: Thiamine 30 to 100 mg twice daily for long-term thiamine replacement.

• Individuals with KP rarely recover; therefore, one must consider the need for additional support and supervision within the home versus placement in a long-term care facility.

• Neurology to confirm the diagnosis and rule out other causes
• Neuropsychiatric testing to assess baseline functioning and further deterioration

• KP is frequently misdiagnosed or underdiagnosed.
• Memory problems may persist even in “recovered” patients.
• Replace thiamine in patients at risk even if clinical symptoms are not evident.
• Prolonged use of dextrose-containing IV fluids without supplemental thiamine may precipitate KP.
• Strengthening of procedural memory and encouragement of procedural learning can help restore some of the patient’s autonomy.

Alcohol Use Disorder (Related Key Topic)

Delirium (Related Key Topic)

Vitamin Deficiency (Hypovitaminosis) (Related Key Topic)

Wernicke Syndrome (Related Key Topic)