Wernicke’s Encephalopathy Flashcards
Wernicke’s encephalopathy (WE): an acute encephalopathy characterised by a triad of confusion, …, and … dysfunction
Wernicke’s encephalopathy (WE): an acute encephalopathy characterised by a triad of confusion, ataxia, and oculomotor dysfunction
Wernicke-Korsakoff syndrome refers to two distinct neurological syndromes resulting from … deficiency
Wernicke-Korsakoff syndrome refers to two distinct neurological syndromes resulting from thiamine (Vitamin B1) deficiency.
The syndromes are most commonly observed in chronic … because of poor dietary intake, although other factors are involved including a possible genetic element. WKS is not restricted to this and may be observed in other conditions (e.g. anorexia nervosa).
The syndromes are most commonly observed in chronic alcoholism because of poor dietary intake, although other factors are involved including a possible genetic element. WKS is not restricted to chronic alcoholism and may be observed in other conditions (e.g. anorexia nervosa).
KS vs WE
KS is essentially the late neuropsychiatric manifestation of WE if it goes unnoticed or untreated. Once KS has been established, patients rarely recover. This means early recognition and treatment of WE with high dose B vitamins (e.g. Pabrinex®) is critical to prevent permanent neurological damage.
… syndrome predominantly occurs in the setting of chronic alcoholism.
Wernicke-Korsakoff syndrome predominantly occurs in the setting of chronic alcoholism.
Other causes of Wernicke-Korsakoff syndrome occur from conditions that result in poor dietary intake or malabsorption of thiamine relative to metabolic requirements. Examples include:
Prolonged fasting or starvation Anorexia nervosa Hyperemesis gravidarum Systemic malignancy End-stage renal failure: on haemodialysis or peritoneal dialysis Gastrointestinal disease & malabsorption
… is an essential cofactor for several metabolic reactions in the body.
Thiamine is an essential cofactor for several metabolic reactions in the body.
Thiamine is present in most foods, but specifically in whole grains, poultry, nuts, peas, brown rice, and fortified food. Once absorbed from the gastrointestinal tract it is stored in the liver. However, storage occurs for a maximum of 18 days meaning a moderate consumption of thiamine is needed to maintain stores.
Recommended daily intake of thiamine (adults >18):
Men: 1.2 mg/day
Women: 1.1 mg/day
Pregnancy: 1.4 mg/day
In Wernicke-Korsakoff syndrome, thiamine deficiency leads to neuronal injury.
In Wernicke-Korsakoff syndrome, thiamine deficiency leads to neuronal injury. Deficiency causes areas of the brain with high metabolic activity to undergo neuronal injury that may be precipitated by the administration of intravenous glucose before thiamine supplementation.
On autopsy, typical findings in acute WE include vascular congestion, microglial proliferation, and petechial haemorrhage. In chronic disease, there is evidence of neuronal loss, most notably in the medial thalamus. Several other histological findings are typical of the syndrome.
Thiamine deficiency may also lead to a condition known as beriberi, which is discussed further below.
Beriberi refers to two classic syndromes known as ‘…’ and ‘…’ that result from thiamine deficiency.
Beriberi refers to two classic syndromes known as ‘dry’ and ‘wet’ that result from thiamine deficiency.
Wernicke-Korsakoff syndrome is not the only manifestation of thiamine deficiency. Beriberi may also develop due to thiamine deficiency. Adult beriberi is divided into two distinct syndromes:
Dry beriberi: symmetrical motor and sensory peripheral neuropathy
Wet beriberi: causes a high-output cardiac failure (fluid overload, cardiomyopathy, tachycardia, warm extremities) due to peripheral vasodilatation from a build-up of pyruvate and lactate
Dry beriberi: symmetrical motor and sensory peripheral …
Wet beriberi: causes a …-output cardiac failure (fluid overload, cardiomyopathy, tachycardia, warm extremities) due to peripheral vasodilatation from a build-up of pyruvate and lactate
Dry beriberi: symmetrical motor and sensory peripheral neuropathy
Wet beriberi: causes a high-output cardiac failure (fluid overload, cardiomyopathy, tachycardia, warm extremities) due to peripheral vasodilatation from a build-up of pyruvate and lactate
WE is characterised by a triad of clinical manifestations that can be remembered by the mnemonic CAN:
WE is characterised by a triad of clinical manifestations that can be remembered by the mnemonic CAN:
Confusion
Ataxia: poor coordination of movement. Predominantly affects gait
Nystagmus: uncontrolled eye movement
WE is characterised by a triad of clinical manifestations that can be remembered by the mnemonic CAN:
Confusion
Ataxia: poor coordination of movement. Predominantly affects gait
Nystagmus: uncontrolled eye movement
This triad of features is only seen in up … of patients
WE is characterised by a triad of clinical manifestations that can be remembered by the mnemonic CAN:
Confusion
Ataxia: poor coordination of movement. Predominantly affects gait
Nystagmus: uncontrolled eye movement
This triad of features is only seen in up to one-third of patients.
Nystagmus may be seen as part of a wider number of abnormalities collectively termed oculomotor dysfunction, which can include:
Lateral rectus palsy (CN VI palsy)
Conjugate gaze palsies: inability to move both eyes in a single horizontal
Nystagmus
