Think CANON for signs of alcohol-induced amnesia

Wernicke’s encephalopathy is often missed in clinical practice.¹ Left untreated, the alcohol-induced amnestic disorder can progress to Korsakoff’s syndrome, a form of permanent short-term memory loss from which four out of five patients do not recover.²

Why Wernicke’s is missed

Lesions in the medial dorsal nucleus of the thalamus, hippocampus, and mammillary bodies cause signs and symptoms of Wernicke’s. Associated psychotic symptoms—including delusions, confusion, agitation, blunted to apathetic affect, and confabulation—may incorrectly suggest delirium tremens, alcohol-induced psychosis, delusional disorder, or dementia.

Key features of Wernicke’s are remembered with the acronym CANON:

Clouded consciousness with impaired orientation and inability to sustain attention to environmental stimuli.

Ataxia, primarily affecting gait

Nystagmus, mainly horizontal

Ophthalmoplegia accompanied by lateral orbital palsy and gaze palsy, which is usually bilateral. Anisocoria and a sluggish reaction to light also are present.

Neuropathy, mainly peripheral.

Early recognition and treatment is essential as early-stage Wernicke’s responds rapidly to parenteral thiamine, 100 mg/d for 5 to 7 days. Oral thiamine, 100 mg two to three times daily, is then given for 1 to 2 weeks.

Wernicke’s encephalopathy is often missed in clinical practice.¹ Left untreated, the alcohol-induced amnestic disorder can progress to Korsakoff’s syndrome, a form of permanent short-term memory loss from which four out of five patients do not recover.²

Why Wernicke’s is missed

Lesions in the medial dorsal nucleus of the thalamus, hippocampus, and mammillary bodies cause signs and symptoms of Wernicke’s. Associated psychotic symptoms—including delusions, confusion, agitation, blunted to apathetic affect, and confabulation—may incorrectly suggest delirium tremens, alcohol-induced psychosis, delusional disorder, or dementia.

Key features of Wernicke’s are remembered with the acronym CANON:

Clouded consciousness with impaired orientation and inability to sustain attention to environmental stimuli.

Ataxia, primarily affecting gait

Nystagmus, mainly horizontal

Ophthalmoplegia accompanied by lateral orbital palsy and gaze palsy, which is usually bilateral. Anisocoria and a sluggish reaction to light also are present.

Neuropathy, mainly peripheral.

Early recognition and treatment is essential as early-stage Wernicke’s responds rapidly to parenteral thiamine, 100 mg/d for 5 to 7 days. Oral thiamine, 100 mg two to three times daily, is then given for 1 to 2 weeks.

Wernicke’s encephalopathy is often missed in clinical practice.¹ Left untreated, the alcohol-induced amnestic disorder can progress to Korsakoff’s syndrome, a form of permanent short-term memory loss from which four out of five patients do not recover.²

Why Wernicke’s is missed

Lesions in the medial dorsal nucleus of the thalamus, hippocampus, and mammillary bodies cause signs and symptoms of Wernicke’s. Associated psychotic symptoms—including delusions, confusion, agitation, blunted to apathetic affect, and confabulation—may incorrectly suggest delirium tremens, alcohol-induced psychosis, delusional disorder, or dementia.

Key features of Wernicke’s are remembered with the acronym CANON:

Clouded consciousness with impaired orientation and inability to sustain attention to environmental stimuli.

Ataxia, primarily affecting gait

Nystagmus, mainly horizontal

Ophthalmoplegia accompanied by lateral orbital palsy and gaze palsy, which is usually bilateral. Anisocoria and a sluggish reaction to light also are present.

Neuropathy, mainly peripheral.

Early recognition and treatment is essential as early-stage Wernicke’s responds rapidly to parenteral thiamine, 100 mg/d for 5 to 7 days. Oral thiamine, 100 mg two to three times daily, is then given for 1 to 2 weeks.