Confusion after thiamine was stopped looked psychiatric. Wernicke's encephalopathy was brewing.

A history of dependence

A 35-year-old man with a history of chronic alcohol dependence and epilepsy was brought to the emergency department. He had experienced an episode of generalized tonic-clonic status epilepticus. Reports indicated he had been drinking heavily in the days before his admission.

At the time, he was known to be prescribed regular oral thiamine to manage his alcohol dependence. However, because he continued to have recurrent seizures despite benzodiazepines, he was intubated for airway protection and moved to the intensive care unit (ICU).

The overlooked supplement

In the ICU, the man was sedated and placed on mechanical ventilation to control the status epilepticus. During this period, several of his regular oral medications were withheld. Among them was his routine thiamine supplementation. It was not replaced with an intravenous or parenteral equivalent. For four days, as he lay sedated, his body was deprived of the essential cofactor needed for neuronal energy production.

Confusion and nystagmus

After four days of care, the patient’s seizures were controlled and he was extubated. As the sedation wore off, he did not return to his baseline. Instead, he exhibited persistent confusion and disorientation. His attention was impaired, and his levels of alertness fluctuated.

Initially, his medical team considered that this might be post-ictal confusion—a common lingering fog that follows severe seizures. However, a neurological examination revealed horizontal nystagmus, an involuntary rhythmic eye movement. The persistence of the mental fog combined with these ocular signs triggered a new suspicion. Given his history of alcohol misuse and the four-day gap in thiamine, the team suspected Wernicke’s encephalopathy.

The actual diagnosis

Wernicke’s encephalopathy is a neurological emergency that can be overlooked because its "classical triad" of confusion, eye abnormalities, and gait ataxia appears in only a minority of patients. In this case, the team did not wait for imaging to act. They immediately initiated high-dose intravenous thiamine therapy.

Subsequent MRI of the brain confirmed the diagnosis. The scans showed symmetrical signal abnormalities—specifically hyperintensities on T2-weighted and FLAIR sequences—in the medial thalami, mammillary bodies, and periaqueductal grey matter. These are the regions of the brain most vulnerable to thiamine depletion.

Recovery and rehabilitation

Following the start of intravenous thiamine, the man's neurological status began to improve. His confusion diminished over several days, and the nystagmus became less prominent. Once he was stable, he was moved from the acute medical unit to a rehabilitation setting.

By the time of his discharge, his cognitive function had continued to improve. He was sent home with ongoing oral thiamine, antiepileptic therapy, and a referral to alcohol support services to prevent a recurrence of the deficiency that had nearly caused irreversible brain damage.