Extreme dieting and thiamin deficiency underlie troubling neurologic changes.
Reprinted from Eating Disorders Review
November/December 2010 Volume 21, Number 6
©2010 Gürze Books
Two cases in a middle-aged and teenaged patient are a reminder that AN patients may develop encephalopathy due to thiamin deficiency.
One case, reported at the University of Campinas, Brazil, involved a 45-year-old woman (J Med Case Reports 2010; 4:217). The woman arrived at an emergency room with marked malnutrition and mental confusion, along with a wobbling gait and ophthalmoplegia. Laboratory tests uncovered low serum magnesium levels and megaloblastic anemia. Brain MRIs showed increased signals in the medial regions of the thalamus and the central and periaqueductal midbrain, and she was diagnosed with Wernicke’s encephalopathy.
Wernicke’s encephalopathy is an acute neuropsychiatric syndrome that results from thiamin deficiency. According to authors Dr. Laura Saad and colleagues, the condition is still greatly under-diagnosed in both adults and children because the telltale signs, including acute onset of ocular abnormalities such as blurred vision, and ataxia and global confusion, are not always present. The condition is a direct result of thiamin deficiency, and may be the aftermath of malnutrition, often paired with alcohol abuse.
The patient was found to have a long history of recurrent thoughts of being overweight and of self-imposed dietary restrictions and self-induced vomiting. The patient’s mother and son reported that the woman had been dieting since she was 30 years old and never allowed herself to weigh more than 88 lb. Every 40 days she spent 10 days vomiting everything she ate and drank. She and been a model as a teenager but remained unemployed after this. She also had been drinking gin daily for the last 8 years. One day after she was admitted to the hospital, her acute global confusion resolved but she continued to have severe memory deficits and confabulation.
The patient was hospitalized for a month for psychiatric treatment and was also given a regimen of 600 mg of thiamin and 450 mg of magnesium oxide orally daily. She also received 4 gm of magnesium sulfate per day for the first 3 weeks and 1 gm per day during the last week of hospitalization. At the end of her hospitalization, her condition was much improved but her memory loss remained.
A case in a 15-year-old
In another instance, Dr. T. E. Peters and colleagues at Brown University reported a case of Wernicke’s encephalopathy in a 15-year-old girl with restricting-type AN (Adolesc Health 2007; 40:376). Just as with the Brazilian patient, the clinical triad of confusion, ataxia, and nystagmus, in addition to MRI scans showing bilateral subthalamic hyperdensities, led to the diagnosis of Wernicke’s encephalopathy. The girl had lost 66 lb over a 6-month period, following a strict diet depleted in thiamin, with no vitamin supplementation. The patient also reported going on a carbohydrate binge for 5 days prior to admission. Nutritional stabilization and parenteral thiamin replacement resulted in rapid improvement of her ataxia and nystagmus and contributed to her recovery.
In both patients, the classical triad of symptoms of Wernicke’s encephalopathy was present, which helped clinicians make the diagnosis. However, nearly one-fifth of patients do not have such clear-cut signs, and as many as 38% of patients with AN have thiamin deficiency. Also, some form of neurologic complications is found in up to 45% of AN patients. The authors recommend that thiamin therapy should be initiated when a patient with AN appears to be confused and disoriented.