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Journal Article
Review
Extend, Pathomechanism and Clinical Consequences of Brain Volume Changes in Anorexia Nervosa.
INTRODUCTION: Brain volume deficits of grey matter (GM) and white matter (WM) are often found in patients with anorexia nervosa (AN). However, until recently, little was known about the influencing factors of these brain volume alterations, nor their exact quantification and rehabilitation.
METHODS: This review addresses these open questions and further explores what is now known about the underlying pathobiology and the clinical consequences including human studies as well as animal studies mimicking anorexia nervosa in rodents.
RESULTS: GM was reduced by 3.7% in adults and 7.6% in adolescents with AN. WM was reduced on average 2.2% in adult patients and 3.2% in adolescents. Most volume deficits in adults are reversible after long-term recovery; for adolescents, data are less clear. The main influencing factors for GM were absolute lowest weight at admission and illness duration. Cerebellar and WM reductions at admission predicted clinical outcome at one year follow-up. New studies found GABA receptor changes in GM and astrocyte loss in both GM and WM, as well as a possible role for oestrogen deficit. All three could partly explain clinical symptoms of anxiety, rigidity and learning impairments in patients with AN.
CONCLUSION: Brain volume deficits in AN seem to play a causal role in the course and the prognosis of AN. A better understanding of these brain changes could lead to more targeted therapies for patients with AN, including astrocyte-directed approaches.
METHODS: This review addresses these open questions and further explores what is now known about the underlying pathobiology and the clinical consequences including human studies as well as animal studies mimicking anorexia nervosa in rodents.
RESULTS: GM was reduced by 3.7% in adults and 7.6% in adolescents with AN. WM was reduced on average 2.2% in adult patients and 3.2% in adolescents. Most volume deficits in adults are reversible after long-term recovery; for adolescents, data are less clear. The main influencing factors for GM were absolute lowest weight at admission and illness duration. Cerebellar and WM reductions at admission predicted clinical outcome at one year follow-up. New studies found GABA receptor changes in GM and astrocyte loss in both GM and WM, as well as a possible role for oestrogen deficit. All three could partly explain clinical symptoms of anxiety, rigidity and learning impairments in patients with AN.
CONCLUSION: Brain volume deficits in AN seem to play a causal role in the course and the prognosis of AN. A better understanding of these brain changes could lead to more targeted therapies for patients with AN, including astrocyte-directed approaches.
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