CNS manifestations of anorexia nervosa are common but varied with most of the imaging features non-specific in their own right.
For a general discussion, and for links to other system specific manifestations, please refer to the article on anorexia nervosa.
Studies have identified that CNS complications may be present in up to 45% of patients with anorexia nervosa although these are based on patients being managed as inpatients 1. The exact frequency of CNS complications in patients being managed in the community is unknown.
CNS complications may manifest with the following 1,2:
- memory impairment
- orthostatic hypotension
- movement disorders
CT scans may show sulcal widening and ventriculomegaly in keeping with generalized cerebral atrophy. The loss of grey and white matter has been shown to improve upon refeeding and restoration of body mass index (BMI) within the 'normal' 18-25 range.
MRI is able to demonstrate the same features as seen on CT. Additionally, features associated with rapid refeeding, namely central pontine myelinolysis 6, and of vitamin B12 deficiency, namely subacute combined degeneration of the cord, may also be seen with MRI of the brain and spinal cord respectively. The features of Wernicke encephalopathy due to thiamine deficiency are also seen in the brain. These are often subtle or not detected on CT.
Patients with anorexia nervosa show increased activity in the medial frontal and anterior cingulate gyri in response to food compared to healthy individuals. The medial prefrontal cortex is responsible for emotional values of stimuli (in this case, food) and influences a response accordingly.
However, despite recovered patients rating food stimuli just as positively as the healthy patients, their brain response to these stimuli is different, suggesting long term neuromodulation.
Dorsal anterior cingulate gyrus activity (which is responsible for attention and motivation) is shown to be proportional to body weight 3.
Single-photon emission computed tomography (SPECT) scanning has revealed temporal lobe hypoperfusion in the acute phase of the illness. This has been correlated with abnormal 5-HT activity in those regions 4,5.
Treatment and prognosis
The treatment for anorexia nervosa involves various forms of psychotherapy including cognitive behavioral therapy and family-based treatment. Acute management includes refeeding, correcting electrolyte abnormalities and monitoring for autonomic and cardiac complications. No specific treatment exists for management of the neurological complications of anorexia, although some studies suggest that antipsychotics like olanzapine may help in quicker restoration of weight and better long term outcomes for patients 7. Despite common practice, there is mixed evidence that antidepressants may be effective in altering the course of the disease 8,9.
- neurological imaging may be indicated in patients with anorexia to screen for CNS complications
- no specific treatment is available for the neurological complications of anorexia nervosa
- correcting nutritional deficiencies and restoring normal body mass index appears to revert the CNS manifestations of anorexia nervosa
- 1. Patchell RA, Fellows HA, Humphries LL. Neurologic complications of anorexia nervosa. (1994) Acta neurologica Scandinavica. 89 (2): 111-6. Pubmed
- 2. Christopher G. Fairburn, Kelly D. Brownell. Eating Disorders and Obesity, Second Edition. (2013) ISBN: 9781462514731
- 3. Uher R, Brammer MJ, Murphy T, Campbell IC, Ng VW, Williams SC, Treasure J. Recovery and chronicity in anorexia nervosa: brain activity associated with differential outcomes. (2003) Biological psychiatry. 54 (9): 934-42. Pubmed
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- 6. Amann B, Schäfer M, Sterr A, Arnold S, Grunze H. Central pontine myelinolysis in a patient with anorexia nervosa. (2001) The International journal of eating disorders. 30 (4): 462-6. Pubmed
- 7. Stephanie J Klenotich, Mariel P Seiglie, Matthew S McMurray, Jamie D Roitman, Daniel Le Grange, Priya Dugad, Stephanie C Dulawa. Olanzapine, but Not Fluoxetine, Treatment Increases Survival in Activity-Based Anorexia in Mice. (2012) Neuropsychopharmacology. 37 (7): 1620. doi:10.1038/npp.2012.7 - Pubmed
- 8. Kaye WH, Nagata T, Weltzin TE, Hsu LK, Sokol MS, McConaha C, Plotnicov KH, Weise J, Deep D. Double-blind placebo-controlled administration of fluoxetine in restricting- and restricting-purging-type anorexia nervosa. (2001) Biological psychiatry. 49 (7): 644-52. Pubmed
- 9. Attia E, Haiman C, Walsh BT, Flater SR. Does fluoxetine augment the inpatient treatment of anorexia nervosa?. (1998) The American journal of psychiatry. 155 (4): 548-51. doi:10.1176/ajp.155.4.548 - Pubmed