Neurobiological Factors

A number of neurotransmitters and appetite-related neuropeptides have been identified as being abnormal in patients with eating disorders. Serotonin has been the neurotransmitter most commonly targeted for investigation, because the 5-hydroxytryptamine (5-HT) systems are known to be involved in disorders of mood, obsessiveness, appetite regulation, and impulse control. Although patients with anorexia nervosa have been found to have low levels of 5-HT metabolites in their cerebrospinal fluid and abnormal hormonal response to 5-HT-specific challenges (Kaye et al. 1991), studies of patients with bulimia nervosa suggest the inverse profile (Jimer-son et al. 1992). The efficacy of selective serotonin

Table 1G-3. Medical complications of eating disorders

Anorexia

Bulimia

Cardiovascular

Bradycardia, hypotension, orthostasis, mitral valve prolapse, decreased left ventricular mass, poor myocardial contractility, pericardial effusion, prolonged QTc, congestive heart failure or arrhythmia due to refeeding syndrome

Bradycardia, hypotension, prolonged QTc, orthostasis, arrhythmia due to hypokalemia, cardiomyopathy due to ipecac

Endocrine/metabolic

Delayed puberty, amenorrhea, ovarian or testicular atrophy, osteoporosis, hypothermia, euthyroid sick syndrome, growth retardation, elevated cholesterol

Oligomenorrhea, amenorrhea, osteoporosis

Gastrointestinal

Delayed gastric emptying, constipation, superior mesenteric artery syndrome, pancreatitis and elevated hepatic enzymes with refeeding

Parotid and salivary gland enlargement, delayed gastric emptying, esophagi tis, Mallory-Weiss tear, esophageal rupture, constipation, laxative dependence, gastric dilatation or rupture due to bingeing

Hematological

Decreased marrow production of all cell types, especially neutrophils

Anemia due to gastrointestinal bleeding

Neurological

Cerebral atrophy, cerebral edema (due to water loading), seizures, muscle weakness (due to low phosphorus), peripheral neuropathy, organic brain syndrome

Pulmonary

Spontaneous pneumothorax due to poor tissue integrity, respiratory failure due to severe inanition or hypophosphatemia

Aspiration pneumonia, pneumomediastinum, subcutaneous emphysema

Renal/electrolytes

Hypokalemia, hypophosphatemia (due to refeeding or vomiting), hypomagnesemia, hyponatremia (due to water loading)

Hypokalemia, hypochloremic metabolic alkalosis, dehydration, fluid retention and peripheral edema on resumption of normal intake

Other

Lanugo, dry skin, brittle hair and nails, impaired thermoregulation

Dental enamel erosion, Russell's sign (abrasions on knuckles)

Source. Katzman 2005; Pomeroy 2004.

reuptake inhibitors (SSRIs) for patients with bulimia nervosa is likely related to this latter finding.

Neuroimaging studies have been conducted in patients with anorexia nervosa using positron emission tomography, single photon emission computed tomography (SPECT), and structural magnetic resonance imaging (MRI). Although findings have not been consistently replicated, several abnormal patterns appear to be related to low weight and normalize following weight gain, and some patterns persist following weight recovery. In patients with anorexia nervosa who are at low weight, SPECT studies demonstrate abnormalities in perfusion of the temporal, parietal, and frontal lobes (Rastam et al. 2001; Ta-kano et al. 2001); the striatum (Rastam et al. 2001);

and the anterior cingulate cortex (ACC) (Naruo et al. 2001). In weight-recovered patients with anorexia nervosa, hypoperfusion is seen in the parietal lobe and orbitofrontal cortex (Rastam et al. 2001). SPECT studies performed both before and after treatment suggest that hypoperfusion of the temporal lobe (I. Gordon et al. 1997) and ACC (Chowd-hury et al. 2003) persists after weight restoration. Volumetric MRI studies show a correlation between decreasing ACC volume and increasing lifetime severity of anorexia nervosa in weight-recovered patients (Muhlau et al. 2007).

Functional MRI (fMRI) tasks have also been used to activate brain circuits relevant to anorexia nervosa symptoms. Neuroimaging studies using food-

relevant paradigms, such as responses to high- and low-calorie food pictures, show elevated temporal lobe activation (C.M. Gordon et al. 2001), while elevated medial prefrontal and ACC activation is found in both underweight and recovered patients with anorexia nervosa (Kurosaki et al. 2006). Tasting sucrose solution versus water decreased activation in the insula and striatum of weight-restored subjects with anorexia nervosa (Kurosaki et al. 2006). Increased striatum activation was found during a non-food-related reward processing task (Wagner et al. 2007). During tasks related to body image distortion, increased activation has been observed in the frontal and parietal lobes (Uher et al. 2005); the ACC (Audenaert et al. 2003); and the brainstem, amygdala, and fusiform gyrus (Wagner et al. 2003). In another study using body image distortion tasks, Uher et al. (2004) found decreased parietal lobe activation. Taken as a group, these studies suggest that patients with anorexia nervosa have differential brain activation in areas related to multiple cognitive functions, including visual-spatial processing, reward processing, and neural responses to food stimuli.

In fMRI studies of patients with bulimia nervosa, food craving-related signal changes have been identified in the hippocampus, insula, and caudate nucleus. These areas are believed to be involved in drug craving (Pelchat et al. 2004). In studies in which images of food are presented, fMRI scans have shown activation in the areas related to mood processing and the control and planning of behavior (i.e., the limbic system, ACC, and prefrontal cortex) in patients with bulimia nervosa, whereas activation occurs in the inferior parietal lobule and left cerebellum in healthy control subjects (Ellison et al. 1998; Uher et al. 2004, 2005). In patients with bulimia nervosa, less activation occurs in the dorsolateral region of the prefrontal cortex, an area that has been linked to inhibition. The finding that the lateral prefrontal cortex is involved in suppressing undesirable behaviors (Aron et al. 2003) suggests that diminished activity in this region may account for the loss of eating behavior control in patients with bulimia nervosa.

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