Eating disorders
Perfectionism has been linked with Anorexia Nervosa in research for decades. A researcher in 1949 described the behavior of the average "anorexic girl" as being "rigid" and "hyperconscious", observing a tendency to "[n]eatness, meticulosity, and a mulish stubbornness not amenable to reason [which] make her a rank perfectionist". So common are such traits as perfectionism and rigidity among anorectics, that they have been referred to in clinical literature as "classical childhood features of patients with anorexia nervosa" or classical premorbid personality descriptors of anorexia nervosa".Regardless of the prevalence of the full-fledged OCPD among eating disordered samples, the presence of this personality disorder or its traits, such as perfectionism, has been found to be positively correlated with a range of complications in eating disorders and a negative outcome, as opposed to impulsive features—those linked with histrionic personality disorder, for example—which predict a better outcome from treatment. OCPD predicts more severe symptoms of Anorexia Nervosa, and worse remission rates, however, OCPD and perfectionistic traits predicted a higher acceptance of treatment, which was defined as undergoing 5 weeks of treatment.People with Anorexia Nervosa who exercise excessively display a higher prevalence of several OCPD traits when compared to their counterparts who did not exercise excessively. The traits included self-imposed perfectionism, and the childhood OCPD traits of being rule-bound and cautious. It may be that people with OCPD traits are more likely to use exercise alongside restricting food intake in order to mitigate fears of increased weight, reduce anxiety, or reduce obsessions related to weight gain.
Diagnosis is difficult, as pathognomonic signs on MRI such as cortical ribboning or hockey stick sign, periodic sharp wave complexes on EEG, and tests for 14-3-3 protein and tau protein are usually not helpful, and no mutations have been observed in the coding region of the PrP gene, unlike CJD and Variant CJD. The diagnosis can be made on pathological examination. There are unique microscopic and immunohistochemical features, and the prions cannot be digested using proteases. Because 8 out of 10 patients had a positive family history of dementia in the original study, a genetic cause was suspected. Some have suggested the disease may be a sporadic form of Gerstmann–Sträussler–Scheinker syndrome (GSS).In 2013, Zou W.Q. and coworkers revealed that the peculiar protease-resistant PrP (PrPres) originally found in VPSPr is also detectable in the brain of patients with a genetic CJD linked to PrP Valine (V) to isoleucine (I) mutation at residue 180 (PrPV180I); moreover, they found that the pathological PrP from both VPSPr and gCJDPrPV180I shares a similar glycoform-selective prion formation mechanism. [8,9] Interestingly, the authors further demonstrated that the protease-resistant PrPres from both VPSPr and gCJDV180I lacks the PrP species glycosylated at the first N-linked glycosylation site at residue 181 and they proposed that the deficiency in PrP glycosylation may be involved in the pathogenesis of the two conditions.