The neurologic findings of the studies suggest that NPD may be related to a compromised (damaged) capacity for emotional empathy and emotional regulation. Management
Treatment for NPD is primarily psychotherapeutic; there is no clear evidence that psychopharmacological treatment is effective for NPD, although it can prove useful for treating comorbid disorders. Psychotherapeutic treatment falls into two general categories: psychoanalytic/psychodynamic and cognitive behavioral. Psychoanalytic therapies include schema therapy, transference focused psychotherapy, mentalization-based treatment and metacognitive psychotherapy. Cognitive behavioral therapies include cognitive behavioral therapy and dialectical behavior therapy. Formats also include group therapy and couples therapy. The specific choice of treatment varies based on individual presentations.Management of narcissistic personality disorder has not been well studied, however many treatments tailored to NPD exist. Therapy is complicated by the lack of treatment-seeking behavior in people with NPD, despite mental distress. Additionally, people with narcissistic personality disorders have decreased life satisfaction and lower qualities of life, irrespective of diagnosis. People with NPD often present with comorbid mental disorders, complicating diagnosis and treatment. NPD is rarely the primary reason for which people seek mental health treatment. When people with NPD enter treatment (psychologic or psychiatric), they often express seeking relief from a comorbid mental disorder,  including major depressive disorder, a substance use disorder (drug addiction), or bipolar disorder.
Causes
APBD is an autosomal recessive disorder that is caused when a person inherits genes from both parents containing one or more loss-of-function mutations in the gene GBE1 which encodes for glycogen branching enzyme, also called 1,4-alpha-glucan-branching enzyme. Mechanism
The GBE1 gene provides instructions for making the glycogen branching enzyme. This enzyme is involved in the production of a complex sugar called glycogen, which is a major source of stored energy in the body. Most GBE1 gene mutations result in a shortage (deficiency) of the glycogen branching enzyme, which leads to the production of abnormal glycogen molecules. These abnormal glycogen molecules, called polyglucosan bodies, accumulate within cells and cause damage. Neurons appear to be particularly vulnerable to the accumulation of polyglucosan bodies in people with this disorder, leading to impaired neuronal function.Some mutations in the GBE1 gene that cause adult polyglucosan body disease do not result in a shortage of glycogen branching enzyme. In people with these mutations, the activity of this enzyme is normal. How mutations cause the disease in these individuals is unclear. Other people with adult polyglucosan body disease do not have identified mutations in the GBE1 gene. In these individuals, the cause of the disease is unknown. Diagnosis
Along with evaluation of the symptoms and a neurological examination, a diagnosis can be made based on genetic testing. Whether or not a person is making sufficient amounts of functional glycogen branching enzyme can be determined by taking a skin biopsy and testing for activity of the enzyme.