Theories to explain these lower rates of eating disorders, lower reporting and lower research rates in include the effects of westernisation, and culture change.Men (and women) who might otherwise be diagnosed with anorexia may not meet the DSM-IV criteria for BMI since they have muscle weight, but have very little fat. In many cases a subclinical "not otherwise specified" diagnosis is made instead; ED-NOS in the DSM-IV, and other specified feeding or eating disorder or unspecified feeding or eating disorder in the DSM-5. ED-NOS was the most diagnosed eating disorder in 2009, and it was also shown that AN did not differ significantly in eating pathology or general psychopathology from EDNOS involving restrictive eating.The elderly population is increasingly experiencing anorexia nervosa, which has been termed the "Anorexia of Aging". The eating disorder is similar to that of typical anorexia nervosa but is more often accompanied by the overuse of laxatives in order to purge the individual of ingested food. Most geriatric anorexia patients limit their food intake to dairy or grains, whereas an adolescent anorexic has a more general limitation.This eating disorder that affects older adults has two types - early onset and late onset. Early onset refers to a recurrence of anorexia in late life in an individual who experienced the disease during their youth. Late onset describes instances where the eating disorder begins for the first time late in life.
Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles". Causes
Pathophysiology
Under persistent activation, the transmission of pain signals to the dorsal horn may produce a pain wind-up phenomenon. This triggers changes that lower the threshold for pain signals to be transmitted. In addition, it may cause nonnociceptive nerve fibers to respond to, generate, and transmit pain signals. The type of nerve fibers that are believed to generate the pain signals are the C-fibers, since they have a slow conductivity and give rise to a painful sensation that persists over a long time. In chronic pain, this process is difficult to reverse or stop once established. In some cases, chronic pain can be caused by genetic factors which interfere with neuronal differentiation, leading to a permanently lowered threshold for pain.Chronic pain of different causes has been characterized as a disease that affects brain structure and function. MRI studies have shown abnormal anatomical and functional connectivity, even during rest involving areas related to the processing of pain. Also, persistent pain has been shown to cause grey matter loss, which is reversible once the pain has resolved.These structural changes can be explained by neuroplasticity. In the case of chronic pain, the somatotopic representation of the body is inappropriately reorganized following peripheral and central sensitization. This can cause allodynia or hyperalgesia. In individuals with chronic pain, EEGs showed altered brain activity, suggesting pain-induced neuroplastic changes.