As summarised in previous chapters, chronic (neoplastic, necrotic, infectious) pathophysiological processes of various systems are frequently accompanied by wasting and cachexia. The pathophysiology of wasting and cachexia is complex [1-10] and multiple brain mechanisms [11-13] can be involved including neurological, psychiatric, psychological, physiological, biochemical/metabolic, immunological, and chemical per se (e.g. neurotransmitter-, neuropeptide-and cytokine-related). These mechanisms can interact/synergise with peripheral/systemic processes or dysfunctions (e.g. gastrointestinal malabsorption and body losses such as via ulcers, effusions, haemorrhage).

Wasting and cachexia may also interact/syner-gise with neuropsychiatric manifestations that frequently accompany chronic disorders [14]. For instance, anorexia, early satiety, chronic pain, depression or anxiety, drowsiness and cognitive impairment and delirium, agitation, hypogeusia and hyposmia (and other taste and olfaction abnormalities), chronic nausea, fatigue and asthenia may in fact exacerbate - or in some cases induce - wasting and cachexia. The symptomatology (e.g. anorexia) may be involved as partly the cause and partly the consequence of wasting and cachexia such as in the cachexia-anorexia syndrome. During treatment (e.g. chemotherapy, radiotherapy, immunotherapy) various neuropsy-chiatric manifestations can be exacerbated.

Conceptually, the profile of brain mechanisms in wasting and cachexia varies depending on the underlying disease condition, but importantly, overlap or interaction of various mechanisms in the pathophysiological dysregulation may be piv otal in dissimilar diseases such as human immunodeficiency virus infection, cancer, chronic inflammatory bowel disease, chronic liver disease, rheumatoid arthritis, chronic bacterial and parasitic diseases, chronic cardiovascular disease, chronic obstructive pulmonary disease and endstage renal disease, all representing conditions associated with wasting and cachexia.

Although multiple peripheral and brain mechanisms may be involved in wasting and cachexia, peripheral mechanisms that affect behavioural responses (e.g. induction of anorexia) could be the result of signalling to a pathway that depends on brain mechanisms (i.e. conscious and decision-making processes). Thus, in specific cases, peripheral mechanisms final operational endpoint would be via brain outputs. Fatigue and asthenia during wasting and cachexia could have underlying peripheral (catabolic) and brain components.

Interaction of autonomic nervous system outflows with peripheral metabolic shifts and catabo-lism is another example of linkage with brain mechanisms.

The output of brain mechanisms would also reflect on many aspects of the quality of life of a patient with wasting and cachexia, including the interactions of these patients with their environment, relatives and caregivers.

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