Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in<unk> . Regions implicated in<unk>  include the prefrontal cortex as a whole, particularly the orbitofrontal cortex (OFC), the striatum, amygdala, anterior cingulate cortex (ACC), hypothalamus, and ventral tegmental area (VTA). Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions. These abnormalities are generally consistent with animal models, except for inconsistent findings with regard to the OFC. This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on<unk> ; a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and<unk> . Researchers theorize that<unk>  may result from the breakdown in the brain's reward system, involving the neurotransmitter dopamine.<unk>  can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness". The conditions of akinetic mutism and negative symptoms are closely related. In akinetic mutism, a stroke or other lesion to the anterior cingulate cortex causes reduction in movement (akinetic) and speech (mutism).
Anhedonia
Sexual anhedonia
Musical anhedonia
Snatiation
Compulsive behavior
Automatism 
Alexithymia
Amnesia