The oldest likely physical evidence of the condition comes from the mummy of Siptah, an Egyptian Pharaoh who ruled from about 1196 to 1190 BCE and died at about 20 years of age. The presence of cerebral palsy has been suspected due to his deformed foot and hands.The medical literature of the ancient Greeks discusses paralysis and weakness of the arms and legs; the modern word palsy comes from the Ancient Greek words παράλυση or πάρεση, meaning paralysis or paresis respectively. The works of the school of Hippocrates (460–c. 370 BCE), and the manuscript On the Sacred Disease in particular, describe a group of problems that matches up very well with the modern understanding of cerebral palsy. The Roman Emperor Claudius (10 BCE–54 CE) is suspected of having CP, as historical records describe him as having several physical problems in line with the condition. Medical historians have begun to suspect and find depictions of CP in much later art. Several paintings from the 16th century and later show individuals with problems consistent with it, such as Jusepe de Riberas 1642 painting The Clubfoot.The modern understanding of CP as resulting from problems within the brain began in the early decades of the 1800s with a number of publications on brain abnormalities by Johann Christian Reil, Claude François Lallemand and Philippe Pinel. Later physicians used this research to connect problems in the brain with specific symptoms. The English surgeon William John Little (1810–1894) was the first person to study CP extensively.
Learning has also been proposed as an independent facet of reward that may be impaired in conditions associated with anhedonia, but empirical evidence dissociating learning from either "liking" or "wanting" is lacking.Anhedonia has also been used to refer to "affective blunting", "restricted range of affect", "emotional numbing", and "flat affect", particularly in the context of post-traumatic stress disorders. In PTSD patients, scales measuring these symptoms correlate strongly with scales that measure more traditional aspects of anhedonia, supporting this association. Causes
Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in anhedonia. Regions implicated in anhedonia 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 anhedonia; 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 anhedonia.