It looks to me as though you've answered your own question. The neurologist is simply being descriptive, the psychiatrist is fitting the phenomenon into a larger framework. If it's part of two different syndromes, we must examine the place where these two sets intersect.

From the psychiatric point of view it is a conceptual problem difficult to overcome, as anhedonia is a core depressive symptom in both classification systems (DSM-5 and ICD-10), and therefore it is inappropriate to compare it with depression (which is often the case of research on patients with Parkinson's disease). Such an approach calls into question the validity of the criteria of depression itself.

Anhedonia is also independently associated with disease prognosis in cardiovascular disease. Indeed, the usefulness of the HADS depression scale is that it taps anhedonia.

I may be jumping the line here, because I am not a psychiatrist nor neurologist, but maybe the case here is that anhedonia occurs in many disorders and diseases (as mentioned above)[1] and is also more easily conceptualized at brain level (like anhedonia in cocaine dependency [2]) than depression which is, I think, more complex on cognitive, behaviour and neural levels.

My thinking may be redundant as depression will always be more complex phenomenon than anhedonia if depression includes anhedonia as one of its symptoms :)

[1] Ho, N., & Sommers, M. (2013). Anhedonia: a concept analysis. Archives of psychiatric nursing, 27(3), 121-129.

[2] Markou, A., & Koob, G. F. (1991). Postcocaine anhedonia. An animal model of cocaine withdrawal. Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology, 4(1), 17-26.

From a purely theoretical point of view, however, the comparison of anhedonia and depression in patients with Parkinson's disease or any other disease can be justified by the fact that anhedonia can be present even in patients without depression and that it is not present in all patients with a depressive disorder, even though it correlates with its severity. Anhedonia is therefore a symptom that may occur outside of depression (as evidenced, for example, by its occurrence in schizophrenia), and many observed correlations of anhedonia with depressive symptomatology can thus be seen as evidence of the validity of the classification criteria of depression.

I think that it is a major sign of depression despite a negative symptom in schizophrenia. Of course it can be seen in dementia or Parkinson's disease or other disorders that had effects on mood. It is better to consider which signs are accompanied with anhedonia.

Anhedonia is not always a part of a patients depression.

Depression is highly co-morbid with both general medical conditions as well as other mental illnesses, hence anhedonia by its very nature can be described in both psychiatry and neurology .

Of course it can. But what I ask is why it is being considered independently of depression. It turns out that anhedonia also occurs outside of depression, which is an extremely interesting topic.

Because many nurologist and psychiatrist don't know what is essential by depression - sadness and guilt feeeling!

According to ICD-10 classification there are only three main (core) symptoms of depression: 1. persistent sadness or low mood, 2. loss of interests or pleasure (anhedonia) and 3. fatigue or low energy. Guilt is only an associated symptom of depression.

"The evaluation of hedonic ability in psychiatry considered both the nature of the stimulus (i.e. physical or social) and the reward-related mechanisms (i.e. wanting or liking). Moreover, pleasure associated with future events could be divided into anticipated (i.e. pleasure expected to be experienced in the future) and anticipatory (i.e. pleasure experienced in the immediate present, imagining future events)".

Article Anhedonia in schizophrenia: The role of subjective experiences

[Shameless self-promotion!]

Probably, as suggested by Berrios, would be more accurate to talk about anhedoniaS.

Article The anhedonias: a conceptual history

To Paolo Ossola:

You're probably right. There are obviously more disorders of hedonic functions that can be neuropsychologically decomposed into multiple classes, not just anticipatory or consumatory anhedonia. It may be appropriate in many cases to talk about hypohedonia or even dyshedonia, with specifying of a particular problem in hedonic tonus or hedonic responsiveness. Anhedonia can also be a trait feature of the individual, a lifelong characteristic, not just a symptom of mental illness. And to the contrary, it may be associated with apathy or motivational disorders.

Neurobiological underpinnings of anhedonia are of a very complex nature.

Thank you for thoughts!

What a smart question.

Parkinson patients show a blunted affect which may suggest anhedonia; it makes sense as Parkinson is related to the deficiency of Dopa, which also regulates the sense of pleasure.

However, Parkinson patients can laugh hearfully or enjoy their daily activities albeit less because of reduced mobility.

Pleasure is generated by the limbic system; does anyone knows if some components of the limbic system are atrophied when there is anhedonia ?

Thanks.

Thank you. The joke is that some parts of the basal ganglia are very close connected to a so-called limbic system. For example, nucleus accumbens is a ventral striatal structure. And there are some works that say that the reduced volume of nucleus accumbens correlates with anhedonia.