Anhedonia As A Symptom

 Anhedonia as a symptom - Crow 19 was an early proponent of modernconcept of anhedonia as a symptom of the schizophrenic state. Taking the clinical approach dichotomous( " Positive symptoms vs.  Negative symptoms " ) proposed by Hughlings -Jackson 20 in neurology, the author hypothesizedthe existence of two different forms of schizophrenia : theType I ( "positive" ), characterized by the predominance ofproductive psychotic phenomena (eg delusions, hallucinations) ,and type II ( "negative" ), dominated by symptomsdifettuale, in which he considered salientflattening of affect and withdrawal from social life. A few years later, Andreasen 13, in order toconstruct valid psychometric instruments to measure thepsychopathology of schizophrenia, inserted the construct of the inabilityhedonic within the subscale " Anhedonia /Anti-social " SANS (Scale for the Assessment of NegativeSymptoms ), defining it as : a) loss of interestand gratification in respect of activities and situationsrecreational normally considered, pleasant, and / or ;b) lack of intimacy and emotional involvement insocial and sexual relationships of various kinds.

Subsequently, Carpenter 14, as part of its redefinitionclinical psychotic symptoms difettuale ,anhedonia placed between the primary and negative symptomsenduring what he called " deficit syndrome " ofschizophrenia.  In SDS ( Schedule for " Deficit Syndrome" )21, developed precisely for the diagnosis of thisspecific schizophrenic subtype, disability was hedonicin fact present in at least three of the six items proposed ( [ A2]decrease in emotional range [to be considered asinability to experience pleasure and / or anger ], [ A4] reductioninterest and [ A6 ] drop in thrust and desirefor social relationships ).

The results of some recent experimental studies seem toconfirm the thesis as a symptom own dell'anedoniastatus schizophrenic.  In particular, Loas et al.  22 ,Blanchard et al.  23 and Kontaxakis et al.  24 foundhigher levels of disability in patients with hedonicschizophrenia ( both acute and chronic ) compared to subjectsnon-psychiatric controls, highlighting how, inboth these samples psychotic, this figure, whilepresenting a significant positive correlation withother negative phenomena of the disease ( flatteningaffect, alogia, avolition / apathy, social withdrawal ), it is showncompletely independent of the size positive, disorganizedand depressive disorder itself.

In a longitudinal study of 127 individuals withchronic schizophrenia (mean follow -up duration of 10years), Herbener and Harrow 25 have also suggested thatanhedonia, being typical of the stages of chronicity ofpsychosis, could be seen as a negative componentstable course of schizophrenic direct expressionfunctional impairment of their evolutionaryof these patients.

In the last decades of the 900, some researchers havedeveloped the idea that the negative symptoms of schizophrenia(and therefore also the inability hedonic ) are due toa deficiency of dopamine (DA) in the offices of projectionmesocortical dopaminergic circuits of the brain to startfrom the ventral tegmental area of the midbrain ,especially those that project in the prefrontal cortexdorsolateral 26-28.  According to this hypothesis, the state ofbehavioral deficits associated with schizophrenic symptomsdifettuali imply hypoactivity (functional) ofthese dopaminergic fibers ascending or a fewexhaustion of their structural neuronal systems. In particular, the deficiency in the functioning of the fibersdopamine may be due to:

1 ) a primary deficit of DA, linked to hyperactivity( " Excitotoxic ") local glutamatergic circuitsmesencephalic, resulting in abnormal activation( RNMDA - mediated) of the mechanisms of apoptosis in loaddopaminergic neurons of the ventral tegmental area( " Neurodegerativa hypothesis " of schizophrenia ) 29. This would be linked to neuronal excitotoxicitya peculiar " individual diathesis stress", forwhich, in a subject predisposed to developing the disorder ,a given biological vulnerability ( iperespressivitàof genes that regulate glutamatergic neurotransmissionbrain ) would apply disproportionatelyunder the influence of numerous environmental stressors( for example toxins, drugs, infectious agents ,high expressed emotion in the family ) 28;

2 ) a deficit of DA secondary to ) an inhibition of theits synaptic release, due to an excess of serotoninmesencephalic level, or b) to a receptor blockadePrefrontal D2, linked to the administration oftypical neuroleptics (eg haloperidol ) 27.  the firstinstead of these mechanisms may help understandingthe clinical efficacy of atypical antipsychotics( eg clozapine ) in reducing the negative symptomsschizophrenia ( selective receptor antagonism5HT2A midbrain ) 30.