According to this model, a number of non-neurocognitive factors influence the performance of individuals with schizophrenia on cognitive tests. Īn alternative model of examining the cognitive deficits has been put forth recently. However, cognitive remediation interventions have modest effect on negative symptoms too. Cognitive remediation interventions do not typically involve negative symptoms as important outcome measure.
Similarly, several studies have found significant association between social cognition and negative symptoms. Several meta-analyses have reported significant but modest association between negative symptoms and specific neurocognitive deficits. Thus, it is understandable that an average clinician, who is faced with the challenge of negative symptoms in his/her patients, feels pessimistic about the prospects of helping them.
However, the optimism raised by these trials gets dampened when one considers the challenges involved in scaling up such therapies and making them accessible to a large number of patients that need such therapies. Cognitive behavior therapy (CBT) and social skills training (SST) have shown some promise in managing negative symptoms. However, no agent has been shown to be consistently effective in sufficiently large studies. Many have shown promise in small, largely preliminary studies. A host of pharmacological agents have been investigated for the treatment of negative symptoms. However, it is unlikely that findings from these studies would translate into development of therapeutic interventions in the foreseeable future. Structural and functional imaging studies on negative symptoms have been largely inconsistent in their findings. Atypical antipsychotics, with affinity towards several neurotransmitter systems other than dopamine, may not add to the burden of negative symptoms, but they are not found to be primarily helpful in treating negative symptoms. Antipsychotic medications, the mainstay of treatment of schizophrenia happen to be dopamine blockers and, as such, are not expected help in the treatment of negative symptoms. Nevertheless, there is consistent evidence that deficient dopamine transmission is associated with negative symptoms. A substantial part of this lack of knowledge is owing to the heterogeneity in the way negative symptoms are conceptualized.
Neurobiology of negative symptoms is a lot less well understood in comparison to that of positive symptoms. Notwithstanding such methodological considerations, one cannot discount the fact that negative symptoms add to the burden of disability associated with schizophrenia. Thus, high association between the two is unsurprising. These very elements of information are used to assess social functioning as well. For instance, in the Positive and Negative Syndrome Scale (PANSS), ‘emotional withdrawal’ (N2) is assessed based on “reports of functioning from primary care workers or family” in addition to observation during the interview ‘passive apathetic withdrawal’ (N4) is assessed based on “reports on social behavior from primary care workers or family”. Assessment of the severity of negative symptoms is, to some extent, based on assessment of the individual’s social functioning, and this may partly explain the association between negative symptoms and social functioning. Affective flattening, alogia, anhedonia, asociality, avolition, etc., frequently last throughout the course of the illness, particularly through the medium and long term, and contribute significantly to disability. However, considerable proportion of individuals with schizophrenia experience long-lasting negative symptoms.
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