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Schizophr Bull. Apr 2006; 32(2): 246–249.
Published online Feb 21, 2006. doi:  10.1093/schbul/sbj054
PMCID: PMC2632226

Subdomains Within the Negative Symptoms of Schizophrenia: Commentary

In an accompanying article in this theme issue, Blanchard and Cohen review the evidence on the relationships among negative symptoms and conclude that meaningful subdomains within negative symptoms may exist.1 Specifically, they suggest that blunted affect and poverty of speech may form one such subdomain, and anhedonia, asociality, and avolition may form another. The authors are appropriately cautious in raising this possibility, and they suggest further studies would be needed before it is confirmed.

Should the independence of these 2 factors be confirmed, it would have implications for research on negative symptoms. At the Consensus Development Conference on Negative Symptoms, sponsored by the National Institute of Mental Health and held in Rockville, Maryland, on January 26–27, 2005, one of us (Kirkpatrick) presented a review of the literature on blunted affect. From the starting point of that presentation, a pattern consistent with the existence of separate subdomains similar to those cited by Blanchard and Cohen emerged. We briefly summarize that presentation and discuss some of the issues involved in conducting research on the existence of separate factors within negative symptoms.

Blunted Affect

All of the widely used negative symptom rating and categorization instruments include blunted or restricted affect. Blunted affect can be considered to have 3 components: (1) decrease in facial expression; (2) decrease in expressive gestures and other body language; and (3) decrease in modulation of the volume, pitch, and speed of speaking. Blunted affect should be distinguished from flat affect, which refers to the extreme end of the spectrum of blunting. Items for “decreased spontaneous movements” and/or “poor eye contact” are included in some blunted affect subscales; in factor analyses these correlate with the core features of blunted affected but are not part of the same construct.

Blunted affect can be found in several disorders other than schizophrenia, including Parkinson's disease, depression, autism, vascular dementia, and multiple system atrophy.2–7 In the context of schizophrenia, antipsychotic medications complicate the assessment of blunted affect, as they can induce this symptom8 (although this is much less of a problem with second-generation drugs than with the first generation).

Data at the Item Level

In Table 1, we summarize the studies that provided data at the item level of the relationships within negative symptoms. Only studies with schizophrenia subjects were included. We omitted studies that used scales that included symptoms other than negative symptoms.

Table 1.
Studies of Blunted Affect and Poverty of Speech

Consistent with the review of Blanchard and Cohen,1 these studies suggest that blunted affect and poverty of speech have a particularly strong relationship and may constitute a domain with some independence from other domains within negative symptoms. Four of 5 publications that were based on 1 negative symptom rating scale found blunted affect loading onto the same factor as poverty of speech9–12,not13; each of these studies found more than 1 negative symptom factor. Another study evaluated 2 scales in the same population; for both scales blunted affect and poverty of speech loaded onto the same factor.14 A study based on the Schedule for the Deficit Syndrome (SDS) that did not use factor analysis found that the blunted affect and poverty of speech items had a (Spearman) correlation of r = 0.84, compared with other bivariate item correlations of 0.48 to 0.68.15

Several aspects of these studies support the generalizability of the finding of a particularly strong relationship between blunted affect and poverty of speech. There is relatively good consistency across these studies, which come from both the United States and Europe and used 4 different instruments. The SDS-based study of Kimhy et al.11—which included only those patients judged to have primary negative symptoms—as well as the study of Kirkpatrick et al.15—which included patients with and without primary negative symptoms—both supported the existence of a particularly strong relationship between blunted affect and poverty of speech. The other studies were based on instruments that are not intended to distinguish primary versus secondary symptoms, providing further support for the generalizability of the conclusion.

Future Research

Taken together, the studies cited above and the review of Blanchard and Cohen1 suggest that blunted affect has a particularly strong relationship to poverty of speech, with these 2 features forming an “expressivity” domain within negative symptoms. The reported independence of social skills and subjective experience from blunted affect16,17 is also consistent with the existence of multiple factors within negative symptoms.

Flat or blunted affect alone has sometimes been used as an independent variable in studies of course, psychopathology, and neurobiology, and in some contexts it has been a significant predictor of other variables.18–22 However, in most studies the potential for confounding by other negative symptoms has not been considered, so the specificity of the relationships with blunted affect is not clear. The study of Gur et al.23 in this issue is a notable exception. We are not aware of any published studies that have considered the correlates of an expressivity factor and an anhedonia/asociality factor separately, although at the Consensus Development Conference, Malaspina presented data suggesting that these factors do have different correlates.

It would not be difficult to test the hypothesis that these factors have different correlates by conducting secondary analyses. In many studies for which negative symptoms are an important dependent variable, expressivity and anhedonia/asociality factor scores can be derived from the Scale for Assessment of Negative Symptoms (SANS) and some other negative symptom rating scales. For instance, blunted affect is very similar to the neurological concept of aprosodia; thus, the anatomical organization of aprosodia provides a conceptual framework for developing hypotheses about the putative expressivity component of negative symptoms.24–30 In most subjects, prosody appears to be under the control of areas in the right hemisphere, with an organization that mirrors that of propositional language in the left, such that separate areas control emotional (versus propositional) expression and comprehension. That is, both expressive and receptive aprosodias exist, with a right-sided anatomical organization that mirrors that of expressive and receptive aphasias in the left hemisphere.

Propositional and affective components of language are thought to be integrated in the brainstem and via the corpus callosum. A smaller volume of the corpus callosum was associated with negative symptoms in two studies,31,32 although not in a third.33 Is the volume of the corpus callosum related to the severity of expressivity factor but not to an anhedonia/asociality/avolition factor?

More generally, are other variables related to negative symptoms linked exclusively or primarily to 1 of the 2 factors described by Blanchard and Cohen?1 What about cognitive function or regional brain activation in schizophrenia, or subclinical negative symptoms in the relatives of probands with schizophrenia?


The psychometric association of blunted affect and poverty of speech raises the possibility that an expressivity factor has an independence from other negative symptoms that extends to course of illness, treatment response, and neurobiology. In analyses of negative symptoms, an additional analysis of an expressivity factor versus other negative symptoms would add little additional work but may improve our understanding of negative symptoms and schizophrenia.


1. Blanchard JJ, Cohen AS. The structure of negative symptoms within schizophrenia: implications for assessment. Schizophr Bull. 2006;32(2) First published on October 27, 2005, doi:10.1093/schbul/sbj013. [PMC free article] [PubMed]
2. Constantino JN, Gruber CP, Davis S, Hayes S, Passanante N, Przybeck T. The factor structure of autistic traits. J Child Psychol Psychiatry. 2004;45:719–726. [PubMed]
3. Fetoni V, Soliveri P, Monza D, Testa D, Girotti F. Affective symptoms in multiple system atrophy and Parkinson's disease: response to levodopa therapy. J Neurol Neurosurg Psychiatry. 1999;66:541–544. [PMC free article] [PubMed]
4. Tremeau F, Malaspina D, Duval F, et al. Facial expressiveness in patients with schizophrenia compared to depressed patients and nonpatient comparison subjects. Am J Psychiatry. 2005;162:92–101. [PubMed]
5. Jouvent R, Le Houezec J, Payan C, et al. Dimensional assessment of onset of action of antidepressants: a comparative study of moclobemide vs. clomipramine in depressed patients with blunted affect and psychomotor retardation. Psychiatry Res. 1998;79(3):267–275. [PubMed]
6. Robertson JM, Tanguay PE, L'ecuyer S, Sims A, Waltrip C. Domains of social communication handicap in autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 1999;38:738–745. [PubMed]
7. Sultzer DL, Levin HS, Mahler ME, High WM, Cummings JL. A comparison of psychiatric symptoms in vascular dementia and Alzheimer's disease. Am J Psychiatry. 1993;150:1806–1812. [PubMed]
8. Van Putten T, May RP. “Akinetic depression” in schizophrenia. Arch Gen Psychiatry. 1978;35:1101–1107. [PubMed]
9. Alphs LD, Summerfelt A, Lann H, Muller R. The Negative Symptom Assessment: a new instrument to assess negative symptoms of schizophrenia. Psychopharmacol Bull. 1989;25:159–163. [PubMed]
10. Keefe RSE, Harvey PD, Lenzenweger MF, et al. Empirical assessment of the factorial structure of clinical symptoms in schizophrenia: negative symptoms. Psychiatry Res. 1992;44:153–165. [PubMed]
11. Kimhy D, Yale S, Goetz RR, McFarr LM, Malaspina D. The Factorial Structure of the Scale for Deficit Syndrome in schizophrenia. Schizophr Bull. 2006;32(2) First published on September 21, 2005, doi:10.1093/schbul/sbi064. [PMC free article] [PubMed]
12. Peralta V, Cuesta MJ. Negative symptoms in schizophrenia: a confirmatory factor analysis of competing models. Am J Psychiatry. 1995;152:1450–1457. [PubMed]
13. Axelrod BN, Goldman RS, Woodard JL, Alphs LD. Factor structure of the Negative Symptom Assessment. Psychiatry Res. 1994;52:173–179. [PubMed]
14. de Leon J, Peralta V, Cuesta MJ. Negative symptoms and emotional blunting in schizophrenic patients. J Clin Psychiatry. 1993;54(3):103–108. [PubMed]
15. Kirkpatrick B, Buchanan RW, McKenny PD, Alphs LD, Carpenter WT., Jr The Schedule for the Deficit Syndrome: an instrument for research in schizophrenia. Psychiatry Res. 1989;30:119–123. [PubMed]
16. Salem JE, Kring AM. Flat affect and social skills in schizophrenia: evidence for their independence. Psychiatry Res. 1999;87:159–167. [PubMed]
17. Myin-Germeys I, Delespaul PAEG, deVries MW. Schizophrenia patients are more emotionally active than is assumed based on their behavior. Schizophr Bull. 2000;26:847–854. [PubMed]
18. Carpenter WT, Jr, Strauss JS. The prediction of outcome in schizophrenia. IV. eleven-year follow-up of the Washington IPSS cohort. J Nerv Ment Dis. 1991;179:517–525. [PubMed]
19. Eaton WW, Thara R, Federman E, Tien A. Remission and relapse in schizophrenia: the Madras Longitudinal Study. J Nerv Ment Dis. 1998;186(6):357–363. [PubMed]
20. Suslow T, Roestel C, Ohrman P, Arolt V. Detection of facial expressions of emotions in schizophrenia. Schizophr Res. 2003;64:137–145. [PubMed]
21. Thara R, Eaton WW. Outcome of schizophrenia: the Madras Longitudinal Study. Aust N Z J Psychiatry. 1996;30:516–522. [PubMed]
22. Yamasue H, Fukui T, Fukuda R, et al. 1H-MR spectroscopy and gray matter volume of the anterior cingulate cortex in schizophrenia. Neuroreport. 2002;13:2133–2137. [PubMed]
23. Gur R, Kohler C, Ragland J, et al. Flat affect in schizophrenia: relation to emotion processing and neurocognitive measures. Schizophr Bull. 2006;32(2) First published on February 1, 2005, doi:10.1093/schbul/sbj041. [PMC free article] [PubMed]
24. Gorelick PB, Ross ED. The aprosodias: further functional-anatomical evidence for the organisation of affective language in the right hemisphere. J Neurol Neurosurg Psychiatry. 1987;50:553–560. [PMC free article] [PubMed]
25. Ross ED. The aprosodias: functional-anatomic organization of the affective components of language in the right hemisphere. Arch Neurol. 1981;38:561–569. [PubMed]
26. Ross ED, Anderson B, Morgan-Fisher A. Crossed aprosodia in strongly dextral patients. Arch Neurol. 1989;46:206–209. [PubMed]
27. Ross ED, Harney JH, deLacoste-Utamsing C, Purdy PD. How the brain integrates affective and propositional language into a unified behavioral function: hypothesis based on clinicoanatomic evidence. Arch Neurol. 1981;38:745–748. [PubMed]
28. Ross ED, Orbelo DM, Cartwright J, et al. Affective-prosodic deficits in schizophrenia: comparison to patients with brain damage and relation to schizophrenic symptoms. J Neurol Neurosurg Psychiatry. 2001;70:597–604. [PMC free article] [PubMed]
29. Wolfe GI, Ross ED. Sensory aprosodia with left hemiparesis from subcortical infarction: right hemisphere analogue of sensory-type aphasia with right hemiparesis? Arch Neurol. 1987;44:668–671. [PubMed]
30. Wymer JH, Lindman LS, Booksh RL. A neuropsychological perspective of aprosody: features, function, assessment, and treatment. Appl Neuropsychol. 2002;9:37–47. [PubMed]
31. Tibbo P, Nopoulos P, Arndt S, Andreasen NC. Corpus callosum shape and size in male patients with schizophrenia. Biol Psychiatry. 1998;44:405–412. [PubMed]
32. Gunther W, Petsch R, Steinberg R, et al. Brain dysfunction during motor activation and corpus callosum alterations in schizophrenia measured by cerebral blood flow and magnetic resonance imaging. Biol Psychiatry. 1991;29:535–555. [PubMed]
33. Mathew RJ, Partain CL, Prakash R, Kulkarni MV, Logan TP, Wilson WH. A study of the septum pellucidum and corpus callosum in schizophrenia with MR imaging. Acta Psychiatr Scand. 1985;72:414–421. [PubMed]

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