In the 1980, to reduce the heterogeneity of schizophrenia, researchers tried to identify homogeneous subtypes in the hope to facilitate the identification of links between symptoms and The division of symptoms as positive or negative and categorization of schizophrenia as positive and negative subtypes became popular. However, researchers noticed that negative symptoms were not inherent to the disorder alone, but may also be due to neuroleptic medications, depression and environmental factors. This was shared by the concept of primary and secondary negative symptoms. To better understand primary negative symptoms, a separate subtype of schizophrenia, deficit and non-deficit schizophrenia was given by Carpenter.According to Carpenter et al. the term ‘deficit symptoms’ should be used to refer specifically to those negative symptoms that are present as enduring traits. These deficit symptoms occur regardless of the patient's medication status and are not specifically responsive to anticholinergic drugs or antipsychotic drug withdrawal. It was further conceptualized that the presence of poor premorbid adjustment preceding initial psychotic episode may be manifestations of the deficit syndrome. In 2001, a review of the literature suggested that deficit schizophrenia is a disease separate from other, nondeficit forms of schizophrenia . The proposal of a separate disease was based on the evidence that deficit and nondeficit schizophrenia differ on five dimensions typically used to distinguish diseases: signs and symptoms, course of illness, pathophysiological correlates, risk and etiological factors, and treatment response.Family history Kirkpatrick et al reviewed studies showing that the deficit/nondeficit categorization has a significant concordance within families and that family members of deficit probands, compared with relatives of nondeficit probands, have more severe social withdrawal and an increased risk of schizophrenia. Genetics A few studies have examined the genetics of deficit and nondeficit schizophrenia, but the results have been disappointing. Hong et al (6) reported that the dihydropyrimidinase-related protein 2 (DRP-2) gene was associated with risk for both deficit and nondeficit schizophrenia; however, after correcting for multiple comparisons, the association with nondeficit schizophrenia was not significant, and for deficit schizophrenia the association was present only for Caucasian but not African-American Deficit patients have a more severe course of illness than nondeficit patients, with a higher prevalence of abnormal involuntary movements before administration of antipsychotic drugs and poorer social function before the onset of psychotic symptoms. The prevalence of deficit schizophrenia has been reported to be about 15% among patients with first-episode schizophrenia and 25%–30% among those with chronic schizophrenia The risk factor of deficit patients differ from those of nondeficit patients. Deficit patients may a

1. DEFICIT SCHIZOPHERNIA
DR.SWATI

2. INTRODUCTION
• In the 1980, to reduce the heterogeneity of schizophrenia, researchers tried to
identify homogeneous subtypes in the hope to facilitate the identification of links
between symptoms and etiology.
• The division of symptoms as positive or negative and categorization of
schizophrenia as positive and negative subtypes became popular. However,
researchers noticed that negative symptoms were not inherent to the disorder
alone, but may also be due to neuroleptic medications, depression and
environmental factors. This was shared by the concept of primary and secondary
negative symptoms. To better understand primary negative symptoms, a separate
subtype of schizophrenia, deficit and non-deficit schizophrenia was given by
Carpenter.

3. CONCEPT OF DEFICIT
SCHIZOPHRENIA
• According to Carpenter et al. the term ‘deficit symptoms’ should be used to refer
specifically to those negative symptoms that are present as enduring traits.
• These deficit symptoms occur regardless of the patient's medication status and are
not specifically responsive to anticholinergic drugs or antipsychotic drug withdrawal.
It was further conceptualized that the presence of poor premorbid adjustment
preceding initial psychotic episode may be manifestations of the deficit syndrome.

4. • By contrast, in non-deficit type of schizophrenia, negative symptoms may be
present but demonstrate greater fluctuation, lack of persistence and temporal
association with possible underlying causes like dysphoric states, drug status, etc.
According to Carpenter et al., this approach to deficit symptoms requires clinical
judgment based on longitudinal observation rather than a cross-sectional
assessment to establish the presence or absence of the symptoms

5. • In 2001, a review of the literature suggested that deficit schizophrenia is a disease
separate from other, nondeficit forms of schizophrenia .
• The proposal of a separate disease was based on the evidence that deficit and
nondeficit schizophrenia differ on five dimensions typically used to distinguish
diseases: signs and symptoms, course of illness, pathophysiological correlates, risk
and etiological factors, and treatment response.

6. RISK AND ETIOLOGICAL FACTORS
• Family history
• Kirkpatrick et al reviewed studies showing that the deficit/nondeficit categorization has a
significant concordance within families and that family members of deficit probands,
compared with relatives of nondeficit probands, have more severe social withdrawal and an
increased risk of schizophrenia.
• Genetics
• A few studies have examined the genetics of deficit and nondeficit schizophrenia, but the
results have been disappointing.
• Hong et al (6) reported that the dihydropyrimidinase-related protein 2 (DRP-2) gene was
associated with risk for both deficit and nondeficit schizophrenia; however, after correcting
for multiple comparisons, the association with nondeficit schizophrenia was not significant,
and for deficit schizophrenia the association was present only for Caucasian but not African-
American subjects.

7. • Long-term prognosis:
• Recent studies confirmed that the diagnosis of deficit schizophrenia is associated
with a worse long-term prognosis, as compared with nondeficit schizophrenia.
• Tek et al , in a prospective study including 46 patients with deficit and 174 with
nondeficit schizophrenia, found that after an average of five years, the deficit
patients had a poorer quality of life, poorer social and occupational functioning, and
more severe negative symptoms, but were less distressed and did not show more
severe positive symptoms.

8. • Response to treatment
• Convincing evidence is available that both old and new generation antipsychotics
may act on secondary negatives symptoms by removing, in part or completely,
some of their causes, such as positive symptoms, depression or extrapyramidal
symptoms. However, the efficacy of these drugs on primary and persistent negative
symptoms has not been proven

9. • Deficit patients have a more severe course of illness than nondeficit patients, with a higher
prevalence of abnormal involuntary movements before administration of antipsychotic drugs and
poorer social function before the onset of psychotic symptoms.
• The prevalence of deficit schizophrenia has been reported to be about 15% among patients with
first-episode schizophrenia and 25%–30% among those with chronic schizophrenia
• The risk factor of deficit patients differ from those of nondeficit patients. Deficit patients may also
be associated with greater familial risk of schizophrenia.
• Deficit schizophrenia is associated with excess of summer birth , whereas non-deficit patients
have an excess of winter birth.
• Within a family of multiple affected siblings the deficit-nondeficit categorization tends to be
uniform.
• The deficit group also has a higher prevalence for men.

10. DIAGNOSTIC CRITERIA FOR DEFICIT
SCHIZOPHRENIA
At least two of the following negative symptoms are present:
• Restricted affect
• Diminished emotional range
• Poverty of speech with curbing of interest and decrease in curiosity
• Diminished sense of purpose
• Diminished social drive
Two or more of the negative symptoms listed above has been present for the preceding 12
months and these symptoms were always present during periods of clinical stability
(including chronic psychotic states) or during recovery from psychotic exacerbation. These
symptoms may not be detectable during transient episodes of acute psychotic
disorganization or decompensation

11. Two or more of these enduring features also idiopathic, that is not secondary to factors
other than the disease process. such factors include
• Anxiety
• Drug effect
• Suspiciousness
• Formal thought disorder
• Hallucinations
• Mental retardation
• Depression
The patient meet DSM criteria for schizophrenia

12. • The psychopathology of deficit patients impacts treatment. Their lack of motivation,
greater cognitive impairment and asocial nature undermine the efficacy of
psychosocial interventions as well as their adherence to medication regimens.

14. • Weinberger (1987) proposed dysregulation of dopamine system . Putative
hypofunction of prefrontal dopamine system could provide a possible
neurobiological mechanism for negative symptom and increased subcortical
dopamine activity might account for positive symptom and movement disorder. The
combination of positive and negative symptom common in schizophrenia could
result from reduced prefrontal dopamine function , leading to relative hyperactivity
of subcortical dopamine , which would normally be modulated by prefrontal system
.

15. STRUCTURAL BRAIN ABNORMALITIES
• The early work of Crow (1980) on negative symptoms proposed a two syndrome
hypothesis and argued that negative symptoms were likely to be tied to a structural
brain abnormality.
• Since the original Crow hypothesis, numerous studies have been done using
computed tomography (CT) scanning to measure ventricular size as an index of
structural brain abnormality.
• Some studies have attempted to seek correlations between negative symptoms and
ventricular enlargement, while others have examined the relationship categorically
and evaluated ventricular size in patients classified as predominantly positive,
negative, or mixed.
• The results of this work are inconclusive, but a review of the literature recently
conducted did seem to indicate that the

16. • majority of studies find a relationship between ventricular size and the presence of
negative symptoms. The review done by Marks and Luchins (1990) concluded that
18 investigations showed a direct relationship between neuroanatomical
abnormalities and positive or negative symptoms,
• 5 found no relationship between structural abnormalities and positive or negative
symptoms ,and 3 revealed a relationship opposite to the predicted direction (i.e.,
normal ventricular size associated with positive symptoms and large ventricles with
negative symptoms as the predicted direction).

18. RATING SCALES
• SELF RATING INSTRUMENTS – 1. Subjective experience of deficits in schizophrenia(SEDS,
Liddle and Barnes , 1988) – consists of 21 items arranged in 6 groups namely abnormal
thinking and concentration , disturbance of affect , impaired will and decreased energy ,
disturbance of perception , intolerance of stress & disturbance of voluntary movements.
• 2. Subjective deficit syndrome scale ( SDSS, Bitter et al 1989 , Jaeger et al 1990 ) - based of
experimental subscale of subclinical symptom scale. Based exclusively on self report.

19. • B . Observer rated instruments –
• 1. Brief psychiatric rating scale ( BPRS , overall and graham 1962) – 7 point scale
based on 16 or 18 items depending on version)
• 2. Positive and negative syndrome scale ( PANSS , kay 1987 ) – it consist of 30 items
scale 18 adapted from BPRS and 12 from psychopathology rating schedule rated on
7 point scale.

20. • 4. Negative symptom rating scale ( NSRS , iager ,1985 ) - 7 point scale based on 10
items divided into 4 subscales, . a. thought process through speech , judgment b.
cognition through memory , attention and orientation. c. volition through grooming
, motivation and motion d. affect and relatedness through emotional response and
expressive relatedness.
• 6. other scales – the schedule for deficit syndrome ( carpenter et al , 1988) , lewin-
fog- melzer scale ( 1983) , pearlson scale (1984) , emotional blunting scale , wing
scale (1961)– giele – harrow scale (1984)

21. TREATMENT
• Treatment begins with assessing factor that can cause secondary negative
symptoms . Treatment of secondary negative symptom will be treating their cause
like antipsychotic for positive symptoms , antidepressant for depression , anxiolytic
for anxiety , antiparkinsonian or antipsychotic dose reduction for extrapyramidal
side effects.
• If they don’t resolve by such treatment than they are primary negative symptom .
For primary negative symptom 2nd generation antipsychotics in low dose are
prescribed.

22. • Low-dose amisulpride should be currently considered first-line treatment for
patients with primary negative symptoms.
• Aripiprazole and olanzapine should be considered second-line treatments.
• Clozapine is not recommended for patients with primary, enduring negative
symptoms.
• Trials with NMDA agonists, mirtazepine and SSRIs are promising but need more
investigation.
• Mirtazepine, fluoxetine, fluvoxamine or paroxetine should be tried as adjunctive
medication in patients resistant to amisulpride and/or aripiprazole/olanzapine.

23. • Psychological interventions should be incorporated into the treatment package.
• Activity based therapy
• Cognitive behavioral therapy
• Integrated therapy
• In one RCT mirtazapine augmentation of risperidone was found to reduce negative
symptom. In another study fluvoxamine has not been found effective . In another
study once weekly dosing of D-cycloserin has been found to improve negative
symptoms. Repeated transcranial magnetic stimulation has also been found to
reduce severity of negative symptoms.

24. • REFERENCES
1. Kraepelin E. Psychiatrie.10th ed.
•
2. Carpenter WT, Jr, Heinrichs DW, Wagman AM. Deficit and nondeficit forms of
schizophrenia: The concept. Am J Psychiatry. 1988;145:578–83. [PubMed]
• 3.Negative schizophrenic symptoms: pathophysiology and clinical implications :By
John F. Greden, Rajiv Tandon
• 4.Deficit schizophrenia: an update: Brian Kirkpatrick1, Silvana Galderisi2