Neuroleptic withdrawal in chronic schizophrenia: CT and endocrine variables relating to psychopathology

Naber, Dieter; Albus, Margot; Bürke, H.; Müller‐Spahn, F.; Münch, U.; Reinertshofer, Thomas; Wissmann, J.; Ackenheil, Manfred

doi:10.1016/0165-1781(85)90108-8

Cited by 34 publications

(10 citation statements)

References 49 publications

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“…These findings in first-episode samples suggest that antipsychotic medication may have less impact on cortisol levels in the early stage of illness. Other studies have identified an increase in cortisol from baseline after a 12-day period of withdrawal from psychotropic treatment (Naber et al 1985;Albus et al 1985). Unlike antipsychotics, mood stabilisers, including lithium carbonate, have been shown to increase cortisol levels in a dose dependent manner (Platman and Fieve 1968;Bschor et al 2011;Eroglu et al 1979).…”

Section: Levels Of Cortisol In Schizophrenia and Bipolar Disordermentioning

confidence: 98%

Stress, Schizophrenia and Bipolar Disorder

Green

Girshkin

Teroganova

et al. 2014

Behavioral Neurobiology of Stress-Related Disorders

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The role of stress in precipitating psychotic episodes in schizophrenia and bipolar disorder has long been acknowledged. However, the neurobiological mechanism/s of this association have remained elusive. Current neurodevelopmental models of psychosis implicate early dysfunction in biological systems regulating hypothalamic-pituitary-adrenal axis and immune function, with long-term effects on the development of the brain networks responsible for higher order cognitive processes and stress reactivity in later life. There is also increasing evidence of childhood trauma in psychosis, and its impact on the development of brain systems regulating stress. These findings are emerging in the context of a new era of epigenetic methods facilitating the study of environmental effects on gene expression. The evidence is thus converging: exposure to stress at critical periods in life may be an important factor in the development of the brain dysfunction that represents psychosis vulnerability, rather than merely interacting with an independent 'biological vulnerability' to manifest in psychosis.

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Section: Levels Of Cortisol In Schizophrenia and Bipolar Disordermentioning

confidence: 98%

Stress, Schizophrenia and Bipolar Disorder

Green

Girshkin

Teroganova

et al. 2014

Behavioral Neurobiology of Stress-Related Disorders

View full text Add to dashboard Cite

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“…They thus continue to act as dopamine antagonists long after the end of their administration. Nevertheless, an endocrine marker of central nervous system dopamine blockade, the level of prolactin in the serum, indicates that dopamine antagonism is substantially lifted within a few days after neuroleptic withdrawal (Kitamura et al 1979;Luchins et al 1983;Naber et al 1985). The studies of Luchins et al (1983) and Naber et al (1985) also show that any change in psychopathology which occurs in this time does not correlate with the fall in prolactin levels.…”

Section: The "Dopamine Hypothesis Of Schizophrenia"mentioning

confidence: 82%

The time course of neuroleptic therapy for psychosis: role of learning processes and implications for concepts of psychotic illness

Miller

1987

Psychopharmacology

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In neuroleptic therapy for psychotic illness, clinical improvement is produced more slowly than is central dopamine blockade, and its time course is highly variable between patients. A theory of neuroleptic-responsive psychotic illness thus requires more than dopamine blockade, though that appears to be the first step in the therapeutic process. Some previous explanations given for the protracted time course of neuroleptic therapy are discussed, with emphasis on the hypothesis of delayed inactivation of midbrain dopamine neurones. For various reasons all explanations are unsatisfactory. An alternative hypothesis is proposed in which neuroleptic-responsive psychoses are seen as arising from a hyperactivity of the associations of thought. Such psychoses thus involve a disorder of a high-level learning process, namely the elaboration of memories of thoughts and beliefs. Neuroleptic drugs are envisaged to remedy this process, but not to eradicate the abnormal memories already formed. Psychotic symptoms may thus outlast the start of neuroleptic therapy by many weeks. It is suggested that the pharmacological characteristics of the hypothetical learning process involved in generating psychotic symptoms are analogous to those of a simpler learning process, defineable in animal experiments - namely, the reward component in instrumental conditioning. A preliminary case is made that the relative potency of different neuroleptic drugs in antipsychotic therapy can better be predicted by their relative potency in retarding such a variety of learning, than by other behavioural tests of these drugs.

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“…Utilizing the BPRS, Breier et al (1987) and Naber et al (1985) reported an exacerbation of positive symptoms, whereas, Dixon et al (1993) found them not to change.…”

Section: ; Unpublished Data)mentioning

confidence: 99%

“…Another approach towards investigating the effect that antipsychotics have on negative symptoms has been to monitor negative symptoms during antipsy chotic withdrawal (Naber et al 1985;Breier et al 1987). These studies assume that the change in negative symp toms associated with antipsychotic withdrawal is op posite the effect on negative symptoms that occurs with antipsychotic treatment (i.e., if negative symptoms worsen following antipsychotic discontinuation, it is assumed that the antipsychotics had previously been effective in reducing negative symptoms).…”

Section: Symptoms [Saps) Scale For Assessment Of Negativementioning

confidence: 99%