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Schizophrenia and Comorbid Substance Abuse – Pathophysiological and Therapeutic Approaches

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Handbook of Schizophrenia Spectrum Disorders, Volume III

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Abstract

Substance use disorder is the most common psychiatric comorbidity in schizophrenic patients, with prevalence rates of up to 65%. Besides the legal substances tobacco and alcohol, cannabis seems to be the most illicit drug abused in schizophrenia patients and has been discussed as an important risk factor for developing schizophrenia. At least substance abuse may contribute to an earlier onset of schizophrenia as seen in many first-episode studies. Common hypothetic models for the increased comorbidity include the concept of increased vulnerability to each individual disorder, the model of a secondary substance use or psychotic disorder, and the bidirectional model. There is no common sense regarding a different neurobiological background for schizophrenia patients with and without substance abuse. Previous substance abuse (primarily cannabis) seems not to lead to pronounced structural brain abnormalities in schizophrenia, but may cause functional changes on cortical inhibition processes and synaptic transmission involving mainly the GABAegic, glutamatergic and dopaminergic system. The key issue in providing treatment for this population is developing a dual disorder approach that integrates treatment of substance abuse and schizophrenia. Many programmes are now providing this integration through interdisciplinary teams with expertise in the treatment of schizophrenia and substance abuse. This form of treatment features assertive outreach, case management, family interventions, housing, rehabilitation and pharmacotherapy. It also includes a stagewise motivational approach for patients who do not recognize the need for treatment of substance use disorders and behavioural interventions for those who are trying to attain or maintain abstinence. Nevertheless, that the evaluation of combined treatment programs with motivational elements, psychoeducation and cognitive-behavioural approaches shows an effect in reducing substance abuse and in decreasing frequency and severity of psychotic decompensations, there is only a slight advantage over routine care. Pharmacotherapy of patients with the dual diagnosis of a schizophrenia and comorbid substance use disorder is a highly challenging topic because this subgroup of patients shows a high relapse rate, low treatment adherence and high rate of side effects. Recommendations for antipsychotic pharmacotherapy in schizophrenia are mainly based on studies that excluded patients with this dual diagnosis. The preferred pharmacological strategy depends on the target symptoms: improvement of schizophrenic psychopathology, reduction of craving and substance use, treatment of concomitant symptoms like depressive mood or management of side effects. Data, mainly based on open studies or case series, suggest superior efficacy for second generation antipsychotics (SGAs) over conventional antipsychotics (FGAs) with regard to improvement of the above mentioned target symptoms. Antidepressants and anti-craving agents (naltrexone) given adjunctive to antipsychotic maintenance therapy showed efficacy in reducing substance use and craving. In conclusion, there is an increasing need to proceed researching the pathophysiological background of this comorbidity to develop new treatment approaches. The insight into the pathomechanisms of the endocannabinoid system may help to find innovative treatment strategies in schizophrenia without substance abuse.

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Abbreviations

2-AG:

2-arachidonoylglycerol

ACC:

Anterior cingulated gyrus

ACT:

Assertive community treatment

AEA:

Anandamide

BDNF:

Brain derived neurotrophic factor

CB1:

Cannabinoid receptor 1

CBD:

Cannabidiol

CBT:

Cognitive behavioural therapy

CM:

Case management

CNR1:

Cannabinoid receptor 1 gene

COMT:

Catechol-O-methyltransferase

CSF:

Cerebro-spinal fluid

D2-receptor:

Dopamine-2-receptor

delta-9-THC:

Delta-9-tetrahydrocannabinol

DRT:

Dual recovery therapy

eCS:

Endogenous cannabinoid system

EPS:

Extra-pyramidal symptoms

ERP:

Event-related potentials

FAAH:

Fatty acid amide hydrolase

FGA:

First-generation antipsychotics

GABA:

Gamma amino butyric acid

ICF:

Intracranial facilitation

MAO:

Monoaminooxidase

MET:

Modified motivational enhancement therapy

MI:

Motivational interviewing

MMN:

Mismatch negativity

MRI:

Magnetic resonance imaging

NMDA:

N-methyl D-aspartate

NRG1:

Neuregulin 1 gene

PANSS:

Positive and negative symptome scale

PFC:

Prefrontal cortex

RCT:

Randomised controlled trial

ROI:

Region of interest

SAMM:

Substance abuse management module

SGA:

Second-generation antipsychotics

SICI:

Short interval cortical inhibition

Smri:

Structural magnetic resonance imaging

ST:

Skills training

STG:

Superior temporal gyrus

SUD:

Substance use disorder

TMS:

Transcranial magnetic stimulation

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  1. Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Georg-August-University Goettingen, Goettingen, Germany

    Thomas Wobrock & Berend Malchow

  2. Department of Clinical Neurophysiology, University Medical Center Goettingen, Georg-August-University Goettingen, Goettingen, Germany

    Dirk Czesnik

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  1. , Rappaport Faculty of Medicine, Technion - Israel Institute of Technolog, Haifa, Israel

    Michael S. Ritsner

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Wobrock, T., Czesnik, D., Malchow, B. (2011). Schizophrenia and Comorbid Substance Abuse – Pathophysiological and Therapeutic Approaches. In: Ritsner, M. (eds) Handbook of Schizophrenia Spectrum Disorders, Volume III. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-0834-1_15

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