Psychomotor Symptoms in Chronic Cocaine Users: An Interpretative Model

Abstract

According to the latest estimates, there are around 24.6 million cocaine users worldwide, and it is estimated that around a quarter of the population worldwide has used cocaine at some point in their lifetime. It follows that such widespread consumption represents a major risk for public health. Long-term use of cocaine, in addition to being related to many cerebral and cardiovascular diseases, is increasingly associated with a higher incidence of psychomotor symptoms and neurodegenerative disorders. In recent years, numerous studies have shown an increased risk of antipsychotic-induced extrapyramidal symptoms (EPSs) in patients with psychotic spectrum disorders comorbid with psychostimulant misuse, particularly of cocaine. In the present paper, we describe the case of a young patient on his first entry into a psychiatric setting with previous cocaine misuse who rapidly presented psychomotor symptoms and was poorly responsive to symptomatic therapy consisting of benzodiazepines and anticholinergics, in relation to the introduction of various antipsychotics (first, second, and third generation). Furthermore, we propose neurobiological mechanisms underlying the hypothesized increased vulnerability to psychomotor symptoms in chronic cocaine abusers. Specifically, we supposed that the chronic administration of cocaine produces important neurobiological changes, causing a complex dysregulation of various neurotransmitter systems, mainly affecting subcortical structures and the dopaminergic and glutamatergic pathways. We believe that a better understanding of these neurochemical and neurobiological processes could have useful clinical and therapeutic implications by providing important indications to increase the risk–benefit ratio in pharmacological choice in patients with psychotic spectrum disorders comorbid with a substance use disorder.

Monoamine Neurotransmitters and Drug Addiction

“…Activation of the mesolimbic DA system is the neurobiological basis of cocaine addiction. Studies have shown that cocaine causes DA neurons in the VTA to release stored DA, increases the concentration of extracellular DA in DA neurons, and then leads to enhance DA release in the striatum and other nerve nuclei (41); the degree of psychomotor activation induced by cocaine is also related to the DA response (42). At the same time, cocaine blocks the re-uptake of DA by DAT (43).…”